Left ventricular regional wall stress in dilated cardiomyopathy.

Abstract

Left ventriculography with simultaneous pressure micromanometry was performed in 11 normal control subjects and 17 patients with dilated cardiomyopathy (DCM). Left ventricular silhouettes in the right anterior oblique projection were divided into eight areas, and regional wall stress was computed by Janz's method in each area excluding the two most basal areas. Wall stress was higher in DCM patients than in control subjects (p<0.01). The percent area changes from end diastole to end systole in each area were lower in DCM patients than in control subjects (mean for six areas, 22+14% versus 54±9%o, respectively, p <0.01), but the coefficient of variation for the percent area changes in the six areas of the left ventricle in DCM patients was greater than that in control subjects (32±17% versus 15±4%, respectively, p<0.01), indicating regional differences in hypokinesis. There was a significant negative correlation between end-systolic regional wall stress and percent area change (r=-0.60 to -0.86, p<0.05) in each area. Thus, excessive regional afterload may play an important role in causing regional hypokinesis in DCM. (Circulation 1990;82:2075-2083 iffuse hypokinesis of the left ventricular wall D motion has been reported in patients with dilated cardiomyopathy (DCM).' However, recent studies on DCM with the use of left ventricular cineangiography2-5or radionuclide ventriculography6,7 suggest that left ventricular wall motion is not always diffusely hypokinetic and that regional differences in the degree of hypokinesis are frequently present. In clinical settings, patients with segmental wall motion abnormality may have better global left ventricular function and better prognosis than patients with diffuse wall motion abnormality.6 Thus, the importance of estimating left ventricular regional wall dynamics in patients with DCM has been emphasized.3-7

Left ventricular aneurysm in patients with idiopathic dilated cardiomyopathy: clinical analysis of six cases

“…Hayashida et al showed that wall stress in patients with IDCM was maximal in the basal segments and minimal in the apical segments. 19 Based on the above findings, we suggest that LVA formation in patients with IDCM occurs when high peak systolic pressure in the left ventricle (as shown in our patients) imposes high levels of stress on a posterobasal wall which is weakened by fibrosis in a manner similar to the expansion of a soap bubble (figure 3). The LVA location in FDCM is mainly at the anterior or apical walls, and the mechanism of cardiac damage differs, which suggests that the pathogenesis of LVA formation in FDCM and IDCM may differ.…”

“…The regional asynergy may be related to the heterogeneity of local wall fibrosis and local wall stress. [17][18][19] Juillière et al demonstrated that regional myocardial perfusion abnormalities were predominant in the myocardial regions delineating the anteroposterior axis of the left ventricle. 17 Local fibrosis occurred more frequently on the anterior wall or posterior wall, while less frequently on the lateral or septal wall.…”

Ischemic etiology of heart failure identifies patients with more severely impaired exercise capacity

“…During exercise, in ischemic heart disease the left ventricle might have a worse preserved adaptation to excessive wall stress than in idiopatic cardiomyopathy, due to the presence of akinetic and dyskinetic cardiac segments [17,18]. A role has been proposed for the presence and severity of mitral regurgitation, which have been shown to negatively influence peak VO2 [7].…”

Predictors of Systolic Augmentation From Left Ventricular Preexcitation in Patients With Dilated Cardiomyopathy and Intraventricular Conduction Delay

“…14,15,17,18,27 We also limited our analysis to DCM patients with widened QRS complexes, and it remains possible that some individuals with more narrow complexes might also benefit. Previous studies have reported regional wall motion abnormalities, heterogeneous wall stress, and myocardial perfusion in DCM patients with normal-appearing epicardial vessels, 28,29 although none reported QRS durations to test correlations with these phenomena. Certainly, surface ECG-based estimates may underestimate the temporal spread of depolarization if early and late portions have relatively low voltages.…”