Effects of the presence or absence of preceding angina pectoris on left ventricular function after acute myocardial infarction.

Left ventricular (LV) function was evaluated in 31 patients, who had total occlusion of the left anterior descending coronary artery and less than 70% stenosis of the other two major coronary arteries or any branch. Fifteen of 31 patients had a history of angina pectoris before acute myocardial infarction (AMI) and 16 of 31 patients had no history of angina pectoris before AMI. The patients with angina pectoris before AMI had a significantly better ejection fraction, percentage of abnormally contracting segment, and regional wall motion than those without angina pectoris before AMI. These data suggest that the symptom of angina pectoris before AMI could be a favorable sign in preserving LV function when the patients subsequently had AMI.

Esophageal echocardiographic left ventricular anterolateral wall motion in normal subjects and patients with coronary artery disease.

Esophageal echocardiography was developed for recording left ventricular anterolateral wall (LVAW) echocardiograms and was applied clinically to 14 normal subjects and 21 patients with coronary artery disease. LVAW echocardiograms were obtained satisfactorily in 11 of 14 normal subjects (75%) and 20 of 21 patients (95%) with coronary artery disease. LVAW echocardiograms were obtained by conventional anterior echocardiography in eight of 21 patients (38%) with coronary artery disease. In 11 normal subjects, mm/sec (mean 34.3 +/- 5.2 mm/sec); and diastolic wall thickness ranged from 9-12.5 mm (mean 11.2 +/- 0.7 mm). In 20 patients with coronary artery disease, LVAW motion obtained by esophageal echocardiography was classified into five groups according to the excursion, and the findings were in good agreement (80%) with those obtained by left ventriculography. Classification of LVAW motion by conventional echocardiography agreed with that of left ventriculography in only three of eight patients, although all eight patients had abnormal LVAW motion by the conventional method. In all patients except one, whose LVAW echocardiograms were obtained by conventional echocardiography, excursion was much less than that obtained by esophageal echocardiography. We conclude that the projection of an ultrasonic beam from the intraesophageal transducer is a better approach for accurate measurement of LVAW motion.

[Exercise echocardiography: II. Interventricular septal wall dynamics in patients with left anterior descending coronary disease during recovery (author's transl)].

Supine ergometer exercise test was performed in 10 healthy subjects and 9 patients who had severe stenosis in the left anterior descending coronary artery [5 patients with stenosis proximal to the septal perforator (proximal LAD disease) and 4 patients with stenosis distal to the septal perforator (distal LAD disease)]. In healthy subjects and patients with distal LAD disease, the increment of septal excursion (IVS Ex) and percent systolic thickening of the septum (% delta Th) during exercise returned to the pre-exercise level with a few minutes after exercise. In patients with proximal LAD disease, IVS Ex decreased to 1.4 +/- 1.2 mm during exercise form the pre-exercise level (7.4 +/- 0.7 mm) and % delta Th decreased to 6.4 +/- 5.1% during exercise from the pre-exercise level (37.2 +/- 8.4%). After exercise, IVS Ex and % delta Th increased to 8.6 +/- 0.9 mm at 2 min and 38.0 +/- 9.8% at 3 min respectively and then returned to the pre-exercise level. End-diastolic wall thickness (WTh) did not change during and after exercise in healthy subjects and patients with distal LAD disease, while in patients with proximal LAD disease, WTh increased for a few minutes after exercise and returned to the pre-exercise level. The change of electrocardiogram and symptom of angina pectoris lasted longer than the abnormal wall motion.

[Exercise echocardiography: interventricular septal thickness and motion in patients with effort angina during ergometer exercise (author's transl)].

To detect abnormal interventricular septal (IVS) motion during exercise-induced ischemia, ergometer exercise echocardiography was performed using a specially devised transducer in 12 patients (pts) with effort angina (left anterior descending artery disease) and 10 normal subjects (N) at rest, and during exercise and recovery. During exercise, percent systolic IVS thickening (% delta T) and IVS excursion (Ex) increased from 52 +/- 13% at rest to 73 +/- 19% and from 7.0 /- 1.3 mm at rest to 10.6 +/- 1.9 mm, respectively, in N, and also from 52 +/- 23% to 67 +/- 36% and from 7.3 +/- 1.9 mm to 9.7 +/- 2.1 mm in all of 3 pts with distal left anterior descending artery disease. On the other hand, in 9 pts with proximal left anterior descending artery disease, % delta T and Ex during exercise decreased from 41 +/- 17+ at rest to 26 +/- 25% and from 7.7 +/- 1.2 mm to 5.1 +/- 4.6 mm. The late systolic wall thickening of IVS was observed during peak exercise in 2 of the 9 pts, one of whom exhibited systolic IVS thinning and a decrease in diastolic thickness (from 6 mm to 4.5 mm). In 5 pts with IVS asynergy during exercise diastolic IVS thickness increased maximally from 10.2 +/- 3.3 mm at rest to 11.4 +/- 3.5 mm during recovery (reactive hyperemia). Exercise echocardiography is useful to predict the location of left anterior descending artery disease and to evaluate IVS performance during exercise-induced ischemia.

Type IV glycogenosis - a study of two cases.

Liver biopsy materials of two siblings with type IV glycogenosis were studied by light and electron microscopy. Biochemical analysis was added using autopsy material in one of the two cases. Two kinds of polysaccharides were noted not only in the cardiac muscle, skeletal muscles, smooth muscles and reticuloendothelial cells, but also in the neutrophils and platelets. One was glycogen and the other was similar to amylopectin. Ultrastructurally, a large amount of fibrils, 60 A in width, glycogen rosettes and glycogen granules were detected in those cells. Branching glycosyltransferase deficiency was biochemically confirmed in one case examined.