Volume-rendered three-dimensional dynamic anatomy of the mitral annulus using a transesophageal echocardiographic technique.

Mitral annulus anatomy and dynamics were evaluated in 12 subjects using a three-dimensional transesophageal echocardiographic technique. The mitral annular area, diameters and distance from the left ventricular apex were measured in end-diastole, mid-systole, end-systole and mid-diastole. The mitral annulus had its largest area in end-systole and the smallest area in end-diastole. The shape of the annulus changed during the cardiac cycle with the maximal change occurring in the diameters passing close to the middle of the mitral leaflets. In the vertical plane, the annulus had a shallow ski-slope shape, with the attachment of the anterior leaflet being farthest from the apex. In other words, the highest point of the annulus was situated anteromedially and was visualized in the long axis imaging plane.

Mechanisms of hypotension during dobutamine stress echocardiography in patients with coronary artery disease.

Fifty-nine consecutive patients with angiographically documented coronary artery disease were prospectively studied during dobutamine stress echocardiography. Twelve patients (20%) developed hypotension, defined as a decrease in systolic blood pressure of > or = 20 mm Hg compared with baseline. The transmitral flow velocities, isovolumic relaxation time (IVRT), and flow in the left ventricular (LV) outflow tract were measured at baseline, at maximal dobutamine dose, or during a hypotensive episode; stroke volume, cardiac output, and systemic vascular resistance (SVR) were computed. Correlates of hypotensive response to dobutamine stress echocardiography included therapy with angiotensin-converting enzyme inhibitors (p = 0.032), a longer IVRT at baseline (121 +/- 25 vs 103 +/- 28 ms, p = 0.047), a greater decrease in LV end-diastolic (-6.0 +/- 3.1 vs -2.2 +/- 2.1 mm, p < 0.0001) and end-systolic (-8.3 +/- 7.0 vs -5.1 +/- 3.7 mm, p = 0.037) dimensions, and a greater decrease in stroke volume (-10 +/- 10 vs -2 +/- 11 ml, p = 0.023) compared with those with a normal response. The groups did not differ significantly with regard to baseline stroke volume, cardiac output, SVR, and LV ejection fraction or LV mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Normal changes in left ventricular filling and hemodynamics during dobutamine stress echocardiography.

During high-dose dobutamine infusion, there is a dose-dependent increase in cardiac output, a reduction in systemic vascular resistance, a reduction in left ventricular size, an increase in the mitral A wave velocity, a reduction in the E/A velocity ratio, and a reduction in the isovolumic relaxation time, with little change in the rate-corrected isovolumic relaxation time. Left ventricular cavity obliteration is common. This information may be useful in defining the mechanism of hypotension commonly seen during dobutamine stress echocardiography. It is speculated that the diastolic behavior of the left ventricle during dobutamine stress echocardiography, especially the isovolumic relaxation time, may provide an additional indicator of early myocardial ischemia, but this needs to be confirmed by larger independent studies.

Dobutamine stress echocardiography for the diagnosis and management of coronary artery disease.

Infusion of dobutamine in low and high doses in combination with echocardiography can be used for the assessment of myocardial viability and functional significance of coronary artery disease. Improvement of contractile function of hypokinetic or akinetic ventricular wall segment with low-dose dobutamine has a high predictive value for the detection of hibernating and stunned myocardium. High-dose dobutamine stress is of value for noninvasive diagnosis of coronary disease, assessment of its clinical significance, risk stratification of patients after myocardial infarction, preoperative evaluation of patients undergoing major noncardiac surgery, and assessment of the efficacy of coronary revascularization. It has an excellent safety record even in the immediate postmyocardial infarction period.

In-hospital and follow-up mortality of patients with acute myocardial infarction.

Patients with definite acute MI who were admitted to Songkla University Hospital between 1982 and 1990 were studied. The 195 patients and 202 admissions were nearly equally distributed between these 65 and older versus those younger than 65. Three quarters were males. The in-hospital mortality was 19.5 per cent and 76.3 per cent of the deaths were from heart failure. Neither age nor gender determined the mortality once corrected for the Killip's staging. There was no difference in mortality when comparing Q versus non-Q MI, anterior versus inferior wall MI or males versus females. One hundred and thirty-eight patients could be followed for and average of 27.1 months. First year mortality was 11 per cent and the first 2 years was 14 per cent. The in-hospital mortality, representing the prethrombolytic era, appeared to be similar to values reported from the Thai and Western literature. The predominance of death from heart failure rather than from arrhythmia may be a consequence of delayed admission whence arrhythmic death had already occurred or patients will seek hospital advice only if highly symptomatic.

Double-blind evaluation of enalapril in patients with systolic heart failure.

Fifty-six patients with a mean age of 58 years, 14 females and 42 males, all with dominant systolic heart failure (33 in functional class 3 and 4) were randomised to receive either added placebo or added enalapril to their heart failure medication. There were 13 patients in this group who had their trial drug switched after a certain period to allow direct but blind comparison between placebo and enalapril. Cardiac mortality with enalapril was 32 per cent compared to 48 per cent with placebo at intervals after initiating therapy of 20.0 +/- 19.4 versus 14.3 +/- 11.5 months respectively. When compared to a preceding control period, 80 per cent of the enalapril patients improved in contrast to 21 per cent of the placebo. However, when a comparison was made directly between enalapril and placebo, enalapril was better in 31 per cent and placebo was better in 8 per cent of the patients. It is concluded that in certain patients with systolic heart failure from non-valvular and non-hypertensive causes, enalapril is beneficial when added to the conventional treatment. An argument is also presented that to cost-effectively identify the group who will benefit, a short term ACE-I trial after the conventional antifailure therapy can be considered in all patients with systolic heart failure.

Embolism and atrial fibrillation. A longitudinal follow-up.

Six hundred and forty-nine patients with proven chronic atrial fibrillation were followed for a total of 1,436 patient-years without anticoagulation. The patient were divided into 7 disease groups with each having an average age ranging from 39 to 69 years. Eleven per cent of the patients had systemic embolism prior to being registered for the follow-up. The diseases which had the highest incidence of embolism prior to being followed were the same as those producing the highest rate of systemic embolism while under observation. The disease groups were rheumatic valvular (predominantly mitral stenosis) and ischemic heart diseases. Their embolic rate were 3.9 to 5.1 emboli per 100 pt-yr. Other disease groups with lower embolic rates of 0 to 0.9 per 100 pt-yr were heart failure, non-rheumatic mitral regurgitation, atrial septal defect and thyrotoxicosis. Since the incidence of systemic embolism varied according to the primary disease, and since the hemorrhagic complication of anticoagulant therapy is finite, it is advised that low risk group may not benefit greatly from anticoagulation. However, the true low risk group has still to be properly determined.

Patients with prosthetic cardiac valves followed in southern Thailand.

Prospective follow-up of 174 post-prosthetic cardiac valves have been done at Prince of Songkla University and Hat Yai Regional hospitals since 1985. The total follow-up time was 549 patient-years (pt-yr). Thirty per cent had been followed for 1 year or less. Eighty-two per cent of the patients had their mitral valves replaced either singly or as part of a multiple replacement. Thirty per cent of the time, the prothrombin time was below therapeutic range. Major events did not appear to be different from other reports: 2.7 embolic events per 100 pt-yr, 3.2 major bleeds and 3.2 deaths which may eventually be as high as 4.4 if a portion of the lost patients was assumed to have died. Events related to prosthetic valves and anticoagulation seemed to occur predominantly 1-2 years after surgery.

Trimetazidine and stable angina a double-blind trial.

The effect of trimetazidine was evaluated in patients with stable angina by adding it to the other antianginal regimen in a double blind crossover design each of 8 week's duration. The method of evaluation made use of symptom recall, daily dairy of the intake of sublingual nitrates or of anginal discomfort and in some, symptom limited treadmill exercise stress test (EST). Thirty-six patients completed the trial. Symptom-wise, 16 patients could not differentiate the effect of the true tablet from the placebo. Eight had less and 12 had more angina while on the drug. Of the 17 evaluable EST, 9 showed no change in the degree of ischemic changes while 4 performed with less and 4 with more ischemia while on the drug. Symptom-wise and taking into account the pre and post trial periods, a placebo effect was not found to be dominant. It is concluded that trimetazidine does not improve angina among those already being treated with conventional doses of nitrates, beta and calcium blockers.