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Hypertensive Heart Disease
- Author: Kamran Riaz, MD; Chief Editor: Yasmine Subhi Ali, MD, FACC, FACP, MSCI more...
The cause of hypertensive heart disease is chronically elevated blood pressure (BP); however, the causes of elevated BP are diverse. Essential hypertension accounts for 90% of cases of hypertension in adults. Secondary causes of hypertension account for the remaining 10% of cases of chronically elevated BP.
According to the Framingham Study, hypertension accounts for about one quarter of heart failure cases.[1] In the elderly population, as many as 68% of heart failure cases are attributed to hypertension.[2] Community-based studies have demonstrated that hypertension may contribute to the development of heart failure in as many as 50-60% of patients. In patients with hypertension, the risk of heart failure is increased by 2-fold in men and by 3-fold in women.
Cardiovascular effects of hypertension
Uncontrolled and prolonged elevation of BP can lead to a variety of changes in the myocardial structure, coronary vasculature, and conduction system of the heart. These changes in turn can lead to the development of left ventricular hypertrophy (LVH), coronary artery disease (CAD), various conduction system diseases, and systolic and diastolic dysfunction of the myocardium, complications that manifest clinically as angina or myocardial infarction, cardiac arrhythmias (especially atrial fibrillation), and congestive heart failure (CHF).
Thus, hypertensive heart disease is a term applied generally to heart diseases, such as LVH (seen in the images below), coronary artery disease, cardiac arrhythmias, and CHF, that are caused by the direct or indirect effects of elevated BP. Although these diseases generally develop in response to chronically elevated BP, marked and acute elevation of BP can lead to accentuation of an underlying predisposition to any of the symptoms traditionally associated with chronic hypertension.
The following conditions should also be considered when evaluating hypertensive heart disease:
Coronary artery atherosclerosis
Athlete's heart (with LVH)
Congestive heart failure due to other etiologies
Atrial fibrillation due to other etiologies
Diastolic dysfunction due to other etiologies
Sleep apnea
Patient education
It is important to educate patients about the nature of their disease and the risks associated with untreated hypertension. In addition, dietary modifications and the importance of regular exercise, taking medications regularly, weight loss, and avoiding medications and foods that can potentially elevate blood pressure should be emphasized.
For patient education information, see the Diabetes Center and the Cholesterol Center, as well as High Blood Pressure, High Cholesterol, Chest Pain, Coronary Heart Disease, and Heart Attack.
The etiology of hypertensive heart disease is a complex interplay of various hemodynamic, structural, neuroendocrine, cellular, and molecular factors.[3] These factors play integral roles in the development of hypertension and its complications; however, elevated BP itself can modulate these factors.
Obesity has been linked to hypertension and LVH in various epidemiologic studies, with as many as 50% of obese patients having some degree of hypertension and as many as 60-70% of patients with hypertension being obese.
Elevated BP leads to adverse changes in cardiac structure and function in 2 ways: directly, by increased afterload, and indirectly, by associated neurohormonal and vascular changes. Elevated 24-hour ambulatory BP and nocturnal BP have been demonstrated to be more closely related to various cardiac pathologies, especially in black persons. The pathophysiologies of the various cardiac effects of hypertension differ and are described in this section.
Left ventricular hypertrophy
Of patients with hypertension, 15-20% develop LVH. The risk of LVH is increased 2-fold by associated obesity. The prevalence of LVH based on electrocardiogram (ECG) findings, which are not a sensitive marker at the time of diagnosis of hypertension, is variable.[4, 5] Studies have shown a direct relationship between the level and duration of elevated BP and LVH.[6]
LVH, defined as an increase in the mass of the left ventricle, is caused by the response of myocytes to various stimuli accompanying elevated BP. Myocyte hypertrophy can occur as a compensatory response to increased afterload. Mechanical and neurohormonal stimuli accompanying hypertension can lead to activation of myocardial cell growth, gene expression (of which some occurs primarily in fetal cardiomyocytes), and, thus, to LVH. In addition, activation of the renin-angiotensin system, through the action of angiotensin II on angiotensin I receptors, leads to growth of interstitium and cell matrix components.[7] In summary, the development of LVH is characterized by myocyte hypertrophy and by an imbalance between the myocytes and the interstitium of the myocardial skeletal structure.
Various patterns of LVH have been described, including concentric remodeling, concentric LVH, and eccentric LVH. Concentric LVH is an increase in LV thickness and LV mass with increased LV diastolic pressure and volume, commonly observed in persons with hypertension; this is a marker of poor prognosis in these patients. Compare concentric LVH with eccentric LVH, in which LV thickness is increased not uniformly but at certain sites, such as the septum.
Although the development of LVH initially plays a protective role in response to increased wall stress to maintain adequate cardiac output, it later leads to the development of diastolic and, ultimately, systolic myocardial dysfunction.
Interestingly, findings from a prospective study (The Multiethnic Study of Atherosclerosis [MESA] trial) also indicate a higher risk of developing systemic hypertension among patients in the higher quartiles of the LV mass at baseline.
Left atrial abnormalities
Frequently underappreciated, structural and functional changes of the left atrium are very common in patients with hypertension. The increased afterload imposed on the LA by the elevated LV end-diastolic pressure secondary to increased BP leads to impairment of the left atrium and left atrial (LA) appendage function, plus increased LA size and thickness.
Increased LA size accompanying hypertension in the absence of valvular heart disease or systolic dysfunction usually implies chronicity of hypertension and may correlate with the severity of LV diastolic dysfunction.
In addition to LA structural changes, these patients are predisposed to atrial fibrillation. Atrial fibrillation, with loss of atrial contribution in the presence of diastolic dysfunction, may precipitate overt heart failure.
Valvular disease
Although valvular disease does not cause hypertensive heart disease, chronic and severe hypertension can cause aortic root dilatation, leading to significant aortic insufficiency. Some degree of hemodynamically insignificant aortic insufficiency is often found in patients with uncontrolled hypertension. An acute rise in BP may accentuate the degree of aortic insufficiency, with return to baseline when the BP is better controlled. In addition to causing aortic regurgitation, hypertension is also thought to accelerate the process of aortic sclerosis and cause mitral regurgitation.
Heart failure
Heart failure is a common complication of chronically elevated BP. Patients with hypertension fall into 1 of the following categories:
Asymptomatic but at risk of developing of heart failure - Stage A or B, per the American College of Cardiology (ACC)/American Heart Association (AHA) classification, depending on whether or not they have developed structural heart disease as a consequence of hypertension
Suffering from symptomatic heart failure - Stage C or D, per the ACC/AHA classification
Hypertension as a cause of CHF is frequently underrecognized, partly because at the time heart failure develops, the dysfunctioning left ventricle is unable to generate the high BP, thus obscuring the heart failure's etiology. The prevalence of asymptomatic diastolic dysfunction in patients with hypertension and without LVH may be as high as 33%. Chronically elevated afterload and the resulting LVH can adversely affect the active early relaxation phase and the late compliance phase of ventricular diastole.
Diastolic dysfunction
Diastolic dysfunction is common in persons with hypertension. It is often, but not invariably, accompanied by LVH. In addition to elevated afterload, other factors that may contribute to the development of diastolic dysfunction include coexistent coronary artery disease, aging, systolic dysfunction, and structural abnormalities such as fibrosis and LVH. Asymptomatic systolic dysfunction usually follows.
Early LV diastolic dyssynchrony may be associated with LV remodeling and contribute to LV diastolic dysfunction in patients with hypertension.[8] The level of diastolic dysfunction appears to correlate with increasing severity of hypertension, and peak myocardial systolic strain rate may be an independent factor in the extent of LV remodeling and diastolic function.[8]
Systolic dysfunction
Later in the course of disease, the LVH fails to compensate by increasing cardiac output in the face of elevated BP, and the LV cavity begins to dilate to maintain cardiac output. As the disease enters the end stage, LV systolic function decreases further. This leads to further increases in activation of the neurohormonal and renin-angiotensin systems, leading to increases in salt and water retention and increased peripheral vasoconstriction. Eventually, the already compromised LV is overwhelmed, and the patient progresses to the stage of symptomatic systolic dysfunction.
Apoptosis, or programmed cell death, stimulated by myocyte hypertrophy and the imbalance between its stimulants and inhibitors, is considered to play an important part in the transition from compensated to decompensated stage. The patient may become symptomatic during the asymptomatic stages of the LV systolic or diastolic dysfunction, owing to changes in afterload conditions or to the presence of other insults to the myocardium (eg, ischemia, infarction). A sudden increase in BP can lead to acute pulmonary edema without necessarily changing the LV ejection fraction.[9]
Generally, development of asymptomatic or symptomatic LV dilatation or dysfunction heralds rapid deterioration in clinical status and a markedly increased risk of death. In addition to LV dysfunction, right ventricular (RV) thickening and diastolic dysfunction also develop as results of septal thickening and LV dysfunction.
Myocardial ischemia
Patients with angina have a high prevalence of hypertension. Hypertension is an established risk factor for the development of coronary artery disease, almost doubling the risk. The development of ischemia in patients with hypertension is multifactorial.
Importantly, in patients with hypertension, angina can occur in the absence of epicardial coronary artery disease. The reason for this is 2-fold. Increased afterload secondary to hypertension leads to an increase in LV wall tension and transmural pressure, compromising coronary blood flow during diastole. In addition, the microvasculature beyond the epicardial coronary arteries has been shown to be dysfunctional in patients with hypertension, and it may be unable to compensate for increased metabolic and oxygen demand.
The development and progression of arteriosclerosis, the hallmark of coronary artery disease, is exacerbated in arteries subjected to chronically elevated BP. Shear stress associated with hypertension and the resulting endothelial dysfunction cause impairment in the synthesis and release of the potent vasodilator nitric oxide. A decreased nitric oxide level promotes the development and acceleration of arteriosclerosis and plaque formation. Morphologic features of the plaque are identical to those observed in patients without hypertension.
Cardiac arrhythmias
Cardiac arrhythmias commonly observed in patients with hypertension include atrial fibrillation, premature ventricular contractions (PVCs), and ventricular tachycardia (VT).[10] The risk of sudden cardiac death is increased.[11] Various mechanisms thought to play a part in the pathogenesis of arrhythmias include altered cellular structure and metabolism, inhomogeneity of the myocardium, poor perfusion, myocardial fibrosis, and fluctuation in afterload. All of these may lead to an increased risk of ventricular tachyarrhythmias.
Atrial fibrillation (paroxysmal, chronic recurrent, or chronic persistent) is observed frequently in patients with hypertension.[12] In fact, elevated BP is the most common cause of atrial fibrillation in the Western hemisphere. In one study, nearly 50% of patients with atrial fibrillation had hypertension. Although the exact etiology is not known, LA structural abnormalities, associated coronary artery disease, and LVH have been suggested as possible contributing factors. The development of atrial fibrillation can cause decompensation of systolic and, more importantly, diastolic dysfunction, owing to loss of atrial kick, and it also increases the risk of thromboembolic complications, most notably stroke.
Premature ventricular contractions, ventricular arrhythmias, and sudden cardiac death are observed more often in patients with LVH than in those without LVH. The etiology of these arrhythmias is thought to be concomitant coronary artery disease and myocardial fibrosis.
The estimated prevalence of hypertension in the United States in 2005 was 35.3 million for men and 38.3 million for women. Hypertension is more prevalent in black persons than in Hispanic and non-Hispanic white persons, and this prevalence is increasing.
Data from 1988-1994 and 1999-2002 demonstrated an increased prevalence of hypertension in black individuals from 35.8% to 41.4%. (Although the prevalence in whites is increasing as well, it is not as dramatic a rise.)[13] This difference between the groups is attributed to factors other than race, because the prevalence of hypertension among blacks and whites is the same in the United Kingdom and because hypertension is not very common on the African continent. In addition, hypertension is the most common etiology of heart failure in black persons in the United States.
Systolic BP increases with age; this increase is more marked in men than in women until women reach menopause, when their BP rises more sharply and reaches levels higher than in men. Thus, the prevalence of hypertension is higher in men than in women younger than 55 years, but the rate is higher in women older than 55 years. The prevalence of hypertensive heart disease probably follows the same pattern and is affected by the severity of BP increase.
In a study by Peacock et al, patients presenting with acute heart failure as a manifestation of hypertensive emergency were more likely to be African American. They were also more likely to have a history of heart failure and were more likely to have higher brain-type natriuretic peptide (BNP) and creatinine levels and lower LV ejection fraction.[14]
Although the exact frequency of LVH is unknown, its rate based on ECG findings is 2.9% for men and 1.5% for women. The rate of LVH based on echocardiographic findings is 15-20%. Of patients without LVH, 33% have evidence of asymptomatic LV diastolic dysfunction.
Patient History
Symptoms of hypertensive heart disease depend on the duration, severity, and type of disease. In addition, the patient may or may not be aware of the presence of hypertension, which is why hypertension has been named "the silent killer."
Left ventricular hypertrophy
Patients with LVH alone are totally asymptomatic, unless the LVH leads to the development of diastolic dysfunction and heart failure.
Heart failure
Although symptomatic diastolic heart failure and systolic heart failure are indistinguishable, the clinical history may be quite revealing. In particular, individuals who abruptly develop severe symptoms of CHF and rapidly return to baseline with medical therapy are more likely to have isolated diastolic dysfunction.
Heart failure symptoms include exertional and nonexertional dyspnea (New York Heart Association [NYHA] classes I-IV); orthopnea; paroxysmal nocturnal dyspnea; fatigue (more common in systolic dysfunction); ankle edema and weight gain; abdominal pain secondary to a congested, distended liver; and, in severe cases, altered mentation.
Patients can present with acute pulmonary edema due to sudden decompensation in LV systolic or diastolic dysfunction. This decompensation can be caused by precipitating factors such as an acute rise in BP, dietary indiscretion, or myocardial ischemia. Patients can develop cardiac arrhythmias, especially atrial fibrillation, or they can develop symptoms of heart failure insidiously over time.
Myocardial ischemia
Angina, a frequent complication of hypertensive heart disease, is indistinguishable from other causes of myocardial ischemia. Typical symptoms of angina include substernal chest pain lasting less than 15 minutes (vs >20min in infarction). Pain is often described as follows:
A heaviness, pressure, and/or squeezing
Radiating to the neck, jaw, upper back, or left arm
Provoked by emotional or physical exertion
Relieved with rest or sublingual nitroglycerin
However, patients may also present with atypical symptoms without chest pain, such as exertional dyspnea or excessive fatigue, commonly referred to as an angina equivalent. Female patients, in particular, are more likely to present atypically.
Patients may present with chronic, stable angina or acute coronary syndrome, including myocardial infarction without ST-segment elevation and acute myocardial infarction with ST elevation. Ischemic ECG changes may be found in individuals presenting with hypertensive crisis in whom no significant coronary atherosclerosis is detectable by coronary angiography.
Acute coronary symptoms can be precipitated by a ruptured atherosclerotic plaque; they can also result from an acute and severe rise in BP that leads to a sudden increase in transmural pressure without a change in stability of the plaque.
Cardiac arrhythmias
Irregular or abnormal heart rhythms can cause a variety of symptoms, including the following:
Near or total syncope
Precipitation of angina
Sudden cardiac death
Precipitation of heart failure, especially with atrial fibrillation in diastolic dysfunction
Physical Examination
Physical signs of hypertensive heart disease depend on the predominant cardiac abnormality and the duration and severity of the hypertensive heart disease. Findings from the physical examination may be entirely normal in the very early stages of the disease, or the patient may have classic signs upon examination.
In addition to generalized findings attributable directly to high BP, the physical examination may reveal clues to a potential etiology of hypertension, such as truncal obesity and striae in Cushing syndrome, renal artery bruit in renal artery stenosis, and abdominal mass in polycystic kidney disease.
The arterial pulses are normal in the early stages of hypertensive heart disease. The cardiac rhythm is regular if the patient is in sinus rhythm; it is irregularly irregular if the patient is in atrial fibrillation. The heart rate is as follows:
Normal in patients in sinus rhythm
Not normal in decompensated heart failure
Tachycardic in patients with heart failure and in patients with atrial fibrillation and a rapid ventricular response
The pulse volume is usually normal, but it is decreased in patients with LV dysfunction. Additional findings may include radial-femoral delay if the etiology of hypertension is coarctation of the aorta
Blood pressure
Systolic and/or diastolic BP is elevated (>140/90mm Hg). Mean BP and pulse pressure are also elevated generally. The BP in the upper extremities may be higher than that in the lower extremities in patients with coarctation of the aorta. BP may be normal at the time of evaluation if the patient is on adequate antihypertensive medications or if the patient has advanced LV dysfunction and the LV cannot generate enough stroke volume and cardiac output to produce an elevated BP.
In patients with heart failure, the jugular veins may be distended. The predominant waves depend on the severity of the heart failure and any other associated lesions.
The apical impulse is sustained and nondisplaced in patients without significant systolic LV dysfunction but with LVH. A presystolic S4 may be felt. Later in the course of disease, when significant systolic LV dysfunction supervenes, the apical impulse is displaced laterally, owing to LV dilatation. In the right ventricle, a lift is present late in the course of heart failure if significant pulmonary hypertension develops.
S1 is normal in intensity and character. S2 at the right upper sternal border is loud because of an accentuated aortic component (A2); it can have a reverse or paradoxical split due either to increased afterload or to associated left bundle-branch block (LBBB). S4 is frequently palpable and audible, implying the presence of a stiffened, noncompliant ventricle due to chronic pressure overload and LVH. S3 is not typically present initially, but it is audible in the presence of heart failure, either systolic or diastolic.
An early decrescendo diastolic murmur of aortic insufficiency may be heard along the mid-parasternal to left parasternal area, especially in the presence of acutely elevated BP, frequently disappearing once the BP is better controlled. In addition, an early systolic to midsystolic murmur of aortic sclerosis is commonly audible. A holosystolic murmur of mitral regurgitation may be present in patients with advanced heart failure and a dilated mitral annulus.
Findings upon chest examination may be normal or may include signs of pulmonary congestion, such as rales, decreased breath sounds, and dullness to percussion due to pleural effusion.
The abdominal examination may reveal a renal artery bruit in patients with hypertension secondary to renal artery stenosis, a pulsatile expansile mass of abdominal aortic aneurysm, and hepatomegaly and ascites due to CHF.
Ankle edema may be present in patients with advanced heart failure.
Central nervous system and ophthalmologic system
Central nervous system (CNS) examination findings are usually unremarkable unless the patient has had previous cerebrovascular accidents with residual deficit. CNS changes may also be seen in patients who present with hypertensive emergency.
Examination of the fundi may reveal evidence of hypertensive retinopathy, the severity of which depends on the duration and severity of the patient's hypertension, or earlier signs of hypertension, such as arteriovenous nicking.
Staging of Hypertension
Although hypertensive heart disease typically is not described in various stages, the disease usually progresses in the following sequence:
Increased wall stress leads to LVH
Which leads to diastolic LV dysfunction
Which can be followed by systolic LV dysfunction
The risks of ventricular ectopy, ventricular arrhythmias, sudden cardiac death, and cardiovascular mortality are increased in patients once LVH develops and are also increased in patients with heart failure. Table 1, below, shows the division of BP and hypertension into stages.
Table 1. Stages of Elevated BP and Hypertension According to The Seventh Report of the Joint National Committee (JNC7) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure[15] (Open Table in a new window)
|Systolic BP,
mm Hg
|Diastolic BP,
mm Hg
|< 120
|< 80
|Stage I
|Stage II
Laboratory Studies
Laboratory studies are helpful in establishing the etiology of hypertension, quantitating the severity of target organ damage, and monitoring the adverse effects of therapy. The tests to be ordered depend on clinical judgment regarding the etiology of hypertension.
Recommendations from the Seventh Report of the Joint National Committee (JNC7) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure include carrying out the following baseline laboratory workup before initiating treatment for hypertension[15] :
Blood glucose and hematocrit levels
Serum potassium, creatinine (or the corresponding estimated glomerular filtration rate [GFR]), and calcium measurements
Lipid profile after a 9- to 12-hour fast - Includes high density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides
Optional tests - Include measurement of urinary albumin excretion or albumin/creatinine ratio
Cardiovascular risk assessment
New guidelines on the assessment of cardiovascular risk, released in late 2013 by the American Heart Association/American College of Cardiology (AHA/ACC), recommend use of a revised calculator for estimating the 10-year risk of developing a first atherosclerotic cardiovascular disease (ASCVD) event, which is defined as nonfatal myocardial infarction, death from coronary heart disease, or stroke (fatal or nonfatal) in a person who was initially free from ASCVD. The calculator uses clinical and laboratory risk factors, including systolic blood pressure and treatment for hypertension.[16]
For patients 20-79 years of age who do not have existing clinical ASCVD, the guidelines recommend assessing clinical risk factors every 4-6 years. For patients with low 10-year risk (< 7.5%), the guidelines recommend assessing 30-year or lifetime risk in patients 20-59 years old.
Regardless of the patient's age, clinicians should communicate risk data to the patient and refer to the AHA/ACC lifestyle guidelines, which cover diet and physical activity.[17] For patients with elevated 10-year risk, clinicians should communicate risk data and refer to the AHA/ACC guidelines on blood cholesterol[18] and obesity.[19]
Evaluating the renal system
Blood urea nitrogen (BUN) and creatinine levels are elevated in patients with renal failure. Other studies include the above-mentioned urinalysis, GFR, and urinary albumin excretion or albumin/creatinine ratio measurements.
Evaluating the endocrine system
Hypokalemia is found in patients with primary hyperaldosteronism and in patients with secondary hyperaldosteronism, Cushing disease, and Bartter syndrome. Hypokalemia is most useful in leading to further diagnostic studies if the patient has not received diuretics.
Plasma renin activity is generally depressed and serum aldosterone level is elevated in patients with primary hyperaldosteronism. Twenty-four–hour urinary catecholamine and metanephrine levels are elevated in patients with pheochromocytoma.
Elevated 24-hour urinary free cortisol and failure to suppress an early morning serum cortisol level after an overnight dexamethasone suppression test are observed in patients with Cushing disease. Thyrotropin levels may be elevated in patients with hypothyroidism and depressed in patients with hyperthyroidism.
Transthoracic Echocardiography
Transthoracic echocardiography (TTE) may be very useful for identifying features of hypertensive heart disease.[20] TTE is more sensitive and specific then electrocardiography for diagnosing the presence of LVH (57% for mild and 98% for severe LVH). LVH is symmetrical, whereas the hypertrophy of hypertrophic cardiomyopathy is asymmetrical. The definition of the LVH based on echocardiography findings is somewhat controversial in the absence of any criterion standards. (See the images below.)
Calculating LV mass
On 2-dimensional (2-D) and M-mode examination, the interventricular septum is thickened, as is the posterior wall (>1.1cm). LVH is defined quantitatively as an increase in the LV mass or the LV mass index (LVMI), which is defined as LV mass divided by body surface area. Various formulas have been used to calculate LV mass, each with inherent drawbacks.
The Troy formula was used in the Framingham Heart study. The American Society of Echocardiography (ASE)–recommended formula for estimation of LV mass from LV linear dimensions (validated with necropsy) is based on modeling the LV as a prolate ellipse of revolution: LV mass = 0.8 × {1.04[(LVIDd + PWTd + SWTd)3 - (LVIDd)3]} + 0.6g, where LVIDd is the internal dimension of the left ventricle at end diastole, PWTd is posterior wall thickness at end diastole, and SWTd is septal wall thickness at end diastole. This formula is appropriate for evaluating patients without major distortions of LV geometry (eg, patients with hypertension).[21]
In various studies, LVH has been defined either as LV mass greater than 215g or greater than 225g. Because LV mass is affected by height, weight, and body surface area, LVMI more accurately sets the limits for LV mass. Framingham Heart Study data indicated that abnormal LVMI limits are 134g/m2 for men and 110g/m2 for women.
Flow velocity pattern
The transmitral flow velocity pattern, characterized by abnormally prolonged isovolumic relaxation time, a reversed "E:A" ratio (ie, reversed velocity of early diastole to peak flow velocity of atrial contraction), and a prolonged deceleration time, is abnormal. The patient may exhibit a pseudonormal pattern during the transition from the impaired relaxation to the restrictive filling phase.
The tissue Doppler indices are abnormal. The tissue Doppler profile shows a reversed E:A ratio, which is especially helpful in patients who have a pseudonormal pattern on transmitral flow velocity Doppler studies.
Systolic dysfunction
Evidence of LV systolic dysfunction includes a dilated LV, low LV fractional shortening, low LV ejection fraction, and the presence of systolic dysfunction, which is commonly associated with some degree of diastolic dysfunction.
Aortic dilatation
LA dilatation may be demonstrated by evidence of right-sided dilatation (right-sided chambers may be dilated with some degree of pulmonary hypertension) and evidence of valvular abnormalities, such as aortic sclerosis (on 2-D TEE) and aortic and mitral insufficiency (on color flow and Doppler examination).
Additional Imaging Studies
Chest radiographs may show notching of the undersurface of the ribs from the development of collateral circulation in coarctation of the aorta; cardiomegaly in late stages of the disease, due to LV dilatation; cephalization of pulmonary blood flow, Kerley B lines, and alveolar infiltrates in the presence of elevated LV end-diastolic pressure and pulmonary congestion; and blunting of the costophrenic angle in the presence of pleural effusion.
Computed tomography (CT) scanning, and magnetic resonance imaging (MRI) of the heart, although not used routinely, have been shown in experimental studies to quantify LVH. CT scanning, MRI, and magnetic resonance angiography (MRA) of the abdomen and chest show the presence of adrenal masses, renal artery stenosis, or evidence of coarctation of aorta. Nuclear imaging may be useful in screening for the presence of coronary artery disease.
A 12-lead ECG may show a variety of abnormalities. For example, ischemic ECG changes may be found in individuals presenting with hypertensive crisis in whom no significant coronary atherosclerosis is detectable by coronary angiography. Evidence of LA enlargement includes broad P waves in the limb leads and a prominent and wide, delayed negative deflection in V1. (See the images below.)
In one series, among patients with left anterior fascicular block on ECG, 50% had hypertension. As many as 70-80% of patients with LBBB have hypertension.
LVH criteria
Various criteria, differing in sensitivity and specificity, have been used to diagnose LVH. Note that the specificities and sensitivities of the different approaches are far less than those of echocardiography. The frequency of LVH on ECG at the time of initial diagnosis varies from 10% to 100%; in one trial, for example, the frequency was 13%. The sensitivity of ECG for diagnosing LVH is limited, approximately 30-57% in patients with severe LVH.
The Cornell criteria (most sensitive) are (1) R wave in aVL plus an S wave in V3 of greater than 2.8 mV in men and greater than 2mV in women. The Cornell and Cornell voltage duration (Cornell voltage multiplied by QRS duration) criteria have a sensitivity as high as 95% and a specificity as high as 50-60%. A Cornell voltage duration of greater than 2440mV/ms-1 particularly identifies the highest-risk patients.
The Sokolow-Lyon criteria are an S wave in V1 plus an R wave in V5 or V6 of greater than 3.5mV or an R wave in V5 or V6 of greater than 2.6mV. The sensitivity of these criteria is 25%, with a specificity of close to 95%. The Gubner-Ungerleider criteria are an R wave in I plus an S wave in III of greater than 2.5mV. Another set of LVH criteria, the Romhilt-Estes criteria, are summarized in Table 2, below.
Table 2. Romhilt-Estes Criteria (A Point Score System*) (Open Table in a new window)
|Voltage Criteria
|R wave or S wave in any limb lead >0.2mV or S wave in lead V1 or V2 or R wave in V5 or V6 >0.3mV
|LV strain (ST and T waves in direction opposite to QRS direction) without digitalis
|LV strain (ST and T waves in direction opposite to QRS direction) with digitalis
|LA enlargement (terminal negativity of P waves in V1 >0.1mV deep and 0.04 seconds wide)
|Left-axis deviation greater than -30°
|QRS duration greater than 0.09 seconds
|Intrinsicoid deflection in V5 or V6 >0.05 seconds
|* Probable LVH is 4 points; definite LVH is 5 points. The sensitivity of these criteria is 50%, with a specificity of close to 95%.
Other Studies
Gross findings
LVH (concentric) occurs without dilatation of the LV (see the image below). The ratio of wall thickness to the radius of the ventricular chamber increases. LV wall thickness may exceed 2cm, and the heart weight exceeds 500g. Dilatation of the ventricular chamber, thinning of the walls, and enlargement of the external dimensions of the heart occur with the onset of decompensation.
Microscopic findings
The earliest changes in hypertensive heart disease include myocyte enlargement, with an increase in the myocytes' transverse diameters. At a more advanced stage, cellular and nuclear enlargement (with variation in cell size), loss of myofibrils, and interstitial fibrosis occur. (See the images below.)
Cardiac catheterization
Cardiac catheterization is used for the diagnosis of coronary artery disease and helps to assess the severity of elevated pulmonary artery pressure in patients with heart failure.
Sleep evaluation
Sleep evaluation and additional tests for excluding other secondary causes of hypertension may be indicated.
Blood Pressure Goals and Consultations
The medical care of patients with hypertensive heart disease falls under 2 categories—treatment of the elevated BP and prevention and treatment of hypertensive heart disease. According to JNC 7, BP goals should be as follows[15] :
Less than 140/90mm Hg in patients with uncomplicated hypertension
Less than 130/85mm Hg in patients with diabetes and those with renal disease with less than 1g/24-hour proteinuria
Less than 125/75mm Hg in patients with renal disease and more than 1 g/24-hour proteinuria
The care and management of patients with hypertensive heart disease include consultations with the following clinicians:
Preventive cardiologist
Hypertension specialist
Heart failure specialist
Heart failure nurse
Electrophysiologist - For treatment of complex arrhythmias
Sleep specialist - If sleep apnea is suspected
Lifestyle Modifications
Emerging data support a target BP goal of less than 150/80mm Hg in patients older than 80 years as a means of reducing the risk of congestive heart failure by 64%.[22] Various treatment strategies include the following:
Dietary modifications
Regular aerobic exercise
Weight loss [23]
Pharmacotherapy directed toward hypertension, heart failure secondary to diastolic and systolic LV dysfunction, coronary artery disease, and arrhythmias
Dietary modifications
Studies have shown that diet and a healthy lifestyle alone or in combination with medical treatment can lower BP and decrease the symptoms of heart failure, as well as reverse LVH. A heart-healthy diet is part of the secondary prophylaxis in patients with coronary artery disease and of the primary prophylaxis in patients at high risk for this disease. Specific dietary recommendations include a diet low in sodium, high in potassium (in patients with normal renal function), rich in fresh fruits and vegetables, low in cholesterol, and low in alcohol consumption.[24, 25, 26]
In a large cohort study of women, the following 6 modifiable lifestyle and dietary factors for lowering the risk of hypertension were identified[27] :
A body mass index (BMI) below 25kg/m 2
Vigorous exercise for a daily mean period of 30 minutes
A high score on the Dietary Approaches to Stop Hypertension (DASH) diet
Modest alcohol intake (up to 10g/day)
Nonnarcotic analgesic use less than once weekly
Intake of 400mcg/day or more of supplemental folic acid
A low-sodium diet, alone or in combination with pharmacotherapy, has been shown by numerous studies to reduce BP in patients with hypertension, with a more prominent response in a subset of patients with hypertension—mainly black individuals—with low renin levels. Restriction of sodium in these patients does not lead to compensatory stimulation of the renin-angiotensin system and thus has a potent antihypertensive effect. Data also indicate that sodium reduction, previously shown to lower BP, may also reduce the long-term risk of cardiovascular events. The recommended daily sodium intake is 50-100mmol, equivalent to 3-6g of salt per day, which leads to an average 2-8mm Hg reduction in BP.[28]
In various epidemiologic studies, a high-potassium diet has been associated with lowering of BP. The mechanism of this action is not clear. Intravenous infusion of potassium has been shown to cause vasodilatation, which is believed to be mediated by nitric oxide in the vascular wall. Fresh fruits and vegetables rich in potassium, such as bananas, oranges, avocados, and tomatoes, should be recommended for patients with normal renal function.
The DASH diet has been shown to significantly lower the BP (8-14mm Hg) in patients with hypertension regardless of whether or not they maintain a constant sodium content in their diet. The DASH diet is not only rich in important nutrients and fiber but also includes foods that contain far more potassium, calcium, and magnesium than are found in the average American diet. This diet should be advised in patients with hypertension.[29, 30, 31, 32, 33]
Heavy alcohol consumption has been associated with high BP and an increase in LV mass.[34] Moderation in alcohol consumption is advised; no more than 1-2 drinks daily is recommended.[35]
Sinha et al concluded that high intakes of red or processed meat were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality.[36] The baseline population was a cohort of one-half million people aged 50-71 years from the National Institutes of Health (NIH)-AARP (formerly known as the American Association of Retired Persons) Diet and Health Study.[36]
Regular dynamic isotonic (aerobic) exercise, such as walking, running, swimming, or cycling, has been shown to decrease BP and improve cardiovascular well-being.[37] It also has additional favorable cardiovascular effects, including improved endothelial function, peripheral vasodilatation, reduced resting heart rate, improved heart rate variability, and reduced plasma levels of catecholamines.
Regular aerobic exercise sessions of at least 30 minutes for most days of the week can produce an average reduction in BP of 4-9mm Hg. Isometric and strenuous exercise should be avoided.
Weight reduction
Studies have shown that weight reduction is one of the most effective ways to reduce BP. A 5-20mm Hg BP reduction occurs with each 10kg of weight loss.[38] Gradual weight reduction (1kg weekly) should be advised. Pharmacologic interventions to reduce weight should be used with great caution, because diet pills, especially those available over the counter, frequently contain sympathomimetics. These agents can raise BP, worsen angina or symptoms of heart failure, and exacerbate tendencies for cardiac arrhythmias. Medications that should be avoided include nonsteroid anti-inflammatory drugs (NSAIDs), sympathomimetics, and monoamine oxidase inhibitors (MAOIs), as these agents can elevate BP or interfere with antihypertensive therapy.
The treatment of hypertension and hypertensive heart disease can involve the following classes of antihypertensive medications:
Thiazide diuretics
Beta blockers and combined alpha and beta blockers
Calcium channel blockers
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin-receptor blockers (ARBs)
Direct vasodilators - Such as hydralazine
Most patients require 2 or more antihypertensive drugs to achieve the BP goal; when the BP is more than 20/10mm Hg above the goal, consideration should be given to initiating therapy with 2 drugs, either as separate prescriptions or in fixed-dose combinations. (Surgical treatment may be necessary for definitive treatment in selected cases of secondary causes of hypertension, such as aortic coarctation or pheochromocytoma.)
Thiazide-type diuretics
Thiazide-type diuretics should be used for most patients with uncomplicated hypertension, either alone or in combination with drugs from other classes, according to the JNC.[15] Updated recommendations from the JNC (JNC-8) were published in 2014.[39]
Calcium channel blockers
Calcium channel blockers are effective for systolic hypertension in elderly patients. In one study, an ACE inhibitor/dihydropyridine calcium channel blocker combination proved to be superior to the ACE inhibitor/thiazide diuretic combination in reducing cardiovascular events in patients with hypertension who were at high risk for such events.[40]
ACE inhibitors and ARBs
ACE inhibitors are the first choice in patients with diabetes and/or ventricular dysfunction. ARBs are a reasonable alternative, especially for patients who suffer adverse effects from ACE inhibitors.
Beta blockers
Beta blockers are the drugs of first choice in patients with heart failure due to systolic LV dysfunction, patients with ischemic heart disease with or without a history of myocardial infarction, and patients with thyrotoxicosis.
Alpha channel blockers
Avoid peripheral alpha channel blockers in patients with hypertension in view of findings that they have an adverse effect on cardiovascular morbidity and mortality rates. Central alpha antagonists have no evidence-based support and have more adverse effects.
Other agents
Intravenous drugs used in patients with a hypertensive emergency include nitroprusside, labetalol, hydralazine, enalapril, and beta blockers (avoided in patients with acutely decompensated heart failure).
Some evidence shows that peroxisome proliferator-activated receptor gamma agonist ameliorates oxidative stress and leads to reversal of systemic hypertension-associated cardiac remodeling in chronic pressure overload myocardium and LVH.[41, 42]
Current guidelines indicate the use of acetaminophen as a first-line analgesic in patients with coronary artery disease. However, a study demonstrated that acetaminophen induced a significant increase in ambulatory BP in these patients.[43]
Treatment of LV Dysfunction and Arrhythmias
Treatment of left ventricular hypertrophy
LVH, a marker of increased risk of cardiovascular morbidity and mortality, should be treated aggressively because patients with LVH represent the subgroup of patients at the highest risk for cardiovascular events and mortality. Whether regression in LVH leads to improvement in cardiovascular mortality and morbidity rates is not clear, although limited data support this hypothesis. Data also indicate that regression of electrocardiographic LVH is associated with less hospitalization for heart failure in hypertensive patients.[41]
Medications for the treatment of hypertension have been shown to reduce LVH. Limited meta-analysis data suggest a slight advantage to ACE inhibitors.
Treatment of left ventricular diastolic dysfunction
Certain classes of antihypertensives—ACE inhibitors, beta blockers, and nondihydropyridine calcium channel blockers—have been shown (although not consistently) to improve echocardiographic parameters in symptomatic and asymptomatic diastolic dysfunction and the symptomatology of heart failure. Candesartan, an ARB, has been shown to decrease hospitalization in patients with diastolic heart failure.[44]
Use diuretics and nitrates with caution in patients with heart failure due to diastolic dysfunction. These drugs may cause severe hypotension by inappropriately decreasing the preload, which is required for adequate LV filling pressures. If diuretics are indicated, delicate titration is necessary. Hydralazine has been shown to cause severe hypotension in patients with heart failure due to diastolic dysfunction.
By increasing the intracellular calcium level, digoxin can worsen LV stiffness. However, a large, randomized trial has not shown any increase in mortality rate.
Treatment of left ventricular systolic dysfunction
Diuretics (predominantly loop diuretics) are used in the treatment of LV systolic dysfunction. Low-dose spironolactone has been shown to decrease the rates of morbidity and mortality in patients in NYHA class III or IV heart failure who are already taking ACE inhibitors. This agent is also recommended for use in post-myocardial infarction patients with diabetes mellitus or who have an LV ejection fraction of less than 40%.[45]
ACE inhibitors are used for preload and afterload reduction and the prevention of pulmonary or systemic congestion. These drugs have been shown to decrease morbidity and mortality rates in patients with heart failure due to systolic dysfunction. The aim should be to use the target dose or the maximum tolerable doses. ACE inhibitors are also indicated in patients with asymptomatic LV dilatation and dysfunction.
Beta blockers (cardioselective or mixed alpha and beta), such as carvedilol, metoprolol XL, and bisoprolol, have been shown to improve LV function and decrease rates of mortality and morbidity from heart failure. Trials have also shown improvement in outcomes for patients in NYHA class IV heart failure with carvedilol administration. These drugs should be started when the patient has no signs of fluid overload and is in compensated heart failure. Therapy should be initiated with low doses, increasing the dose of the beta blocker very slowly and closely monitoring the patient for signs of worsening heart failure.
Treatment of cardiac arrhythmias
The treatment of these conditions depends upon the specific arrhythmia and the underlying LV function, Anticoagulation should be considered in patients with atrial fibrillation. In addition, treat anxiety, stress, sleep apnea, and other contributing or precipitating factors.
Treatment-Resistant Hypertension
The Symplicity HTN-2 trial assessed the effectiveness and safety of catheter-based renal denervation to reduce BP in patients with treatment-resistant hypertension. The findings suggested that this approach can safely reduce hypertension in these patients.[46] In addition, some data suggest that baroreflex activation therapy (BAT) using an implantable stimulator can potentially reduce systolic BP safely over the long term in patients with resistant hypertension.[47]
Mortality and morbidity rates from hypertensive heart disease are higher than those of the general population and depend on the specific cardiac pathology.[1] Data suggest that increases in mortality and morbidity rates are related more to the pulse pressure than to the absolute systolic or diastolic BP levels, but all are important.
Left ventricular hypertrophy
The development of LVH is clearly related to an increase in the cardiovascular mortality rate. In fact, studies have shown an increase in the risk of sudden cardiac death in patients with LVH.[48]
The increased risk of cardiovascular events with LVH depends on its type. Concentric LVH poses the greatest risk of such events, as much as a 30% risk over a 10-year period in one study, compared with a 15% risk with eccentric remodeling and a 9% risk without any LVH. The degree of LVH, as assessed by LV mass index (LVMI), is also related to the cardiovascular mortality rate, with a relative risk of 1.73 for men and 2.12 for women for each 50g/m2 increase in the LVMI over a 4-year period. With LVH, the relative risk of mortality is increased 2-fold in patients with coronary artery disease and 4-fold in patients without coronary artery disease.[49]
Although not proven, limited data suggest a reduction in LVH results in a reduction in cardiovascular events. Regression of the LVMI has been demonstrated with several different antihypertensive medications.
Left ventricular diastolic dysfunction
The prognosis of patients with diastolic dysfunction is poor and is affected by the presence of underlying coronary artery disease. In one study, survival rates at 3 months, 1 year, and 5 years in patients with heart failure due to diastolic dysfunction were 86%, 76%, and 46%, respectively. In another study, the 7-year cardiovascular mortality rate approached 50% in patients with heart failure due to diastolic dysfunction and concomitant coronary artery disease; some also had hypertension.
Even in patients with asymptomatic diastolic dysfunction due to hypertension, the risk of all-cause mortality and cardiovascular events is significantly increased, particularly with an increase in the pulmonary artery wedge pressure (PAWP). LV diastolic dysfunction and the heart failure symptoms associated with it have been shown to improve with treatment aimed at lowering BP and reducing LVH. Whether such treatment has any effect on the mortality rate is not clear.
Left ventricular systolic dysfunction
The mortality rate from heart failure due to systolic LV dysfunction is high and depends on the symptoms and NYHA heart failure classification. The 5-year mortality rate for patients with heart failure due to systolic dysfunction approaches 20%, whereas the 2-year mortality rate in patients with NYHA class IV classification is as high as 50%. Mortality rates have decreased with the use of ACE inhibitors and beta blockers, which improve LV function.
Long-Term Monitoring
The long-term follow-up of patients with hypertensive heart disease includes monitoring of several factors. For example, patients with heart failure require daily measurement of weight and evaluation of accurate fluid balance. Furthermore, the effectiveness and choice of antihypertensive treatment, medication effectiveness and compliance, the presence or absence of coronary artery disease and degree of LV systolic function, and the patient's dietary habits and exercise pattern require assessment. In addition, it is important to reinforce dietary advice and advice regarding the importance of regular exercise.
Workup for secondary causes of hypertension should be performed if not already done. In addition, screen for complications related to hypertension, such as cerebrovascular disease, hypertensive retinopathy, worsening heart failure, and renal failure, and assess for LVH by electrocardiography or echocardiography.
When evaluating the adverse effects of various medications, obtain a urinalysis and BUN result, creatinine level, and electrolyte levels to rule out renal insufficiency and electrolyte imbalances secondary to medications and to quantitate proteinuria. A study by Leung et al found a 30% incidence of hyponatremia (Na < 130mmol) in long-term follow-up of patients who were exposed to thiazide diuretics for treatment of hypertension.[50]
In addition, advise the patient to avoid taking over-the-counter medications, such as commonly used NSAIDs, cough suppressants, and decongestants containing sympathomimetics, which can potentially raise BP.
Kannel WB, Cobb J. Left ventricular hypertrophy and mortality--results from the Framingham Study. Cardiology. 1992. 81(4-5):291-8. [Medline].
Yamasaki N, Kitaoka H, Matsumura Y, et al. Heart failure in the elderly. Intern Med. 2003 May. 42(5):383-8. [Medline].
Patel SK, Velkoska E, Freeman M, Wai B, Lancefield TF, Burrell LM. From gene to protein-experimental and clinical studies of ACE2 in blood pressure control and arterial hypertension. Front Physiol. 2014. 5:227. [Medline]. [Full Text].
Cabezas M, Comellas A, Ramon Gomez J, et al. [Comparison of the sensitivity and specificity of the electrocardiography criteria for left ventricular hypertrophy according to the methods of Romhilt-Estes, Sokolow-Lyon, Cornell and Rodriguez Padial]. Rev Esp Cardiol. 1997 Jan. 50(1):31-5. [Medline].
Kahn S, Frishman WH, Weissman S, et al. Left ventricular hypertrophy on electrocardiogram: prognostic implications from a 10-year cohort study of older subjects: a report from the Bronx Longitudinal Aging Study. J Am Geriatr Soc. 1996 May. 44(5):524-9. [Medline].
Shimbo D, Muntner P, Mann D, Barr RG, Tang W, Post W, et al. Association of left ventricular hypertrophy with incident hypertension: the multi-ethnic study of atherosclerosis. Am J Epidemiol. 2011 Apr 15. 173(8):898-905. [Medline].
von Lueder TG, Atar D, Krum H. Current role of neprilysin inhibitors in hypertension and heart failure. Pharmacol Ther. 2014 Oct. 144(1):41-49. [Medline].
Sun JP, Xu TY, Lee AP, et al. Early diastolic dyssynchrony in relation to left ventricular remodeling and function in hypertension. Int J Cardiol. 2015 Jan 20. 179:195-200. [Medline].
Gandhi SK, Powers JC, Nomeir AM, et al. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med. 2001 Jan 4. 344(1):17-22. [Medline].
Ghali JK, Kadakia S, Cooper RS, Liao YL. Impact of left ventricular hypertrophy on ventricular arrhythmias in the absence of coronary artery disease. J Am Coll Cardiol. 1991 May. 17(6):1277-82. [Medline].
Jouven X, Desnos M, Guerot C, Ducimetiere P. Predicting sudden death in the population: the Paris Prospective Study I. Circulation. 1999 Apr 20. 99(15):1978-83. [Medline].
Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA. 2001 May 9. 285(18):2370-5. [Medline].
Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB, Flegal K, et al. Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2009 Jan 27. 119(3):e21-181. [Medline].
Peacock F, Amin A, Granger CB, et al. Hypertensive heart failure: patient characteristics, treatment, and outcomes. Am J Emerg Med. 2011 Oct. 29(8):855-862. [Medline].
Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003 May 21. 289(19):2560-72. [Medline].
[Guideline] Goff DC Jr, Lloyd-Jones DM, Bennett G, Coady S, D'Agostino RB Sr, Gibbons R, et al. 2013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013 Nov 12. [Medline]. [Full Text].
[Guideline] Eckel RH, Jakicic JM, Ard JD, de Jesus JM, Houston Miller N, Hubbard VS, et al. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014 Jul 1. 63(25 Pt B):2960-84. [Medline].
[Guideline] Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014 Jul 1. 63(25 Pt B):2889-934. [Medline].
[Guideline] Jensen MD, Ryan DH, Apovian CM, Ard JD, Comuzzie AG, Donato KA, et al. 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society. J Am Coll Cardiol. 2014 Jul 1. 63(25 Pt B):2985-3023. [Medline].
Hoey ET, Pakala V, Teoh JK, Simpson H. The role of imaging in hypertensive heart disease. Int J Angiol. 2014 Jun. 23(2):85-92. [Medline]. [Full Text].
Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986 Feb 15. 57(6):450-8. [Medline].
Beckett NS, Peters R, Fletcher AE, Staessen JA, Liu L, Dumitrascu D, et al. Treatment of hypertension in patients 80 years of age or older. N Engl J Med. 2008 May 1. 358(18):1887-98. [Medline].
Elmer PJ, Grimm R Jr, Laing B, et al. Lifestyle intervention: results of the Treatment of Mild Hypertension Study (TOMHS). Prev Med. 1995 Jul. 24(4):378-88. [Medline].
Hajjar IM, Grim CE, George V, Kotchen TA. Impact of diet on blood pressure and age-related changes in blood pressure in the US population: analysis of NHANES III. Arch Intern Med. 2001 Feb 26. 161(4):589-93. [Medline].
Hypertension Prevention Trial Research Group. The Hypertension Prevention Trial: three-year effects of dietary changes on blood pressure. Arch Intern Med. 1990 Jan. 150(1):153-62. [Medline].
Aguilera MT, de la Sierra A, Coca A, et al. Effect of alcohol abstinence on blood pressure: assessment by 24-hour ambulatory blood pressure monitoring. Hypertension. 1999 Feb. 33(2):653-7. [Medline].
Forman JP, Stampfer MJ, Curhan GC. Diet and lifestyle risk factors associated with incident hypertension in women. JAMA. 2009 Jul 22. 302(4):401-11. [Medline]. [Full Text].
Cook NR, Cutler JA, Obarzanek E, Buring JE, Rexrode KM, Kumanyika SK. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJ. 2007 Apr 28. 334(7599):885. [Medline].
Conlin PR, Chow D, Miller ER 3rd, et al. The effect of dietary patterns on blood pressure control in hypertensive patients: results from the Dietary Approaches to Stop Hypertension (DASH) trial. Am J Hypertens. 2000 Sep. 13(9):949-55. [Medline].
Conlin PR. The dietary approaches to stop hypertension (DASH) clinical trial: implications for lifestyle modifications in the treatment of hypertensive patients. Cardiol Rev. 1999 Sep-Oct. 7(5):284-8. [Medline].
Moore TJ, Vollmer WM, Appel LJ, et al. Effect of dietary patterns on ambulatory blood pressure : results from the Dietary Approaches to Stop Hypertension (DASH) Trial. DASH Collaborative Research Group. Hypertension. 1999 Sep. 34(3):472-7. [Medline].
Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med. 2001 Jan 4. 344(1):3-10. [Medline].
Svetkey LP, Sacks FM, Obarzanek E. The DASH Diet, Sodium Intake and Blood Pressure Trial (DASH-sodium): rationale and design. DASH-Sodium Collaborative Research Group. J Am Diet Assoc. 1999 Aug. 99(8 Suppl):S96-104. [Medline].
Manolio TA, Levy D, Garrison RJ, et al. Relation of alcohol intake to left ventricular mass: The Framingham Study. J Am Coll Cardiol. 1991 Mar 1. 17(3):717-21. [Medline].
Klatsky AL, Friedman GD, Armstrong MA. The relationships between alcoholic beverage use and other traits to blood pressure: a new Kaiser Permanente study. Circulation. 1986 Apr. 73(4):628-36. [Medline].
Sinha R, Cross AJ, Graubard BI, Leitzmann MF, Schatzkin A. Meat intake and mortality: a prospective study of over half a million people. Arch Intern Med. 2009 Mar 23. 169(6):562-71. [Medline].
Kokkinos PF, Papademetriou V. Exercise and hypertension. Coron Artery Dis. 2000 Mar. 11(2):99-102. [Medline].
Mahamat A, Richard F, Arveiler D, et al. Body mass index, hypertension and 5-year coronary heart disease incidence in middle aged men: the PRIME study. J Hypertens. 2003 Mar. 21(3):519-24. [Medline].
[Guideline] James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014 Feb 5. 311(5):507-20. [Medline].
Jamerson K, Weber MA, Bakris GL, Dahlöf B, Pitt B, Shi V, et al. Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients. N Engl J Med. 2008 Dec 4. 359(23):2417-28. [Medline].
Henderson BC, Sen U, Reynolds C, Moshal KS, Ovechkin A, Tyagi N. Reversal of systemic hypertension-associated cardiac remodeling in chronic pressure overload myocardium by ciglitazone. Int J Biol Sci. 2007. 3(6):385-92. [Medline].
Baradaran A, Nasri H, Rafieian-Kopaei M. Oxidative stress and hypertension: Possibility of hypertension therapy with antioxidants. J Res Med Sci. 2014 Apr. 19(4):358-67. [Medline]. [Full Text].
Sudano I, Flammer AJ, Périat D, Enseleit F, Hermann M, Wolfrum M, et al. Acetaminophen increases blood pressure in patients with coronary artery disease. Circulation. 2010 Nov 2. 122(18):1789-96. [Medline].
Weir RA, McMurray JJ, Puu M, Solomon SD, Olofsson B, Granger CB, et al. Efficacy and tolerability of adding an angiotensin receptor blocker in patients with heart failure already receiving an angiotensin-converting inhibitor plus aldosterone antagonist, with or without a beta blocker. Findings from the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM)-Added trial. Eur J Heart Fail. 2008 Feb. 10(2):157-63. [Medline].
Okin PM, Devereux RB, Harris KE, Jern S, Kjeldsen SE, Julius S. Regression of electrocardiographic left ventricular hypertrophy is associated with less hospitalization for heart failure in hypertensive patients. Ann Intern Med. 2007 Sep 4. 147(5):311-9. [Medline].
Esler MD, Krum H, Sobotka PA, Schlaich MP, Schmieder RE, Böhm M. Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomised controlled trial. Lancet. 2010 Dec 4. 376(9756):1903-9. [Medline].
Bisognano JD, Bakris G, Nadim MK, et al. Baroreflex activation therapy lowers blood pressure in patients with resistant hypertension results from the double-blind, randomized, placebo-controlled rheos pivotal trial. J Am Coll Cardiol. 2011 Aug 9. 58(7):765-73. [Medline].
Burke AP, Farb A, Liang YH, et al. Effect of hypertension and cardiac hypertrophy on coronary artery morphology in sudden cardiac death. Circulation. 1996 Dec 15. 94(12):3138-45. [Medline].
Liao Y, Cooper RS, Mensah GA, McGee DL. Left ventricular hypertrophy has a greater impact on survival in women than in men. Circulation. 1995 Aug 15. 92(4):805-10. [Medline].
Leung AA, Wright A, Pazo V, Karson A, Bates DW. Risk of Thiazide-induced Hyponatremia in Patients with Hypertension. Am J Med. 2011 Nov. 124(11):1064-72. [Medline].
|Systolic BP,
mm Hg
|Diastolic BP,
mm Hg
|< 120
|< 80
|Stage I
|Stage II
|Voltage Criteria
|R wave or S wave in any limb lead >0.2mV or S wave in lead V1 or V2 or R wave in V5 or V6 >0.3mV
|LV strain (ST and T waves in direction opposite to QRS direction) without digitalis
|LV strain (ST and T waves in direction opposite to QRS direction) with digitalis
|LA enlargement (terminal negativity of P waves in V1 >0.1mV deep and 0.04 seconds wide)
|Left-axis deviation greater than -30°
|QRS duration greater than 0.09 seconds
|Intrinsicoid deflection in V5 or V6 >0.05 seconds
|* Probable LVH is 4 points; definite LVH is 5 points. The sensitivity of these criteria is 50%, with a specificity of close to 95%.


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Style Note
A driving shoe that understands your feet and gives your look a refined twist, this pair from red tape is a closet essential. The slip-on styling helps you wear this pair with ease and keeps your feet comfy as well.
Product Details
Brown square toed slip-on shoes with stitch detail at the seams of the toe box
Has a cushioned insole
TPU outsole in the form grooved geometrical lugs
Material and Care
Clean with a leather brush
Do not store under sunlight or wash

subset: commoncrawl


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Electronics & Wiring
Electronics & Wiring
Electronics & WiringIf you're looking to add electronic devices to enhance the safety and comfort of your motorcycle, you're in the right place. Browse from a large selection of wiring, fuse blocks, device mounts and cradles made for your motorbike that will get the job done. We carry the best, most innovative and high quality motorcycle electronic and wiring products from tried, tested and true brands like 3BR Power Sports, AdMore Lighting, Battery Tender, Denali, DrySpec, Garmin, GoPro, Interphone, RAM Mounts, Sena, SW-MOTECH and many more. Shop with us to stay powered up and connected with wiring and electrical components made for motorcyclists and their motorcycles.
Techmount GEN 4 Universal Wide Top Plate Kit with Velcro in Black, Silver or Chrome$23.88
Techmount GEN 4 Top Plate for mounting Garmin Zumo 660 GPS to GEN 4 in Black, Silver or Chrome$23.88
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Techmount GEN 4 Mount for LifeProof iPhone 5/S Cases$31.44
Techmount GEN 4 Mount for LifeProof iPhone 4 & iPhone 4s Cases$31.44
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23rd March 1931: Shaheed is a 2002 Hindi film directed by Guddu Dhanoa which depicts the events leading up to the hanging of Indian freedom fighter Bhagat Singh and his companions Rajguru and Sukhdev on 23 March 1931. The film stars Bobby Deol as Bhagat Singh, his elder brother Sunny Deol as Chandrashekhar Azad and Amrita Singh in her comeback role as Bhagat Singh's mother. Aishwarya Rai has a special appearance in a song. Wikipedia
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Athletics are just as important to faculty and students as academics are.
Students come out and support their friends at sporting events. Because the school is so small, almost everyone is friends with an athlete or an athlete themselves. The facilities are better than average, plus the addition of a new Varsity Weight Room allows athletes to train separately from the non-athlete population. For a Division III school, our athletics rank as some of the best in the nation in many different sports.
overrated and overexaggerated athletes are rude at times
Honestly I forget that we have sports at Rhodes.
I'm not an athletic person nor do I find sports very entertaining so my opinion isn't really valid. I can go a long time without hearing about our athletics if that means anything.
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Rhodes is a school that's not very sports-oriented. No one really knows exactly why that is. Maybe it's because it's Division III, or maybe everyone gets too hyped up about SEC (Southeastern Conference) football teams to focus any excess energy on Rhodes' team. Either way, varsity sports are mainly only important to the people who play them or to those with friends on the team. Some students will make it out to a few games each year, but usually the stands are pretty bare. It's unfortunate for the players, especially since Rhodes does in fact have some great teams, but that's just how it is.
Intramurals and club sports are much more popular. That could be because they're a good balance for students who are unable or unwilling to try to deal with varsity athletics with a full, intensive course load. Ultimate Frisbee, soccer, basketball, and even Quidditch have big followings, and students love getting involved to take a break from working and to meet new people. Intramurals are the way to go if the lack of real sports drama is killing you. You could drive to Ole Miss (University of Mississippi) an hour and a half away to see a real SEC game, but if that's too much effort, you're out of luck. Technically, Sewanee is the school rival, but few people are even aware of that, let alone care enough to get truly competitive. Rhodes Activities Board (RAB) has started creating events to try to bring students into the stands and make everyone more involved, and it is working a little bit. You can also try to create school spirit on your own by putting on the red and black, and getting out into the stands, but you might have some trouble trying to drag your friends out with you. It's sad that the sports teams don't get enough credit because they do produce wins, and they're a great thing to be a part of. You don't need to be recruited to get involved—one of the pros to being Division III!
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Welcome orioles; beware fleas
July's end brings out all sorts
8:09 p.m., July 28
Abrahim Ah Saed wore a white t-shirt for sentencing. Photo Weatherston.
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June 28, 2013
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Freda Charcilia Payne (born September 19, 1942) is an American Soul/R&B singer and actress best known for her million selling 1970 hit single, "Band of Gold". She was also an actress in musicals and film, as well as the host of a TV talk show. Fr...eda is the older sister of former Supreme Scherrie Payne.
Connect any celebrity with Freda Payne to see how closely they are linked... romantically!
Freda, I found through my father's record collection a "test pressing album along with a M-G-M/VERVE RECORDS REFERENCE RECORDING RECORD" from the year "1966" ... also, my brother's finance' Lisa who used to work for a radio station played one of your songs and she told me that you had called her and thanked her for playing one of your songs......would love to hear from you in regards to why my father has one of your "1st" pre-cut albums before they were distributed....please contact me at (248) 320-4803...would "LOVE" to hear from you.....respectfully, cindy aqwa-burke
Hello Freda I just had thought about your hit song Band of Gold today and I remember see you on PBS Singing that song !!! I was too young to rember the song when it first came out ,but when I saw you on PBS YOU WERE SO BEAUTIFUL AND LOVELY AND TALENTED that I just has to respond to this websight and say thank you for your years of entertainment I am a fan as well!!
thats a good record but where`s judge joe brown
Love you much! Let`s talk soon.
Hi Freda you are a fantastic singer and you would have been even bigger if better songs were available .Band of Gold was an example of the right talent and the right song.I am a big fan of yours.


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Seducing the Succubus (A Sisters of Darkness Novel #1)
October 5, 2010 | Language: English | ISBN-10: 0425236846 | EPUB | 336 pages | 318.86 Kb
First in a sexy new series featuring four succubus sisters fighting demons and desires.
Jezebeth is living out the centuries as any succubus must-seducing men to survive and corrupting souls to make her quota with her queen, Lilith. But, when she's attacked by a bounty hunter demon, it's a handsome human who saves her.
Noah Halston is a horror writer who owes his life to Lilith. Now he must pay up by eluding the fearsome beasts of hell while escorting a very attractive and tempting succubus safely to Lilith's lair-or else he will forfeit his soul to an eternity of torture.
Trouble is, if he spends too much time with the all too tempting Jezebeth, he may just lose his heart-or, even worse, his life.
[Fast Download] Seducing the Succubus (A Sisters of Darkness Novel #1)
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Dark Guardian: Dark Series, Book 9
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text:
12" Aluminum Fry Pan
- Quantity Discounts!
Other Available Sizes:
- 3.5mm aluminum thickness
- Riveted-on handle ensures longevity and a secure connection
You May Also Need
"You May Also Need" items are guaranteed to work with the item you are viewing, such as lids that will fit a cup or casters that will fit a piece of equipment. If an item is not listed in this section, we do not guarantee that it will work with the product you are viewing and do not recommend that you purchase them for use together.
"You May Also Need" items are guaranteed to work with the item you are viewing, such as lids that will fit a cup or casters that will fit a piece of equipment. If an item is not listed in this section, we do not guarantee that it will work with the product you are viewing and do not recommend that you purchase them for use together.
|2 3/4 Inches
|Top Diameter
|12 Inches
|10 Gauge
|Handle Type
|NSF Listed
|Fry Pans
|Entry Level
Customer questions about this product
- How can I properly care for this aluminum item?
- Hand washing is always the best option to ensure that your aluminum stays in best working order. However, if you decide to clean these in a dishwasher, we strongly recommend using metal-safe detergents and sanitizers to eliminate any flaking or tarnishing that could occur from some harsher cleaners.
- What's the difference between a riveted and a welded handle?
- A riveted handle is connected by small metal pieces (called rivets) that are crushed between the handle and the pan body to attach them together. This type of handle is more common on copper and aluminum cookware.
For a handle to be welded, the metal must first be melted and then adhered to the pan body. This creates a strong bond that leaves little to no space in between, so bacteria and other food crumbs can't collect and cause sanitation issues. Both are long lasting solutions for fry and sauce pan handles because they are durable and can withstand heat.
Fry, sear, scramble, and saute all of your signature dishes in this versatile 12" aluminum fry pan! With a shallow, curved wall design, this pan allows for easy stirring and prevents steam from forming in the pan.
This pan's professional quality, heavy-duty 3004 10 gauge series aluminum alloy construction distributes heat evenly, while its satin finish is perfect for restaurants and caterers alike. A large hole at the end of the aluminum handles makes for easy storage, and since the handles are riveted on, they ensure a very rigid connection between handle and vessel, guaranteeing longevity even in a commercial kitchen.
Overall Dimensions:
Top Diameter: 12"
Height: 2 3/4"
NSF Listed
This item meets the standards imposed by NSF International, which focuses on public safety, health, and the environment.
Related Items
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Customer Reviews
Arrange by
Nice fry pans. They work just fine for us and they are so reasonable in price that they can be replaced as needed. They are not a thin pan.
Patricia H. Posted on 01/06/2016
One of the best 12" Aluminum Fry Pan that i got i like the durability of this fry pan great to use for everything love it !!!
Alexander I. from ashlexdrei tradings /sweets by chef jhay Posted on 10/19/2015
These are nice. The coating could be a little bit better on the. Will probably get a year maybe a bit more out of these pans.
Elise M. from backwater Posted on 06/24/2015
Amazing value at this price. Ordered a few to see the quality and was satisfied with them I will be ordering more of these for sure!!
William P. from Funky fresh food truck Posted on 06/18/2015
Would not recommend this, constructed well, but, the pan heats too quickly and is not reliable in overall cooking, hard to clean, just not good for our restaurant.
Christopher R. from the black fig Posted on 06/11/2015
This fry pans are absolutely amazing for the price. They are heavy duty. They have lasted great under heavy use with no sign of a problem.
Matt B. from rollin' coal bbq and catering Posted on 03/28/2015
This a well made, heavy duty frying pan made out of thick metal. It is great for larger meals, and it cooks fast and even.
John S. Posted on 03/26/2015
My first all aluminum pan. Works great for sauces and sautéing. Quality through and through. I highly recommend it! Haven't had much luck with eggs and "sticky" foods but I'm still learning. I love this online store. Great prices and quality products!
Rick L. from Tbones Smoke House Posted on 03/09/2015
Great quality thick bottomed pan. You cannot beat it for the price. we use it on a daily basis and is a great size for multiple portion cooking.
James M. from Daily Grinders Posted on 08/15/2014
If you want to get a silicone handle to slip over the exposed metal handle of this pan, then you should probably buy the handles designed for 14" pans instead of the ones designed for 12" pans. I wasn't able to fit the 12" handle cover, but the 14" cover went on nicely.
Nicholas O. Posted on 06/23/2014
I ordered this pan for my home use as I needed a bigger pan than my regular 12 inch. The pan has held up wonderfully as I have been putting it to use with several dishes at different heat levels. A very nice pan for my uses.
Mike S. Posted on 04/16/2014
This is the workhorse of the 407 series in my book , super heavy duty. When you step up from the 10" to the 12" there is a big difference. I use this bad boy on my outdoor 135,000 btu burner with no problems or warping.
Anthony L. Posted on 03/10/2014
If you are planning to buy this fry pan, you will make a very good decision. I would recommend this good fry pan to everyone.
Shawn H. from S & H Gourmet LLC Posted on 11/12/2013
Purchased this frying pan along with a number of other similar items and was impressed with the level of quality in it's construction. A sturdy cooking tool that does it's job well and at a phenomenal price!
Louis R. from Jim R Posted on 07/13/2013
This aluminum pan is pretty big and is great for sauting, sauces, gravies and other like things. They are also durable and price just right.
David D. Posted on 08/14/2012
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text:
Tribal Organization: Tule River Tribe of Yokuts
681 South Tule Road
Porterville, California 93258
(800) 903-3353
(559) 788-6220
Gaming at Eagle Mountain Casino
Open 24 hours daily
70,000 square foot casino
1,400+ slots
13 table games
Bingo Hall - 450 seats
Oak Tree Buffet: Serving breakfast and lunch Sun - Thurs. Open for breakfast, lunch & dinner on Fri and Sat.
The Acorn Room: Signature steaks, fish, and poultry. Open Wed - Sun, 5PM - 10PM. Reservations: (559)788-1816
Grizzly's Food Court: soups, sandwiches, hot dogs, nachos, pizza and more. Open 24 hours, 7 days a week.


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A New Map of the Brain: What Does It Mean?
2 days ago
A brave attempt to think out loud about theories of psychology until we get some
Funny story. One day, I got a text from Sabrina that said "Holy crap. I think ecological information is a representation." "...


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This Business is not BBB Accredited
Edward Jones InvestmentFind a Location
(903) 583-5462308 N Main St, Bonham, TX 75418-4321http://www.edwardjones.com
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Find aggregate BBB complaint information for Edward Jones. BBB located in Saint Louis, MO has the full report as that BBB handles all complaints for Edward Jones.
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BBB has not received a sufficient volume of requests for information, nor has BBB received complaints on this firm to warrant the maintenance of a report. The information provided, however limited, is presented to assist you in your purchasing decisions or for any other purpose you deem relevant.
BBB suggests you read and understand company promotional materials and contracts and check company references and licensing, where applicable.BBB file opened: 02/27/2012Business started: 11/01/1995Business started locally: 06/18/1992
Licensing, Bonding or Registration
This company is in an industry that may require licensing, bonding or registration in order to lawfully do business. BBB encourages you to check with the appropriate agency to be certain any requirements are currently being met.
These agencies may include:State Securities Board
1800 San Jacinto St, P O Box 13167
Austin, TX 78711-3167
(512) 305-8300
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Check License Status: http://www.finra.org2245482
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Contact InformationPrincipal: Mr. Brent Speck (Investment Representative)
Business Category
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text:
Spanish Word for uncle
English Word: uncle
Spanish Word: el tío
Now you know how to say uncle in Spanish. :-)
Interested in travelling to a Spanish-speaking country? Read the travel blog below:
Food experiences (Guadalajara, Mexico)
Hola! I cannot believe that I have been here for almost a month! Time flies even in this nice settle routine that I have become adapted quite well to. I had a hard time adjusting to the big breakfast of beans, eggs, fruit, yogurt and granola or sometimes taquitos. However, I do know what I'm going to do without it when I return home. : ( Lunch time is between 1-3 PM and our host mom...
[ view entire travel blog ]
Popular Phrase: sentarse present tense | Language schools | Conjugated Verb: facturar - to invoice, to bill for [ click for full conjugation ]


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Skrillex has designed a series of limited-edition phone cases for Android.
The new By Atelier collection for iPhone 6 is composed of 7 luxury cases, customised with calf leathers and alligator skins in contemporary colours.
French brand Christian Lacroix has introduced its first line of smartphone and tablet cases, which will be available in the fall, starting from €24.90.
Gresso has launched the Titanium Bumper, a collection of protective cases for iPhone 5 with prices ranging from $1,000 to $10,000.
Jean Paul Gaultier has unveiled a range of five different mobile phone and tablet accessories, working with French company Bigben connected, which already creates accessories for Kenzo and Swarovski.
Apple's first gold-colour iPhone sold out immediately in Hong Kong and mainland China, according to reports and online buyers desperate to snap up the new status symbol.
British luxury designer Stuart Hughes has created a £10 million, solid-gold bodied, diamond-encrusted iPhone 5.
Omega has brought old-world craftsmanship to one of the world's most popular high-tech devices. The brand has introduced a fine leather case for the iPhone 5.
The Just Cavalli I Lock Your Love and Python accessories (for iPhone4, 4S, 5 and for iPad 2) are available online at PURO.
On Sep. 27, Gold & Co is set to unveil what it claims is the world's first 24-karat gold-plated iPhone 5 at the Collector's Palace in Dubai Mall.
As the world waits for the launch of Apple iPhone 5, Gresso, a manufacturer of luxury accessories, has rolled out a bumper case for the iPhone 5.
Marc by Marc Jacobs and Incase have released a new collection of cases for the iPhone 4 and iPhone 4S, available exclusively at the Apple Store.
Miansai have unveiled this gorgeous iPhone 4 case made of solid gold. It can be purchased either in yellow or rose gold. Crafted by hand at Miansai, it can be customized according to the client's tastes. Every case is engraved with its limited edition number. Price: $10,000.
De Bethune has released the Dream Watch IV, an iPhone 4S case that features a mechanical clock as well as protection for your phone… and your brain! Clearly inspired by the unique piece made for Only Watch 2011 (below), the pocket watch face is made from blued titanium with gold and diamond stars. The Dream … Continued
Luxury design company Brikk will launch a series of limited edition luxury iPhone cases, profits from which will benefit those in need around the world. The limited edition collection revolves around the theme of "Altruistic Precision" and is launched with the Trim series of luxury titanium cases for the iPhone 4. The luxury cases are … Continued
The Maison Martin Margiela has released this two-piece smartphone holder for autumn/winter 2011 – seen here in brown. Made from two pieces of richly-coloured leather, the phone holder is lined with a soft and fluffy shearling, mirroring pieces from the Margiela mainline collection. The holder is the perfect size for an iPhone (both 3 and … Continued
Valentino iPhone case is made from black leather with silver pyramid studs, gold designer stamp and topstitch detail. It features snap-fastening fold-over tab – $245.
Louis Vuitton has released four different cases for the iPhone 4. There is the Damier Azur Canvas, Damier Ebene Canvas, and of course the Monogram canvas cases. Each one sports an ultra soft microfiber interior, so there is no threat of scratches and is ultra slim so it fits into your pocketbook or pants pocket … Continued
Bentley and its luxury leather partner Ettinger have devised a range of modern must-have personal accessories to be launched at this year's Geneva Motor Show. Inspired by the Beluga and Hotspur interior trim colours of the Bentley Continental Supersports, the capsule collection of leather items in black and red leather with contrast stitching includes keyrings … Continued
Swiss luxury watch maker Franck Muller has designed a special case for the iPhone, which is now available for pre-order in Japan for a whopping $1,270. The cases will be sold as a limited edition, with Japanese iPhone provider SoftBank offering a total of 6 different models that will be produced 500 times each.


text:
email@example.com us • +44 1534 725501
All Special Offers can be booked either online or direct with the hotel. "Early Bird" discounts can apply.
Summer Midweek Indulgent BreakMake the most of the long hot days! From £160 per person per night - fourth night free!
Summer BreakSun drenched beaches and poolside cocktails.
From £182.50 per person per night - fifth night free! ...
October BreakA slower pace so relax and indulge!
From only £195 per person per night - fourth night free!
Consult "Book Online" for all our best available Bed & Breakfast rates
Most rates offer an "Early Bird" discount for full pre-payment made at the time of booking:
10% discount for full pre-payment made 60 days or more in advance.
20% discount for full pre-payment made 120 days or more in advance (selected rates only).
An "Early Bird" pre-payment is strictly non-refundable and non-transferable
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text: Aberdeen Asian Income Fund Company Profile (LON:AAIF) Analyst Ratings Earnings Estimates Dividends Insider Trades Headlines Company Profile Chart Analyst Ratings Consensus Ratings for Aberdeen Asian Income Fund (LON:AAIF) (?) The ratings breakdown includes the most recent rating from each analyst that has rated the stock within the last twelve months. The ratings score is a calculation of the average number of sell, hold, buy and strong buy ratings (0-1.5 = Sell, 1.5-2.5 = Hold, 2.5-3.5 = Buy, >3.5 = Strong Buy). The consensus price target is a mean average of the most recent price target set by each analyst that has set a price target for the stock in the last twelve months.Ratings Breakdown: No ratings tracked in the last 12 months.Consensus Rating:N/A (Score: NaN)Consensus Price Target: N/A Analysts' Ratings History for Aberdeen Asian Income Fund (LON:AAIF) Show: All Ratings For This Stock Only the Most Recent Rating From Each Brokerage No equities research coverage for this company has been tracked by MarketBeat.com Earnings Earnings History for Aberdeen Asian Income Fund (LON:AAIF)No earnings announcements for this company have been tracked by MarketBeat.com Estimates Earnings Estimates for Aberdeen Asian Income Fund (LON:AAIF)No earnings estimates for this company have been tracked by MarketBeat.com Dividends Dividend History for Aberdeen Asian Income Fund (LON:AAIF)AnnouncedPeriodAmountYieldEx-Dividend DateRecord DatePayable DateShare4/14/2016GBX 21.18%4/21/20164/21/20165/23/2016 1/14/2016GBX 2.501.73%1/21/20161/21/20162/18/2016 10/13/2015GBX 21.19%10/22/201510/22/201511/17/2015 7/9/2015GBX 21.04%7/16/20157/16/20158/21/2015 (Data available from 1/1/2013 forward) Insider Trades Insider Trading History for Aberdeen Asian Income Fund (LON:AAIF)Transaction DateInsider NameTitleBuy/SellNumber of SharesAverage Share PriceTotal TransactionActions6/22/2016Arthur,PeterInsiderBuy303GBX 165£499.95 5/24/2016Arthur,PeterInsiderBuy267GBX 159£424.53 5/23/2016Arthur,PeterInsiderBuy311GBX 161£500.71 4/22/2016Arthur,PeterInsiderBuy290GBX 173£501.70 4/5/2016Nowak,KrystynaInsiderBuy4,423GBX 158£6,988.34 3/22/2016Arthur,PeterInsiderBuy307GBX 1,625£4,988.75 2/22/2016Arthur,PeterInsiderBuy338GBX 148£500.24 2/19/2016Arthur,PeterInsiderBuy345GBX 144£496.80 1/22/2016Arthur,PeterInsiderBuy347GBX 144£499.68 12/22/2015Arthur,PeterInsiderBuy327GBX 153£500.31 11/23/2015Arthur,PeterInsiderBuy318GBX 157£499.26 11/18/2015Arthur,PeterInsiderBuy241GBX 155£373.55 10/23/2015Arthur,PeterInsiderBuy305GBX 164£500.20 9/23/2015Arthur,PeterInsiderBuy320GBX 156£499.20 8/25/2015Arthur,PeterInsiderBuy581GBX 146£848.26 8/24/2015Baxter,DuncanInsiderBuy20,000GBX 147£29,400 7/23/2015Arthur,PeterInsiderBuy263GBX 190£499.70 6/23/2015Arthur,PeterInsiderBuy262GBX 1.91GBX 500.42 5/26/2015Krystyna NowakInsiderBuy7,596GBX 198.79£15,100.09 (Data available from 1/1/2013 forward) Headlines Latest Headlines for Aberdeen Asian Income Fund (LON:AAIF)DateHeadline07/19/16 07:40 PMABERDEEN ASIA PACIFIC INCOME INVESTMENT : ANNOUNCES NORMAL COURSE ISSUER BID07/15/16 06:28 PMAberdeen Asia-Pacific Income Investment Company Limited Announces Normal Course Issuer Bid06/06/16 11:48 AMS&P Scorned by Investors for Keeping Asia's Best Debt at Junk05/19/16 08:29 AMAberdeen Asia-Pacific Income Fund, Inc. : Announces Performance Data And Portfolio Composition - However, the figures are unaudited and neither the Fund, the Administrator, Aberdeen Asset Management Asia Limited (the Investment Manager ... http://www.prnewswire.com/news-releases/aberdeen-asia-pacific-income-fund-inc-announces-performance-data ...05/11/16 08:06 AMAAIF passes all resolutions at AGM - has announced that, at the Annual General Meeting of the Company held today, all resolutions were unanimously passed on a show of hands. At 12:08pm: [LON:AAIF] Aberdeen Asian Income Fund Ltd share price was +0.5p at 162.5p04/14/16 07:51 AMAAIF declares interim divi - StockMarketWire.com - The Directors of Aberdeen Asian Income Fund (AAIF) have declared a first interim dividend, in respect of the year ending 31 December 2016, of 2.0p per Ordinary share (2015: 2.0p). The dividend will be payable on 23 May 2016 to ...04/04/16 04:41 PMAberdeen Asian IncFd (AAIF) - In accordance with UKLA Listing Rule 15.6.8 Aberdeen Asian Income Fund Limited announces the following portfolio disclosures as at 31 March 2016 in other UK listed investment companies (including investment trusts) which themselves do not have a stated ...03/22/16 04:03 PMAberdeen Global Income Fund : Announces Performance Data And Portfolio Composition - PHILADELPHIA, March 21, 2016 /PRNewswire/ -- Aberdeen Global Income Fund, Inc. (the "Fund ... However, the figures are unaudited and neither the Fund, the Administrator, Aberdeen Asset Management Asia Limited (the Investment Manager), Aberdeen Asset ...03/10/16 03:49 PMAberdeen Asia-Pacific Income Investment Company Limited Announces Election Of Directors - Shares of closed-end funds may trade above (a premium) or below (a discount) the net asset value (NAV) of the fund's portfolio. There is no assurance that the Company will achieve its investment objective.02/13/16 06:02 AMAberdeen Asian IncFd: Portfolio Disclosures - Aberdeen Asset Management PLC announces that the unaudited monthly portfolio listings of the following investment companies, as at 31 January 2016, are now available on the respective company websites. Unless otherwise disclosed financial assets have ...01/16/16 02:23 PMAberdeen Asian Income buys back shares - StockMarketWire.com - Aberdeen Asian Income Fund bought back 50,000 ordinary shares yesterday at an average price of 144.9p apiece to be held in treasury. At 1:07pm: [LON:AAIF] Aberdeen Asian Income Fund Ltd share price was -1.25p at 143.25p Social About Aberdeen Asian Income Fund Aberdeen Asian Income Fund Limited is a closed-end investment company. The investment objective of the Company is to provide investors with a total return primarily through investing in Asian Pacific securities, including those with an above average yield. The Company invests in the Asia Pacific region through investment in companies listed on stock exchanges in the Asia Pacific region; Asia Pacific securities, such as global depositary receipts (GDRs), listed on other international stock exchanges; companies listed on other international exchanges that derive significant revenues or profits from the Asia Pacific region, and debt issued by governments or companies in the Asia Pacific region or denominated in Asian Pacific currencies. It invests in all types of securities, including equity shares, preference shares, debt, convertible securities, warrants and other equity-related securities. Aberdeen Asset Management Asia Limited is the investment manager of the Company. Industry, Sector and Symbol: Sector: N/A Industry: N/A Sub-Industry: N/A Exchange: LON Symbol: AAIF CUSIP: Key Metrics: Previous Close: $2.5750 Day Moving Average: $1.898200 Day Moving Average: $1.753P/E Ratio: N/AP/E Growth: 0.000Market Cap: $N/ACurrent Year EPS Consensus Estimate: $nan EPSNext Year EPS Consensus Estimate: $N/A EPS Additional Links: View AAIF on Google FinanceView AAIF on Yahoo FinanceView AAIF's Company Profile on ReutersSearch for Aberdeen Asian Income Fund Ltd. on Google