Left Ventricular Stress and Compliance in Man

Abstract

Left ventricular circumferential end-diastolic stress (Sed), peak systolic stress (Sps), and compliance at end-diastole ([dV/VdP]ed) were estimated in 13 subjects with normal left ventricles (N group), nine subjects with inappropriate hypertrophy (IH group), five with aortic valvular stenosis (AS group), and six with congestive cardiomyopathy (CC group). The product of Sed and (dV/dP)ed was employed as an index of (<muscle fiber stretch" and related to systolic indices of ventricular performance. Compliance was significantly less than normal in IH (P < 0.001), in AS (P < 0.01), and in CC (P < 0.001), while end-diastolic volumes were smaller than normal (P < 0.05), normal (P = NS), and larger than normal (P < 0.001) in the three groups, respectively. Sed was normal in IH and AS but elevated in CC (P < 0.001), while Sps was decreased in IH and normal in AS and CC. "Muscle fiber stretch," however, was substantially less than normal in IH (P <0.001), indicating that the low Sps is due at least in part to short sarcomeres. In CC, despite a markedly elevated preload, "muscle fiber stretch" was normal (P = NS), while work indices of the ventricle were diminished indicating depressed ventricular function. Thus, the product of Sed and (dV/VdP)ed provides a normalized index of "muscle fiber stretch," which permits one to compare length-tension or length-work relationships in diseased ventricles of varying dimensions and compliance.Additional Indexing Words: Length-tension relationships Pressure-volume relations Inappropriate hypertrophy Congestive cardiomyopathy STUDIES OF ISOLATED heart muscle have demonstrated that sarcomere length is directly proportional to muscle length along the ascending limb of the length-active

Alterations in left ventricular diastolic function in conscious dogs with pacing-induced heart failure.

“…The indices employed encompassed both active and passive aspects of diastole and were consistent with abnormalities which have been described in the advanced stages of human dilated cardiomyopathy (30)(31)(32)(33)(34). In hamber Stiffness LV End, Diastolic Volume (ml addition, we observed that the LV diastolic abnormalities develop in close temporal relationship with the LV systolic abnormalities and were evident within 24 h of initiating the insult of RV pacing.…”

“…Abnormalities in LV diastolic function are characteristic of heart failure (1, 2) in both patients (30)(31)(32)(33)(34)(35)(36) and in experimental models (12,17,37). Prior studies have suggested that alterations in LV diastolic function in heart failure are due to intrinsic properties of the cardiac myocytes (38) or to intracellular calcium regulation (39)(40)(41), concomitant myocardial ischemia (17), or alterations in collagen content (42,43).…”

Ventricular performance, pump function and compensatory mechanisms in patients with aortic stenosis.

“…Our data show no evidence that inadequate hypertrophy accounts for the failure state since, in our AS-CHF group, systolic wall stress was relatively normalized, ventricular mass was highest, and the ratio of left ventricular mass to enddiastolic volume was not depressed. We confirmed previous studies that demonstrate that wall stress is relatively normal despite increased intracavitary pressure in patients with aortic stenosis.16 [27][28][29] Gunther and Grossman's conclusions about myocardial contractile performance may be questioned because ejection fraction and mean velocity of fiber shortening, which they used to estimate ventricular function, are sensitive to alterations in afterload. Further, if their data are used to plot stroke work index vs end-diastolic volume as a Frank-Starling relationship, findings that may be contrary to their conclusions become evident.…”

Beneficial effect of salbutamol on cardiac function in severe congestive cardiomyopathy. Effect on systolic and diastolic function of the left ventricle.

“…The decision of whether a given therapeutic agent is an inotropic agent or a vasodilator can be difficult when a study is carried out in Alterations in LV compliance are affected by many factors other than elastic properties of the myocardium. Most accepted factors related to the left ventricle itself altering compliance are ventricular geometry, initial volume, hypertrophy, wall thickness, ventricular filling rate 15,17,19,[24][25][26] and ventricular stiffness. Changes in the behavior of the anatomical constraints to the LV distension, including right ventricular chamber,27 the pericardium and the pleural cavity28 associated with altered pressure and volume-loading conditions, have also been suggested to contribute to the observed displacement of the LV pressure-volume curves.…”