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Previous studies from our laboratory have shown that the position of the ventricular septum relative to the two ventricles at end-diastole is determined by the instantaneous transseptal pressure gradient (TSG) defined as left ventricular minus simultaneous right ventricular pressure. Since patients with mitral stenosis often have exaggerated leftward (paradoxic) motion of the ventricular septum during early diastole, we studied seven patients with mitral stenosis undergoing cardiac catheterization to determine if position (and therefore motion) of the ventricular septum was determined by TSG throughout diastole. M Mode echocardiograms derived from a two-dimensional parasternal short-axis view were recorded with simultaneous micromanometer measurements of left ventricular and right ventricular pressures. Six of seven patients demonstrated abnormal early diastolic leftward motion of the ventricular septum in at least one cardiac cycle. TSG measured at intervals throughout diastole ranged from -2.5 to +20 mm Hg, with abnormal TSG observed in most of the 40 cardiac cycles selected for analysis. The intracardiac position of the ventricular septum, defined as the distance from the right ventricular epicardium (RVEpi) to the left surface of the ventricular septum normalized for total cardiac dimension (RVEpi-VS), was plotted against left ventricular pressure, right ventricular pressure, and TSG. Linear regression of pooled data from all patients (164 observations) demonstrated a highly significant correlation between the instantaneous TSG and the relative intracardiac position of the ventricular septum (RVEpi-VS = 1.52 TSG + 42.7; r = .79, p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Nitroglycerin has been shown to cause a downward shift in the left ventricular (LV) pressure-volume relation in patients. To test the hypothesis that this shift is mediated by an alteration in pericardial pressure, 13 patients undergoing diagnostic cardiac catheterization were studied. LV and right ventricular (RV) pressure (micromanometers) and LV diameter (2-dimensional echocardiography) were measured simultaneously before and after sublingual administration of 0.3 to 0.6 mg of nitroglycerin. In the 11 patients with hemodynamic effects from nitroglycerin, mean LV end-diastolic pressure decreased from 12.7 +/- 5 mm Hg (mean +/- standard deviation) to 7.3 +/- 3 mm Hg (p less than 0.002) and mean RV end-diastolic pressure declined from 7.7 +/- 3 mm Hg to 5.0 +/- 1 mm Hg (p less than 0.001). However, nitroglycerin caused only a slight (6%) reduction in LV minor axis diameter, from 52 +/- 8 mm to 49 +/- 9 mm (p less than 0.05). Diastolic pressure-diameter plots constructed from early and late diastolic measurements demonstrated a downward shift in the relation. However, when RV end-diastolic pressure was used as an estimate of pericardial pressure (a procedure validated by studies in our laboratory), the transmural pressure-diameter points before and after administration of nitroglycerin defined a single curve. These observations are in keeping with the conclusions that nitroglycerin did not alter the elastic properties of the myocardium and that the decrease in LV end-diastolic pressure induced by nitroglycerin was primarily attributable to a reduction in external constraint.

To assess cardiac status in end-stage renal disease, we compared clinical, ECG, and echocardiographic data from 37 patients on maintenance hemodialysis with data from 42 patients with functioning renal transplants. Cardiovascular symptoms and abnormal cardiovascular findings were more common in dialysis-maintained patients than in those with transplants. Follow-up studies indicated that despite a high prevalence of cardiac symptoms, abnormal physical signs, and dilated left ventricles among patients with end-stage renal disease, systolic left ventricular function was generally well preserved irrespective of renal failure therapy. Compared with maintenance hemodialysis, however, successful renal transplantation is associated with an overall enhancement of cardiac status, the majority of which is probably secondary to transplant-associated improvement in hemoglobin level and control of intravascular volume.

In a prospective study of the results of 5582 consecutive two-dimensional echocardiographic examinations, hypertrophy of a localized region of the basal ventricular septum was identified in 26 patients. Proven diagnoses were coronary disease in five patients, coronary plus valvular disease in three, valvular disease in seven, and miscellaneous in four. Localized septal hypertrophy was the only cardiac diagnosis in seven patients. The ratio of the thickness of the hypertrophied area to that of the adjacent septum was greater than or equal to 1.7 (mean 1.93 +/- 0.19) in all patients. The ration of the length of the hypertrophied portion (mean 0.34 +/- 06) to the length (apex to base) of the septum was less than 0.39 in all but one patient. Although the mitral valve tended to be more anterior than expected in 20, other features of hypertrophic cardiomyopathy were generally lacking. Of four patients undergoing left ventricular angiography, the bulge was identified in only one in whom cranial-caudal angulation was added to the 60-degree left anterior oblique view. An autopsy was performed in one patient; the hypertrophy was identified, although results of microscopic examination showed no fiber disarray. These data suggest that, in most instances, localized septal hypertrophy is an incidental echocardiographic finding. The diagnosis of hypertrophic cardiomyopathy should generally not be made on the basis of this feature alone.