[Left ventricular ejection and ejection reserve during isoproterenol infusion in hypertrophic obstructive cardiomyopathy (author's transl)].

Abstract

In 10 patients with hypertrophic obstructive cardiomyopathy (HOCM) and in 10 patients without heart disease (normals) left ventricular function and myocardial reserve under isoproterenol (Iso) infusion (0.3 microgram/kg B.W./min) were measured. From the monoplane cineangiography of the left ventricle diastolic wall thickness as well as ejection phase contractile indices, ejection fraction (EF) mean velocity of fiber shortening (VCF) and mean normalized systolic ejection rate (MNSER), were calculated. Maximum total load (TL) served as measure for afterload. Wall thickness in HOCM was higher by 73% as compared to normals (p less than 0.001). Hemodynamic values for normals at rest were as follows: EF 68.9 +/- 8.0%, VCF 1.22 +/- 0.19 circ/sec, MNSER 2.25 +/- 0.25 vol/sec and TL 228.6 +/- 37.4 dynes . 10(5). Values for HOCM at rest were as follows: EF 77.4 +/- 7.71% (p less than 0.05), VCF 1.53 +/- 0.3 circ/sec (p less than 0.05); MNSER 2.66 +/- 0.35 vol/sec (p less than 0.01) and TL 288.5 +/- 55.5 dynes . 10(5) (p less than 0.01) as compared to normals. The values under Iso in normals resulted in a significant fall of the TL (p less than 0.05), the enddiastolic volume (EDV, p less than 0.05) and of the enddiastolic pressure (EDP, p less than 0.05), VCF rose by 89% (p less than 0.001), MNSER by 66% (p less than 0.001) and EF by 23% (p less than 0.001). In HOCM under Iso TL rose by 45% (p less than 0.05), EDV and EDP did not change (p less than 0.05), VCF and MNSER rose by 23% (p less than 0.05 respectively p less than 0.01). VCF and MNSER in HOCM with Iso were reduced by 17% respectively by 13% (p less than 0.01) as compared to normals, the EDP was increased by factor 4, while EDV showed no significant difference (p less than 0.05). Our results indicate that the left ventricle in HOCM in spite of its marked hypertrophy is unable to adequately compensate for an acute gain of afterload as induced by the effect of catecholamines. Therefore, we assume stress-related congestive symptoms in HOCM to be caused--aside from other mechanisms--by diminished ejection reserve.