Severe Left Ventricular Diastolic Dysfunction Research Articles

Transesophageal pulsed Doppler echocardiographic evaluation of left atrial systolic performance in hypertrophic cardiomyopathy: combined analysis of transmitral and pulmonary venous flow velocities.

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. 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. 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. 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. 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.

756-2 Long Term Results of Dual Chamber (DDD) Pacing in 114 Adult Patients with Obstructive Hypertrophic Cardiomyopathy and Severe Drug-Refractory Symptoms

Several studies indicate that short term, dual chamber (DOD) pacing relieves symptoms and reduces LV outflow tract (LVOT) obstruction in hypertrophic cardiomyopathy (HCM). We evaluated the long term outcome of DDD pacing in 114 adult patients (age, 47 ± 15 yrs) with obstructive HCM and symptoms refractory to β -blocker and verapamil therapy. Three sudden deaths occurred during a follow up period of 34 ± 10 months, maximum, 52 months (98% 3-year survival rate). At the last follow up evaluation, the NYHA functional class improved significantly (3.1 ± 0.54 versus 1.7 ± 0.72, p &lt; 0.0001). Thirty-seven patients (32%) became asymptomatic. Symptoms were improved in a further 62 patients (54%). However, 12 patients (10%) continued to have disabling symptoms for various reasons: 8 had persistent LVOT obstruction (in 3 patients an aberrant papillary muscle contributed to the LVOT obstruction and in 3 patients, rapid AV node conduction prevented RV pacing), 3 patients had severe LV diastolic dysfunction, and 1 patient had mitral valve prolapse and regurgitation. Seven of the 12 patients underwent corrective cardiac surgery, and two patients are being considered for cardiac transplantation. At a follow up cardiac catheterization after 14 ± 8 months of pacing, there were significant reductions in LVOT gradient (79 ± 45 mmHg versus 26 ± 31 mmHg, p &lt; 0.0001) and LV systolic pressure (188 ± 44 mmHg versus 147 ± 32 mmHg, p &lt; 0.0001) comparing baseline and follow up measurements. Aortic pulse pressure increased (45 ± 17 mmHg versus 52 ± 14 mmHg, p &lt; 0.01). These results suggest that long term, DDD pacing relieves symptoms and LVOT obstruction in most HCM patients who would otherwise have been candidates for cardiac surgery.

Noninvasive detection of left ventricular diastolic dysfunction using M-mode echocardiography to assess left ventricular posterior wall kinetics in hypertrophic cardiomyopathy

In patients with hypertrophic cardiomyopathy (HC), it is difficult to determine the severity of left ventricular (LV) diastolic dysfunction. Three different patterns of LV posterior wall motion were found by M-mode echocardiography in patients with HC, and the use of these patterns is proposed as a new noninvasive index of the severity of LV diastolic dysfunction. M-mode echocardiograms were recorded prospectively from 35 patients with HC, and the posterior wall motion pattern in late systole and early diastole was classified into the following 3 types: (1) normal motion (n = 9); (2) flat motion — flat motion from late systole to early diastole, followed by rapid backward movement (n = 13); and (3) downward motion — slow backward movement from late systole (n = 13). There were no differences in the severity or type of hypertrophy, LV systolic function and pulsed Doppler indexes of LV filling among these 3 groups. However, LV end-diastolic pressure was increased in the groups with flat (15 ± 6 mm Hg) and downward (16 ± 9 mm Hg) motion. Furthermore, the maximal rate of decrease in LV pressure (normal 1,450 ± 300, flat 1,250 ± 300 and downward 860 ± 80 mm Hg/s) and the time constant of LV pressure reduction (normal 60 ± 15, flat 70 ± 25 and downward 101 ± 34 ms) showed a stepwise deterioration from the normal to the flat and then to the downward motion groups. Determination of the pattern of LV posterior wall motion appears to be useful for semiquantitatively assessing the presence and severity of LV diastolic dysfunction in HC, especially during relaxation and early diastolic filling.

Doppler echocardiographic patterns of left ventricular filling in patients early after acute myocardial infarction

Diastolic function is routinely assessed using Doppler-derived left ventricular (LV) filling patterns. Ratios between peak flow velocities during early filling and atrial contraction ( E A ) of <1 are considered pathologic and diagnostic of impaired relaxation. Myocardial stiffness can normalize the E >A ratio, and thus, in some clinical settings, a normal E A ratio may identify patients with high filling pressures. LV filling patterns were studied with Doppler echocardiography in 15 healthy subjects and 38 patients with recent acute myocardial infarction. The results were correlated with clinical and hemodynamic variables. E A ratio <1 was found in 14 patients (37%) and in only 1 control subject; E A ratio >2 was found in 5 patients (13%) and in only 1 control subject; 19 patients (50%) had an apparently normal E A ratio. No correlation was found between LV filling pattern and ejection fraction or presence of diabetes or arterial hypertension. LV end-diastolic pressures were low to normal in patients with an E A ratio <1 and were usually >15 mm Hg in those with normal or abnormally increased (>2) E A ratios. Thus, an apparently normal E A ratio in patients after myocardial infarction may identify those with more severe LV diastolic dysfunction and increased LV filling pressure.