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Pathophysiology and management of right heart ischemia
Author + information
- Received December 27, 2001
- Revision received April 26, 2002
- Accepted May 24, 2002
- Published online September 4, 2002.
Author Information
- ↵*Reprint requests and correspondence:
Dr. James A. Goldstein, Director, Research and Education, Division of Cardiology, William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, Michigan 48073, USA.
Acute right coronary artery occlusion proximal to the right ventricular (RV) branches results in right ventricular free wall dysfunction, exerting mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function decreases transpulmonary delivery of left ventricular (LV) preload, resulting in diminished cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction and septally mediated alterations in LV compliance, which are exacerbated by elevated intrapericardial pressure. Under these conditions, RV pressure generation and output are dependent on LV-septal contractile contributions, governed by both primary septal contraction and paradoxical septal motion. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling and performance, resulting in more severe hemodynamic compromise. Bradyarrhythmias limit output generated by the rate-dependent noncompliant ventricles. Hemodynamic compromise may respond to volume resuscitation and restoration of physiologic rhythm. Vasodilators and diuretics should generally be avoided. In some patients, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and recovers even after prolonged occlusion. The term RV "infarction" appears to be somewhat of a misnomer, for in most patients acute RV dysfunction represents ischemic but predominantly viable myocardium. Although RV performance improves spontaneously even in the absence of reperfusion, recovery of function may be slow and associated with high in-hospital mortality. Reperfusion enhances recovery of RV performance and improves the clinical course and survival.
On the basis of early experimental studies of right ventricular (RV) performance, it was felt for many years that RV contraction was unimportant in maintenance of the circulation (1). However, recognition of the profound hemodynamic effects of RV systolic dysfunction became evident with the description of severe right ventricular infarction (RVI) (2–9). Significant RVI typically occurs in association with acute transmural inferior-posterior left ventricular (LV) myocardial infarction (MI), and the right coronary artery (RCA) is almost always the culprit vessel (3,7–13). Necropsy studies demonstrate pathologic evidence of RVI in 14% to 60% of patients dying of inferior MI (3,4), typically inscribing a "tripartite" pathologic signature consisting of LV inferior-posterior wall, septal, and posterior right ventricular free wall (RVFW) necrosis contiguous with the septum, with less frequent extension into the anterolateral RVFW (3). In patients with anterior MI, the RV apex may be infarcted, but the extent of RVFW involvement is small and clinically insignificant (4). It must be emphasized that these patterns of RVI are derived from autopsy studies and do not necessarily reflect the status of the right ventricle in the vast majority of patients who survive acute RV ischemic dysfunction.
Noninvasive studies demonstrate RV ischemic dysfunction characterized by RV dilatation and RVFW motion abnormalities in 40% to 50% of patients with acute inferior MI (6,11), although hemodynamic compromise develops in fewer than one-half of such cases. Patients with predominant severe RVI develop a distinct hemodynamic syndrome characterized by severe right heart failure, clear lungs, and low output despite intact global LV systolic function (2,5–9). Although in general the magnitude of hemodynamic derangements in patients with RVI is related to the extent of RVFW contraction abnormalities (7,8,9,11–13), some patients tolerate severe RV systolic dysfunction without hemodynamic compromise whereas others develop life-threatening low output, emphasizing that additional factors modulate the clinical expression of RVI.
Although acute ischemic RV dysfunction may result in hemodynamic compromise associated with higher in-hospital morbidity and mortality (12,14–17), most patients manifest spontaneous early hemodynamic improvement and later recovery of RV function, even in the absence of reperfusion of the infarct-related artery (7,18–21). In fact, chronic right heart failure attributable to RVI is rare (11). Thus, the term RV "infarction" is to an extent a misnomer, for in most cases acute RV ischemic dysfunction appears to represent viable myocardium. These responses are in marked contrast to the effects of ischemia on the left ventricle (22–25). This review will clarify the present understanding of fundamental issues regarding the pathophysiology, natural history, and clinical management of right heart ischemic dysfunction.
RV mechanics and oxygen supply-demand
Given that the right and left ventricles face dramatically different loading conditions, it should not be surprising that they differ markedly in their anatomy, mechanics, and metabolism. The left ventricle is a thick-walled bullet-shaped pressure pump ejecting into the high-resistance systemic arterial system. In contrast, the pyramidal-shaped right ventricle has a triangular base with a thin crescentic free wall and is designed as a volume pump, ejecting into the lower resistance pulmonary circulation. Under physiologic conditions, RV systolic pressure and flow are generated by RVFW shortening and contraction toward the septum from apex to outflow tract (26–28). The septum is an integral architectural and mechanical component of the RV chamber and, even under physiologic conditions, LV-septal contraction contributes to RV performance (26–28). The right ventricle has a more favorable oxygen supply-demand profile than the left ventricle. The RVFW has less myocardial mass and faces lower preload and afterload; therefore, RV oxygen demand is lower (29–31). Less oxygen extraction at rest also imparts to the right ventricle greater extraction reserve capabilities during stress (30). Right ventricular perfusion also is more favorable, in part because of a dual anatomic supply system whereby nearly one-third of RVFW flow is derived from left coronary branches (32,33). In addition, because the RVFW is thinner, develops lower systolic intramyocardial pressure, and faces less diastolic intracavitary pressure (29,31), it receives relatively homogeneous transmural perfusion in systole as well as diastole, both under physiologic conditions and with collateral perfusion during RCA occlusion. Furthermore, there is a comparatively greater likelihood of acute collateral development to the RCA (34–36), attributable in part to lower coronary resistance that favors a left-to-right transcoronary pressure gradient. The propensity for bridging ipsilaterals and the frequent presence of an independently arising conus branch further impart a greater anatomic reserve capacity for maintenance of perfusion.
Patterns of coronary compromise resulting in RVI
Although proximal RCA occlusion is accepted as the culprit commonly responsible for RVI (3,4,7–11), some patients with proximal occlusions develop minimal or no RVI ischemic dysfunction, whereas in others RVI develops in association with more distal occlusion. Furthermore, in those who develop RV ischemic involvement, the severity of RV dysfunction ranges broadly from mild RVFW contraction abnormalities to profound global depression of RV pump function. Recent observations from our laboratory have delineated the patterns of coronary compromise that determine the magnitude of RV ischemic dysfunction (12,13). In patients undergoing primary angioplasty for acute inferior-posterior MI, the RCA was the culprit vessel in all cases with RV ischemic dysfunction, the vast majority of whom showed proximal high-grade occlusion compromising flow to the major RV branches (Fig. 1). In contrast, patients without RVI tended to have more distal RCA lesions or circumflex culprits that spared RV branch perfusion (13). Although the proximity of the culprit lesion and its relationship to RVFW perfusion correlates with the presence or absence of RVI in most patients, there are exceptions in which proximal occlusions do not result in RV ischemic dysfunction, attributable in most cases to restoration of RVFW perfusion through prominent collaterals or spontaneous antegrade reperfusion. In the rare cases in which RV ischemic dysfunction occurs in association with culprit lesions distal to the major RV branches, RV branch flow is impaired by adjacent thrombus or RV branch stenosis. Occasionally, isolated RVI may develop from occlusion of a nondominant RCA (37) or selective compromise of RV branches during percutaneous coronary interventions (38).
Effects of RV systolic and diastolic dysfunction
The pathophysiologic mechanisms contributing to hemodynamic compromise with severe RVI are now well documented. In experimental animal models and in patients (9,12,34,35,39–45), proximal RCA occlusion compromises RVFW perfusion, resulting in RVFW dyskinesis and severely depressed global RV performance (Fig. 2), reflected in the RV waveform by a sluggish upstroke, depressed and broadened systolic peak, delayed relaxation phase, and markedly diminished RV stroke work (Figs. 3 and 4). ⇓⇓ Right ventricular systolic dysfunction diminishes transpulmonary delivery of LV preload, leading to decreased cardiac output despite intact LV contractility.
Biventricular diastolic dysfunction contributes to hemodynamic compromise associated with acute right heart ischemia (9,34,35,39–45). Depressed RV contractility results in RV dilation and ischemia intrinsically impairs RV relaxation. Therefore, the ischemic right ventricle is stiff and dilated early in diastole, resulting in increased impedance to initial RV inflow. As filling progresses, the noncompliant right ventricle ascends a steep pressure-volume curve, leading to a pattern of rapid diastolic pressure elevation. Right ventricular diastolic dysfunction adversely affects LV diastolic properties through diastolic interactions mediated by the reversed curved septum and exacerbated by elevated intrapericardial pressure (9,39–45). Acute RV dilation and elevated RV diastolic pressure shift the interventricular septum toward the volume-deprived left ventricle, thereby impairing LV compliance and further limiting LV filling. Abrupt RV dilation within the noncompliant pericardium leads to elevated intrapericardial pressure. The resultant pericardial constraint further impairs both RV and LV compliance and filling, both directly and by intensifying the adverse effects of diastolic ventricular interactions. Furthermore, as both ventricles fill and compete for space within the crowded pericardium, the effects of pericardial constraint contribute to the pattern of equalized diastolic pressures and RV "dip-and-plateau" characteristic of RVI (5,9,39).
The hemodynamic importance of abnormal RV compliance has been recognized in patients with significant RVI (2,5,6,9,46), who manifest distinctive alterations in right atrial (RA) waveform morphology, at one time thought to be characterized by a blunted X and prominent Y descent (5,46). However, given that progressive increments in diastolic impedance imposed by the stiff dilated right ventricle reduce inflow velocity across the tricuspid valve, a blunted rather than a rapid Y descent would be expected. In contrast to these previous interpretations, in experimental animal studies (34,35,43–45) and patients with severe RVI (9), when RA waveform components are timed to mechanical correlates rather than the electrocardiogram alone, the RA Y descent is blunted (Figs. 3 and 4), reflecting pandiastolic RV dysfunction.
Determinants of RV performance in severe RVI
Importance of systolic ventricular interactions
For many years it was felt that under conditions of loss of RV contraction, pulmonary flow could be generated by passive gradient from a distended systemic venous system and by active RA contraction. Experimental and clinical studies of acute severe RVFW dysfunction now demonstrate that despite the absence of RVFW motion, an active albeit depressed RV systolic waveform (Fig. 3) is generated by global LV-septal contractile contributions transmitted through systolic interactions mediated by the septum (9,34,35,43–45). The septum constitutes an important anatomic component of the RV chamber and even in normal hearts is responsible for one-third of RV stroke work (26–28). When RVFW contraction is depressed, RV systolic pressure is generated by primary septal contraction and through mechanical displacement of the septum into the RV cavity associated with paradoxical septal motion (Fig. 2). The systolic behavior of the septum is fundamentally influenced by the instantaneous trans-septal gradient, and under conditions of severe RVFW dysfunction, paradoxical septal motion reflects the development of an early left-to-right systolic trans-septal gradient because depressed RV contraction allows unopposed LV septal tension development (34,35,43–45). Global RV performance is influenced by the extent of mechanical disadvantage imposed by the ischemic dyskinetic RVFW (34,35,43–45). Dyssynergic segments must be stretched to their maximal systolic length before providing a stable buttress upon which actively contracting segments can generate effective stroke work. Dyssynergic segments in the left ventricle undergo passive systolic lengthening and thereby impose a mechanical disadvantage on nonischemic zones because of regional intraventricular interactions that diminish the contribution of the contracting regions to overall ejection (47,48). The ischemic dyskinetic RVFW behaves in an analogous manner, and must be stretched through interventricular interactions that reduce their contributions to both RV and LV performance (34,35,44,45). The critical compensatory contributions of LV-septal contraction to global RV systolic are emphasized by the deleterious effects of depressed LV septal function, which diminishes these compensatory systolic interactions, thereby further depressing both RV and LV performance (45). Not surprisingly, LV-septal contractile dysfunction exacerbates hemodynamic compromise associated with RVI. In contrast, inotropic stimulation enhances LV-septal contraction and thereby augments RV performance through augmented compensatory systolic interactions (45).
Compensatory role of augmented RA contraction
Augmented RA booster pump transport is an important compensatory mechanism that optimizes RV performance and thereby improves cardiac output (9,43–45). Under conditions of RVI attributable to occlusions compromising RV but sparing RA branches, RV diastolic dysfunction imposes increased preload and afterload on the right atrium, resulting in enhanced RA contractility reflected in the RA waveform as a "W" pattern characterized by a rapid upstroke and increased peak A-wave amplitude, sharp X descent reflecting enhanced atrial relaxation, and blunted Y descent owing to pandiastolic RV dysfunction (Fig. 3) (9,43–45). Conversely, more proximal RCA occlusions compromising the atrial as well as the RV branches result in ischemic depression of atrial function (9,43–45), manifesting as more severely elevated mean RA pressure and inscribing an "M" pattern in the RA waveform characterized by depressed A-wave and X descent, as well as blunted Y descent (Fig. 4). Under conditions of acute RV dysfunction, loss of augmented RA transport because of ischemic depression of atrial contractility or AV dyssynchrony precipitates more severe hemodynamic compromise (9,43,49). Right atrial dysfunction decreases RV filling, which impairs global RV systolic performance, thereby resulting in further decrements in LV preload and cardiac output. Interventions that augment ventricular filling reduce the extent of systolic lengthening in the dyskinetic zone and the magnitude of isovolumetric shortening in the nonischemic zone, reducing regional dyssynergy and thereby improving ventricular performance (34,35,44,45,47,48). Because the end-diastolic length-tension relationship is steeper in ischemic segments, such zones are especially sensitive to changes in filling in general and more dependent on atrial transport in particular (50,51). Thus, depression of RA contractility further impairs RV performance not only because of the absolute reduction in RV preload resulting from diminished atrial transport, but also because of the increased mechanical disadvantage imposed on the septum by the dyskinetic right ventricle (34,35,44,45). Venous return is inversely proportional to the instantaneous RA pressure, which is itself dependent on atrial compliance and relaxation (52,53). Augmented RA contractility, by enhancing atrial relaxation, facilitates atrial inflow (9,44,45,52,53). Conversely, depressed atrial performance impairs relaxation, an effect evident by a diminished X descent (9,44,45). These effects, together with abnormalities induced by ischemia on RA compliance directly, impede venous return to the preload-dependent right heart. Furthermore, the increased loading conditions imposed on the right atrium by the stiff dilated right ventricle increase atrial oxygen demand at a time when the compressive effects of increased intracavitary filling pressure tend to diminish transmural perfusion (9,44,45), thereby increasing the ischemic burden on the thin-walled atrium. Not surprisingly, ischemic atrial involvement is not rare, with autopsy studies documenting atrial infarction in up to 20% of cases of ventricular infarction, with RA involvement five times commoner than left (9,54,55).
Rhythm disorders and reflexes associated with RVI
High-grade atrioventricular (AV) block and bradycardia-hypotension without AV block commonly complicate inferior myocardial infarction (56–58) and have been attributed predominantly to the effects of AV nodal ischemia and cardioinhibitory (Bezold-Jarisch) reflexes arising from stimulation of vagal afferents in the ischemic LV inferoposterior wall (59–61). We and others have documented that in patients with acute RVI there is an increased incidence of high-grade AV block compared to those without right heart involvement (12,15,62–64). Recent observations from our laboratory now also document that bradycardia-hypotension without AV block is also more common in patients with RVI (65,66). Given that the AV nodal artery and branches to the inferoposterior LV wall typically arise distally from the dominant RCA, if reflexes arising from the ischemic LV alone or together with AV nodal ischemia were responsible for bradycardia-hypotension and high-grade AV block, then occlusions just proximal to the origin of the AV nodal and LV branches should result in an incidence of these phenomena no different from more proximal RCA occlusions resulting in RV and LV ischemia. Recent findings from our laboratory document that both bradycardia-hypotension and AV block are far more common in patients with proximal RCA occlusion inducing right heart and LV inferior-posterior ischemia, compared to more distal occlusions compromising LV perfusion but sparing the RV branches (65,66). These findings suggest that the ischemic right heart may also be a trigger for cardioinhibitory-vasodilator reflexes. Receptors and reflexes arising from the RV have received little attention. Although fewer in number, there are both myelinated and nonmyelinated nerves that terminate in the right ventricle, and some experimental studies suggest that RV afferents stimulated by RV distention can result in bradycardia-hypotension (67–69).
It is important to consider separately bradycardia-hypotension induced by RCA reperfusion. Following successful thrombolysis or primary angioplasty of the acutely occluded RCA, transient but profound bradycardia-hypotension may paradoxically develop in a patient whose rhythm and blood pressure were stable during occlusion (66,70,71). Based on its abrupt and transient nature, reperfusion induced bradycardia-hypotension appears to be reflex mediated and, based on recent findings, also appears to be more common with proximal versus distal RCA occlusions (65,66), suggesting a right heart mechanism.
Patients with RVI are prone to ventricular tachyarrhythmias (12,14–17,72). In-hospital ventricular tachycardia should not be unexpected, given that the ischemic RV is often massively dilated. Autonomic denervation in the peri-infarct area may also play a role (72). However, RVI is unlikely to portend late ventricular arrhythmias, as RV function tends to recover completely. Supraventricular tachycardias including atrial fibrillation may develop, attributable to atrial ischemia/infarction, distension, and elevated atrial pressures (73).
Natural history of RV ischemic dysfunction
Although RVI may result in profound acute hemodynamic effects, arrhythmias, and higher in-hospital mortality, many patients manifest spontaneous clinical improvement within 3 to 10 days regardless of the patency status of the infarct-related artery (7,19). Furthermore, global RV performance typically recovers over several weeks, with subsequent return of RV ejection fraction to near-normal levels within 3 to 12 months (18–20). Moreover, chronic unilateral right heart failure secondary to RVI is rare. This favorable natural history of RV performance is in marked contrast to the effects of coronary occlusion on segmental and global LV function (20–25). Observations from experimental animal studies document that the spontaneous recovery of RV function despite chronic RCA occlusion is attributable to the more favorable oxygen supply-demand characteristics of the RV in general and the beneficial effects of collaterals in particular (34,35). In a canine model of persistent RCA occlusion (34), we demonstrated that despite persistent RCA occlusion, collateral restoration of RCA perfusion facilitates complete recovery of RVFW function and global RV performance, with minimal infarction by gross and histologic analysis. Although most previous clinical studies of chronic RCA occlusion demonstrate that resting RV performance is preserved (18–20), other studies suggest that a significant subset of patients exhibit RV contraction abnormalities during stress (74,75). Until recently, no study of chronic RCA occlusion has analyzed the site of RCA occlusion relative to the nutritive RV branches or the presence of collaterals, nor documented and correlated with detailed angiographic data the response of the RV to stress. We have recently shown that in patients with chronic proximal RCA occlusion, RV function is typically maintained at rest and augments appropriately during stress (21). This dramatic spontaneous recovery of RV function and trivial infarction contrast sharply with the response of the left ventricle to equivalent ischemic insults (76–78). The relative resistance of the RVFW to infarction is undoubtedly attributable to more favorable oxygen supply-demand characteristics. In fact, in patients with acute inferior MI, preinfarction angina is an independent risk factor that predicts the absence of RVI (79), an effect likely mediated by the development of protective collaterals.
Effects of reperfusion on ischemic RV dysfunction
It thus appears that acute ischemic RV dysfunction is largely reversible. Nevertheless, acute RV ischemia contributes to early morbidity and mortality (9,14–16). Furthermore, spontaneous recovery of RV contractile function and hemodynamics may be slow. The salutary effects of timely reperfusion on myocardial function and infarct size in the ischemic left ventricle are well documented in both experimental models (76–78) and in patients (22–25,80–83). Given the more favorable oxygen supply-demand characteristics of the right ventricle and the strength of observations supporting the notion that the preponderance of acutely dysfunctional RV myocardium is viable, it would be expected that reperfusion (even late) could have salutary effects on recovery of RV function and clinical outcome. Observations from our laboratory in experimental animals (35) and in humans (12) now demonstrate the beneficial effects of reperfusion on recovery of RV performance. In experimental models, RCA occlusion results in depressed RVFW function and global RV performance (35). Reperfusion after 1 h of occlusion reperfusion leads to immediate improvement in RVFW function and consequently global RV performance, with prompt resolution of the pattern of equalized diastolic filling pressures and lesser reversed septal curvature, indicating diminished effects of hemodynamically adverse diastolic ventricular interactions. These effects contribute to enhanced LV filling and performance. Reperfusion after 4 to 8 h of ischemia also results in acute improvement in global RV performance, but to a lesser extent. However, even after prolonged ischemia, reperfusion results in striking, albeit slower, improvement in function over time with minimal RV infarction (35).
Until recently, there were scant clinical data regarding the effects on ischemic RV myocardium of interventions designed to achieve reperfusion. In recent studies of patients with RVI undergoing primary angioplasty (12), we have now documented that successful complete reperfusion of the main RCA and the major RV branches leads to immediate improvement in and later complete recovery of RVFW function and consequently global RV performance (Figs. 1 and 2). Most importantly, reperfusion-mediated recovery of RV performance is associated with excellent clinical outcome. In contrast, failure to restore flow to the major RV branches was associated with lack of recovery of RV performance and refractory hemodynamic compromise leading to high in-hospital mortality, even if flow was restored in the main RCA (Fig. 1). These findings emphasize not only the crucial relationship between reperfusion-mediated recovery of RV performance and clinical outcome, but documents for the first time the importance of RV branch reperfusion. Previous definitions have largely ignored the reperfusion status of the RV branches (24,25,81,82). The dramatic recovery of RVFW function and global RV performance contrasts sharply with the response of the left ventricle. Despite comparable degrees of initial regional dysfunction in the ischemic RVFW and inferior LV wall, in patients undergoing successful reperfusion the pace and extent of recovery of contraction in the left ventricle lags behind the right ventricle (12), undoubtedly related to oxygen supply-demand differences between the ventricles that influence resistance to ischemic damage (12,29–36).
Although evidence suggests that patients with inferior myocardial infarction benefit from timely thrombolytic reperfusion, the specific short- and long-term responses of the right ventricle have not been adequately evaluated. Some thrombolytic studies suggested that RV function improves only in patients in whom RCA patency is achieved (84–87), whereas others report little benefit (88,89). More recent prospective reports of patients with inferior MI undergoing thrombolytic therapy demonstrate that successful thrombolysis imparts survival benefit in those with RV involvement (90) and that failure to restore infarct related artery patency is associated with persistent RV dysfunction and increased mortality (90,91). Although successful thrombolysis appears to exert beneficial effects on RV function and mortality in patients with RVI, it is precisely such patients who may be resistant to fibrinolytic recanalization (89–92), due to proximal RCA occlusion with extensive clot burden which, together with impaired coronary delivery of fibrinolytic agents attributable to hypotension, leads to a higher incidence of primary thrombolytic failure in such patients. There also appears to be a higher incidence of reocclusion following thrombolysis of the RCA (89). In contrast, primary angioplasty is more likely to result in successful recanalization of the acutely occluded RCA (12,82,91) and has established salutary effects on RV performance and clinical outcome (12). Future controlled trials are needed to better define the role of thrombolysis in patients with RV infarction.
In aggregate, these results support the concept that, under conditions of ischemia and reperfusion, the right ventricle is more resilient than the left ventricle, consistent with the notion that RV "infarction" is to a great extent a misnomer, for the acutely ischemic dysfunctional right ventricle appears to represent predominantly viable myocardium which responds favorably to successful reperfusion, even late after the onset of occlusion (35).
Mechanical complications associated with RVI
Patients with acute RVI may suffer additional mechanical complications of acute infarction that may compound hemodynamic compromise and confound the clinical-hemodynamic picture. Ventricular septal rupture is a particularly disastrous complication, adding substantial overload stress to the ischemically dysfunctional right ventricle (93,94). As in other postinfarction myonecrotic septal ruptures, acute left-to-right shunting reduces effective forward LV output, precipitates pulmonary edema, and elevates pulmonary pressures and resistance. In aggregate, these effects exacerbate the RV dysfunction and low output associated with RVI. Surgical repair is imperative, but may be technically difficult. Furthermore, timing of repair, typically a challenging decision in the peri-infarction period, is further complicated in patients with RVI owing to RV dysfunction, which substantially increases the risks of any cardiac procedure and for which most surgeons prefer to wait to allow for recovery of RV performance, a luxury that may not be possible with acute septal rupture. Severe right heart dilation and diastolic pressure elevation associated with right heart ischemia may stretch open a patent foramen ovale, precipitating acute right-to-left shunting manifest as systemic hypoxemia or paradoxic emboli (95,96), which may resolve as right heart pressures diminish with recovery of RV performance, although some may require closure (97). Severe tricuspid regurgitation may also complicate RVI (98,99), developing as a result of primary papillary muscle ischemic dysfunction or rupture as well as secondary functional regurgitation attributable to severe RV and tricuspid valve annular dilation. Severe tricuspid regurgitation further impairs forward RV output and exaggerates right heart volume overload, thereby exacerbating low output, worsening systemic venous congestion and, owing to gross right heart dilation, impeding recovery of right heart performance. Although in most cases functional tricuspid regurgitation will improve as RV function recovers, some patients with severe papillary muscle dysfunction and dilated annulus require surgical repair, as do most with frank papillary muscle rupture.
Clinical presentations and evaluation
Although nearly 50% of patients with acute transmural inferior-posterior MI have ischemic RV involvement by echocardiography, RVI is often silent, as only 25% of patients overall develop clinically evident hemodynamic manifestations (6–8). Patients with inferior MI may initially present without evidence of hemodynamic compromise characteristic of RVI, but subsequently develop hypotension precipitated by preload reduction attributable to nitroglycerine (100) or associated with bradyarrhythmias (9,49,63,64). The physical exam provides important insights regarding the hemodynamic effects of RVI (101). Significant RV ischemic dysfunction results in increased mean RA pressure (>10 mm Hg), reflected as elevated jugular venous pressure (JVP). Pulsus paradoxus and Kussmaul sign have been reported in patients with RVI (101). Although the mechanisms underlying these phenomena in patients with RVI have not been delineated, they are likely related to the pericardial crowding and marked diastolic ventricular interactions evident in such patients. Under these conditions, it would not be unexpected that inspiratory augmentation of filling of the already distended right ventricle would intensify the adverse right-to-left septal mediated diastolic interactions, thereby resulting in respiratory oscillations of LV filling and output, resulting in pulsus paradoxus. In other cases, the stiff dilated right heart chambers, together with the effects of elevated intrapericardial pressure, may act to constrain the right heart such that inspiratory augmentation of right heart filling is blunted while venous return to the extrapericardial great veins is enhanced which, analogous to constrictive pericarditis, results in Kussmaul's sign (102).
Patients with severe RVI but preserved global LV function may be hemodynamically compensated, manifest by elevated JVP but clear lungs, normal systemic arterial pressure, and intact perfusion. When RVI leads to more severe hemodynamic compromise, systemic hypotension and hypoperfusion result. However, because LV preload is reduced, the lungs typically remain clear, even though LV filling pressure may be moderately elevated owing to adverse diastolic interactions. In patients with RVI and intact LV function, the carotid upstroke is intact but its volume is diminished. The precordial exam reveals an unimpressive LV impulse. Surprisingly, despite RV dilation, a RV heave is often not appreciated, likely owing to the constraining effects of the acutely noncompliant pericardium. Auscultation may reveal an RV S3 or S4 reflecting diastolic dysfunction. The presence of a holosystolic murmur suggests the development of ventricular septal rupture or tricuspid regurgitation. It is important to note that RVI may occur in the setting of global LV dysfunction, especially in patients with prior anterior myocardial infarction. In such cases, RVI may be masked by a presentation dominated by ischemic LV dysfunction characterized by low output and pulmonary congestion, with right heart failure ascribed to biventricular failure typical of ischemic cardiomyopathy.
Noninvasive and hemodynamic evaluation
The chest X-ray is not particularly helpful in detecting RVI. Although ST-segment elevation and loss of R-wave in the right-sided electrocardiographic leads (V3R and V4R) are sensitive indicators of the presence of RVI (15,90,103–105), they are not predictive of the magnitude of RV dysfunction or its hemodynamic impact. Two-dimensional echocardiography is the most effective tool for delineation of the presence and severity of RVI, demonstrating RVFW dysfunction and depression of global RV performance, the extent of RV dilation, and reversed septal curvature, which confirms the presence of significant adverse diastolic interactions, the degree of paradoxical septal motion indicative of compensatory systolic interactions, and the presence of severe RA enlargement that may indicate concomitant ischemic RA dysfunction and/or tricuspid regurgitation. Invasive hemodynamic assessment of the extent and severity of right heart ischemic involvement (Figs. 3 and 4) has been extensively discussed.
Therapeutic options for management of right heart ischemia follow directly from the pathophysiology discussed. Treatment modalities include: 1) restoration of physiologic rhythm; 2) optimization of ventricular preload; 3) optimization of oxygen supply and demand; 4) parenteral inotropic support for persistent hemodynamic compromise; 5) reperfusion; and 6) mechanical support with intra-aortic balloon counterpulsation and RV assist devices.
Optimization of rhythm
Patients with RVI are particularly prone to the adverse effects of bradyarrhythmias. The depressed ischemic right ventricle has a relatively fixed stroke volume, as does the preload-deprived left ventricle (9,34,35,44,45). Therefore, biventricular output is exquisitely heart-rate dependent, and bradycardia even in the absence of AV dyssynchrony may be deleterious to patients with RVI. Severe RV systolic and diastolic dysfunction limit RV stroke volume and render RV output rate-dependent; the left ventricle is also stiff and has limited stroke volume reserve attributable to reduced preload. Therefore, chronotropic competence is critical in patients with acute inferior MI and ischemic RV dysfunction. However, not only are such patients notoriously prone to reflex-mediated frank bradycardia, they often manifest a relative inability to increase sinus rate in response to low output, owing to excess vagal tone, ischemia, or pharmacologic agents. Given that the ischemic right ventricle is dependent on atrial transport, the loss of RA contraction due to AV dyssynchrony further exacerbates difficulties with RV filling and contributes to hemodynamic compromise (9,43,49). In addition, AV dyssynchrony may precipitate tricuspid regurgitation, a mechanical defect likely to be devastating to performance of the ischemic right ventricle. Although atropine may restore physiologic rhythm in some patients, temporary pacing is often required. Ventricular pacing alone may suffice in some, especially if the bradyarrhythmias are intermittent. However, some patients require AV sequential pacing (9,49). Unfortunately, transvenous pacing can be difficult in patients with right heart ischemia because of problems in ventricular sensing, presumably related to diminished generation of endomyocardial potentials in the ischemic right ventricle, as well as difficulties in lead positioning and capture in the atrium, which may be ischemic and dilated. Reports suggest that rapid administration of intravenous aminophylline may restore sinus rhythm in some patients with acute AV block unresponsive to atropine (106,107), a response likely reflecting reversal of the adverse bradycardic effects of ischemia-induced adenosine elaboration. This pharmacologic maneuver may restore AV synchrony and thereby obviate the technical challenges of temporary AV sequential pacing.
Optimization of ventricular preload
In patients with RVI, the dilated noncompliant right ventricle is exquisitely preload dependent, as is the left ventricle, which is stiff but preload deprived. Therefore, any factor that reduces ventricular preload will tend to be detrimental, whereas measures that optimize cardiac filling tend to be beneficial. Accordingly, vasodilators and diuretics are contraindicated. Although experimental animal studies of RVI demonstrate hemodynamic benefit from volume loading (40), clinical studies have reported variable responses to volume challenge (2,6,7,9,108–110). These conflicting results may reflect a spectrum of initial volume status in patients with acute RVI, with those patients who are relatively volume depleted benefiting, and those who are more replete manifesting a flat response to fluid resuscitation. Nevertheless, an initial volume challenge is appropriate for patients manifesting low output without pulmonary congestion, particularly if the estimated central venous pressure is <15 mm Hg. For those unresponsive to an initial trail of fluids, determination of filling pressures and subsequent hemodynamically monitored volume challenge may be appropriate. Caution should be exercised to avoid excessive volume administration above and beyond that documented to augment output, as the right heart chambers may operate on a "descending limb" of the Starling curve, resulting in further depression of RV pump performance as well as inducing severe systemic venous congestion. Abnormalities of volume retention and impaired diuresis may be related in part to impaired responses of atrial natriuretic factor (111,112).
Anti-ischemic therapy
Although hemodynamic compromise often dramatically dominates the clinical picture in severe RVI, it is important to keep in perspective the underlying ischemic pathophysiology that ultimately dictates recovery of both LV and RV function. Therefore, treatment of RVI should focus on optimizing oxygen supply and demand. However, given that virtually all anti-ischemic agents exert hemodynamic effects, caution must be exercised in administering these drugs to patients with RVI. Specially, beta-blockers and some calcium channel blockers may reduce heart rate and depress conduction, thereby increasing the risk of bradyarrhythmias and heart block in these chronotropically dependent patients. The vasodilator properties of nitrates and calcium-channel blockers may be deleterious to the stiff volume-dependent ventricles (100). Because in such patients RV performance is dependent on LV-septal systolic contraction, the potentially negative inotropic effects of beta-blockers and some calcium channel blockers can also be deleterious. Accordingly, these drugs should be avoided in patients with RVI resulting in manifest hemodynamic compromise, and in stable patients used only when clearly indicated and with careful monitoring to detect adverse hemodynamic effects.
Reperfusion therapy
The beneficial effects of successful reperfusion on RV function and clinical outcome, as well as the demonstrated efficacy and advantages of primary angioplasty versus thrombolysis in patients with acute right heart ischemic dysfunction, have been discussed.
Inotropic stimulation
Parenteral inotropic support is usually effective in stabilizing hemodynamically compromised patients not fully responsive to volume resuscitation and restoration of physiologic rhythm (9,108). The mechanisms by which inotropic stimulation improves low output and hypotension in patients with acute RVI have not been well studied. However, experimental animal investigations from our laboratory suggest that inotropic stimulation enhances RV performance by increasing LV-septal contraction, which thereby augments septal-mediated systolic ventricular interactions (43,45). Whether this mechanism is responsible for the improvement in patients treated with inotropic stimulation has not been delineated. Although an inotropic agent such as dobutamine that has the least deleterious effects on afterload, oxygen consumption, and arrhythmias is the preferred initial drug of choice, patients with severe hypotension may require agents with pressor effects (such as dopamine) for prompt restoration of adequate coronary perfusion pressure. The "inodilator" agents such as milrinone have not been studied in patients with RVI, but on the basis of their vasodilator properties, could exacerbate hypotension.
Mechanical assist devices
Intraaortic balloon pumping may be beneficial in patients with RVI and refractory low output and hypotension. Although balloon assist does not directly improve RV performance, it will improve coronary perfusion pressure in severely hypotensive patients. Because RV myocardial blood flow is dependent on perfusion pressure, balloon pumping may therefore also improve RV perfusion and thereby benefit RV function, particularly if the RCA has been recanalized or if there is collateral supply to an occluded vessel. Intra-aortic balloon pumping may also improve LV performance in those patients with hypotension and depressed LV function. As performance of the dysfunctional RV is largely dependent on LV septal contraction, RV performance may also benefit. Right ventricular assist devices have not been well studied in patients with RV infarction, but may improve hemodynamics and, in patients with life-threatening low output refractory to all other measures, such assist devices may be life-saving and serve as a bridge to transplant. Successful treatment of RV failure by atrial septostomy to augment left heart filling (113,114) should be considered only as a desperation intervention when all other measures have failed.
Acute RCA occlusion proximal to the RV branches results in RVFW dysfunction. The ischemic, dyskinetic RVFW exerts mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function leads to a decrease in transpulmonary delivery of LV preload, resulting in diminished cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction and septally mediated alterations in LV compliance, which are exacerbated by elevated intrapericardial pressure. Under these conditions, RV pressure generation and output are dependent on LV-septal contractile contributions, governed by both primary septal contraction and paradoxical septal motion. When the culprit coronary lesion is distal to the RA branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling, thereby resulting in further depression of RV performance and more severe hemodynamic compromise. Bradyarrhythmias limit the output generated by the rate-dependent noncompliant ventricles. Patients with RVI and hemodynamic compromise often respond to volume resuscitation and restoration of a physiologic rhythm. Vasodilators and diuretics should generally be avoided. In some patients, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and has a remarkable ability to recover even after prolonged occlusion. Therefore, the term RV "infarction" appears to be somewhat of a misnomer, for in most patients a substantial proportion of acute RV dysfunction represents ischemic but viable myocardium. Although RV performance improves spontaneously even in the absence of reperfusion, recovery of function may be slow and associated with high in-hospital mortality. Reperfusion enhances the recovery of RV performance and improves the clinical course and survival of patients with ischemic RV dysfunction.
- Abbreviations
- atrioventricular
- jugular venous pressure
- left ventricular
- myocardial infarction
- right atrial
- right coronary artery
- right ventricular
- right ventricular free wall
- right ventricular infarction
- Received December 27, 2001.
- Revision received April 26, 2002.
- Accepted May 24, 2002.
- American College of Cardiology Foundation
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text:
It is what it is
It is what it is
How one reflects upon the past in relation to the present is based on personal perception and philosophy. From another standpoint, the matter is also about temporal reality. Regardless, whatever life one lives, at the time, it is what it is.
As a child in Hungary, I didn't know anything about owning a telephone, a television, never mind an automobile. Nor did I know that there were other races in my world besides people who cared about me; that included the man who had black skin and was the porter at the railway station. Yet, my personal perception of my world was just fine.
As a child refugee, coming to Canada, I didn't know that not having a telephone, nor a television, nor an automobile meant I was poor. I didn't know that I shouldn't play with Johnathan who was a Native, because he was not the same colour as I was. I didn't know any of that, until another child pointed these out to me. And sadly, owing to influences from others, the personal perception of my world shifted, to some degree.
Looking back, it was somewhat akin to being cast out of Eden. Unsolicited, inflicted impressions, continued to be an ongoing challenge in how I viewed my world, and me in it.
Both as a child and later as a working wife, I did want my family to acquire such items as the telephone, the television, the automobile, the computer and the purchased home.
All of these kinds of procurements became common place in our western world of wealth. In fact, having only one telephone, one television, one computer and one automobile became insufficient in many households – largely because communication and travel needs escalated, and also because professional positions spiraled. Living in an all too fast paced, competitive world became a norm. Expectation of increased net worth, meant enhanced status hence a heightened requirement of additional acquisitions.
The temporal reality aspect of course also played and continues to sustain a significant role. The telephone, television, computer and automobile are major innovations upon which today's technological world continues to be built. We may not like the speed with which moment by moment transformation is cast out to the masses.
At this point in time, however, any of us could cut off connection to these items and live an alright life. A caveat nevertheless: one must act in haste, because before long, disconnecting will not be an option, as more and more facets of our daily dealings become computerized. Realistically, it is likely too late to disengage.…
As early as the 1960s, Canadian philosopher Marshall McLuhan coined the term 'global village'. The concept was based on the notion that cultures would focus on communicating and moving towards personal interactions. In that way the different parts of the world would form one community linked by the internet.
I consider that proposition to have become a remarkable reality. Clearly, there are parts of technology that are frustrating, problematic and some even dangerous. Vigilance is a key both from a state, public and a private approach. Nonetheless, on the whole, what an interesting and progressive time we live in!
Personally, technology has strengthened my awareness as to how I think about my fellow humans, my environment, my belief system, my commitments, my creativity and my place in this world. I need to believe that what is ahead will continue to bring humanity to a closer understanding as McLuhan had hoped.
One can easily view some aspects of one's life as the golden years, and other parts, including today's as undesirable. At best and at worst, it is what it is.
Soren Kierkegaard wisely stated: "Life can only be understood backwards; but it must be lived forwards."
Katalin Kennedy
June, 2019
When one is little –
Wishes flow expectantly.
Some, even come true.
When one is older –
Miracles are not for free.
Life, comes at a cost.
Katalin Kennedy
November, 2018
And so it goes
And so it goes
Hottest summer ever! Cold inside. Broiling oven outside. And so it goes.
Finally, when there was a reprieve for a few days, my foot found a small hole in the sidewalk, the exact shape of my shoe. The hole was marked with a pink circle, which the rose-coloured sun glasses clearly missed. The fall was a heavy thud. What hurt most was the left hand. Tried heat, then cold. Still hurt. Bruising spread.
Five days later drove to Emergency at the insistence of 92-year-old mother. Having been there a couple of years before by cab, I knew where to park. Didn't know the rules inside. Observing my confusion, a smiling man came to help obtain a number from the electronic information gizmo. Right away, the number 259 was called. Reporting the fall and injury, a first question by the first nurse attendant was a screening about woman abuse.
Happy to hear that. Years ago, I had a project on hospital triage screening on this critical subject, at the Vancouver General Hospital. The protocol became nation wide.
She said she ordered an X-ray, then onto the identification intake. Afterwards – sitting and waiting. Oddly pleasant and serene! It had been weeks since I remembered simply resting without any other commitment than to me. The white noise of the television overhead on some unidentifiable channel and far behind from view at any area seating, mumbled on as background noise. The walls covered with various required signs melted into each other.
Opened the Kobo to continue the wretched book I had begun two days before to be finished in two days for the monthly book club meeting.
The frantic single sound from an infant interrupted the reading – as did the voice of a young girl who took a seat too close by. She was accompanied by a well-dressed woman. A pungent odour of stale cigarette smoke wafted over the free seat between us.
"Oh, dear lord no!" I heard my inner thoughts. "But, I can't just get up and move," though that was foremost on my mind.
The need to do so, quickly passed as my concentration shifted. The young girl took out a sheet on which she had created a naive coloured something. She rifled through her stuffed back pack…
"There's a fly on me!" her child voice was frantic. "I hate flies!" She brushed it off her shoulder. "But I like butterflies. They're nice. I'll draw one."
The woman said, "That's a good idea."
"I'll also print the butterfly's name, Barbara. How do you spell that?"
"B- A-R- B-A- R-A" the woman's voice was calm and encouraging as she helped form the letters.
"That's a long name. A lot of As. Maybe I'll just print BARB," came the voice now sounding louder and more shrill.
"Yes. It is long. Alright to shorten it." Said the woman. "Soon we'll go up to that window. See number 3 over there?"
"I see. Number 3. There's a person in there. Can she come out? Does she have a name? Everyone has a name! Can I ask her, Marilyn?"
"Yes, you may." Came the continued kind response to the persistent inquiry.
And when the call came, the woman went first to identify some group home. The young girl with the child like voice gathered up her belongings and followed. She was taller than her companion. Could have been 12 or 18. A challenge to guess her age.
The first nurse came to advise she should have instructed me to go straight to X-ray. She apologized. Too bad. The hospital's average stay wait-time might have been reduced – had she not erred. So then, onto the blue triangle route which meandered on and on, hall after hall.
In that waiting area, an older man was holding court about his knee surgery recovery and his sixty-two stitches. He wore beige shorts revealing his now healed knee. A woman far in the corner wanted details; she was scheduled for the same operation. Having found his audience, he continued disclosing alarming caveats:
"The worst part was, you have to sleep on your back. I'm a side sleeper. Didn't sleep much for the duration."
He eagerly showed unsolicited photos to everyone on his cell camera, taken straight after the surgery. Really! Impossible to turn him off. Impossible to tune him out.
"Dear lord, help keep my knees in tact!" I offered a silent prayer to the great beyond.
The woman beside me was youngish. Sharing a camaraderie smile between us about the man, we chatted quietly. She fell from her bicycle. Cast on her left arm. Accidents. Incidents… Sigh.
More waiting for Emergency doctor to read the X-ray. Tiny fracture in an odd place on the hand. Unhappy diagnoses and advice. Then, dismissed to another attendant who located a left-hand medium size hand-arm brace
"So, what's next?"
"I think you can leave."
"Are you sure?"
"I'll check with the Dr."
Emerge Dr. appeared across the hallway. "Wait for a call from Dr. X, the specialist."
"You mean by phone?"
"Yes. You can leave."
Intake time 9:40 am. Out time 11:40 am. Parking ticket $6. Waiting for follow up.
It's hot again. And so it goes.
Katalin Kennedy, September, 2018
Seeking a new dwelling
Seeking a new dwelling
Falling, falling, falling …
Hurling through the cosmos,
His ineffable wings unfurl to catch the wind
As he searches with radar eyes
For the perfect place
To unearth his new dwelling.
Lower and lower he descends
Overlooking the ancient structures of worship:
First being Gobeldi Tebe near Sanhurfa.
Then onto the Palace of Knossos in Crete,
And the Temple of Amas in Nubia.
Soaring onward to the Ggantija Temple and the
Megalithic Hagar Qim of Malta
He next heads off to the Temple of Hatshepsut
Beneath the cliffs at Deir el-Bahri of Egypt –
And later across to Stonenehenge.
Attaining no shelter in any, he frantically ascends
Back to the Temple Mount of Jerusalem
Where like the Phoenix
He attempts to arise once more and surmount the
Three faiths of Judah, Jesus and Mohammed –
Yet none will give him sanctuary!
Cast out by the sacred trinity
He yearns to establish where he might reign.
Then out of the tumultuous whirlwind
The sound of almighty fire and fury
Penetrates his dejected spirit.
"You were once my son," the mighty resonance proclaims!
"I Am – of compassion.
Fly then, into the new world.
Seek out a place called the domed Capitol of the Americas.
There, have I been abandoned.
There, will you find followers to rule."
Katalin Kennedy
August 2018
The Knock
The Knock
The knocking woke her! Dazed from the unexpected rousing, she checked the clock. The numbers looked hazy. Had she forgotten to place the 'Do Not Disturb' sign on the door? Didn't matter. She had examined the lock the required number of times. Even if hotel staff tried to get in, she had also bolted the door. Who could be bothering her?
Her mind raced to another place where there had been a knocking. It too had been a surprise. New in St. John's, only the administrative staff at Memorial had been given her address. She had found a charming house on Water Street: one of the brightly coloured attached buildings. She was thrilled that hers was maroon, her favourite colour. She had been told that the name for them was Jellybean Row. The legend was that the luminous colours shone like a lighthouse. That way, fishermen could find their way home. And then she realized this legend was exactly the same she had experienced while visiting the Venetian Island of Burano in Italy, on another trip with Malcolm. There too, fishermen could see the vivid, different colours of each painted building even through thick fog and thus avoid crashing into the shore.
At that instant, the buildings were as clear to her as if she was walking on the very streets of the colourful row houses. Such fanciful folksy tales, so typical of both these friendly places. "Good morning to you!" greeted the voices of two young girls with their lilting accent. Everyone had that accent – except for Edwin. His was British. Like her, he too was a visiting professor. She was a little disappointed in him when he disclosed why the houses were really painted that way. The legend had been simply that ˗ he had told her ˗ a legend. In fact, the Jellybean houses were part of a 1970 heritage project to restore Victorian homes.
The knocking bothered her at the Water Street house. Her bedroom was upstairs on the second floor. Although she knew the front door had been triple tested, she couldn't help wondering how safe the locks were on these old houses. The knocking persisted. Finally, she screwed up her courage. She pulled on her jogging pants and tee shirt and went down the stairs…. She remembered being terrified to open the door.
Her fear stemmed from another image ˗ a passage that floated into her thoughts of Tolstoy's War and Peace. Natasha was still in the room nursing the wounded weak Prince Andrei. He was dreaming that he was lying in a room with a closed door. He too had gone to the door to bolt and lock it. But had he been in time to secure it properly? He was in agonizing terror. Something on the other side was pushing against the door, trying to force its way across the threshold. With all his strength he thrust his suffering body against it – to no avail. The door opened. It was death. Prince Andrei was dead. That haunting story was as real to her as if she had stepped into the very pages of the epic novel.
Stirred to reality, she could not avoid the knocking that persisted at her hotel room door. There was nothing else to do but to see who was causing it. She found her glasses and pulled on her overcoat at the desk chair. Slowly, cautiously she peered through the peek hole but could not distinguish anything. The knocking continued. She unbolted, unlocked and slowly opened the door ˗ to darkness, to a black empty hole ˗ into which she fell with a thump ˗ and woke with a start, to the knocking!
July 2018
Katalin Kennedy
Her Story
Her Story
If you were to journey to her haven, far from the city gates, what questions would you ask of her? And if she were to look deep into your eyes with her piercing dark ones and respond with that enigmatic smile, how could you be satisfied with her words, "It was long ago. It no longer matters." Instead, I believe you would persuade her with other questions, until she would finally relent and tell her tale:
I was born in a fishing town where my father held a prominent position. Being the only child, he encouraged me to study as though I were a boy. I learned the languages of those who sailed to our shores and heard their stories about far off lands.
It was how I met him. His party of followers landed the small boat. He led them to the hillside. Then the strangest occurrence took place. Masses of people from other boats and from the town made their way to be near him. I saw him from afar in his long cloak, arms outstretched and welcoming, face glowing not from the sun but what seemed like – from within. I meandered through the seating multitudes and found a place close by. His words were simple but powerful. I was touched by his sincerity.
My father later sent me to his brother's home in the city, to further my education about the real world. My Uncle Joseph was learned, honourable and also well off. When I asked him about the man on the hillside, he was aware of him. "A Teacher", he told me. My uncle feared for him. The times were difficult with the occupation of the army. Rebellion and chaos were imminent.
One day, I heard that the man whom I had seen on the hillside had also traveled to Jerusalem. My uncle knew I wanted to hear him once more; he went with me to the city square where again a crowd surrounded him. His words of meek wisdom still cling in my heart. After the others dispersed, Uncle introduced me. In our private talks I learned from the Teacher about his joys and his struggles.
He had spent several years in the desert, living among the Essenes. He revered their humble, pure and spiritual life. They were well versed about Hebrew Scriptures. They taught that there was virtue in poverty, honouring the Almighty above worldly riches. They did not worship in the temple, considering the priests to be negligent in spiritual discipline. He respected many of their doctrine including that they would help usher in a new era. One aspect of their teaching which he rejected was celibacy.
We were wed in Canaan. I too became his follower. He encouraged me to understand the authentic meaning of his teachings. His male supporters either ignored me or were jealous of me. He knew them to be unaware folk who nevertheless championed him until his final hour.
He died. A horrible death! Mistaken identity or martyrdom? His devotees all scattered to distant parts. Fearing my life to be in danger, my Uncle Joseph of Arimathea sailed me to this place where I have now lived for over thirty years. I teach his words to all who will listen. Our child chose to return to the land of her father – where she lives in anonymity.
I hear that his disciples, including new ones, relate their stories ˗ keeping him alive. Many of these accounts will become retold and eventually some versions will be written down, including perhaps by me.
It has also come to my attention that references about me are varied: that he performed a miracle by releasing seven demons from within me; that I was a sinful woman; that I was saved from stoning having been 'taken in adultery'; that I was a harlot ˗ and that I was a witness of his crucifixion and his burial. No mention ever ˗ that I ˗ Miriam of Magdala was his beloved wife. Where else would I have been, but by his side?
As time goes on, there will continue to be many speculations. Keeping him alive may become the ongoing mission of some who come after me.
And so my friend, to answer your very first question, "Is the story a myth or is it the truth?" my answer is still the same. "It was long ago. It no longer matters". You must be the judge.
June 2018
Katalin Kennedy
In the Tall Grass
In the Tall Grass
Stretched long in the tall grass
Embraced by yellow dandelions
And wild purple violets flown from
Grandmother's heavenly garden ˗
His Cat nose sores high
To sense the lilac scented breeze
While his green Cat eyes
Survey his tame domain.
The creak of a near-by opening door
Distracts his Cat ears ˗
Searching for the gay women
And the two young girls
Home schooled,
Playing in mid-day alone
On unsteady roller blades
Along the lazy street.
Echoing through the cacophony
Of whirls and shouts and giggles
The man in the balcony spews
Guttural cough from his throat
To which his primitive Cat response reacts
With a tiger's roar –
Until another day, maybe to chase a squirrel.
May 2018
Katalin Kennedy
She used to love old black and white films: especially the horror ones, produced in the late thirties and forties. By the time they were released for television, the sound was slow and eerie and the character movements were jerky and mechanical. The most intriguing, scary aspect of these films was the interaction among the various ranges of the colour spectrum – from white to grey to black. All these traits were precisely part of the attraction. When the production worked most effectively, with hovering, menacing shadows and piercing shrieks that penetrated her entire nervous system, she would grab onto her father with one hand and shield her eyes with the other. It was this unexpected thrill of fear that kept her body glued to the sofa and her eyes to the television set.
Saturday afternoons were the best time for watching these movies. For one thing, prowling, creeping silhouettes were not as foreboding in daylight. For another, her father was a willing partner, ready to humour her. He too enjoyed haunting movies. He was a connoisseur of the works of such actors as the Hungarian Lugosi Béla, most notably famous for his portrayal of Dracula. He admitted, however, to draw the line on watching the 1922 silent film Nosferatu. That one, he was confident, slithered from the energy of another world.
A highpoint of their comradery in this venture was that her father knew her triggers – those delicate moments when she was most vulnerable to be spooked. "Watch out!" He would yell. Afterwards they would laugh and laugh about the absurdity of a harmless scare – until their sides were near to bursting.
But that was then… another lifetime ago. There came a day when she could no longer watch any film that included ghostly, frightening themes. Even the idea of watching one worried her; she could not deal with the possibility of having a nightmare resulting from a monster movie. She had enough nightmares already. These were strange dreams that intertwined from slivers of images or experiences she had encountered.
They were often of daunting women trying to subject her to suffering. Sometimes the dreams were about searching for a place and sometimes about almost getting there – but something always blocked the entrance.
And yet, for whatever enigmatic reason, her life-work was about mythology and superstition: probing the various folk tales ˗ often dark tales – from different cultures and identifying their root beginnings and ongoing influences.
Against her father's persuasion, she was convinced she was called to this field of study, by some force she couldn't decipher.
Perhaps it was Malcolm's influence that lead her to this domain. "Look for the essence of the thing" he had instructed. That had also become her philosophy. From the moment they met, she grasped that the two of them had a connection. The eerie part of her intuition was that she also understood they had known each other ˗ forever. She clung to him as her rock, whenever her life shifted. Where was he now? Not knowing was her darkest fear.
Katalin Kennedy
April 2018
The climb through meandering rocky paths
In open sandals for forty days ˗
Who does that? And why?
I ask siting in his rose patterned wing back chair,
Now my chair.
Here, I expect messages of consolation.
The dark nights of the soul on sunny mornings
Are incongruous.
Can't get beyond the desolate brown hills
Without greenery –
Even my green walls give a sense of serenity
But the image on the projector screen in the bare church hall,
Of the Wanderer,
Does not give comfort – only questioning….
Oh, these days we are far more enlightened ˗
Who quotes passages from that ancient book?
And aren't there many ancient books?
Though most ˗ in the Land of White ˗
Believe in only the one ancient book
Written by ancient people, but with divine inspiration:
In the beginning was the Word, and the Word was with God, and the Word was God.
Those in the know, say all that writing is poppycock because
As creative beings in the here and now, we are privy to scholarly and intuitive insight:
In the beginning was the Big Bang – which came out of what? Nothingness?
These day, we don't talk god stuff –
Even when we contemplate with like minded folk, in the know ˗
God words are taboo.
Science has taught us to see the Universe,
Not just the Wanderer on rocky paths in an ancient story.
Talk of god is off-limits,
Reminding of church and institutions
And dark sermons on sin, hell, fire and damnation –
And memories of nuns with straps curbing any questioning.
Yet, sitting in my rose patterned wing back chair
I do little more than question ˗ and contemplate
About the massive rough-hewn cross
Standing at the front of the sanctuary
Draped in black on the day that marks his death.
Each good Friday,
I used to say to Husband the Minister
Get off your cross, it's been done!
And I remember those words,
Maybe blasphemous –
As I sit in his rose patterned wing back chair
Wondering if he too is wandering
Through meandering rocky paths,
In open sandals.
Katalin Kennedy
March 2018
March Snow
March Snow
White cotton clumps clung on the tree branches beside
Her new place, in her new life.
The snow had come ˗ again ˗
Just as he had come ˗ the evening before,
With only the words: and so it goes,
And ready for bed ….
Not their long bed at the other place
But a normal length one in this her place
His feet dangling at the base ˗
His lingering arms wrapped round her until she slept ˗
Only woken to the affable aromas:
Of eggs sizzling in the blue porcelain-lined frying pan,
Of rosemary focaccia toast and
Of dark roasted coffee
Hers ˗ with frothy milk in her china cup,
His ˗ black in his bottomless tucked away mug
He reclaimed ˗
From deep in her cupboard….
Just as he had been tucked away deep in her heart,
Until he might come ˗ again –
Just as the march snow.
Katalin Kennedy
March 2018

subset: commoncrawl


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Children aren't the only ones who like to dress up as their favorite Disney characters for Halloween. Adults like them, too! Profiled below is one website that offers adult Disney Halloween costumes.
Disney Halloween Costumes for Adults – Princess, Pirate, Evil Queen
Annie's Costumes offers a nice selection of adult Disney Halloween costumes and accessories from popular Disney / Pixar movies, including several Disney princess costumes and outfits for men. Below are the costumes available, grouped by movie.
- Cinderella – Prince Charming and Cinderella character outfits are available.
- Peter Pan – Adults can dress up like the movie's main characters, Captain Hook, Peter Pan, or Tinkerbell.
- Pirates of the Carribean – Adults may become cool Captain Jack Sparrow, pretty Elizabeth, or creepy Davy Jones for a night.
- Sleeping Beauty – Evil Maleficent and Sleeping Beauty are the two characters available from this movie.
- Snow White and the Seven Dwarfs – The site offers three different adult size Snow White costumes. All three of these Disney princess outfits have blue bodices, but only two of them have capes. Two different Evil Queen costumes are also offered.
- The Incredibles – Adults can transform into Mr. or Mrs. Incredible (Elastigirl). The outfits consist of tight-fitting red and black leotards with masks.
Adult Size Disney Halloween Costumes – Other Outfits for Men & Women
Other Disney character Halloween outfits for women and men offered on this site include Buzz Lightyear, Jafar, and Minnie Mouse. Prices fall anywhere between $39.95 to $109.95. On average, the men's costumes are more expensive than the women's costumes. Accessories like wands and gloves cost extra.
Scary Adult Activities – Fun Things to do for Halloween
Don't know what to do on Halloween? Trick-or-treating is not the only fun thing to do for Halloween. Adults aren't always welcome to trick-or-treat on their own anyway (a young child is usually a prerequisite for an adult to trick-or-treat). Here are some scary activity ideas for adult Halloween fun:
- Go to a haunted house. Several local organizations in every town are bound to host haunted houses. Expect to pay to be frightened!
- Walk through a corn maze. These are especially easy to find in farm towns. Rows of corn and hay bales typically serve as barriers and pathways. Look for spooky ghouls and creatures of the night to jump out and scare you at any second. Don't get cornered by anyone with a chainsaw!
- Visit a theme park. Disneyworld and Disneyland host a Halloween party every year. This isn't the cheapest option, but it would be fun.
- Go to a Halloween party. If you're not invited to one, host one!
- Visit a haunted graveyard or actual haunted house. Some people are lucky enough to live close to a graveyard or house rumored to be haunted. These are sometimes even tourist attractions.


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and Receive Complimentary E-Books of Previous Editions
The present society, based on knowledge and modern information and communication technologies, is shaping the global economy. Now knowledge becomes the most value commodity to the economy and also to the society. Thus, knowledge society that we are experiencing has shown that having capacity to manipulate, transmit, and store large quantities of knowledge is an advantage. Therefore, knowledge has increased at a staggering rate over recent years. At the same time, digitization process of services and resources as a result of advanced information and communication technologies assist in making available that knowledge freely and instantly.
Therefore, in the increasing global economy knowledge becomes the main attribute to competitiveness, innovation, and sustainability. Fundamentally, innovations base on knowledge commodities that make a stronger society towards a sustainable social and economic development process. If society is based on knowledge then there is no argument that society comes up with new ideas in better and faster ways. This idea shows that knowledge society is serving us mainly on knowledge-based products and services that no one had thought of before. Further, it is about putting new ideas to workforces to engage with new insights. However, though experiencing a very successive knowledge society right now, the way of engaging with it by educational institutes such as universities to grab and enhance knowledge is questionable. A proactive engagement in knowledge exploring is very low. But as someone said, we are quite late as academicians to fully engage with this buzz knowledge society. We believe that even this stage is not too late to langue a new journey to engage with by identifying main components of the society as a whole. On that journey, we believe that universities can be a good starting point to work with because one of the main roles of universities is to explore new knowledge. However, to deal with knowledge society within the conventional frame of universities may pose problems. Therefore, re-framing our way of thinking of its roles will create more opportunities and might assist in enhancing knowledge of its communities. It is necessary to introduce and use appropriate mechanisms to explore knowledge because only introducing sophisticated technologies may not mean that will meet requirements of communities of universities and society as a whole. It is better to introduce knowledge sharing and knowledge communication culture. For that, we have to think of universities as an eco-system because different species of the eco-system live coherently for success and sustain their inhabitants. That is what universities have to do.
Therefore, in this chapter we are aiming to introduce a concept of knowledge ecology, a field of theory and practice that focuses on discovering better social, organizational, behavioral, and technical conditions for knowledge creation and utilization, using knowledge exploration in universities, how universities can identify and work with knowledge ecology and adjust existing roles and functions assigned either by policies or norms. We believe universities can enhance knowledge to compete with knowledge competitors, and to take advantage of knowledge component to betterment of universities. As we said, because knowledge ecology is an inter-disciplinary subject including business innovation, skill development, communication and information systems, learning relationships, professional practice, education policy development, knowledge management, and communities of practice, etc., it assists new knowledge creation and utilization. Therefore, keeping in mind that universities are social institutions, we discuss roles that have to be played to explore new knowledge on knowledge ecology perspectives by universities.


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This time I would like to just share some pretty pictures. These were sent to me by Ely-based Patricia Kreyer. She kindly let me reproduce some of her remarkable images.
The Ouse Washes landscape – and the Fens as a whole – lends itself perfectly for photography, as this previous post also clearly demonstrated.
Ely Cathedral, taken from the SSSI at Kiln Lane. Photo by Patricia Kreyer, all rights reserved.
I am happy to showcase other people's work as well, to show people the beauty of the Ouse Washes landscape – feel free to contact me to discuss further.
Related articles
- Family Adams shop: a true Fen Treasure Chest (ousewasheslps.wordpress.com)
- High in the Sky: Heritage & Landscape Photography from above (ousewasheslps.wordpress.com)


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Film Review: Red Joan
Trevor Nunn's mystery drama Red Joan is a broadly entertaining watch, although it is not quite the tense narrative the premise suggests. Joan Stanley, a retired civil servant, is arrested at her home in a surprising turn of events. She is accused of being a spy for Russia following World War II. As the police question her, Joan looks back […]Read more


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A fierce rivalry was re-ignited as long jumpers Chris Tomlinson and Nathan Morgan fought out another duel.
Tomlinson, coached by Lanchester-based Peter Stanley, who also coaches world triple jump record holder Jonathan Edwards, broke the long-standing British record last year but it was Morgan who won the Commonwealth title after emerging from his opponent's shadow with perfect timing.
Tomlinson produced a series of consistent jumps to take the title with a mark of 7.90m with Commonwealth silver medallist Gable Garenamotse jumping a season's best of 7.79m to clinch second place. Morgan was third with 7.59m.
Tomlinson was pleased to have won the AAAs title but was disappointed not to have beaten the eight-metre mark. Although he recognises it will be a tall order to get a medal at the World Indoor Championships, he believes that anyone who jumps over 8m will have a chance of finishing in the top three.
European 100 metres gold medallist Dwain Chambers claimed his narrow defeat by Mark Lewis-Francis in their 60m showdown at the Norwich Union World Indoor Championships trials in Birmingham had been "a race too soon".
Chambers faced local favourite Lewis-Francis in the most high-profile race at the trials which were marred by the absence of the majority of Britain's potential medallists.
Chambers said: "I knew it was going to be hard for me. I only had my first race last week."
The race was the most keenly-contested of the weekend with Lewis-Francis finishing just one-hundredth of a second ahead in 6.58secs to secure a spot on the British team with the absent Jason Gardener.


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Darren, who is your dr there? They should shedule the appointment, or call trusty Sue!
Type: Posts; User: Jim
Darren, who is your dr there? They should shedule the appointment, or call trusty Sue!
Happy Thanksgiving!
3) I have not heard of any issue with opening the dura and injecting more than once. In fact, Wise has said, more than 1 injection may be necessary, he doesn't know. It is very likely that a...
We had a meeting yesterday working on finalizing the budget for the six weeks of outpatient PT. This has to be done with each center, almost complete. One IRB has been approved, 2 are pending. Almost...
In the trial, 15/20 subjects walked at Kunming level IV or better. (Person walking behind locking knees with rope.)
Yes, it's legit. I know some of the Dr's in the video from when I visited...
Didn't work in Chrome, does in Firefox.
This person was not in our ChinaSCINet Clinical trial. When the video says, 'Three Months After Surgery', don't know what surgery they are referring to.
It has been discussed whether a second round of cells may be necessary. Neurosurgeons said it wouldn't be a big deal to repeat.
the link takes me here. Ironic, i have a mac, China ...
i don't see a video
I'll ask Wise
The nine who are randomized to the 6-6-6 only group will be offered the cells after the trial, followed by 6 more months of training. This group will probably do the best.
The 6 weeks of...
I have seen the videos because I work for Dr Young. He does show them at Open Houses, and sometimes when he gives talks.
I'll be there!
No vid bro
I got it already installed in my last two cars.
Incredible Bob, we are fortunate to know you all these years. I shared your story wit the Medical Director at Kessler. He was amazed.
I'll see want I have to post abou the surgery and 6-6-6.
I haven't been specific about our upcoming trial?
You need to be more specific about the the procedure.
I've seen the videos, read the published paper- https://journals.sagepub.com/doi/10.3727/096368916X691411
Hi Naty,
I am told that anyone can apply for the trial. The surgeons choose who will be in the trial. A critical part is returning for follow up exams at 1 and 2 years. If they are concerned you...


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The National Counterterrorism Center: What Is a Terrorist and How Do We Know Who They Are?
In reaction to the 911 attacks on New York City, President George W. Bush issued Presidential Executive Order 13354 on August 27, 2004, thereby creating the National Counterterrorism Center (NCTC). The precursor of this center was the Terrorist Threat … Continue reading
Posted in Posts for the Cause Tagged Architecture, Current Events, guns and violence, intelligence reform and terrorism prevention act, libya, middle-east, monuments to the fallen, monuments to victims of terrorism, national counterterrorism center, national pride, News, peace, Politics, terrorist threat integration center, terroristic violence, violence, world brotherhood, World News Leave a comment


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10 MUST HAVES for Spring
Good afternoon :)
It is finally spring and I am stoked about it. It seemed like winter lasted FOREVER. I am so excited about a change in the weather. Ever since I can remember, spring has been my favorite season because it's not too hot/cold; it's just right.
I decided to write about the top 10 things I think every girl needs for spring. I have found all of these items to be essential for the spring season. I feel like we can bring in spring 2018 with justice if you own these 10 items;)
1.) Denim Jacket.
Yes mam!!! I am in love with denim jackets. They add style to any outfit. I feel like denim is a hot fashion trend, especially for this spring season. You can go to Target, American Eagle, and also Old Navy. Always make sure you peek in thrift stores as well.
I found this one at the Goodwill thrift store; such a steal!
Goodwill- $3.00
2.) Morphe 35O- 35 Eyeshadow Palette.
I am in love with all of the Morphe palettes, but I think this one defines the spring season colors. It contains lots of neutral tones and bright orange/ red colors. Top it all off with the light shade of highlighters and you're all set. Did I mention this palette is only $23.00? It is amazing!
Morphe- $23.00- https://www.morphebrushes.com/products/35o?utm_medium=cpc&utm_source=googleshopping&variant=4982012353&gclid=EAIaIQobChMI7rTbydOR2gIVk-DICh0fXwqPEAQYASABEgLIZfD_BwE
3.) Bondi Sands Self Tanner.
This stuff is literally the greatest thing since sliced bread. Self tanner is the way to go. Tanning beds damage your skin and if you have sensitive skin like mine, it is hard to get out in the sun without getting burned. Have a tan this spring by using Bondi Sands. It will last you months and you can bring in spring with glowy, tan skin!
Bondi Sands- $24.00
4.) JORD Watch.
Does JORD watches sound familiar? I did a blog post on it a few weeks ago. I am in love with my JORD watch. I think they make the perfect statement piece for spring. The company is incredible and I am a huge fan of this item. I am obsessed with my watch; I never want to take it off!
5.) Mac Waterproof Foundation.
I have tried every foundation known to man and this is by far this best that I have found. I have been wearing Mac Foundation for 2 years. I tell everyone about it; it is just that good! As the weather gets warmer, pool (and sweat LOL) days are in the near future. Mac Waterproof foundation stays on your skin and lasts all throughout the day.
6.) Hoop Earrings.
Hoop earrings are so in right now. They make for any outfit. I always think Claire's or Agaci has the best selections.
7.) Romper
I know that rompers were pretty big last summer, but I still think they make for a great outfit for spring. As the weather is getting warmer, shorts are gonna be worn soon and what is not to love about a romper? It's shorts and a shirt all in one!
8.) Statement Sunglasses.
Although I am a fan of Rayban sunglasses, I find myself in the cheaper sunglasses section every time I go shopping. I believe with sunglasses, the more the merrier! They don't necessarily have to be top name brand; there are so many cute sunglasses out there!
I found these for $6.99 at Target :)
9.) Maxi Dress.
I think Maxi Dresses scream spring season. I have always loved maxi dresses. They are so comfortable and you can just throw them on and go. Plus, I always wear my wedges with them. A maxi dress makes me look 5x taller, LOL.
Ross- $15.99


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Governing Board
The OPC is governed by the Older Persons' Commission Governing Board, which consists of eight commissioners representing the City of Rochester, City of Rochester Hills and Charter Township of Oakland. The OPC Governing Board adopts and monitors policies under the provisions of the Interlocal Agreement, which establishes the basic purpose, organization, structure, and operation of OPC.
The Commissioners consist of:
- City of Rochester Hills - 2 Elected Officials / 2 Senior Representatives
- City of Rochester – 1 Elected Official / 1 Senior Representative
- Charter Township of Oakland - 1 Elected Official / 1 Senior Representative
The Elected Officials and Senior Representatives are appointed by their corresponding council or board.
The meetings are held at the Older Persons' Commission, 650 Letica Dr., Rochester, Michigan on the first Thursday of the month, with the exception of the July and August meeting. The agenda is posted the Friday before the meeting in the main lobby, and on the website.
Meeting dates for 2019: January 3, February 7, March 7, April 4, May 2, June 6, July 11, August (no meeting), September 5, October 3, November 7, and December 5.
The next OPC Governing Board meeting is: December 5, 2019, at 5:00 p.m.
Board Members:
Stuart Bikson
Micheline Sommers
Lucy Strand
William Jandeska
Dale Hetrick
David Walker
Mike Bailey
John (Jack) Dalton


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Syracuse routs Duke 49-6, snaps 4-game slide
- Ben McKeown
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DURHAM, N.C. (AP) — Tommy DeVito threw for two touchdowns and rushed for another, and Syracu…
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text: Blossom Walk is officially sold out! However not to worry we have a new community in Hacienda Heights – Manzanita Walk. With everything from traditional townhomes to carriage units, and single-family detached homes, Manzanita Walk's unique variety and open floor plans are built to exceed all your home expectations. These homes offer up to 4 bedrooms and 3.5 baths with up to 1,788 square feet of living space. Stop by Manzanita Walk today to tour our beautiful model homes.


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Interesting point on heirlooms. It's hard to get into this mindset, but to a previous generation pieces like a watch or women's jewellery were bought perhaps once or twice a lifetime, or given to one that often - for example on your wedding day. And…
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Why wont my computer boot up?
my computer was giving messages of memory error when shutting down. now my computer wont boot up. montor dosent light up until I unplug it. so I replaced video card still no response. Do I need to get new memory chips
This question was answered on February 12, 2003. Much of the information contained herein may have changed since posting.You have to upgrade in memory so your computer would boot up or you may try to boot up with the boot up disk first and if that dont work then upgrade in memory but is more likely that you my have to upgrade in memory.You need to increase RAM on the Motherboard
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Posted by erik of Katharine Gibbs School - New York on February 12, 2003


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Stunning custom Chandler home in the desirable Ryan Estates is now on the market! This is your chance to own over 4000sqft with 6bedrms/4.5bath, tile flooring throughout the main living areas, bamboo in the bedrooms, gorgeous upgrades in every corner and a kitchen/living great room ready for entertaining! Enjoy the chefs kitchen with matching appliances, a large eat at island with granite counters, an additional sink, ample cabinets and the show piece of kitchen the gas stove with its own pot filler. The master suite is a true getaway with the soaring ceilings & luxurious on suite. Step outside and indulge the Arizona evenings under the covered patio relaxing by the fireplace or taking a swim in the pool. The boojum trees are the fine touch that makes this place unique! This is must see
Listing courtesy of My Home Group Real Estate.
All information should be verified by the recipient and none is guaranteed as accurate by ARMLS. Copyright 2019 Arizona Regional Multiple Listing Service, Inc. All rights reserved.


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