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Sudden Cardiac Death in Adult Congenital Heart DiseaseClinical Perspective
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Background—Sudden cardiac death (SCD) is a major cause of mortality in adults with congenital heart disease (CHD). The aim of this study was to determine the adult CHD population at risk of SCD and the clinical parameters associated with SCD.
Methods and Results—We performed a multicenter case-control study. Patients who died suddenly as a result of proven or presumed arrhythmia were included (cases). For each case, 2 controls matched on diagnosis, type of surgical intervention, age, and gender were included. From 3 databases including 25 790 adults with CHD, 1189 deaths (5%) were identified, of whom 213 patients (19%) died suddenly. Arrhythmic death occurred in 171 of 1189 patients. The underlying cardiac lesions were mild, moderate, and severe CHD in 12%, 33%, and 55% of the SCD cases, respectively. Clinical variables associated with SCD were supraventricular tachycardia (odds ratio [OR], 3.5; 95% confidence interval [CI], 1.5–7.9; P=0.004), moderate to severe systemic ventricular dysfunction (OR, 3.4; 95% CI, 1.1–10.4; P=0.034), moderate to severe subpulmonary ventricular dysfunction (OR, 3.4; 95% CI, 1.1–10.2; P=0.030), increased QRS duration (OR, 1.34 [per 10-ms increase]; 95% CI, 1.10–1.34; P=0.008), and QT dispersion (OR, 1.22 [per 10-ms increase]; 95% CI, 1.22–1.48; P=0.008).
Conclusions—The clinical parameters found to be associated with SCD in adults with a broad spectrum of CHD, including systemic right ventricles, are similar to those in ischemic heart disease. Moreover, even those patients with mild cardiac lesions are potentially at risk for SCD. This highlights the need for further prospective studies as well as vigilant ongoing follow-up of the adult with CHD.
Sudden cardiac death (SCD) accounts for 15% of total mortality and 5.6% of annual mortality in the Unites States, and the vast majority is due to fatal arrhythmia. Similar event rates have also been reported in Europe. Approximately 70% of SCD cases are attributable to coronary heart disease and 10% to acquired or hereditary cardiac diseases.1–3 In patients with ischemic and nonischemic cardiomyopathy, left ventricular ejection fraction (EF) ≤35% is the most important predictor of SCD, and implantable cardioverter-defibrillator (ICD) therapy has been proven to be effective in primary and secondary prevention of SCD in these patients.4,5 Similarly, in adults with congenital heart disease (CHD), SCD is a prominent cause of death (19–26%).6,7 During the past few decades, life expectancy has remarkably improved in CHD as a result of better surgical and interventional techniques.8,9 The annual incidence of SCD in the entire CHD population is relatively low (0.09%/y) but much higher than in age-matched controls. When applied to adults with CHD in the United States and Canada, ≈765 and 90 SCD events will occur annually, respectively.10,11 Additionally, because the majority of infants born with CHD will now survive into adulthood, the prevalence of SCD will steadily increase. Adults with repaired tetralogy of Fallot (TOF) and/or Mustard or Senning repair for complete transposition of the great arteries (TGA) have been studied previously, and several potential risk factors for SCD have been identified.12–15 Unfortunately, the predictive value of these risk factors is relatively low, and it is uncertain whether these proposed risk factors are relevant to other forms of CHD. Moreover, because the CHD population is growing and aging, the risk profile for SCD may have changed. Therefore, we performed a multicenter case-control study to investigate patients with various types of CHD who died suddenly. Our primary objective was to define clinical parameters associated with SCD. We studied the cause of SCD in this population and determined the circumstances under which SCD occurred.
Clinical Perspective on p 1954
Study Design and Population
This was an international, retrospective, case-control study of adults (aged ≥18 years) with CHD and proven or presumed arrhythmic death. Cases were defined as adult CHD patients with SCD, and controls were alive adult CHD patients without SCD. Patients with moderate or severe heart failure were not excluded. Those patients with nonarrhythmic causes of sudden death were excluded. For each SCD case, 2 control patients who were alive were matched to (1) age (plus or minus 5 years of corresponding SCD case); (2) gender; (3) diagnosis; (4) type of surgical intervention (eg, prior shunt, palliative or corrective surgery, valve replacements); (5) date of surgical repair (within 5 years of corresponding SCD case); and (6) center (when available). Cases and controls were recruited from the CONCOR (CONgenital CORvitia) database, the Toronto Congenital Cardiac Centre for Adults, and the University Hospital Leuven. CONCOR is a Dutch registry of adults with CHD since 2001 and included 11 535 patients.16 The Toronto Congenital Cardiac Centre for Adults serves as the adult continuity clinic in Toronto for CHD in Ontario, Canada, and all consecutive patients seen in the clinic have been entered into a database since 1980. This database contains ≈8000 adults with CHD. University Hospital Leuven registered ≈6255 adults with CHD since 1970. Data collection was completed in March 2011.
SCD is historically defined as (1) death due to cardiovascular causes within 1 hour of onset or significant worsening of the symptoms or (2) unwitnessed death during sleep. In this study, SCD included (1) proven or documented arrhythmic death (instantaneous death with documented ventricular fibrillation [VF] or ventricular tachycardia [VT]); (2) arrhythmic death by exclusion (instantaneous death or circumstances compatible with SCD, without severe disease that would lead to death soon and in the absence of a nonarrhythmic cause of death at autopsy); and (3) arrhythmic death by default (abrupt loss of consciousness and disappearance of pulse but no further data).17
Data Collection
Information about circumstances of SCD, location, cardiopulmonary resuscitation, or autopsy was collected from general practitioners, relatives, hospitals involved in follow-up, and ambulance care in the region. On the basis of this information, the actual or probable cause of SCD was determined. Medical records were reviewed, and the most recent data before the event were obtained and compared with data on controls at the same time frame. The median time between last outpatient or clinical visit and death was 4 months for the SCD cases (25th percentile, 1 month; 75th percentile, 9 months), and the median time since last outpatient or clinical visit was 2 months for the controls (25th percentile, 0 months; 75th percentile, 12 months). The complexity of the congenital defect was classified as mild, moderate, and complex.18 Eisenmenger syndrome was defined as the presence of systemic pulmonary arterial pressures or high pulmonary vascular resistance with reversed or bidirectional shunts or in a single ventricle through a large defect between the systemic and pulmonary circulation at ventricular, atrial, or aortopulmonary levels.19 All patients were considered to have contraindications for cardiac surgery because of high pulmonary vascular resistance. Patients with progressive or severe pulmonary hypertension after surgical repair of defects were not considered to have Eisenmenger syndrome.
Arrhythmias were classified according to the American College of Cardiology/American Heart Association/European Society of Cardiology guidelines.20 Arrhythmic symptoms included palpitations or (pre)syncope. Rhythm (spontaneous or paced), RR interval, QRS duration, QT interval, and QT dispersion were analyzed manually from standard (25 mm/s and 1 mV/cm) 12-lead ECGs. Moreover, investigators examining the ECGs were blinded to case status. Ventricular paced rhythms for both SCDs and controls were compared. Heart failure symptoms included decreased exercise tolerance, dyspnea, and peripheral edema. Chest x-rays were studied for cardiomegaly (defined as cardiothoracic ratio >50%) and redistribution of the pulmonary flow. Ventricular function was assessed by 2-dimensional echocardiography and classified as normal (EF ≥50%) or mildly (EF, 40%–49%), moderately (EF, 30%–39%), and severely (EF <30%) impaired. Because the aorta does not always arise from the morphological left ventricle, we classified the ventricles as systemic and subpulmonary throughout the article instead of as left and right ventricles. Left ventricular enlargement was defined as end-diastolic diameter ≥60 mm. Right ventricular size was qualitatively assessed as normal or enlarged from the echocardiography reports. Valvular dysfunction was graded as absent or mild, moderate, and severe from continuous wave Doppler tracings and Doppler color flow mapping.21
Statistical Analysis
Data analyses were performed with SPSS software for Windows (18.0 for Windows; SPSS Inc, Chicago, IL). For all analyses, 2-tailed P values <0.05 were considered statistically significant. Descriptive statistics for nominal data were expressed in absolute numbers and percentages. After normality was confirmed, mean values and SDs were calculated for normally distributed continuous variables. When frequencies and means were compared, the χ2 test and Student t test were used, respectively. To identify clinical parameters associated with SCD, univariate and stepwise multivariate conditional logistic regression models were used. Variables with P values ≤0.10 in univariate analyses were considered in multivariate models (backward stepwise; entry threshold, P=0.05; removal threshold, P=0.10). Holter monitoring and exercise tests were lacking in more than half of the cases and were therefore excluded from the multivariate analysis. The clinical parameters associated with SCD among the different CHD conditions were also assessed. In the present study, no multivariate analysis was performed because of the small number of cases in each underlying CHD condition. Results were reported as odds ratios (ORs) with 95% confidence intervals (CIs).
Overall, 1189 of 25 790 adults (5%) died, of whom 213 died suddenly (19%). The causes of sudden death were proven or presumed arrhythmia in 171 (80%), aortic dissection or aneurysm rupture in 19 (9%), cerebrovascular accident in 8 (4%), pulmonary embolism/hemorrhage in 8 (4%), myocardial infarction in 4 (2%), and upper gastrointestinal bleeding in 3 patients (1%). Patients who died from a nonarrhythmic cause of sudden death were excluded from further analysis. Of the remaining 171 SCDs, 131 (77%) experienced an out-of-hospital cardiac arrest, and cardiopulmonary resuscitation was performed in 84%. One hundred eighteen events (69%) occurred at rest, 19 (11%) during sleep, and only 17 (10%) during exercise. No information was available regarding the circumstances at time of cardiovascular collapse in 17 patients (10%). Autopsy reports were available for 38 SCD cases (22%) and showed known clinical cardiac defects only, with no explanation for sudden death other than a fatal arrhythmia. Rhythm documentation at the time of event was available for 37 patients (22%) and showed VF in 23 (62%), VT in 4 (11%), combined VT/VF in 4 (11%), supraventricular tachycardia (SVT) in 3 (8%), and bradyarrhythmia in 3 (8%) patients.
Characteristics of SCD Cases Versus Controls
The underlying cardiac lesions were mild, moderate, and severe CHD in 12%, 33%, and 55% of the SCD cases, respectively. The more specific underlying cardiac defects of the 171 SCDs are shown in Figure 1. Characteristics of SCD cases versus controls are summarized in Table 1. For 165 SCDs, 310 suitable control patients were identified. For 20 SCDs we were able to find only 1 control patient, and for 6 SCDs we were able to find none. These 6 SCDs were excluded from further analyses. SCD cases were more often in a worse functional class (24% versus 5%; P<0.005) than controls and subsequently were more likely to be using heart failure drugs (42% versus 14%; P<0.001). Both SVTs (40% versus 25%; P=0.001) and nonsustained VT (15% versus 9%; P=0.032) occurred more frequently in SCD cases than in controls, and antiarrhythmic medication was also used more frequently (24% versus 12%; P=0.001). Amiodarone was the most frequently prescribed drug for SCD cases (65%), followed by sotalol (20%). In contrast, controls used sotalol (46%) more frequently than amiodarone (38%). Table 2 shows the clinical parameters of the SCD cases and controls.
Clinical Parameters Associated With Sudden Arrhythmic Death
Univariate and multivariate analyses are summarized in Table 3. Clinical parameters associated with SCD in multivariate analysis were documented SVTs (OR, 3.5; 95% CI, 1.5–7.9; P=0.004), QRS duration (OR, 1.34 [per 10-ms increase]; 95% CI, 1.10–1.34; P=0.008), QT dispersion (OR, 1.22 [per 10-ms increase]; 95% CI, 1.22–1.48; P=0.008), moderately to severely impaired systemic ventricular function (OR, 3.4; 95% CI, 1.1–10.4; P=0.034), and moderately to severely impaired subpulmonary ventricular function (OR, 3.4; 95% CI, 1.1–10.2; P=0.030). Neither heart failure symptoms, worse New York Heart Association functional class, nor documented ventricular arrhythmias and antiarrhythmic medication altered the risk of SCD. Cardiac surgery with subsequent ventriculotomy with myocardial scar was not found as a specific risk factor for SCD because this was a matching criterion for controls.
SVTs were more common in the SCD cases before death than in controls. SVT was documented during cardiopulmonary resuscitation in 3 patients. Patient 1 had a repaired TOF, accessory pathway, and atrial tachycardia and used propafenone for his arrhythmias. This patient also showed pauses of >2.1 seconds during Holter monitoring but did not have any protection for bradycardia. Patient 2 had a univentricular heart and documented nonsustained VTs and SVTs but used only digoxin for arrhythmia management. Patient 3 also had a univentricular heart but without documented arrhythmias or antiarrhythmic medication use in the patient's history. Given these data, we are not able to draw any firm conclusions with respect to drugs used to control SVT resulting in unprotected bradycardia leading to VT or VF or ischemia and SCD.
Figure 2A depicts the QRS duration and Figure 2B depicts the QT dispersion in individual SCD cases and controls (with ventricular pacing excluded). Mean QRS duration was significantly longer in SCD cases than in controls (129±30 versus 114±25 ms; P=0.001). A complete right bundle-branch block was present in 34% versus 23% of SCD cases and controls, respectively. Even when these patients were eliminated from the analysis, mean QRS duration was still significantly increased in SCD cases compared with controls (P=0.007). A complete left bundle-branch block was rare in SCD cases and controls (4% versus 1%). In patients with ventricular paced rhythms (25 SCD cases and 39 controls), the mean QRS duration in SCD cases (177±29) and controls (188±34) was not significantly different (P=0.161). QT dispersion was increased (≥70 ms) in 50% of SCD cases and in only 16% of controls (P<0.001). Figures 3 and 4 show that mean QRS duration and QT dispersion were greater in SCD cases than in controls regardless of ventricular function.
We also analyzed the patients with proven SCD (n=37) and presumed (n=128) SCD separately. The determinants for SCD were the same in proven and presumed SCDs.
Clinical Parameters Associated With Sudden Arrhythmic Death Among Various CHD Conditions
Table 4 summarizes the statistically significant factors associated with SCD among the various cardiac conditions in univariate analysis. Results of exercise testing and 24-hour Holter monitoring, of which the majority were performed in TOF and (congenitally corrected) TGA patients, were not associated with the risk of SCD. Figure 5 shows the age at time of death according to underlying cardiac defects. Overall, 33 SCD cases (58% male) had Eisenmenger syndrome. Eisenmenger syndrome resulted predominantly from septal defects (58%) and univentricular heart physiology (27%).
The underlying cardiac defects were complete TGA in 18 SCD cases (70% male) and congenitally corrected TGA in 12 patients. Fifteen of the 18 complete TGA patients (83%) were treated with Mustard or Senning repair, 2 with an arterial switch procedure (11%), and 1 with a Rastelli procedure (1%). Seven of the 18 complete TGA patients (39%) also had repaired ventricular septal defect. Nine of the 12 congenitally corrected TGA patients (75%) had associated cardiac defects (7 with ventricular septal defect and pulmonary stenosis and 2 with Ebstein-like malformation of the tricuspid valve). Of these, 6 patients were treated with ventricular septal defect closure and 5 also with a left ventricular–to–pulmonary artery conduit. After surgical repair, 27 of the 30 SCD cases with complete TGA or congenitally corrected TGA (90%) had a systemic right ventricle.
Overall, 26 patients with SCD (69% male) had surgically repaired TOF, of whom 12 had a previous palliative shunt (46%). Surgical repair took place at a mean age of 12±14 years, and pulmonary valve replacement with a homograft was performed in 31% of the patients during follow-up. Four of 26 TOF patients had complete atrioventricular block requiring permanent pacemakers in the late postoperative period. A history of complete atrioventricular block was not associated with the risk of SCD (P=0.439).
Left-sided outflow tract lesions were present in 21 SCD cases. These included isolated aortic valve stenosis (n=9; mean age, 33±8 years), isolated bicuspid aortic valve (n=5; mean age, 46±23 years), and coarctation of the aorta (n=7; mean age, 35±18 years). All coarctation of the aorta cases were complex; 5 had bicuspid aortic valve, and 2 had ventricular septal defect. Overall, 18 of 21 patients had undergone surgery for severe aortic valve stenosis. The incidence of moderate to severe aortic valve stenosis was similar for SCD cases and controls. In this subgroup, no clinical variables associated with SCD were found.
Nineteen SCD cases (11%) had septal defects, including atrial septal defect (n=8), ventricular septal defect (n=9), and atrioventricular septal defect (n=2). Thirteen patients had surgical closure, and 4 patients had percutaneous closure of the defect. Only 2 patients (1 atrial septal defect, 1 ventricular septal defect) were untreated because their shunt was not hemodynamically relevant. Patients with atrial septal defect were older (mean age, 60±21 years) than patients with a ventricular septal defect or atrioventricular septal defect (mean age, 29±8 years), and 2 of them had documented coronary artery disease. Postoperative atrioventricular block was present in 3 SCD cases and was not associated with SCD. Moderately to severely impaired systemic ventricular function and subpulmonary ventricular function were present in 18% and 1% of SCD cases and controls, respectively.
Overall, 25 SCD cases had a cyanotic cardiac condition without Eisenmenger physiology, of which 7 were palliated with a Fontan procedure (4%; 86% male). There was no significant difference in baseline characteristics and clinical parameters between SCD cases and controls with a Fontan procedure. Of the remaining 18 cyanotic SCD cases (11%; 61% female), 7 were palliated with an aortopulmonary shunt and 3 with a bidirectional cavopulmonary anastomosis.
To the best of our knowledge, this is the largest international study investigating the circumstances of SCD in adults with CHD. This study defines clinical parameters associated with SCD in a large cohort of adults with CHD and among various cardiac defects. The majority of patients were male and died suddenly at rest; only 10% died during active physical exertion. The rhythm most often recorded at time of sudden cardiac arrest was VF. Not only were adults with severe cardiac conditions at risk of SCD but also adults with less complex CHD such as septal defects and left ventricular outflow tract obstruction. Clinical parameters independently associated with SCD were documented prior SVTs (predominantly atrial flutter or fibrillation), increased QRS duration, QT dispersion, and moderately to severely impaired systolic function of the systemic and/or subpulmonary ventricle. The clinical variables associated with SCD differed among the various underlying cardiac defects.
Ventricular Dysfunction
The relationship between left ventricular systolic dysfunction and death due to heart failure and ventricular arrhythmias in patients with ischemic heart disease is well established.22,23 This study shows that systemic ventricular dysfunction is associated with SCD in a general CHD population, particularly in adults with (congenitally corrected) TGA, cyanotic patients with or without Eisenmenger physiology, and surgically repaired TOF patients. Published results of the predictive value of systemic ventricular dysfunction in repaired TGA are conflicting.24,25 In the present study, impaired systolic function of the systemic and subpulmonary ventricle was associated with SCD in Eisenmenger syndrome patients and surgically repaired TOF patients. In one of the largest cohorts of subjects with Eisenmenger syndrome (n=171), impaired ventricular function, neither systemic nor subpulmonary, was predictive of death. In that study, 20 patients died, of whom 11 died suddenly.26 The association of impaired systolic function of the systemic and subpulmonary ventricle with SCD has been described earlier in TOF patients.14 Left ventricular dysfunction in TOF may be explained in part by older age at repair with longer periods of volume overload and chronic hypoxemia, right ventricular dysfunction leading to left ventricular dysfunction, and regurgitation of the aortic or mitral valve. However, further studies are needed to identify the exact mechanism of left ventricular dysfunction in these patients.
In this study, none of the SCD cases with moderately to severely impaired systemic ventricular function who may have been considered at "high risk" of SCD received an ICD for primary prevention of SCD. This may be attributable in part to the era in which these deaths occurred. Secondary ICD prophylaxis for SCD via the transvenous route has been available since the mid-1990s, and the benefit of primary prophylaxis for SCD was appreciated with the publication of the results of the Multicenter Automatic Defibrillator Implantation Trial (MADIT)4 and the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT)27 over the past decade. The lack of evidence-based criteria for prophylactic ICD implantation in CHD may explain in part the conservative approach to ICD implantation in more recent years. Left ventricular EF <35% is a powerful prognostic factor and indication for ICD therapy in adults with ischemic and dilated cardiomyopathy. In CHD, the right ventricle is often impaired and might create an arrhythmogenic substrate. In this study, left or right ventricular dysfunction was associated with an at least 3-fold increased risk of SCD. Therefore, ICD therapy should be considered in adults with CHD and an at least moderately impaired ventricular function after elimination of reversible causes of ventricular dysfunction.
In this study, one fifth of the SCD cases had pacemaker implantation for complete atrioventricular block. Chronic right ventricular pacing may contribute to left ventricular dysfunction. One might speculate that biventricular pacing may improve ventricular function and prevent SCD in CHD.
QRS Duration and QT Dispersion
Increased QRS duration is associated with an increased risk of all-cause mortality and SCD in patients with ischemic cardiomyopathy.28 In adults with CHD, an association between QRS duration and SCD was reported in patients with TOF, TGA, and Eisenmenger syndrome.12,13,26 Although QRS duration was significantly increased in SCD cases, we were not able to demonstrate an association between QRS duration and SCD in TOF and TGA, which might be explained by the low number of SCDs in these subgroups.
In healthy control subjects, QT dispersion ranges from 10 to 70 ms. However, overlaps in values between healthy controls and cardiac patients or between patients with and without adverse outcome have been reported.29 Prognostic information on QT dispersion in CHD is limited.30 In this study, increased QT dispersion was associated with SCD and was above the upper normal limit in 50% of SCD cases. The QT dispersion was within the normal range in the majority of controls (84%).
Documented Arrhythmias
In the present study, atrial flutter or fibrillation was associated with SCD, especially in patients with TGA and TOF. This association has been described earlier in patients with TGA but not in those with TOF.13 Further studies are needed to clarify whether atrial tachyarrhythmias are a surrogate marker for SCD or a consequence of ventricular dysfunction. Documented nonsustained VTs were uncommon in SCD cases (18%) and not associated with SCD. Antiarrhythmic drugs were used more often by the SCD cases than controls because arrhythmias were more often present in SCD cases. One might speculate that lack of back-up pacing in these patients might have been a contributing factor, with bradycardia-induced ventricular arrhythmias leading to SCD.
Sudden Arrhythmic Death in Septal Defects
Although repaired septal defects are considered benign and ventricular arrhythmias or SCDs have been reported as uncommon,31 in the present cohort, 11% of SCD cases had septal defects (89% were closed). The few untreated septal defects were not hemodynamically relevant. Patients with atrial septal defect repair were older, and potentially coronary artery disease rather than CHD might have been the cause of SCD. Almost half of the SCD cases with ventricular septal defect/atrioventricular septal defect had pacemaker insertion for complete atrioventricular block, and the remaining cases had associated cardiac anomalies.
Study Limitations
This study has limitations inherent to any retrospective study. Data collection was limited to data in medical records. Rhythm documentation at the time of event or autopsy reports was not available for all SCD cases, and thus it is not possible to ascertain that their deaths were solely arrhythmic in nature. On the other hand, the actual incidence of SCD might have been underestimated because of the strict definitions applied in this study. Data on syncope were lacking in the majority of the SCD cases and could therefore not be used for risk stratification. Patients were retrieved from 3 databases with different inclusion periods, which precluded determination of the annual incidence rate of SCD in the general CHD population. Moreover, the prognosis of patients and thus the incidence of SCD might have been influenced by changes in treatment recommendations during the study period. Assessment of ventricular function may be challenging in CHD because of abnormal ventricular geometry. Cardiac magnetic resonance imaging is more accurate in measuring EF in some cardiac lesions (eg, the systemic right ventricle). Unfortunately, quantification of ventricular EF by cardiac magnetic resonance imaging was frequently lacking in this study, in which case qualitative data were used. Furthermore, a cutoff value for pulmonary arterial blood pressure to define Eisenmenger syndrome was not used in this study. The number of patients among the various cardiac defects was small, and therefore multivariate analyses were not performed for these subgroups. A prospective analysis of the risk factors reported here would be preferable but is extremely difficult to achieve because of the low incidence of SCD and the heterogeneity within the CHD population.
We have identified several clinical parameters associated with SCD in adults with a broad spectrum of CHD including systemic right ventricles. These parameters may be helpful for identifying high-risk patients and may guide clinicians in their treatment strategy. The identified clinical parameters are similar to the risk factors for SCD in ischemic cardiomyopathy and include documented SVTs, impaired ventricular function, increased QRS duration, and prolonged QT dispersion. It is important to be aware that SCD occurs at a relatively young age in patients with CHD. The treating cardiologist should focus on preserving ventricular function as a means of reducing the risk of SCD. Reversible causes of ventricular dysfunction should also be treated at a young age. Although patients with repaired cyanotic and left-sided outflow lesions have previously been identified as at risk for SCD, this study reveals that a broader spectrum of adults with CHD, even those with cardiac lesions traditionally considered mild, are potentially at risk for SCD. This highlights the need for further prospective studies as well as vigilant ongoing follow-up of the adult with CHD.
Sources of Funding
Dr de Groot is supported by the Netherlands Heart Foundation (grant 2009T021). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the article apart from those disclosed. No writing assistance was utilized in the production of this manuscript.
Continuing medical education (CME) credit is available for this article. Go to http://cme.ahajournals.org to take the quiz.
- Received March 9, 2012.
- Accepted September 7, 2012.
- © 2012 American Heart Association, Inc.
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- 31.↵
Clinical Perspective
Sudden cardiac death (SCD) is a major cause of mortality in adults with congenital heart disease (CHD). As this population ages, the population at risk and the risk factors associated with SCD may be changing. Therefore, we conducted a multicenter case-control study to determine the adult CHD population at risk of SCD and the clinical parameters associated with SCD. From 3 databases including 25 790 adults with CHD, 1189 deaths (5%) were identified, of which 213 patients (19%) died suddenly. The cause of sudden death was proven or presumed arrhythmia in 171 of 1189 patients (14%; 64% male; mean age, 36±15 years). Most cases of SCD occurred at rest (69%) or during sleep (11%). The underlying cardiac lesions were mild, moderate, and severe CHD in 12%, 33%, and 55% of the SCD cases, respectively. We have identified several clinical parameters associated with SCD in adults with CHD that may be helpful in identifying high-risk patients and may guide clinicians in their treatment strategy. The identified clinical parameters are similar to the risk factors for SCD in ischemic cardiomyopathy and include documented supraventricular tachycardias, impaired ventricular function, prolonged QRS duration, and increased QT dispersion. Although patients with repaired cyanotic and left-sided outflow tract lesions have been identified previously as at risk for SCD, this study reveals that a broader spectrum of adults with CHD, even those with cardiac lesions traditionally considered mild, are potentially at risk for SCD. This highlights the need for further prospective studies as well as vigilant ongoing follow-up of the adult with CHD.
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- Sudden Cardiac Death in Adult Congenital Heart DiseaseClinical PerspectiveZeliha Koyak, Louise Harris, Joris R. de Groot, Candice K. Silversides, Erwin N. Oechslin, Berto J. Bouma, Werner Budts, Aeilko H. Zwinderman, Isabelle C. Van Gelder and Barbara J.M. MulderCirculation. 2012;126:1944-1954, originally published October 15, 2012https://doi.org/10.1161/CIRCULATIONAHA.112.104786
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- Sudden Cardiac Death in Adult Congenital Heart DiseaseClinical PerspectiveZeliha Koyak, Louise Harris, Joris R. de Groot, Candice K. Silversides, Erwin N. Oechslin, Berto J. Bouma, Werner Budts, Aeilko H. Zwinderman, Isabelle C. Van Gelder and Barbara J.M. MulderCirculation. 2012;126:1944-1954, originally published October 15, 2012https://doi.org/10.1161/CIRCULATIONAHA.112.104786


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Project management project
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A fair amount of my time has been spent writing computer program how-tos for my mom in the hopes of nurturing her e-commerce independence. I thought it may be a good idea to post only slightly modified versions of these tutorials, or as I call them, "cutetorials," here for all the world to see. There are most likely superior Photoshop and Cafepress tutorials discoverable with the help of the great Google god, but this seems to work well for my mom - a woman who seems fairly intimidated by computers. Enjoy.
P.S. I will do a secondary edit of this post at a later date, to make up for any gaps in logic. My apologies for any inconvenience in the meantime.
How to use Photoshop Elements to prepare a scanned image for Cafepress.
First you will need to go to the CafePress website to find out the required size of the image for your calendar/mug/etc. Later, you will upload your edited image to CafePress
The login page is located here: https://www.cafepress.com/cp/members/login.aspx?passthru=yes
Login Name: firstname.lastname@example.com
Pasword: pass1234
Click on "Your Shop Name"
Click on "Manage Sections and Products"
Click on "A section your daughter already made for you, probably Ginger the Gopher"
Now click on whichever product you would like to create a new image for. For the sake of our cutetorial, let's use the pre-made calendar. So, click on "Ginger the Gopher Calendar Print."
On the middle-left part of the page, you should see "Image Guidelines." They should look something like this:
Image Guidelines
11 x 8.5 in. Full BleedH: 11.5 x 9 in. (trimmed on calendar to 11 x 8.5 in.)
DPI: 150 minimum
These are the specifications we will use in Photoshop Elements.
Go to Photoshop Elements and click on "File" then "New" then "Blank File."
Change the "Width" to be measured in "inches" instead of "pixels." Do the same for the "Height."
Now set the width and height to match the image guidelines you got from cafepress. In this case, it will be 11.5 x 9 inches. (The end product will be trimmed to 11 x 8.5.)
Change the "Resolution" to 200.
Click "OK"
Now go to "File" then "Save As" and name the file. Change the file format to ".PNG"
Now go to "File" then "Open" then choose to open the image you want to use for the product. (This is the image you scanned in earlier, or one that already exists on your computer.)
Now that you have both your new file and the image you want to edit open, click and hold the image you want to use, and drag it over to the window with the blank Photoshop file. It should drop the image you want to use into the formerly blank file.
Now we get to adjust the image.
If the image is facing the wrong direction, you can rotate it until it is aligned properly. To do this, go to "Image" then "Rotate" then rotate it using the tools they provide until it looks okay.
As an alternative (but this is not required), you can put your mouse button very very close to the outline of the new image – then the mouse arrow should become a little arc with two points. If you hold down the left mouse button when this little arc pops up, you can drag the mouse around and rotate the picture (keeping the mouse button pushed the whole time). If you hold the "Shift" key while doing this, the image will snap into place in increments of about 30 degrees.
Now we should resize the image.
At each of the corners of the image is a little tiny box. Click on one of the tiny boxes and drag (hold down the mouse button as you drag). This will let you resize the image to fit the print area. You can also click on the image itself and drag it to move it around. When you have adjusted it to your liking, hit "Enter"
Now we should fix the rough edges:
If there are rough edges you need to delete, look to the lefthand menu in the Photoshop screen. It is the menu with little pictures of arrows and stars and Ts and such. These are your tools. Click on the box that looks like a rectangle with a white dashed line running around it. It should be the fourth button down from the top. Now create a rectangle around the area you would like to remove by clicking and dragging your mouse. This should make a small box. To finish removing the area, click the "Backspace" button on your keyboard. Make sure that you create a really looong rectangle – that goes all the way from one side of the picture to the other We prevent rough or jagged edges by making sure to go all the way across with our rectangle.
We can now fix the colors of the image in a few ways:
At the top of the screen go to "Enhance" then "Adjust Lighting" then "Brightness/Contrast." Fiddle with these settings until you find a balance you like. You can always click "Cancel" to undo any of your fiddling.
If these results aren't good enough, go to the top of the screen and select "Enhance" then "Adjust color" then "Adjust Hue/Saturation" or, if you feel like having some fun, "Replace Color." You can fiddle with those settings as much as you like. If you want more detailed instructions, give me a call and we can go over them on the phone. Don't be afraid to try them on your own – you can always click the "Cancel" or "Undo" buttons if you don't like the results.
Don't forget to zoom in and make sure there aren't any weird fuzzies or scratches on the picture.
You can zoom in by holding down the "Ctrl" key on your keyboard, then, while still holding that button down, push the "+" key. This should zoom you in. If this is too tricky, go to the menu at the top of the screen and click on "View" then "Zoom In" or "Zoom Out" respectively.
If there are little fuzzy or dusty-thing issues, we will use the clone stamp to fix them. The "Clone Stamp" button is in the lefthand menu we used earlier. It is in the lower half of that menu and is just above the pink eraser, and right below the bandaid. Here's a hint for the tools – if you let your mouse pointer hover (meaning not moving!) over each of the little tool buttons, in a few seconds, a little line of text will pop up, telling you the name of the tool!
Once you find it, click on the "Clone Stamp" button. Then zoom WAY in on the spot you want to fix. The closer up you get to it, the less any fiddling will show once we get the image to print. Now, find a good spot that you would like to essentially "copy" and "paste" over the spot that looks icky. Click on it and, at the same time, push the "Alt" key on your keyboard. This will copy the spot you want to use. Now drag (while holding down) the mouse button over the icky spot. Now release the mouse button. Next hold down the mouse button and drag again. Repeat. The icky spot should gradually begin to disappear, the more you repeat the dragging-and-clicking-then-release action. You can repeat this process with several different "good" spots to copy over the one "bad spot." The goal is to fiddle until you have something that look completely blended in with the surrounding area.
If the mouse button on the screen is too large or too small, you can adjust it. It is like switching out your current paintbrush with one of a different size.
Just under the menu at the top of the screen (the one that says things like "File" or "Image") is a second menu. There will be a small button that says, "Size." Next to size, it will say something like, "22 px." Next to "22 px" there will be a tiny little black arrow. Click on it. A slider bar will come up. Grab the rectangle in the slider bar to make the mouse button larger or smaller. Then hold the mouse button over the image to see if you like the new size. This works with a lot of the other tools as well.
If the area you copied contrasts too much with the area you are pasting it over, you can adjust the opacity of the copied part.
First we should undo the part that was too opaque. Go to the menu at the top of the screen and click on "Edit" then "Undo." You can click "Undo" several times until you have gotten rid of the problem. If you accidentally click "Undo" too many times, don't worry! Go back to "Edit" then click on "Redo." You're all set.
Go back up to the menu at the top. Just under the menu at the top is the area where you adjusted the clone stamp (mouse button) size. A few sections over to the right is "Opacity." Decrease the percentage of "opacity" to make the copied part more subtle when you are placing it over the icky part we want to cover up.
Now go back and cover up that pesky fuzzy spot.
If there are white rectangles around the image, we can now fill them in with a pretty color (if you want).
Make sure you are zoomed out so that you can see the whole image. On the lower right hand part of the screen there is a box called "Layers." Click on the layer that says, "Background."
Look over to the lefthand toolbar – go to the very bottom where there are two little boxes filled with color. Click on the one that says, "Set Foreground Color" on it when you let your mouse hover above it. This should be the leftmost color box. Now you can choose a color for the white spaces. There are two ways to do this.
Click on different areas of the painting itself. You will see the colors in the preview box of the color selector that popped up when you clicked on "Set Foreground Color." If you find one you like, click "OK."
You can also click around for colors in the color selector box. You can also adjust the color by clicking in different spots on the horizontal rainbow rectangle. When you find one you like, click "OK."
Now look over to the lefthand tool bar and find the "paint bucket" tool. This one is near the bottom, just above the rectangle that is rainbow colored and a few tools below the pink eraser. Click on the paint bucket tool. Now, take the tool and click once in the white part of the picture that you want to make a color. If you like it, great! If not, go and find a new color!
If the "Paint bucket" tool is misbehaving , one option is to go to the tools on the lefthand side and select the "Custom Shape Tool." This is also sometimes called the "rectangle tool." It will be whichever tool is just below the rainbow rectangle and just above the raindrop. Click on the button for the tool and hold down. This will open up a list of tools you can use. Select the rectangle tool. Now click and drag so that the rectangle complete covers up the white space. Make sure that it goes all the way from one edge to the other. This way it will look nice for press! If this doesn't work, give me a call!
Now we need to finish the file for uploading to cafepress.
Go to the menu at the top and click on "Layer." Then click on "Flatten Image." Now click on "Save" and make sure it has been saved as a ".PNG" file.
Now you can upload this to Cafepress! Yay!
Your tutorial for uploading to Cafepress is coming soon...


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Ever since I put my wardrobe on the Economy Diet, I haven't been able to update my look in my usual indulgent fashion. But I've learned that adding an accent piece to basics already in your closet can make a big difference. With that in mind, I've found a new appreciation for the accessories department at Target. I'm particularly in lurrrve with their fashion scarves. Spring doesn't always mean warm weather right away, and their lightweight scarves available in the season's hot, vibrant hues like lemon yellow will warm you up and rev up your look.
Nebraska Dobby Scarf, $16.99
Wednesday, February 18, 2009
A Sunny Outlook
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Monday, July 31, 2006
Old Misery Guts
There was a time when I'd enjoy being in these joyless, characterless shitholes. I'd enjoy meeting up with friends, enjoy a creamy headed pint of Guinness or five, enjoy the conversation, the catching up, the odd laugh.
And I'd also enjoy the goodbyes at 11.30 and the see you soons.
That was when friends were local.
Now, apart from the fact that beer is too belchy and voluminous for me, because friends aren't local, a night out is once in a blue moon and is followed by after hours drinks in front of the telly or stereo. And here I'm struggling.
I keep going because I always drink until the night peters out. So I'm drinking lager at 2.30 in the morning, outstaying my welcome, fed up with myself, fed up with other people, knowing I'm going to get four hours sleep, wanting my own comfortable bed 160 miles away, two hours ago. Wanting a belly nicely warmed with red wine rather than full to bursting with gassy beer.
I'm just not a social animal. I'm a good listener, yes. If you've got a story or ten to tell me, I'll listen and maybe even remember some of them the next day. You just won't get much out of me. The more I drink, the less able I am to tell my own stories. My vocabulary shrinks. I stop talking and carry on listening.
So when this carries on after midnight, I want my daddy to ring on the bell and take me home in his car. But my daddy's dead and he wouldn't be able to take me home if he was alive because if he was alive he'd be more pissed than me.
And he would've been drinking alone.
19 comments:
I found that pubs lost their appeal when I stopped smoking. Yeah, and none of my friends are local, either. What this really means is that I stopped making friends around the time that I stopped smoking. Or something.ReplyDelete
Rob - It used to be every Friday, Saturday, Sunday and Wednesday. Then it was every Friday and Saturday. Then every Saturday. Now once every three months. And that feels like too much. No wonder I'm losing what friends I had. I think I'd rather pop round for a cup of tea but it's a bloody long way to go for a cup of tea.ReplyDelete
Dick - At parties I'd just stand still and wait for people to come to me. They never did. Which was for the best for everybody.
I know what you mean about pubs. Even if you're going to a dive of a boozer you still have "get ready" as it were and booze is loads cheaper from the offie.ReplyDelete
I don't mind parties (I go for the kitchen myself) but the one I can't stand (and is making me feel funny as I type this) is large gatherings. For example a birthday meal in Pizza Express or something. *shudder*
I enjoy the company of people who don't really want to be in other peoples' company. Because we all understand that it's okay if there are long pauses in the conversation. And we understand that not everyone is "on" all the time. And that if one or more of us is quiet that evening, there's not necessarily something wrong with them.ReplyDelete
A 'Good listener' is hard to find. That's why we blog. I used to be in the pub every single night of my life. Then I realised I was listening to bores, talking rubbish and being too scared to leave first.ReplyDelete
New Years eve is the worst time. I just long for an early night to avoid all the sociable drunks.
Btw, instead of dredging this one up from a couple of weeks back I'll do it here: we had the British Acoustic Festival just down the road last weekend. Apparently Sandi Thom was originally booked to appear but my step-daughter says that she pulled out because she's now had a number 1 and got a bit big for it.ReplyDelete
Here's a few of the folk off the running order:
Steve Harley, Paul Jones and the Blues Band, The Stranglers, Glenn Tilbrook, The Animals,Dennis Lacorriere from Dr Hook, Hayseed Dixie, Ezio, Chumbawumba, Elkie Brooks, Mike Peters, Roddy Radiation and Pauline Black. How many did she sell?
I'm thinking it's probably not the SAME Animals it used to be. At least one of them's dead, and another lives in California.ReplyDelete
Mine's a small JD, on its own please (no ice); and a glass of water on the side. I find that does my digestion no end of good.
Pint of cooking lager for me please...ReplyDelete


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Dec 30, 2007
The raging throat plague of death
Case in point: The Raging Throat Plague of Death. It starts with the typical itchy-throat, sneezing, congestion symptoms. Then it moves on to stabbing pain in the larynx, extremely irritated/swollen bronchial passages, uncontrollable coughing that causes more stabbage in the larynx area, and then when the fever pitch of the illness passes,you're left with a deluge of awful goo to somehow rid yourself of,mostly through mintues-long, uncontrollable bouts of coughing.
Do I sound like I'm whining? Well, I am. I'm so glad I'm almost done with this... what a nasty bug it was. I can't remember having been ill like this, at least, not in a long time. It will be nice to be able to be a normal, 9-month-pregnant woman again and not a bedridden, 9-months-pregnant-woman who cannot do much more than keep the kids from stabbing each other with blunt paintbrush ends, barely keep up with the dishes(forget the laundry, I have an everest of clean clothes awaiting folding in my bedroom) and serve PBJ's and grapes for every meal.
The saddest thing of all,though.... Skywalker's coming down with it now. As we speak, he's lying in the middle of the floor, listening to itunes on his headphones, his head propped up on a santa-claus hat. It doesn't look very comfortable. I'll have to offer him my pillow in just a second.
At any rate, this illness is going around. Everyone's getting it—the two- week chest cold. Called, by the way, bronchiolitis(or, conversely, RSV if contracted by a baby). This worries me... we'll have to keep our newborn close and out of contact with the public for a while. And hopefully Skywalker's two- week bout will be over by the time I deliver... maybe a small prayer or two would be good.
Thanks for listening to my whining.
6 comments:
I feel for you. Really, I do. Back "in the day" when I was having my babies, we didn't know quite as much as we do now about how medications could hurt a fetus so expectant mothers (in ignorance) took whatever was available to get rid of the bugs and viruses or whatever. Although it's probably no comfort to you at the moment, remember that "This too shall pass."
- December 30, 2007 6:44 PM
- Lucy Stern said...
Boy, that is no fun!! Whenever I get a cough, it seems to linger for about a month....I hope all of this is over when you deliver. Keep taking your natural remedies and get well. The olive leaf is really good for getting rid of a cough. It works for me.
- December 31, 2007 10:05 AM
- Janell said...
Whining would be bemoaning a simple sniffle. This plague of death sounds absolutely miserable! Miserable!
I hope everyone feels better soon.
- December 31, 2007 11:06 AM
- NoSurfGirl said...
LOl, thank you Janell! You sure know how to be sympathetic! Lucy-- I didn't do olive leaf this time... I think i forgot and then was too lazy to get to the HF store. But I think I'll go get some today. Marla, thanks for the reminder... going on 3 weeks I sort of forget what it feels like to feel well. :)
- December 31, 2007 3:05 PM
- maren said...
Not fun at all. We are all just recovering ourselves. Glad to be on the recovery end of things.
Happy New Year!!!!
- January 01, 2008 7:13 AM
- Sherpa said...
Oy, no fun. My sympathies. This sounds like the cold I'm just giving over. Hopefully, this virus moves on by the time the baby is here.
- January 01, 2008 4:06 PM


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Purchase this article with an account.
Anthony N. Kuo, Ryan P. McNabb, Francesco LaRocca, Sina Farsiu, Joseph A. Izatt; Distributed Scan SDOCT for Post Refractive Surgery Corneal Power Measurement. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3632.
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© ARVO (1962-2015); The Authors (2016-present)
Anterior segment tomographic imaging offers the ability to optically characterize the cornea without the limitations inherent to topographic imaging. This is especially important in corneas that have been surgically altered by laser refractive surgery and which no longer maintain the topographic assumptions. Spectral domain optical coherence tomography (SDOCT) offers the highest axial resolution of the clinically available tomographic imaging systems. However, due to its sequential imaging nature, SDOCT volumes of the cornea can be affected by motion artifacts. To mitigate these motion artifacts, we previously developed Distributed Scan SDOCT (DSOCT). In DSOCT, patient motion is encoded into high spatial frequencies by high-speed distribution of individual A-scans across the cornea; the motion artifacts can then be filtered . In previous work, we found DSOCT to be comparable to existing clinical imaging in determining corneal power in normal corneas. In this study, we examined the ability of DSOCT to characterize the corneal power in eyes after laser refractive surgery.
Under an IRB approved protocol, subjects undergoing myopic LASIK had corneal imaging prior to and 3 months after surgery. The corneal imaging consisted of DSOCT, topography, and Scheimpflug photography. DSOCT used a commercial SDOCT system with =840nm, Δ=50nm, 10 kHz A-scan rate and a telecentric scanner in the sample arm (Bioptigen; RTP, NC). The portable telecentric scanner was mounted on a modified slit-lamp base with a chin and forehead rest for subject stability. A custom waveform was applied to the galvanometer scanners for high-speed distribution of A-scans across the central 6mm of the subject's cornea. The change in pre to post-operative corneal powers obtained from the three imaging modalities was then compared to the manifest refraction change.
6 eyes of 5 subjects were imaged. The mean spherical equivalent pre-operative refraction was -3.75 D ± 1.49 D; the mean spherical equivalent post-operative change in refraction was 3.14 D ± 1.60 D.The mean differences between the clinical refractive power change and that reported by the imaging modalities was 0.19 D ± 0.51 D (DSOCT), 0.55 D ± 0.61 D (topography), and 0.32 D ± 0.46 D (Scheimpflug photography).
Compared with topography and Scheimpflug photography, distributed scan SDOCT potentially better reflects the change in corneal refractive power after LASIK. However, there is similar variability in the comparison of DSOCT measurements to refractive change with respect to the other imaging modalities.
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Only five teams, including defenders BMW Oracle and challengers of record Mascalzone Latino, have committed to the event which is due to kick off next June with a series of preliminary regattas in smaller versions of the official America's Cup 72ft wing-masted catamarans.
Each was due to stump up a sequence of entry fees and performance bonds amounting to £2.6 million by next July but, following a meeting of existing and potential competitors, the event organisers, America's Cup Racing Management, reduced those payments to just £710,000 in total.
They also gave teams another five months to make those payments in recognition of the difficult economic climate which is said to be preventing campaigns from raising the necessary sponsorships funds, said to be at least £15 million a year.
Other changes to the protocol include concessions on the amount of equipment that ACRM will ship to regattas on behalf of competitors and extra time for teams to share knowledge on designing their AC72s and building them, all of which should result in reduced costs.
"These changes are designed to allow the teams to put their initial investments into building their teams and boats," said Iain Murray, regatta director for the 34th America's Cup and head of ACRM.
"Our target when we opened entries was that we would be delighted to have eight, we would be ecstatic to have 10 and we would be doubly ecstatic if we got 12.
"With the changes I have announced about the protocol, we are expecting entries six to eight to follow quite quickly."
An announcement is expected on Dec 31 confirming the venue.
Attempts to sell the event to the authorities in San Francisco where wealthy BMW Oracle boss Larry Ellison is based have been received coolly, resulting in a lower than expected hosting offer.
Efforts to sell it into Newport Rhode Island or even Europe are now gaining ground.


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Brand Label: Givenchy Beauty
Available for Purchase Online at Barneys New York for $62.00Pin It
The ideal creamy texture to help dry skin rediscover its radiance. Enriched with SWC® and a nourishing cocktail of ingredients (shea butter, luffa oil and a derivative of jojoba oil), this ideal creamy texture helps dry skin regain its radiance. Rich Luminescence Moisturizing Cream offers a cocoon of comfort to very dry skin thanks to the Sparkling Water Complex® (SWC®) with its dual "light moisturizing" and "light energizing" technology that adds "the effervescence of sparkling water" in the skin for a dazzling light effect. This generous cream gently soothes skin that easily pulls and becomes irritated. Nourished and moisturized, the skin recovers its supple appearance, its velvety feel and its radiant appearance. Nourished and moisturized, the skin recovers its suppleness, its velvety feel comfort and is illuminated with new radiance. After removing all traces of make-up, apply morning and/or evening to the face and neck in gentle upward movements. Dry Skin. 1.7 fl oz/50ml.
Shop other brand label items from Givenchy Beauty on FashionStylist.com.
This item was published for sale online by Barneys New York on July 29, 2017 1:21 am and last updated by us June 4, 2018 3:05 pm.
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No.. I wish.
But I am graduating with a first class cgpa :)
Not to boast or anything (pffttt..) but I have been holding my #1 rank in my class standings for my entire degree. I have also tried really hard to graduate with a 3.75 cgpa, but a 3.7 is good enough for me.
To be honest, I'm not a smart student. In high school, I was an average student, sometimes below average. I never scored all A's, nor did I do well in my final exam. But when I entered university, I was finally studying something I was interested in and I started to take more effort.
Throughout the 4 years, I have never been late for a submission, unless it is a group assignment (we all know how mishaps happen in group assignments). I made sure to take my work seriously, and I actually studied for exams (which I rarely did in my final years at high school.)
On top of that, God has always been there to help me out. No relational problems, or personal issues ever came between me and my studies. God made sure of it. I'm also pretty sure he helped me with my assignments and my exams; by being my inspiration and expanding my memory bank.
Though I may not be receiving any awards, but the greater reward that I got from the end of my studying phase, is the knowledge that God has the ability to create success and lighten burdens.
Besides, what better satisfaction is there than knowing you made it, and you made it excellently.
I have definitely learnt more than just theories and practicality in the course that I studied; I have learnt to trust God more, and to push through tough times. I have learned about determination, focus, and will power.
University was more than head and hand knowledge, it was also heart knowledge.
Now moving on towards a new phase in life, it may seem big and scary, but from all the heart knowledge I have learned, I know I can overcome and achieve my dreams.
Nothing is ever too hard with God and passion :)


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I *finally* got back my Holga pictures that I left at Wolf Camera. Remember how it took 2 months to get the ones back from Wal-Mart? These didn't take 2 months but they cost me an obscene amount of money to get them developed and put on a disc. This development trip cost me more money than the actual camera. Thanks for the heads up Wolf Camera. Needless to say, I will be investigating cheaper ways to develop my Holga pics. Regardless of how expensive they were, I love them. Here are a few from the two rolls. [The photos are actually square but Blogger doesn't like to reflect that. No matter how hard I try.]
[port at Cayman. that's our snorkel guide]
[beach club dock]


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Tuesday, November 11, 2014
Awesome Jumper Lady
This ^ horse was a total boss today over fences with lots witnesses to verify our sane jumping-ness. The extra EXTRA short reins are working, we had a great jump school today. It was so nice to be able to ride in the daylight during the week and with warm temps. Another wonderful day. :)
If you're getting sick of the "EVERYTHING IS WONDERFUL!!Q11!" posts, feel free to change the channel. I'm blogging the shit out of this stuff, man.
Posted by War Horse at 9:19 PM
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In case you are searching for short term rentals in Bamako, Mali you have come to the right place. We have designed this webpage to make it easy as possible for you to find a suitable and affordable accommodation in this city.
There are many fully-furnished short stay rentals in Bamako, Mali available via this page. We have a varied selection of temporary accommodations in Bamako which can cater to every budget and vacation style so we're sure that you won't have any problems finding a suitable apartment to stay in this city.
Another great thing is that all of the vacation rentals in Bamako are owned by friendly local people who will be happy to help you have a great experience during your stay in Bamako. Those who plan on visiting this city on their own would do well to check out the private rooms in Bamako, Mali as that way they will have enough space and comfort for an affordable price.
We also have luxurious private apartments for rent in Bamako, Mali, available via this page. They are located on the banks of the Niger River which flows through the city centre allowing for a great view of the surrounding area and gives you an opportunity to experience life in the downtown of the city.
For those who plan on bringing a larger group of friends with them, there are entire houses for rent in Bamako, Mali. These temporary rentals has several bedrooms and can accommodate large groups of travelers that came in Bamako for a few days.
Also, you can count on many amenities to make your stay an even more enjoyable experience and the rental you opt for will determine which amenities you will have at your disposal. As we said all available studios are advertised by owners.
Local people lease their properties in Bamako to travelers which is great because you'll have a chance to meet some locals. You can find cheap condos in Bamako in almost each part of the city, so if you are traveling for a business purpose or just want to explore Mali, you'll be able to rent an apartment near any place which is important to you.
About Bamako
Bamako is the largest city and capital of Mali, boasting a population of 1.8 million people and branded as the fastest growing city in Africa. It is situated on the Niger River close to the rapids which divide the upper and middle Niger valleys. Local industry relies mostly on processed meat, metal goods, textiles and there is also commercial fishing on the Niger River. The city got its name from the Bambara word which means "Crocodile river".


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Busy today, so briefly...
I'll cover the first three (of five!) stories together today...
1) VIOLENT DISORDER - As violent disorder spread across London and other parts of the UK, we ask: Why are our cities on fire and our youth engaged in civil disorder?
2) FIGHTING THE RIOTERS - It's said that we're a nation of shop keepers and it's small shops and businesses which have been burned and looted. But now a group of shop owners are saying they will not be defeated. Find out more in this video from the Guardian.
3) ARMY - The leader of Croydon Council has called for the army to be brought in
I was perhaps a little dismissive of the riots yesterday, but fortunately I am far enough away to not be directly affected by what is going on. However, we have two family members living in north London, and we are anxious for their safety. My thoughts go out to everybody who has been hurt, made homeless or lost property. Action obviously needs to be taken, not just by the police but by the residents of these areas. Somebody must know who the rioters are. I know what I would do but, and like you, I have no influence on what happens.
It is good to see that item 2 uses the word "rioters". The BBC has been rightly criticised for referring to the participants as "protesters" yet it was not made clear what they were protesting about. The Daily Telegraph covers this here http://www.telegraph.co.uk/culture/tvandradio/bbc/8690267/London-riots-BBC-criticised-for-branding-thugs-as-protesters.html. Is this the BBC's own version of political correctness gone mad? Next...
4) BURIED ALIVE - A 15 year old girl is buried alive on the beach after digging a tunnel in the sand : Good to read that she survived. Banning the digging of holes on sandy beaches is surely the only answer. Or maybe not. Next...
5) NANCY WAKE - Resistance fighter Nancy Wake dies at the age of 98. She fought the Nazis with her bare hands. Was your granny a war hero? : Sorry, but no. They were both heroines.
Welcome to my blog! I listen to Radio 2 all day but I absolutely hate The Jeremy Vine Show. On most days I send Jeremy an email explaining why his show is irrelevant to me and why I will not be listening. This blog is a record of those emails, which I hope you will enjoy. IMPORTANT NOTE : I do not hate Jeremy Vine, only his radio show. My communications with him have always been respectful of each other's viewpoint, and I thank him for that.
Please click here for more information about who I am and why I do this.
The text shown after 1), 2), 3) and 4) is copied exactly from the BBC's daily JV Show web page and I acknowledge their copyright of this text.
The "Find out more..." links to web pages referred to by the JV Show web page are available by clicking on the text following 1), 2), 3) and 4).
"Find out more..." text is only included here when it refers to a non-BBC web page link.
You can follow my occasional postings on Twitter at @JVineBlogMan although @TheJeremyVine has blocked me from following him.
I am subject to the BBC's "expedited complaints handling process" (meaning I'll be ignored) for two years from 25/01/12.
Tuesday, 9 August 2011
Today's show 09/08/11
1 comment:
crikey, JV goes on holiday and it all kicks off. Seriously 'tho, we could do with a few more Nancy Wakes at the moment
- 9 August 2011 at 12:01
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Dear Diary:
I am weak with anticipation of the upcoming trip home to Seattle, and on to Ohio for the Truth For Life weekend. And yet, I have misgivings. Will I be given a bath before I go–I haven't bathed since Israel, and that was 2007.Will I be stuffed in a sack and left somewhere to ponder my fate while The Others go to the conference? Will I have a place at the table?
I am hopeful, but not unwise. I have been disappointed before.
More later, I hear her coming.
NOTE: I found a copy of "Little Ida's Flowers," a story by Hans Christian Anderson, here. It *does* remind one of me, yes? http://hca.gilead.org.il/li_ida_f.html


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Download Angry Birds Star Wars Mod APk for android. New update with version 1.2.2 Unlimited purchase.
Rebel birds, striking from a hidden base, have won their first victory against the evil Imperial Pigs. During the battle, Rebel spies managed to steal secret plans to the Empire's ultimate weapon, the PIG STAR, and are racing to deliver the plans to the Rebel Birds. Now they need your help!
Join an epic adventure with the Angry Birds in the legendary Star Wars™ universe! Use the Force, wield your lightsaber, and blast away Pigtroopers on an intergalactic journey from the deserts of Tatooine to the depths of the Pig Star -- where you'll face off against the terrifying Darth Vader, Dark Lord of the Pigs! Can you become a Jedi Master and restore freedom to the galaxy?
Version: 1.2.2 mod free Shopping
Size: 49 MB
Required android: 2.2 and up
Playstore Link: https://play.google.com/com.rovio.angrybirdsstarwars
Playstore Link: https://play.google.com/com.rovio.angrybirdsstarwars
Instruction: install apk and play
Download Zippy Link:
Thanx for your visited..Take around and see another games or application for your droid.
Please share my little blog to your friends at facebook,twitter,or google +..im very appreciate with it.:)
Come back tomorrow and see new application and amazing games


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Wednesday, September 10, 2008
Family Photos
We had BM's picture taken at a photography shop specializing in babies (not mentioning the name on purpose). We paid way too much for pictures that we didn't even like and felt obligated to sign up for a "special package."
Later that evening, while we were at the Box Elder Fair, I was drawn into a booth that was covered in adorable pictures. I talked to the photographer, Amanda Laing, and got her card. I was blown away with her quality work and affordable prices.
Early Saturday morning, the entire Halhouse and UnderRoos gang met at the Ogden Union Station for a photo shoot. We had a blast! The kids cooperated at various times but I love how Amanda captured it all. I am so happy that we found someone who not only has a gift for photography but also makes her prices affordable. I love her, love her, love her!
You're getting a sneak peak at possible Christmas cards.
Check out her blog http://www.amandalaingphotography.blogspot.com
13 comments:
- Mike and Gin said...
Jennie! Your pics are too cute! I love love love your red peep toe shoes! Can't wait for the X-mas card!
- September 10, 2008 at 7:21 PM
- Jamie said...
What beautiful pictures! Your photographer is a great find.
- September 10, 2008 at 8:25 PM
- megan said...
Adorable pictures!
- September 10, 2008 at 9:11 PM
- KT said...
love them!
- September 10, 2008 at 9:21 PM
- Greg & Torrey said...
the pictures are beautiful... max is adorable! loving your darker hair, you're lookin' ssssssexy! and your rack looks incredible. i'm sure both baby and hubby are in heaven. love you.
- September 10, 2008 at 10:43 PM
- Grandma Beaner said...
I love every single photo!! I especially love Grandma Reta's red hair and BM's cute hat. You're all just too precious. Hugs from Utah's Dixie.
- September 10, 2008 at 11:07 PM
- The Idahoans said...
I love the pictures they are so cute! I especially liked the one of BM with the hat it is adorable- he is adorable!!
- September 11, 2008 at 10:34 AM
- Jenny said...
really cute pics. I love them all.
- September 11, 2008 at 1:26 PM
- Brittany said...
I love them!!! You little boy is a little man now!!!!!! He is growing so fast!!
- September 13, 2008 at 9:19 PM
- k8 said...
oh i loooove these! family photos are my favorite.
- September 16, 2008 at 3:25 PM
- Tupea said...
This is Luisa- Mounu's sister. I'm loving your fam pics! You guys looks so good esp your adorable little boy. Since you raved about your photographer and I was looking to do some, I'm going to see if she can do ours when we are there next month.
- September 17, 2008 at 7:49 PM
- porterpies said...
Those pictures turned out beatifully!
- September 26, 2008 at 3:11 PM
- Shauna said...
What awesome pictures! You are such an adorable family! Thanks for sharing :)
- October 11, 2008 at 9:00 PM


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Wednesday, September 1, 2010
I can't wait to get my hands on this issue. I like to get 2 copies for my stash. I have stitched so many ornaments out of these over the years.
For about 4 or 5 years I was involved in a swap based on this issue. I have at least a dozen kits based on the last few years. The exchange has gone away and I really missed it this year. I have been trying to work on getting them stitched up. I have finished all my kits from the 2004 issue, now I am working on the 2005 issue. I am struggling with the Handwork ornament that I have been working on. The piece of linen is hardly big enough. I am also raiding my stash for floss. Hopefully I will have an updated pic this weekend.
I have EGA tomorrow night. The group is continuing the mystery band sampler. I will try and snap a picture tomorrow. Right now I am not attempting to stitch the piece, I am just collecting the chart. It will be great seeing everyone since I missed last month due to my surgery. I am looking forward to seeing what everyone has been stitching.
Well, I am going to try and stitch a little.
Good Night.
5 comments:
- Andrea said...
My friend and I were at the LNS today and I reserved my copy. Then, when we got back to our homes later in the afternoon, there was a message on our voice mail, the issue was in! So now we have to go back...bummer, lol!
Anyway, it's always an exciting time, can't wait to see this years ornaments!
- September 1, 2010 at 6:41 PM
- Myra said...
I love the JCS ornament issue too Chris. I was just looking at my 2008 and 2009 issues last night. They are dog eared I have looked at them so many times. I think I am going to order mine online as it takes forever for the bookstore at the mall to get it in. I can hardly wait to see the beauties in it this year.
Have fun at EGA!
- September 1, 2010 at 7:25 PM
- robindefender said...
I'm counting on Mom to let me 'borrow' her issue. Hopefully, she'll get hers soon. You should start your own ornament exchange! I'll bet lots of folks would enjoy participating (insert devilish smile here).
- September 2, 2010 at 4:49 AM
- Carol said...
I know what you mean, Chris! I always look forward to the latest JCS ornament issue. I usually order mine through 123 Stitch because they will notify you via email as soon as they're ready to ship... Hope this issue is a good one)
- September 2, 2010 at 7:21 AM
- Beth said...
Like you, I can't wait for the ornament issue! It's so much fun and a year's worth of projects too!
- September 2, 2010 at 8:36 PM


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Artist's description:
This is one of my series of "West Country Harbour" paintings. It is painted in gouache on a prepared stretched canvas, and varnished. The painting continues around the sides of the canvas. It is signed with my initials, and features my "trademark" seagull. It is ready to hang or can be framed.
Size 30X25 cm
Materials used:
canvas, gouache, pencil
Sunlit Harbour (2017)
Gouache painting by Linda Bartlett
$118.42 Sold
- Gouache painting on Canvas
- One of a kind artwork
- Size: 9.84 x 11.81 x 0.79 in (unframed) / 9.84 x 11.81 in (actual image size)
- Signed on the front
- Style: Naive
- Subject: Landscapes, sea and sky
This artwork is sold by LInda Bartlett from United Kingdom


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Proposal to make Silverless Street one-way in move to stop damaging juggernauts
The latest incident involving a juggernaut taking a short cut along Silverless Street resulted in damage to the lower roofing of Dormy House - a listed building - as its driver tried to turn out into Kingsbury Street.
This has intensified moves to prevent these mammoth trucks obeying their satnavs and travelling down unsuitably narrow streets to avoid the traffic build-up at the war memorial roundabout - as Marlborough News Online has reported.
Marlborough Town Council's planning committee (September 21) has endorsed a plan to try and solve the problem by making Silverless Street a one-way street - with no entry from the Herd Street/Barn Street/St Martins crossroads.
This had been raised at the Community Area Transport Group and Councillor Fogg said it was 'the only solution on offer': "Wiltshire Council Highways have said they'll review the issue - which means they'll do nothing. It's only a matter of time before something severe happens."
"The one-way solution is not ideal, but as an alternative to catastrophe, that's all we've got."
Councillors also wanted Wiltshire Council to remove the out of scale 'Unsuitable for HGV' sign that is supposed to catch the eye truck drivers coming from the High Street up Kingsbury Street and deter them from turning into Silverless Street.
It was also announced that Wiltshire Council is about review the request made by the Town Council to put an HGV weight limit on George Lane. It was pointed out that this would have to be waived whenever the High Street was closed for Mop Fairs and other events. This request was made - with others across the Marlborough area - in 2007-2008.
With timescales like this it might take sometime for the one-way order to come through the Wiltshire Council decision-making system.


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Monday, January 18, 2010
growing old
posted for Carry on Tuesdays
9 comments:
- Larry said...
Shame on you and I hope your wife catches you too. no wonder there aren't any posts here.
For My Wife
- January 18, 2010 at 8:59 PM
- linda may said...
Hahahaha. Good for you, when you find the right formula I want some too.
- January 19, 2010 at 3:35 AM
- sg beatty said...
Larry..... I am shameless but I love the power of words and the ability to say something that isn't obvious.
Linda....I believe the right formula is what we are doing. Putting life to words is creating the fountain of youth.
- January 19, 2010 at 8:01 AM
- madeline d. murray said...
I'm with you, Old Grizz. Flip that script! (But I hear your wife's gone and got herself a boy-toy.) Great post.
- January 19, 2010 at 9:15 AM
- Andy Sewina said...
Yeah, yeah, yeah! What was the address of that mail-order bride, again?
- January 19, 2010 at 2:57 PM
- Stan Ski said...
Growing young sounds good to me.
- January 19, 2010 at 3:39 PM
- sg beatty said...
madeline - I wondered where she has been lately. thanks for the tip. Now he gets to rub her feet.
- January 20, 2010 at 6:20 AM
- sg beatty said...
andy -00I812 Vodka Lane, Siberia
- January 20, 2010 at 6:22 AM
- sg beatty said...
stan - we can do it together. It will be the same as when went ot High School together. We can giggle and laugh and dream about old ladies growing young with us.
- January 20, 2010 at 6:25 AM


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Now I will admit that I am an organized person. I'm efficient and hardworking. But this place gets to be a mess. I'm betting everybody's place gets to be a mess sometimes.
Here's an example from today. I took my three lovies to the grocery store. We are blessed to live in the land of Wegmans, and one store close by actually has a free childcare service called WKids. So we dropped off my son, and I proceeded to shop with my two-year-old daughter in the cart and my new-baby-daughter strapped to me. She cried on and off while we navigated the produce section. I was steering with one hand and holding a binkie in her mouth with my other hand. I earned a lot of graces as numerous people passed me and thought "God bless that poor woman!" I know people were thinking that because several of my fellow shoppers commented on how I had my hands full. And I thought it was funny because usually there's a super-lively three-year-old boy in tow. But I didn't want to brag.
I digress.
We got home and the baby started to cry. So I started chucking bags full of groceries into the fridge and freezer. Bags, not items, I mean plastic grocery bags full of yogurts, butter, and cheeses. I had to leave the rest of the stuff on the floor and then keep a really good ear on my two-year-old to make sure she wasn't getting into anything dangerous (e.g. plastic bags) while I fed the baby.
Are you getting an image of this mess? On the floor are crushed up leaves, shoes, groceries, empty bags, a diaper bag, and my purse. The fridge is booby-trapped with plastic bags of food that I'll have to put away later.
So I'm feeding the baby, reading Little Pig Robinson to my son, and listening to my daughter run around playing with all the groceries I left on the floor. I'm calling "Come out here! Mommy will read to you!" in my funnest voice. But she kept playing.
Then she got organized with a real game. Carry all of the groceries to the basement door and make a mountain of food. And then my son joined her.
So I sat back and enjoyed their happy giggles and mentally went through the things I had bought to think if there was anything there that would be destroyed (and fortunately there wasn't). At least I had a moment to sit quietly. They were so busy in their "naughtiness" that they weren't trying to kill each other, so that was good.
This was the end result.
So this house that is called "spotless" is actually a place of controlled chaos. If I know someone is coming over, I do a quick once over so things look picked up. But most of the time there is some sort of crazy thing like this going on. The perfection (and it's really not perfection, it's perceived perfection) is merely a facade.
When a friend looks at my house, she sees things picked up and clean. When I look at the same house I see blinds that need to be replaced, trim that needs a good scrub, hand prints on the windows, a closet that I need to clean out... There's the constant to-do list in my head. But it's in my head-not anyone else's.
So the point of this post is to say Relax. Every house with children has crazy messes. No one has it together. That's impossible. It's not like the groceries magically float themselves into the cupboards. It's not like there aren't dirty dishes and piles of clothes ready to be laundered.
Now, obviously there are times when things get really out of control. Sometimes for good reasons (e.g. a newborn, an injury) and sometimes for bad reasons (e.g. laziness). And we need to make sure things are sanitary. But I bet a lot of us are doing better than we think. The goal can not be to have a perfect home all the time. That's just ridiculous.
But I must admit, I wish it were that way. It's like in the Weezer song "Beverly Hills":
Look at all those movie stars
They're all so beautiful and clean
When the housemaids scrub the floors
They get the spaces in between
I do sing that quite often when I'm scrubbing. It's a nice idea. But I'll never have a housemaid.
We need to let ourselves off the hook. We can't let this desire for perfection steal our peace. It shouldn't keep us from playing with our kids or having enough energy to love our husbands. For me, the goal is controlled chaos.