How the left and right sides of the heart, as well as pulmonary venous drainage, adapt to an increasing degree of head-up tilting in hypertrophic cardiomyopathy: Differences from the normal heart

OBJECTIVES We aimed to assess the differences in the adaptive response of p atients with hypertrophic cardiomyopathy (HCM) compared with normal subject s, as well as any association with increased susceptibility to the test. BACKGROUND Diastolic function contributes importantly in the adaptation of the normal heart to head-up tilting. This mechanism may be disturbed by an impaired relaxation in HCM. METHODS Twenty-one male patients with HCM (46 +/- 6 years old) and 22 healt hy men (44 +/- 8 years) were studied using Doppler echocardiography after 1 and 10 min of head-up tilting at 20 degrees, 40 degrees and 60 degrees. RESULTS In control subjects, tilting was associated with 1) a predominance of diastolic pulmonary venous flow and early left ventricular (LV) filling (atrium functioning as an open conduit); 2) right ventricular (RV) shrinkag e; and 3) no LV dimensional variations. In patients with HCM, tilting was a ssociated with 1) a prevalence of systolic pulmonary venous flow (atrium fu nctioning as a reservoir in which filling depends on atrial relaxation and compliance) and late diastolic transmitral flow (atrium working as a booste r pump); 2) LV shrinkage; and 3) no RV dimension variations. These mechanis ms did not prevent stroke volume (SV from decreasing at 40 degrees and 60 d egrees in both groups. Because of a lower increase in heart rate (HR), a re duction in cardiac output (CO) was greater in patients with HCM. The respon ses were similar after 1 and 10 min of tilting in control subjects, whereas in patients, blood pressure (BP), SV and LV dimension fell more after 10 m in. CONCLUSIONS Adaptation of the normal heart to tilting is based on a ventric ular interaction and LV diastolic properties; HCM relies on left atrial dia stolic and systolic functions. An inadequate HR reaction to a fall in BP an d SV in HCM (depressed reflexogenic activity) contributes to making CO more vulnerable by greater and more prolonged displacements. (C) 2000 by the Am erican College of Cardiology.