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.
OBJECTIVE
We aimed to assess the differences in the adaptive response of patients with hypertrophic cardiomyopathy (HCM) compared with normal subjects, 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 healthy 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) shrinkage; and 3) no LV dimensional variations. In patients with HCM, tilting was associated with 1) a prevalence of systolic pulmonary venous flow (atrium functioning as a reservoir in which filling depends on atrial relaxation and compliance) and late diastolic transmitral flow (atrium working as a booster pump); 2) LV shrinkage; and 3) no RV dimension variations. These mechanisms did not prevent stroke volume (SV) from decreasing at 40 degrees and 60 degrees in both groups. Because of a lower increase in heart rate (HR), a reduction in cardiac output (CO) was greater in patients with HCM. The responses 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 min.


CONCLUSIONS
Adaptation of the normal heart to tilting is based on a ventricular interaction and LV diastolic properties; HCM relies on left atrial diastolic and systolic functions. An inadequate HR reaction to a fall in BP and SV in HCM (depressed reflexogenic activity) contributes to making CO more vulnerable by greater and more prolonged displacements.
Guazzi
M
M
Istituto di Cardiologia dell'Università degli Studi, Centro Cardiologico, IRCCS, Centro di Studio Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Milano, Italy. Maurizio.Guazzi@unimi.it
Maltagliati
A
A
Tamborini
G
G
Celeste
F
F
Pepi
M
M
Muratori
M
M
Berti
M
M
Guazzi
M D
MD
D000222:Adaptation, Physiological / Q000502:physiology*; D001783:Blood Flow Velocity; D002302:Cardiac Output; D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging / Q000503:physiopathology*; D015150:Echocardiography, Doppler; D006339:Heart Rate; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D011187:Posture / Q000502:physiology*; D011379:Prognosis; D011652:Pulmonary Circulation; D011667:Pulmonary Veins / Q000000981:diagnostic imaging / Q000503:physiopathology*; D018667:Tilt-Table Test; D016277:Ventricular Function, Left / Q000502:physiology*; D016278:Ventricular Function, Right / Q000502:physiology*