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Background: Hypertrophic cardiomyopathy (HC) is characterized by impaired left ventricular (LV) diastolic function due to an increase in LV wall thickness. The severity of this disease varies depending on the localization and extent of the hypertrophied myocardium and the presence and extent of myocardial disarray or fibrosis., Hypothesis: The purpose of this study was to examine the background of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole in patients with HC using pulsed Doppler echocardiography., Methods: Hemodynamic abnormalities between the left atrium and left ventricle during atrial systole were evaluated in patients with HC using transmitral flow (TMF) and pulmonary venous flow (PVF) velocities obtained by transesophageal pulsed Doppler echocardiography. The study population included 50 patients with HC, including 39 with asymmetric septal hypertrophy and 11 with apical hypertrophy, and showing fractional shortening of the left ventricle > or = 30%. They were classified into three groups: (1) Group A (n = 11): the ratio of the late to early TMF velocity < 1, and peak atrial systolic PVF velocity (PVA) < 25 mm/s; (2) Group B (n = 13): their ratio < 1, and PVA > or = 25 mm/s; and (3) Group C (n = 26): their ratio > or = 1. The mean age of patients in Group A was lower than that in Groups B and C., Results: Left atrial dimension in Group B was significantly greater than that in the other HC groups and the control group. Furthermore, left atrial volume changes during atrial systole in Group B were significantly smaller than those in the other HC groups and the control group. Peak atrial systolic PVF velocity in Group B was significantly higher than that in the control group and in Group C. The duration of the atrial systolic waves of the TMF and PVF in Group B was significantly shorter and longer, respectively, than that in Group A. Left ventricular end-diastolic pressure (LVEDP) decreased in descending order with Group B > Group C > Group A. In all patients there was a significant positive correlation between the LVEDP and peak atrial systolic PVF velocity or the difference in duration between the atrial systolic waves of PVF and TMF. Plots of these values shifted toward the left and inferiorly in Group A, and toward the right and superiorly in Group B., Conclusion: Peak velocity and duration of TMF and PVF during atrial systole by transesophageal pulsed Doppler echocardiography are useful indices of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole, particularly a forceful atrial contraction mismatched to the left atrial afterload and severity of LV diastolic dysfunction, in HC.

Systolic ejection murmurs of the left heart usually have their peak during early to mid-systole. Few reports have addressed ejection murmurs with their peak at late systole. We evaluated the clinical significance of an apical systolic ejection murmur with a peak intensity during late systole using Doppler and two-dimensional (2-D) echocardiography and phonocardiography. The apical late systolic ejection murmur was observed in 9 of 13 consecutive patients with mid-left ventricular obstruction. We investigated the ejection flow velocity and the timing of maximum velocity at the three different sites of the left ventricle, the left ventricular cavity shape, and the timing of the peak murmur intensity in these nine patients (late-murmur group). The same parameters were also examined in 8 consecutive patients with mid-systolic ejection murmurs (mid-murmur group), 10 with early systolic ejection murmurs (early-murmur group), and 7 controls without murmurs. Patients with aortic stenosis were excluded. The mid-ventricular ejection flow velocity was significantly higher in the late-murmur group than in the other three groups; that of the outflow tract was markedly higher in the mid-murmur group. The ejection flow velocity at the aortic orifice of patients in the early-murmur group was significantly high compared with that of the controls. The timing of the peak murmur intensity in each group correlated with that of the peak flow signal at the corresponding site with maximum velocity. In all patients in the late-murmur group, 2-D echocardiography revealed a systolic narrowing of the cavity at the mid-ventricle. Amyl nitrite inhalation induced a marked increase in the intensity of the murmur without evidence of appearing or increasing mitral regurgitation. It was concluded that the apical ejection murmur with a late systolic peak intensity is a new phonocardiographic sign indicative of dynamic, mid-left ventricular obstruction. This murmur should be differentiated from the mitral regurgitant murmur.

The aim of the present study was to assess the changes of left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities during preload alteration in 30 patients with dilated heart (LV end-diastolic dimension > or = 6.0 cm) and impaired LV systolic function (% fractional shortening of the LV < or = 25%). We performed transesophageal pulsed Doppler echocardiography during lower body negative (LBNP, -40 mmHg) and positive pressure (LBPP, +40 mmHg) in 10 patients with dilated cardiomyopathy, in 20 with old myocardial infarction, and in 22 healthy controls. Eight of the patients showed a pseudonormalization (compliance failure) pattern, and 22 showed a decreased early diastolic wave and compensatorily increased atrial systolic wave (relaxation failure) pattern of LVIF in the control state. Mean pulmonary capillary wedge pressure (PCWP) was greater in the compliance failure group than in the relaxation failure group in the control state. LVIF in 6 of the 22 patients with the relaxation failure pattern changed to the compliance failure pattern during LBPP, and that in 3 of 8 patients in the compliance failure group changed to the relaxation failure pattern during LBNP. The 6 patients with a change from the relaxation failure to the compliance failure pattern showed significantly higher peak diastolic and atrial systolic PVFs during LBPP than in the control state, and significantly higher PCWPs in the control state than the 16 patients with no change in LVIF. These findings suggest that the compliance failure and relaxation failure patterns of LVIF are readily interchangeable in various hemodynamic conditions, and that pattern analysis of LVIF and PVF during preload alteration is useful for understanding the hemodynamic severity and for evaluating preload reduction therapy in the dilated heart.