It has been reported that panic attacks might cause mitral valve prolapse (MVP) via haemodynamic or indirect effects. Such prolapse can be classified as being physiological (benign course) or pathological (poor course). It is therefore important to consider whether panic attacks, as a risk factor for MVP, are associated with its physiological or pathological type. Our study sample consisted of two groups of patients with panic disorder (PD), one having onset within 1 year (n=24) and the other with a history of more than 10 years (n=21). Demographic data, symptom presentations, auscultatory and echocardiographic findings of both groups were compared, but no significant difference was found except with regard to anticipatory anxiety. It is concluded that panic attack exerts no significant effect on mitral valve prolapse.

In conclusion, this study demonstrates, in an animal model, that analysis of the digitized two-dimensional echocardiogram may detect the acute changes in mean gray level (occurring as early as 30 minutes after coronary artery ligation) caused by myocardial ischemia. The clinical application of our findings to humans requires further study.

This study showed that (1) the prevalence of MVP in patients with Wolff-Parkinson-White syndrome and AV nodal reentrant tachycardia was similar to that of the general population; (2) the location of accessory pathways was not related to the presence of MVP; and (3) MVP was persistently present after elimination of preexcitation. These findings suggest that MVP may have an independent association with PSVT. The study limitations are: (1) Acquisition bias should be noted because the prevalence of PSVT in patients found to have MVP was not obtained. (2) Comparison between patients with PSVT and an ageand sex-matched population sample in whom MVP was assessed by identical methods was not performed; thus, the association between MVP and this family of arrhythmias was not obtained. Furthermore, the higher prevalence of MVP in patients with both accessory pathway-mediated and AV nodal reentrant tachycardia must be reassessed.

A group of consecutive 180 veteran patients with mild to moderate essential hypertension were chosen to participate in clinical antihypertensive trial for the purpose of defining the role of converting enzyme inhibitors and renin-angiotensin-aldosterone system in the management of mild to moderate hypertension patients. After a two-week placebo period, these patients were randomly assigned to regimens of converting enzyme inhibitors (enalapril or captopril with or without diuretics) or conventional therapy (diuretics with or without traditional vasodilators with or without beta-blockers). Each patient was regularly followed up every two weeks and doses were added until the diastolic blood pressure was equal to or lower than 90 mmHg. After 1 year of follow-up, only 162 patients completed the study. All high blood pressure was significantly reduced by these three regimens, but no significant difference of blood pressure control was noted. The mean left ventricular ejection fraction increased from 55.9 +/- 6.2 to 57.5 +/- 5.3% in captopril group (P less than 0.05, n = 59) and from 54.8 +/- 6.8 to 57.2 +/- 5.8% enalapril group (P less than 0.01, n = 53), in contrast to the insignificant change in control group (n = 50) (56.5 +/- 7.7 to 56.6 +/- 5.9%). The exercise duration also significantly increased only in converting enzyme inhibitors group (P less than 0.01). Furthermore, the plasma aldosterone level was significantly reduced by converting enzyme inhibitors therapy, whereas conventional therapy had no beneficial effect (P less than 0.01). Furthermore, the plasma aldosterone level was significantly reduced by converting enzyme inhibitors therapy, whereas conventional therapy had no beneficial effect (P less than 0.001). Concomitantly, antidiuretic hormone and plasma norepinephrine levels were also significantly reduced by converting enzyme inhibitors. In addition, converting enzyme inhibitors had a favorable trend to affect the metabolism of lipid in contrast to the conventional therapy. These results show that a first-step treatment of hypertension with converting enzyme inhibitors permits better left ventricular function and improves exercise tolerance by way of renin-angiotensin-aldosterone system inhibition. Thus, converting enzyme inhibitors might be suggested as the first step regimen in the treatment of hypertension.

Mitral regurgitation (MR) was evaluated by Doppler echocardiography in 59 patients with mitral stenosis before, immediately after and 1 year after balloon mitral valvuloplasty (BMV). The severity of MR was graded on a scale from 1+ to 4+. Echocardiographic and hemodynamic variables were analyzed to study the potential factor(s) that might predict the long-term persistence of MR. Echocardiographic variables were mitral valve thickness and motion, subvalvular change, left atrial dimension, commissural calcification and effective balloon/mitral anular diameters. Hemodynamic variables were mitral pressure gradient, pulmonary arterial pressure, ejection fraction, mitral valve area index, age, gender and cardiac rhythm. Mitral valve area index increased from 0.9 +/- 0.5 to 1.5 +/- 0.8 cm2/m2 immediately after BMW, and to 1.4 +/- 0.3 cm2/m2 at 1 year follow-up (p less than 0.01). Immediately after BMV, MR grading did not change in 30 patients (51%), increased by 1+ in 23 patients (39%), by 2+ in 2 patients (3.3%) and by 3+ in 2 patients (3.3%), and decreased by 1+ in 2 others. At 1-year follow-up, only 1 patient with severe MR required valve replacement. Fifty-one patients (88%) had no change in the extent of MR (less than or equal to 1+) and 6 patients (10%) had a 1-grade decrease in their MR; only 1 patient had a 1-grade increase in MR. No clinical or hemodynamic variables or morphologic characteristics of the mitral valve could predict the development of significant MR after BMV. It is concluded that an increment in MR severity less than or equal to 2+ is frequently seen after BMV.(ABSTRACT TRUNCATED AT 250 WORDS)

The study tested whether an experimental myocardial infarction can be detected from two-dimensional echocardiograms (2DE) by analysis of regional gray levels. The mid-left anterior descending coronary artery was ligated for 3 hours in 14 dogs (group 1) and for 5 hours in 6 dogs (group 2). 2DE were performed before, and after 3 and 5 hours of coronary artery ligation. The ultrasonic amplitude of the control and infarcted regions were obtained from digitized 2DE in the short axis view, at the mid-papillary muscle level. The mean gray levels (+/- SD) of the control and infarcted regions were compared during end-diastolic stop frames. After sacrifice, the hearts were cut into 1 cm thick slices and stained with 1% triphenyl tetrazolium chloride (TTC) solution. The myocardium was then studied by light microscopy. Computerized tomographic scans were also obtained in vitro from 3 hearts of both groups. There was no difference in mean gray levels of the control region during the experiments. However, in the region of wall motion abnormality (area of infarction), the mean gray levels increased from 49.9 +/- 3.5 (before ligation) to 62.0 +/- 7.4 (after 3 hours of ligation, p less than 0.005) in 10 group 1 dogs, but no differences were seen in mean gray levels (49.6 +/- 3.8 vs 50.4 +/- 4.0) in those without a myocardial infarction in 4 group 1 dogs; gray levels also increased from 50.4 +/- 2.9 (before ligation) to 58.6 +/- 6.1 (after 3 hours of ligation, p less than 0.05) and to 65.0 +/- 4.2 (after 5 hours of ligation, p less than 0.005) in group 2 dogs. The area of left ventricular asynergy corresponded precisely to the area of myocardial infarction, determined by both TTC staining and the computerized tomographic scans. The light microscopy of the infarcted area also demonstrated interstitial edema and polymorphonuclear cell infiltration.