Naito Foundation

The effects of pharmacologically induced changes in myocardial properties on diastolic mitral valve mechanics were studied in five open-chest dogs. After the induction of complete atrioventricular block, the dogs were subjected to a protocol of programmed pacing. During prolonged diastolic pauses, programmed atrial contractions were induced at progressively increasing coupling intervals. Echocardiographically determined mitral valve reopening time was established for each coupling interval in the control state as well as under the influence of calcium or verapamil. Compared with control, calcium caused an increase in myocardial tension from 23.8 +/- 3.0 to 30.0 +/- 4.6 g/cm2 (mean +/- SD, p less than .005) as well as an increase in mean septal contraction and relaxation velocities from 142 +/- 25.9 and 144 +/- 15.2 mm/sec to 188 +/- 21.7 and 174 +/- 19.5 mm/sec, respectively (each p less than .001). Conversely, verapamil caused a decrease in mean myocardial tension from 23.8 +/- 3.0 to 19.4 +/- 5.3 g/cm2 (p less than .001) and in mean septal contraction and relaxation velocities from 142 +/- 25.9 and 144 +/- 15.2 mm/sec to 112 +/- 32.7 and 112 +/- 21.6 mm/sec, respectively (each p less than .001). At every coupling interval, calcium significantly (p less than .01 to .001) prolonged, whereas verapamil significantly shortened (p less than .01 to .001), mitral reopening time compared with the control state. These pharmacologically induced changes in mitral valve mechanics occurred despite variations in left ventricular volume, as well as left ventricular and left atrial pressures that under normal conditions exert opposite effects on mitral valve mechanics.(ABSTRACT TRUNCATED AT 250 WORDS)

Ninety-nine adult mongrel dogs underwent acute ligation of the proximal left anterior descending coronary artery. Thirty minutes later, the occlusion was released to evaluate the effectiveness of five antiarrhythmic protocols in eliminating reperfusion ventricular fibrillation. The five protocols included: protocol 1 --i.v. lidocaine, preligation and prerelease (n = 19); protocol 2 -- i.v. lidocaine, prereperfusion only (n = 22); protocol 3 -- chronic, oral, daily amiodarone for 2 weeks preligation (n = 19); protocol 4 -- i.v. procainamide, preligation and prereperfusion (n = 21); and protocol 5 -- i.v. verapamil, prereperfusion (n = 18). Each regimen was evaluated with respect to the incidence of reperfusion ventricular fibrillation in dogs that survived to reperfusion, and the results were compared to 77 control dogs that underwent identical coronary artery occlusion and release procedures without drug therapy. The incidence of reperfusion ventricular fibrillation was as follows: protocol 1 -- seven of 15 dogs (47%); protocol 2 -- six of 18 (33%); protocol 3 -- 11 of 16 dogs (69%); protocol 4 -- eight of 17 dogs (47%); and protocol 5 -- 10 of 17 dogs (59%), compared with 36 of 60 (60%) in control dogs. Using chi-square analysis, protocol 2 was beneficial (p < 0.05). The dogs were then stratified into high- and low-risk subgroups based on the arrhythmic events of the antecedent coronary artery ligation periods, and predictive risk indexes for the occurrence of reperfusion ventricular fibrillation were developed. the Mantel-Haenszel method of statistical analysis revealed that none of these protocols resulted in a statistically significant reduction in the incidence of reperfusion ventricular fibrillation. Thus, use of these predictive indexes plus appropriate statistical methods has revealed, unexpectedly, limitations in the efficacy of a spectrum of antiarrhythmic agents in preventing reperfusion ventricular fibrillation.

We attempted to detect mitral deformities in ostium primum atrial septal defect using real-time cross-sectional echocardiography. Transverse sections of the anterior mitral leaflet echo were examined in 11 patients with this malformation who subsequently received surgical treatment. The section for observing the transverse view of te anterior leaflet was along the sagittal plane of the body, because of the deformity of the mitral annulus. Each echocardiographic finding was compared with the surgical and angiographic findings. On the echocardiogram, the superior and inferior parts of the anterior mitral leaflet separated into two parts during diastole in all patients with mitral cleft. Thin linear echoes connected the ridges of the cleft and the ventricular septum in seven patients in whom the accessory chordae at that area were revealed at surgery. The systolic configuration of the anterior leaflet echo varied among the patients. The severity of the miral regurgitation seemed to relate not only to the size of the cleft but also to the systolic configuration of the anterior mitral leaflet. After surgery, diastolic separation of the anterior leaflet echo was no longer observed. However, the abnormal systolic configuration of the anterior leaflet was unchanged.