Takaharu Saito

Left ventricular midwall mechanics in systemic arterial hypertension. Myocardial function is depressed in pressure-overload hypertrophy.

BackgroundLeft ventricular (LV) midwall geometry has been described conventionally as the sum of the chamber radius and half of the wall thickness; this convention is based on the assumption of uniform transmural thickening during systole. However, theoretical considerations and experimental data indicate that the inner half (inner shell) of the LV wall thickens more than the outer half (outer shell). Thus, an end-diastolic circumferential midwall fiber exhibits a relative migration toward the epicardium during systole. As a result, the conventional method provides an overestimate of the extent of the midwall fiber shortening. Methods and ResultsWe developed an ellipsoidal model with a concentric two-shell geometry (nonuniform thickening) to assess midwall fiber length transients throughout the cardiac cycle. This modified midwall method was used in the analysis of LV cineangiograms from 15 patients with systemic arterial hypertension and 14 normal subjects. Study groups were classified according to LV mass index (LVMI): 14 normal subjects (group I), eight hypertensive patients with a normal LVMI (group II), and seven hypertensive patients with an increased LVMI (group III). There were no significant differences in LV end-diastolic pressure or volume among the three groups; the ejection fraction was slightly greater in group 11 (70 + 5%) than in groups I (65±8%) and III (664±4%), but this trend did not achieve statistical significance. Values for endocardial and conventional midwall fractional shortening (FS) were also similar in the three groups. By contrast, FS by the concentric two-shell geometry (modified midwall method) in group III (16±2%) was significantly less than that seen in groups I and II (21±4% and 21 + 5%, respectively; both p < 0.05). This difference achieves greater importance when it is recognized that mean systolic circumferential stress was lower in group III (151±22 g/cm2) than in groups I and 11 (244±37 g/cm2 and 213+38 g/cm2, respectively; both p<0.01). The midwall stressshortening coordinates in six of the seven group III patients were outside the 95% confidence limits for the normal (group I) subjects. Thus, despite a normal ejection fraction, systolic function is subnormal in hypertensive patients with LV hypertrophy. ConclusionsChamber dynamics provide an overestimate of myocardial function, especially when LV wall thickness is increased. This is due to a relatively greater contribution of inner shell thickening in pressure-overload hypertrophy.

Functional and histopathologic correlation in patients with dilated cardiomyopathy: An integrated evaluation by multivariate analysis

To correlate left ventricular function and histologic features in patients with dilated cardiomyopathy, precise indexes of hemodynamics and semiquantitative histologic data were combined for multivariate analysis. Right endomyocardial biopsy was performed at the time of cardiac catheterization. Five hemodynamic indexes were used for functional assessment: ejection fraction, ratio of end-systolic stress to volume index, end-diastolic stress, time constant (T) of left ventricular pressure fall, and end-systolic stress. Six histologic findings (disarray of myofibers, hypertrophy of myofibers, scarcity of myofibrils, nuclear changes of myofibers, vacuolization of myofibers and proliferation of collagen fibers) were graded from (-) to (4+). Each finding was assigned to category (-) or (+) according to the absence or presence of significant abnormality. Ordinary statistical analysis revealed that, although ejection fraction was lower in category (+) for proliferation of collagen fibers, ratio of end-systolic to volume index was reduced for category (+) of hypertrophy of myofibers. A significant correlation was present between hypertrophy of myofibers and proliferation of collagen fibers by Spearman rank correlation. When principal component analysis was applied to the hemodynamic data, two principal components could be extracted. Fishers discriminant analysis could clearly differentiate two categories (-) and (+) in the semiquantitative histologic finding of proliferation of collagen fibers. The analysis indicated that contractility was reduced with elevated afterload in that category (+). Thus, proliferation of collagen fibers may play a pivotal role in deteriorating contractility in patients with dilated cardiomyopathy.

Mechanisms of compensation and decompensation in dilated cardiomyopathy

Left ventricular (LV) function was evaluated in 32 patients with dilated cardiomyopathy (DC) who underwent cardiac catheterization during the past 6 years (group 4), and the results were compared with the data of 30 normal subjects (group 1). The patients were divided into mildly (group 2, 12 patients) and severely symptomatic subgroups (group 3, 20 patients). DC was characterized by dilated and poorly contracting left ventricle with increased muscle mass, reduced cardiac output and elevated systemic vascular resistance. LV volume was larger, ejection fraction was lower, and end-diastolic and end-systolic stresses were higher in group 3 than in groups 1 and 2. No significant differences were seen in LV muscle mass and wall thickness between groups 2 and 3. A significant inverse correlation was seen between ejection fraction and end-systolic stress in patients with DC (Y = -0.05x + 48.7, r = 0.57, p less than 0.01). The slope of the correlation line between end-systolic stress and volume in DC (Y = 1.20x + 135, r = 0.52, p less than 0.02) was less steep than that of normal subjects (Y = 3.68x + 40, r = 0.64, p less than 0.001). These observations indicate that the primary problem of DC is depressed contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Nifedipine on Cardiovascular System, with Special Reference to Coronary Circulation

Hypertrophic cardiomyopathy (HCM) has been believed to be a disease of diastole, while systolic functions are normal or supernormal (Goodwin 1970; Wynne and Braunwald 1984). As such, the disease involves impaired left ventricular (LV) relaxation and reduced compliance. The traditional concept of supernormal systolic function has been questioned recently by some investigators (Hirota et al. 1982; Pouleur et al. 1983), and the development of congestive heart failure associated with dilated and poorly contracting left ventricle has received substantial attention (Fujiwara et al. 1984; Yutani et al. 1985; Fighali et al. 1987). Inadequate blood supply to the myocardium due either to elevated LV diastolic pressure or to the presence of small-vessel disease may be responsible for the clinical deterioration (Fujiwara et al. 1984; Maron et al. 1986).