Masako Matsuda

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.

Sphingosylphosphorylcholine induces cytosolic Ca2+ elevation in endothelial cells in situ and causes endothelium‐dependent relaxation through nitric oxide production in bovine coronary artery

Sphingosylphosphorylcholine (SPC) increased intracellular Ca2+ concentration ([Ca2+]i) and nitric oxide (NO) production in endothelial cells in situ on bovine aortic valves, and induced endothelium‐dependent relaxation of bovine coronary arteries precontracted with U‐46619. The SPC‐induced vasorelaxation was inhibited by N ω‐monomethyl‐L‐arginine, an inhibitor of both constitutive and inducible NO synthase (NOS), but not by 1‐(2‐trifluoromethylphenyl) imidazole, an inhibitor of inducible NOS (iNOS). Immunoblotting revealed that endothelial constitutive NOS, but not iNOS, was present in endothelial cells in situ on the bovine aortic valves. We propose that SPC activates [Ca2+]i levels and NO production of endothelial cells in situ, thereby causing an endothelium‐dependent vasorelaxation.

Familial isolated noncompaction of ventricular myocardium

AbstractWe report a family in which two male sibs were affected with isolated noncompaction of ventricular myocardium (INVM). The familial occurrence of INVM suggests a genetic basis. We review the literature of familial and nonfamilial cases and discuss the inheritance pattern of INVM.

Coronary angiography during exercise-induced angina with ECG changes

Coronary angiography was performed at rest and during bicycle exercise immediately after the onset of angina and significant ST segment elevation or depression in the ECG. Of 11 patients, six showed significant reduction of coronary lumen diameter at the site of organic stenosis; mean values of stenosis (range) before and during exercise were 55% (25% to 88%) and 98% (89% to 100%), respectively. Five patients did not have any diameter change of the organic lesion; mean values of stenosis (range) before and during exercise were 84% (74% to 89%) and 84% (73% to 92%), respectively. Excluding the areas of these stenoses, diameters of left main coronary artery, proximal, middle, and distal left anterior descending, circumflex, and right coronary artery segments were measured before and during exercise. Diameter in each coronary artery segment during exercise was not significantly changed from that before exercise, both in the groups with and without diameter reduction. Exercise provoked a localized worsening of coronary artery stenosis without changing the diameter in the remaining artery. These findings suggest that the worsening of stenosis might be caused by a regional abnormality of the coronary artery that is not necessarily related to the degree of organic stenosis.

Angina pectoris before and during acute myocardial infarction: Relation to degree of physical activity

One hundred ninety-seven patients with a history of acute myocardial infarction (AMI) were interviewed to evaluate the character of angina pectoris relative to physical activity before AMI and at the onset of AMI. Ninety-two patients had no angina before AMI and 105 had angina. Among the 105 patients with angina, 58 had chronic stable angina that did not change before AMI, 22 noted worsening of symptoms within 2 weeks before AMI, and 25 had onset of angina within 2 weeks before AMI. In the 92 patients without angina before AMI, AMI occurred during heavy exertion in 10 (11%), mild exertion in 43 (47%), at rest in 28 (30%), and during sleep in 11 (12%). In the 58 patients with chronic stable angina, 47 had angina during exertion, 7 during rest and 4 during both. However, subsequent AMI occurred during heavy exertion in 9 (15%), during mild exertion in 16 (28%), at rest in 25 (43%), and during sleep in 8 (14%). In the patients without angina, or with chronic stable angina without worsening of symptoms, AMI occurred unpredictably or differently from the mode of physical activity precipitating angina before AMI.

Response of the coronary artery to a small dose of ergonovine in variant angina

The response of the coronary artery to a small dose (0.01 mg) of ergonovine was observed in nine patients without variant angina and in 10 patients with variant angina. Coronary angiograms were obtained before and after small and larger (routinely used) doses of ergonovine. With the larger dose, all 10 patients with variant angina had total or subtotal spastic occlusion accompanied by angina and ECG changes. Excluding the site of spastic occlusion produced by the larger dose of ergonovine, diameters of proximal, middle, and distal segments in each major coronary artery were measured before and after a small dose of ergonovine. The mean percentage of change in diameter (diameter before - diameter after a small dose of ergonovine)/diameter before a small dose of ergonovine X 100% in patients without variant angina was not significantly different from that in patients with variant angina (5.2 +/- 9.5% vs 7.0 +/- 11.9%, respectively). However, in patients with variant angina, a small dose of ergonovine produced a percentage of change in diameter of 39.8 +/- 15.3% at the site of spastic occlusion included by a larger dose of ergonovine, compared with that of 7.0 +/- 11.9% in the remaining non-spastic coronary arteries (p less than 0.05). These results indicate that patients with variant angina have local segments which respond differently to ergonovine from the remaining segments of coronary arteries. Clinically, this observation might be helpful in determining the angiographic positivity to ergonovine.

Transient appearance of collaterals during vasospastic occlusion in patients without obstructive coronary atherosclerosis

Coronary angiography of both right and left coronary arteries, using the Sones technique, was performed during the attack of total spastic obstruction in 11 patients with clinically documented history of variant angina. None of the patients had more than 70% stenosis of organic atherosclerosis in any coronary artery and none had a history of myocardial infarction. Total spastic obstruction occurred spontaneously in 3 of 11 patients, and was provoked by ergonovine maleate in eight patients. Six patients had total spastic obstruction in the left anterior descending coronary artery, four patients had total obstruction in the right coronary artery, and one patient had total obstruction in the left anterior descending and right coronary arteries. In 7 of 11 patients, the coronary artery distal to the total spastic obstruction received collaterals from the nonspastic artery. The collaterals disappeared promptly when the spastic coronary artery was patent. These patients had ST segment elevation in the ECG during the attacks. In the remaining four patients, the spastic artery did not receive any collaterals from the nonspastic artery, associated with ST segment elevation during the attacks. These findings suggest that the brief, repetitive total occlusion of the coronary artery may stimulate the enlargement of collaterals. These collaterals may not always function to prevent the ischemia of the myocardium on the ECG.

Longitudinal study of a health education program for Japanese women in menopause.

In this longitudinal intervention study, a 6 week health education program consisting of lectures and exercises was implemented for 39 Japanese menopausal women. The effects of the program were assessed by measuring their exercise participation, climacteric symptoms, and quality of life immediately before, 6 weeks after, and 1 year after the program. The Simplified Menopausal Index was used to assess the climacteric symptoms and the Medical Outcomes Study 36-Item Short-Form Health (SF-36) Survey was used to assess the quality of life. Significant improvements were observed in the subscale score for general health perception and the summary score for the physical component summary in the SF-36 Survey. Favorable results also were found for women without a previous exercise habit before the program but who participated in regular exercise 1 year after the program. No improvements were observed in the climacteric symptoms. We concluded that our program was effective for menopausal women in spite of the intervention period being relatively short.

Clinical characteristics of unstable angina before acute myocardial infarction

Four hundred and seventy-six patients with acute myocardial infarction (AMI) were interviewed to evaluate the clinical features of angina before AMI. Two hundred and sixty-six of the 476 patients had angina before AMI, of which 137 had new onset of angina within 2 months before AMI, and 129 had chronic angina of more than 2 months before AMI. Forty of the 129 chronic angina patients noted worsening of symptoms within 2 months before AMI. Of the 177 patients with new onset angina or worsening angina such as unstable angina, the incidence of new onset angina was higher than that of worsening angina. Twenty-eight (70%) of the 40 patients with worsening of symptoms had started with effort angina, 16 of whom turned to resting angina from effort angina at the onset of unstable angina in spite of the fact that 12 had worsening of effort angina. Of the 137 patients with new onset angina, 65 (40%) started with resting angina and 72 (53%) with exertional angina. In the former group, 43 (66%) developed AMI within 1 week after the onset of angina, which was greater than 19 (26%) in the latter group. These results may suggest that the appearance of the resting angina would herald AMI in both groups of unstable angina. The onset of resting angina in the group of new onset angina could be the warning of AMI development within a shorter interval than those of exertional angina.

Left ventricular wall motion at rest in patients with organic coronary artery disease vs coronary spasm.

Left ventricular ejection fractions and regional ejection changes obtained from left ventriculograms at rest were analyzed in 15 normal subjects, in 17 patients with isolated, organic left anterior descending coronary artery disease, and in 11 patients with isolated left anterior descending coronary artery spasm. Patients with coronary artery spasm did not have significant organic lesions at the site of spasm. All patients with organic coronary artery disease and coronary artery spasm had a history of angina pectoris without myocardial infarction. No significant differences in ejection fraction were observed among the three groups. The regional ejection change of the anterolateral and apical wall supplied by the left anterior descending coronary artery was significantly decreased in patients with organic coronary artery disease compared with those in normal subjects (anterolateral 39.5 +/- 10.3% vs 48.4 +/- 7.7%, p less than 0.05; apical 48.4 +/- 8.8% vs 55.6 +/- 7.8%, p less than 0.05). However, the anterolateral and apical wall motion was not impaired in patients with coronary artery spasm. Thus, patients with organic coronary artery disease had impairment of left ventricular wall motion, while those with coronary artery spasm did not, although both groups of patients had symptoms of angina. These results suggest that patients with organic coronary artery disease may have had coronary blood flow disturbances through stenosed vessels and chronic active ischemia that produced left ventricular impairment.