Intravenous propranolol and verapamil did not alter LV diastolic stiffness in HCM patients, but verapamil significantly improved LV relaxation (T decreased from 53 to 43 ms, P<0.05).
In patients with hypertrophic cardiomyopathy (HCM), impaired left ventricular (LV) relaxation and diastolic filling have been reported. Therefore, we determined LV diastolic stiffness in nine patients with HCM before and 10 to 15 min after 0.15 mg/kg propranolol i.v. (group 1) and in six patients with HCM before and 10 to 15 min after 0.1 mg/kg verapamil i.v. (group 2). Simultaneous LV cineangiography and high-fidelity pressure measurements were performed in group 1 and simultaneous M-mode echocardiography and high-fidelity pressure measurements in group 2. Passive LV chamber stiffness was determined in group 1 from the diastolic pressure-volume data using an exponential three-parameter model: P = ae beta V + C, where P = pressure, alpha = intercept, beta = constant of chamber stiffness, V = volume and C = baseline pressure. Passive LV myocardial stiffness was estimated in group 2 from the diastolic stress-strain data using a viscoelastic model: sigma = alpha' (e beta' epsilon -1) + eta epsilon, where sigma = meridional wall stress, alpha = intercept, beta' = constant of myocardial stiffness, epsilon = midwall strain, eta = constant of myocardial viscosity and epsilon = strain rate. LV relaxation was assessed from the time constant of LV pressure decay (T) by plotting LV pressure versus negative dP/dt. LV diastolic filling was evaluated from peak and mean LV filling rate in group 1 and from peak and mean midwall lengthening rate in group 2. LV chamber and myocardial stiffness, respectively, remained unchanged before and after administration of propranolol (beta = 0.054 and 0.047) and verapamil (beta' = 14.8 and 12.6); however, the time constant of LV pressure decay T increased significantly in group 1 from 45 to 66 ms (P less than 0.05) and decreased significantly in group 2 from 53 to 43 ms (P less than 0.05). Parallel to the changes in LV isovolumic relaxation, mean LV diastolic filling rate decreased significantly in group 1 from 257 to 196 ml m-2 s-1 (P less than 0.025) and mean LV midwall lengthening rate increased significantly in group 2 from 2.37 to 4.31 cm/sec (P less than 0.05). It is concluded that LV diastolic stiffness remains unchanged in patients with HCM after propranolol and verapamil. LV relaxation and mean diastolic filling, however, are impaired in patients with HCM following propranolol but are improved after verapamil. Thus, the beneficial effect of verapamil on diastolic mechanics is related to improved relaxation and diastolic filling rather than to changes in LV diastolic stiffness.
Hess et al. (Wed,) conducted a other in Hypertrophic cardiomyopathy (n=15). Propranolol and Verapamil vs. Baseline (before administration) was evaluated on LV diastolic stiffness. Intravenous propranolol and verapamil did not alter LV diastolic stiffness in HCM patients, but verapamil significantly improved LV relaxation (T decreased from 53 to 43 ms, P<0.05).