Changes of the degree of hypertrophy in hypertrophic obstructive cardiomyopathy under medical and surgical treatment.

The aim of our study was to establish the extent to which therapy of hypertrophic obstructive cardiomyopathy (HOCM) can influence the degree of hypertrophy. By means of two-dimensionally guided M-mode echocardiography, 120 patients with HOCM (age range 4-72 years, mean age 41 years) were observed over an average period of 49 +/- 41 months. Depending on the respective therapy, we formed four patient groups: group 1: 13 patients without any therapy (follow-up period 31 +/- 30 months); group 2: 27 patients receiving propranolol (follow-up period 47 +/- 34 months); group 3: 50 patients receiving verapamil (follow-up period 39 +/- 27 months), and group 4: 30 patients with myectomy (follow-up period 34 +/- 32 months). In group 4, as expected, the thickness of the interventricular septum (IVS) decreased postoperatively (from 24.2 +/- 4.5 to 19.8 +/- 6.7 mm, p less than 0.05), and the left ventricular posterior wall (LVPW) thickness also decreased later postoperatively (from 13.0 +/- 2.6 to 11.9 +/- 2.3 mm, p less than 0.05). The left ventricular diameters increased. In groups 2 and 3 treated with pharmacotherapy as in the untreated patients of group 1, on average there was no change in IVS and LVPW thickness nor in the left ventricular diameters (with the exception of increasing left ventricular end-diastolic diameter in the propranolol-treated group). In contrast to group 1, in occasional cases there were substantial decreases of IVS thickness (11% of the patients in group 2, 13% in group 3) or LVPW thickness (13% of the patients in group 2, 12% in group 3).(ABSTRACT TRUNCATED AT 250 WORDS)

[A new Doppler echocardiography parameter of diastolic ventricular function]. / Ein neuer dopplerechokardiographischer Parameter der diastolischen Ventrikelfunktion.

The evaluation of flow velocities in left ventricular inflow tract (LVIT) by Doppler echocardiography gives information about the diastolic ventricular function. In late diastole, shortly after the flow velocity of atrial contraction V(A), we notice in the left ventricular outflow tract (LVOT) a laminar flow velocity directed to the aortic valve. The purpose of this study was to compare this flow velocity V(A*) in the LVOT with the flow velocity of the atrial contraction V(A), and the flow velocity of early diastole V(E) in LVIT, to determine whether such comparison would provide information concerning diastolic function. We studied three groups: 39 patients with left ventricular hypertrophy (HY) (mean age 56 +/- 12 y, 77% male), 41 patients with coronary heart disease (KHK) (mean age 53 +/- 10 y, 85% male) and 41 healthy subjects (N) (mean age 50 +/- 16 y, 51% male); all three groups were studied by pulsed Doppler from apical 4 chamber view in LVOT for maximal velocity (Vmax-A*) and time velocity integral of A* (TVI-A*), and in LVIT for maximal velocity of early diastole (Vmax-E), maximal velocity of atrial contraction (Vmax-A), ratio Vmax-E/Vmax-A, and the time velocity integrals (TVI-E, TVI-A). A slight correlation between Vmax-A* and Vmax-A was found (r = .60), being nearly the same as for TVI-A* and TVI-A (r = .64).(ABSTRACT TRUNCATED AT 250 WORDS)

[Diastolic left ventricular volume flow in patients with arterial hypertension before and following acute antihypertensive medication]. / Diastolischer linksventrikulärer Volumenfluss bei Patienten mit arterieller Hypertonie vor und nach akuter antihypertensiver Medikation.

Parameters of diastolic left ventricular (LV) function were studied noninvasively in 15 hypertensive patients without coronary heart disease (HY) vs 15 age- and sex-matched normotensive controls (CO). The maximal mitral valve area (2-D-Mode), the diastolic change in mitral valve area (M-mode), and diastolic velocity profiles in the LV inflow tract (pw-Doppler) were obtained in each patient using echocardiography. In HY the early diastolic volume flow (371 +/- 125 vs 492 +/- 134 ml/s, p less than 0.01) and the early diastolic filling volume (38 +/- 12 vs 48 +/- 15 ml, p less than 0.0125) were significantly diminished compared to CO. However, the early diastolic maximal flow velocity was not altered due to a smaller maximal early diastolic mitral valve area. At the time of active filling, volume flow and filling volume in HY were not significantly increased, whereas--due to a smaller mitral valve area (5.8 +/- 1.4 vs 6.9 +/- 1.7 cm2, p less than 0.01)--maximal flow velocity was higher than in controls (65 +/- 20 vs 55 +/- 9 cm/s, p less than 0.05). One hour following oral medication of 20 mg nifedipine, diastolic wall stress dropped significantly in HY. The diastolic flow velocity, the volume flow, and the filling volume during rapid and active filling were unchanged. Conclusively, we found a drop in early diastolic volume flow and filling volume due to an alteration of relaxation in patients with hypertension. Acute pharmacological interventions leading to lowering of the arterial blood pressure and systolic wall stress do not reverse these alterations.(ABSTRACT TRUNCATED AT 250 WORDS)