Hemodynamically important right ventricular infarction: follow-up evaluation of right ventricular systolic function at rest and during exercise with radionuclide ventriculography and respiratory gas exchange.

Dell'Italia, L. J.; Lembo, Nicholas; Starling, Mark R.; Crawford, Michael H.; Simmons, R. S.; Lasher, J. C.; Blumhardt, Ralph; Lancaster, Jack L.; O’Rourke, Robert A.

doi:10.1161/01.cir.75.5.996

Cited by 80 publications

(28 citation statements)

References 43 publications

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“…One can estimate that at least 25% of the right ventricular cardiomyocytes are under the direct control of the EE; the remaining 75% will comprise the right ventricular compact myocardium, where they are under the control of the coronary perfusion and the MyoCapE. The substantial potential influence of the EE on right ventricular contractile performance may at least partly explain why considerably fewer cases of right ventricular dysfunction result from occlusion of the right coronary artery than there are of left ventricular dysfunction resulting from occlusion of the left coronary artery, and, why right ventricular function can improve remarkably after right ventricular infarction even in the absence of documented revascularization (112,113). Reperfusion of the right coronary artery will, obviously, enhance further recovery of right ventricular function, even after prolonged ischemia (49, 535).…”

Section: The Endothelial System: Conjectural Role Of Cardiac Endotmentioning

confidence: 99%

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Brutsaert

2003

Physiological Reviews

613

544

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Experimental work during the past 15 years has demonstrated that endothelial cells in the heart play an obligatory role in regulating and maintaining cardiac function, in particular, at the endocardium and in the myocardial capillaries where endothelial cells directly interact with adjacent cardiomyocytes. The emerging field of targeted gene manipulation has led to the contention that cardiac endothelial-cardiomyocytal interaction is a prerequisite for normal cardiac development and growth. Some of the molecular mechanisms and cellular signals governing this interaction, such as neuregulin, vascular endothelial growth factor, and angiopoietin, continue to maintain phenotype and survival of cardiomyocytes in the adult heart. Cardiac endothelial cells, like vascular endothelial cells, also express and release a variety of auto- and paracrine agents, such as nitric oxide, endothelin, prostaglandin I2, and angiotensin II, which directly influence cardiac metabolism, growth, contractile performance, and rhythmicity of the adult heart. The synthesis, secretion, and, most importantly, the activities of these endothelium-derived substances in the heart are closely linked, interrelated, and interactive. It may therefore be simplistic to try and define their properties independently from one another. Moreover, in relation specifically to the endocardial endothelium, an active transendothelial physicochemical gradient for various ions, or blood-heart barrier, has been demonstrated. Linkage of this blood-heart barrier to the various other endothelium-mediated signaling pathways or to the putative vascular endothelium-derived hyperpolarizing factors remains to be determined. At the early stages of cardiac failure, all major cardiovascular risk factors may cause cardiac endothelial activation as an adaptive response often followed by cardiac endothelial dysfunction. Because of the interdependency of all endothelial signaling pathways, activation or disturbance of any will necessarily affect the others leading to a disturbance of their normal balance, leading to further progression of cardiac failure.

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Section: The Endothelial System: Conjectural Role Of Cardiac Endotmentioning

confidence: 99%

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Brutsaert

2003

Physiological Reviews

613

544

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“…Because the RV is thin walled and functions at low oxygen demands and low pressure with coronary perfusion throughout systole and diastole, extensive irreversible RV damage is unusual. 27 The prognosis of RV infarction is largely determined by the degree of associated LV infarction. 28 Volume therapy (200-1000 mL over the first several hours following the acute infarction) that has become standard on the basis of animal and human data 29 is only of benefit in the presence of low right atrial pressures.…”

Section: Treatment Of Rv Infarctionmentioning

confidence: 99%

Management of acute and chronic RV dysfunction

Lang

2007

European Heart Journal Supplements

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The aim of this article was to outline contemporary treatments of right ventricular (RV) dysfunction and failure. Despite the heterogeneity of disorders underlying RV failure, RV function is a main determinant of long-term prognosis. Therefore, the unique therapeutic goal is to preserve or ameliorate RV function. Although, in advanced stages of RV failure, there is a considerable overlap of pathophysiological mechanisms, the principle targets of treatment are RV contractility, RV pressure overload, and RV volume overload. Apart from surgical strategies such as pulmonary endarterectomy, lung transplantation, closure of shunt lesions, and interventional structural cardiology procedures such as closure of abnormal communications and defects, or graded blade balloon atrial septostomy, targeted pharmacological treatments have become available over the past years. In addition, global strategies such as exercise training, arrhythmia correction, and synchronization treatments may become a new standard of care in the near future. KEYWORDS Right ventricular dysfunction; Right ventricular failure DefinitionRight ventricular (RV) dysfunction has been defined as a state where stroke volume still increases in the presence of increased RV end-diastolic volume. In contrast, RV failure is present when stroke volume cannot increase any further in parallel to increased RV end-diastolic volume. The compromise of the systemic circulation by the septal shift and interventricular dependence causing a severe left ventricular (LV) filling disorder, offsets a vicious cycle. On a molecular basis, it appears that there is a recapitulation of the fetal gene pattern with a decrease in the a-myosin heavy chain gene and an increase in the expression of the fetal b-myosin heavy chain in dysfunctional or failing RV myocardium. Although excessive and longstanding elevation of RV afterload is a major and prevalent cause of RV dysfunction/ failure, evidence accumulates that RV ischemia, 2 excessive sympathetic and renin-angiotensin system stimulation, 3 and volume overload that is accelerated by tricuspid regurgitation 4 contribute. This transition from dysfunction to failure may be ongoing fast or slowly over years, with an unknown genetic component underlying the ability of the RV to resist pressure and volume overload and to maintain stroke volume. RV hypertrophy is a mechanism accounting for preserved RV function. Recent work has demonstrated that in COPD, concentric RV hypertrophy is the earliest sign of RV pressure overload. However, this early structural adaptation of the heart does not yet compromise RV and LV systolic function. 5In practice, the distinction between RV dysfunction and failure can be revealed by a short-time inhalation of NO which, because of its high pulmonary vascular selectivity, 6 will increase RV stroke volume only in the case of a predominantly pulmonary vascular alteration, i.e. in the presence of RV dysfunction.Taken together, pressure, volume, and contractility are main determinants of RV function, and as such, are ...

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“…These functional changes improved after the acute event [24] in some sub jects but not in others [25]. Even in subjects without myocardial infarction a decreased right ventricular ejec tion fraction has been noted on radionuclide angiogra phy [26], A correlation between hypokinesis, reduced ejection fraction and right ventricular dilatation at rest with electrocardiographic evidence of ST segment eleva tion in the V4R leads has been observed with nonin vasive techniques during acute myocardial infarction [11,24,26], and with hemodynamic studies as well [12], Croft et al [ 13] found that the sensitivity and specificity of electrocardiography was improved when V4R to V6R were employed in comparison to Vj, C4R or V4R alone (leads previously studied by others) [9-12, 24] during infarction.…”

Section: Limitations Of the Studymentioning

confidence: 99%

Exercise Testing Postmyocardial Infarction Using Right-Sided Chest Leads (V(4)R and V(6)R) to Detect Right Ventricular Ischemia

Rubler¹,

Glasser²,

Sedlis³

et al. 1988

Am J Noninvas Cardiol

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A study was conducted with 41 male subjects (mean age 60.9 ± 7.3 years) who had sustained myocardial infarctions, to elicit electrocardiographic evidence of right ventricular ischemia or dysfunction during maximal exercise on a treadmill (35 subjects) or with arm-crank (6 subjects). V(4)R and V(6)R leads were substituted for the V(1) and V(2) leads in a 12-lead electrocardiogram. Eighteen patients developed ST segment elevations in the V(4)R and V(6)R leads (group 1) whereas 23 patients had no changes in these leads (group 2). In group 1, 14/18 subjects (77.7%) had inferior infarcts, 2 had old anterior damage and 2 had a recent non-Q wave involvement. In group 2, 12/23 (52.2%) had inferior infarcts, 8 anterior and 3 had non-Q wave damage. All group 1 subjects with inferior infarcts had V(6)R ST segment elevation (6 had V(4)R changes as well). Standard leads demonstrated ST segment alterations in 13/18 (72%) in group 1 and in only 8/23 (34.8%) in group 2 (p < 0.05). Ten (66.6%) of 15 patients with right-sided ST segment elevations had a severe proximal right coronary artery stenosis and/or stenosis of a right ventricular branch. Another 3 subjects had a 50% right coronary artery narrowing in association with severe distal disease of the right coronary artery. In those with no ST segment changes, 7/16 patients (43.8%) had severe proximal right coronary disease. The difference between the groups was significant (p < 0.005). The sensitivity for the detection of right coronary pathology in those with 50% stenosis was 65%; the specificity 81.8%. On echocardiography, right ventricular diastolic dimensions were significantly greater in the group 1 subjects. Myocardial scintigraphy in 14 group 1 patients revealed that 50% had inferior or inferoseptal scars or ischemia and that only 4 had inferolateral ischemia. Of the 20 patients in group 2, a similar number (4) had inferolateral ischemia and 1 had lateral wall ischemia. Therefore, it appears that reciprocal changes due to lateral wall ischemia was not the cause of the ST elevations in V(4)R and V(6)R observed in group 1. On radionuclide angiography performed in 7 group 1 subjects, 4 had abnormal right ventricular ejection fractions and/or wall motion abnormalities at rest, and of 14 group 2 patients studied, 6 were abnormal at rest. With exercise, 3 out of 4 subjects thus tested in group 1 (2 of whom were normal at rest) had abnormal responses, 1 patient who was initially abnormal deteriorated further. Similarly, of 5 group 2 subjects who exercised, only 1 had a normal response. Thus, wall motion abnormalities alone could not explain the ST segment changes in the right precordial leads since patients with and without abnormal wall motion had V(4)R and V(6)R segment changes. We conclude that ST segment elevations in V(6)R and V(4)R leads during exercise in patients with inferior infarction often are associated with severe proximal right coronary and/or right ventricular branch artery disease and that this may represent either right venricular ischemia or dysfunction. The ...

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Hemodynamically important right ventricular infarction: follow-up evaluation of right ventricular systolic function at rest and during exercise with radionuclide ventriculography and respiratory gas exchange.

Cited by 80 publications

References 43 publications

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Management of acute and chronic RV dysfunction

Exercise Testing Postmyocardial Infarction Using Right-Sided Chest Leads (V(4)R and V(6)R) to Detect Right Ventricular Ischemia

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