Variant angina in two brothers with left anterior descending coronary arterial spasm.
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Biomedical subjects
Publications and source records attributed to F Yoshino.
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Diurnal change of plasma atrial natriuretic peptide (ANP) concentration was observed in 14 patients with congestive heart failure (CHF) and in eight healthy control subjects. Blood pressure, heart rate, and plasma concentration of ANP were obtained at intervals of 4 hours beginning immediately after midnight. In the CHF group, plasma ANP concentrations at the time of blood sampling were all higher than those in the control group. Patients with severe CHF had higher plasma ANP concentrations than those in patients with less severe CHF. Plasma ANP concentration in the control group was highest at 4:00 AM and was lowest at 4:00 PM. The percent change of ANP secretion (% delta ANP): [(ANP at 4:00 AM-ANP at 4:00 PM)/ANP at 4:00 PM] x 100%, increased in the control group, while it decreased in the CHF group. Moreover, % delta ANP was much lower in patients with severe CHF than it was in patients with less severe CHF. There was a possible relation between the severity of CHF and the increase of ANP secretion associated with the relative diminution of nocturnal ANP secretion. Thus the present data imply that the diurnal change in ANP was lost in patients with CHF.
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To compare two expressions of the time constant for ventricular relaxation, 39 patients with various heart diseases (six normal, six angina pectoris [AP], 13 myocardial infarction [MI], eight hypertrophic cardiomyopathy [HCM], and six congestive cardiomyopathy [CCM]) were studied. One time constant was obtained by the method of Weiss et al. (T1) and the other was the ratio of left ventricular pressure at peak (-) dP/dt (Pm) to peak (-) dP/dt (T2). The deviation of T2 from T1 was expressed as 100 X (T2 - T1)/T1 (delta %). In normal subjects, T1 was nearly equal to T2 (32 +/- 3 and 32 +/- 6 msec, respectively), resulting in a low value of delta (-1 +/- 9). However, delta values in AP (20 +/- 23, p less than 0.05), MI (24 +/- 26, p less than 0.05), HCM (37 +/- 21, p less than 0.001), and CCM (46 +/- 24, p less than 0.001) were significantly higher than in normal subjects. Thus T1, T2, or delta separated the patient groups from the control subjects, and there were significant differences between T1 and T2 among the types of heart disease.
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.
The effects of nitroprusside (NP) on hemodynamics, especially on venous flow velocity of the inferior vena cava (IVC) were evaluated in 20 remote myocardial infarction patients. NP was given beginning at 10 micrograms/min, with subsequent increments of 10 micrograms/min every 5 minutes until the systolic blood pressure was reduced to about 30 mmHg. Pressure was measured by a catheter-tip micromanometer. Flow velocity of IVC was measured by a catheter-tip flow velocity probe. NP significantly decreased left ventricular systolic pressure, left ventricular end-diastolic pressure, mean aortic pressure, right ventricular systolic pressure, right ventricular end-diastolic pressure, mean pulmonary arterial pressure, mean pulmonary capillary wedge pressure, systemic vascular resistance index (SVRI) and left ventricular volume. Cardiac index (CI) was unchanged and stroke volume index was decreased. IVC pressure was unchanged, while right atrial (RA) pressure decreased. Subsequently, the pressure difference between IVC and RA increased significantly. The amplitude of IVC flow velocity decreased significantly. Twenty patients were classified into two groups according to whether or not the CI increased by NP. CI increased in 9 patients (group I) and decreased in 11 patients (group D). Compared to group D, control CI and the slope of end-systolic pressure-volume relation were less and the difference between IVC pressure and RA pressure was greater in group I. The patients with higher control SVRI had greater increase in CI during NP. In our study, the greater the depression of cardiac performance and the higher the SVRI, the greater the improvement of left ventricular pumping function during NP.
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The present study is an angiographic demonstration of coronary artery spasm during both spontaneous and exercise-induced angina in three patients with variant angina. In each case, clinical, ECG, coronary angiographic, and left ventriculographic observations were made at rest, during spontaneous angina, and during exercise-induced angina. The character of chest pain was similar during spontaneous and exercise-induced episodes. ST segment elevation was present in the anterior ECG leads during both episodes. The left anterior descending coronary artery became partially or totally obstructed during both types of attacks. When coronary spasm was demonstrated during both types of attacks, left ventriculography disclosed akinetic or dyskinetic wall motion in the area supplied by the involved artery. In those patients with reproducible exercise-induced ST segment elevation and chest pain, thallium-201 scintigraphy showed areas of reversible anteroseptal hypoperfusion. Thus in selected patients exercise-induced attacks of angina were similar to spontaneous episodes.
Left atrial function was evaluated in patients with and without remote myocardial infarction. The simultaneous left atrial pressure recording and left atrial and left ventricular cineangiograms were obtained with a catheter-tip micromanometer. The pressure-volume curve of the left atrium was composed of an A-loop and a V-loop. The ratio of active atrial emptying to left ventricular stroke volume in patients with myocardial infarction was significantly larger than that in normal subjects (42 +/- 12% vs 29 +/- 10%, p less than 0.05). The left atrial work was also significantly greater in patients with myocardial infarction (1690 +/- 717 mm Hg X ml) than in normal subjects (940 +/- 426 mm Hg X ml, p less than 0.05). The ratio of active atrial emptying to left ventricular stroke volume and left atrial work were significantly related in both normal subjects and patients with myocardial infarction (gamma = 0.72, p less than 0.01). The left ventricular ejection fraction correlated inversely with left atrial work (gamma = -0.5, p less than 0.05). Left atrial work also showed a significant linear correlation with left atrial volume before active atrial emptying (gamma = 0.82, p less than 0.01). We conclude that the left atrial contribution to left ventricular function is increased in patients with remote myocardial infarction. This left atrial contribution to the left ventricle is attributed to the Frank-Starling mechanism in the left atrium.
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A patient with an islet cell tumor of the pancreas that produced the watery diarrhea, hypokalemia, achlorhydria (WDHA) syndrome is presented. On celiac angiography an extremely vascular mass was seen in the body of pancreas with hypertrophied arteries and persistent, dense tumor staining.
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