Assessment of left ventricular contractility from late systolic stress-volume relations.

Pouleur, H.; Rousseau, Michel F.; Eyll, Christian van; Mechelen, Henri Van; Brasseur, L.; Charlier, Aa.

doi:10.1161/01.cir.65.6.1204

Cited by 28 publications

(8 citation statements)

References 44 publications

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“…Finally, alterations in LV volume, pressure, shape, and morphology are consistent with the increased peak systolic and diastolic wall stress reported in severe CAD (33,(132)(133)(134)164). Such increased wall stress would tend to alter myocardial energetic and mechanical performance.…”

Section: Myocardial Wall Stresssupporting

confidence: 71%

Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning

Mazzadi

André‐Fouët²,

Costes³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Croisille, Didier Revel, and Marc F. Janier. Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning. Am J Physiol Heart Circ Physiol 291: H2570 -H2582, 2006. First published July 21, 2006 doi:10.1152/ajpheart.01249.2005.-Patients with severe chronic coronary artery disease (CAD) exhibit a highly altered myocardial pattern of perfusion, metabolism, and mechanical performance. In this context, the diagnosis of stunning remains elusive not only because of methodological and logistic considerations, but also because of the pathophysiological characteristics of the myocardium of these patients. In addition, a number of alternative pathophysiological mechanisms may act by mimicking the functional manifestations usually attributed to stunning. The present review describes three mechanisms that could theoretically lead to reversible mechanical dysfunction in these patients: myocardial wall stress, the tethering effect, and myocardial expression and release of auto-and paracrine agents. Attention is focused on the role of these mechanisms in scintigraphically "normal" regions (i.e., regions usually showing normal perfusion, glucose metabolism, and cellular integrity as assessed by nuclear imaging techniques), in which stunning is usually considered, but these mechanisms could also operate throughout the viable myocardium. We hypothesize that reversion of these three mechanisms could partially explain the unexpected functional benefit after reperfusion recently highlighted by high-spatial-resolution imaging techniques. stunned myocardium; hibernating myocardium; inotropic reserve; cardiac imaging; myocardial wall stress; ventricular remodeling SUMMARY OF CLINICAL PROBLEMIN RECENT YEARS, WIDESPREAD utilization of noninvasive cardiac imaging methods has greatly improved the synergy between clinical and basic investigation of cardiac ischemic pathophysiology. Thus imaging methods have shown that the reversible left ventricular (LV) dysfunction arising from brief coronary occlusion and reflow (myocardial stunning), first described in animal models (80), occurs in humans. Two major hypotheses explain this phenomenon: 1) the oxyradical hypothesis, which proposes that oxidant stress impairs LV function (18), and 2) the calcium hypothesis, which postulates that stunning results from disturbed myocyte calcium homeostasis (98). On the other hand, the hibernating myocardium (136, 137) was first discovered by imaging methods in humans, and it was originally defined as "resting LV dysfunction due to reduced coronary blood flow that can be partially or completely reversed by myocardial revascularization and/or by reducing myocardial oxygen demand" (136). The concept was refined when ultrastructural investigations showed a distinctive morphology for hibernating myocardium, generally without necrosis, but with loss of sarcomeres and myofibrils (suggesting a "dedifferentiation" process toward an embryonic phenotype), with loss of mitochondria and increased glycogen storage (9,19,27,162)...

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Section: Myocardial Wall Stresssupporting

confidence: 71%

Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning

Mazzadi

André‐Fouët²,

Costes³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…These different methods remain valid for the equatorial region of the latter; however, they lead to systematic overestimation of the thickness of the left ventricular wall and underestimation of the radius of curvature (4), as we have reported in the normal subject (2). In myocardial infarction, Pouleur et al (21), in utilizing the Janz formula, found that the precision of the method decreases in the apical region of the left ventricle, where there are considerable variations in the radius of curvature. Our tridimensional approach allows the best possible assessment of the regional variations of the wall thickness and the radius of curvature in the three planes of space (2).…”

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confidence: 67%

3-D MRI assessment of regional left ventricular systolic wall stress in patients with reperfused MI

Delépine¹,

Furber²,

Beygui³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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. 3-D MRI assessment of regional left ventricular systolic wall stress in patients with reperfused MI. Am J Physiol Heart Circ Physiol 284: H1190-H1197, 2003. First published October 10, 2002 10.1152/ajpheart.00106.2002The goal of this study was to assess the regional variations of end-systolic wall stress in patients with reperfused Q wave acute myocardial infarction (AMI), with the use of a three-dimensional (3-D) approach. Fifteen normal volunteers and fifty patients with reperfused AMI underwent cardiac MRI that used a short-axis fastgradient-echo sequence. The end-systolic wall stress was calculated with the use of the Grossman formula with the radius and the wall thickness defined with a 3-D approach using the tridimensional curvature. The mean wall stress was significantly increased at each level of the short-axis plane only in patients with anterior AMI. When calculated at a regional level in patients with anterior AMI, wall stress significantly increased in anterior sector as well as normal sector. In patients with inferior AMI, wall stress significantly increased only in inferior and lateral sectors. In conclusion, the quantification of regional wall stress by cardiac MRI is better with the 3D approach than other methods for precise evaluation in patients with AMI. Despite early reperfusion, the wall stress remained high in patients with anterior AMI. left ventricular remodeling; left ventricular function; cardiac imaging LEFT VENTRICULAR REMODELING, a factor of poor prognosis (29), begins on formation of the infarction (11) and can continue after the cicatrization phase (13). The modifications of ventricular geometry concern the infarcted zone, which is subjected to a phenomenon of expansion associated with wall thinning, and the healthy zone, which will hypertrophy and then dilate (17). Remodeling intensity is a function of neurohormonal factors linked with activation of the renin-angiotensin system (19) and the sympathetic nervous system (6), together with mechanical factors, depending on the size and the localization of the infarction (28) and on the afterload evaluated by the end-systolic wall stress (20).The end-systolic wall stress is the product of the systolic pressure of the left ventricle (or its estimation) and a geometric factor dependent on the shape of the left ventricle (5). The geometry of the left ventricle in infarction is complicated, and only a tridimensional approach, excluding the use of a geometric model, is valid in the presence of ventricular deformations, which can occur after myocardial infarction. Because of good spatial resolution and an absence of a geometric hypothesis, the MRI allows precise definition of the epicardial and endocardial borders of the left ventricle (1,8).Several mathematical models have been used to calculate the wall stress. Some (10) depend on the shape of the left ventricle and are only valid in the presence of a ventricle of spheroid or ellipsoid shape and only allow calculation of the global wall stress. Others are applicable whatever the shape of...

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“…The conspicuous reduction of contractil ity is therefore matched by an important recruitment of the preload, which allows ac ceptable performance of the pump [16,21].…”

Section: Aortic Insufficiencymentioning

confidence: 99%

Myocardial Function in Heart Failure

Dalla‐Volta

Razzolini²,

Scognamiglio³

et al. 1988

Cardiology

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Overt cardiac failure usually presents with constant clinical features as consequences of the reduced pump action, associated with an increased adrenergic drive, independent of the underlying disease. However, the study of left ventricular function, before and during the phase of cardiac insufficiency, shows that different pathophysiological mechanisms are responsible for the symptoms and signs of reduced cardiac action. It is possible to recognize that cardiac failure is caused primarily by: (1) early severe depression of the inotropic state, i.e. dilated cardiomyopathies; (2) late inadequate level of ventricular hypertrophy, with normal contractility, i.e. aortic stenosis; (3) early inadequate level of hypertrophy and slightly reduced inotropic state, i.e. mitral insufficiency, and (4) late inadequate level of hypertrophy and severe progressive reduction in contractility, i.e. aortic insufficiency. The possibility of an ‘in vivo’ assessment of the different determinant parameters of left ventricular function (contractility, afterload, preload, fiber and chamber compliance) through echocardiography enables a better understanding of the mechanisms leading to the cardiac failure and a more efficient therapeutic approach.

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Assessment of left ventricular contractility from late systolic stress-volume relations.

Cited by 28 publications

References 44 publications

Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning

Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning

3-D MRI assessment of regional left ventricular systolic wall stress in patients with reperfused MI

Myocardial Function in Heart Failure

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