Kikuo Sakai

Effect of nitroglycerin on coronary collateral function during exercise evaluated by quantitative analysis of thallium-201 single photon emission computed tomography

A noninfarcted, entirely collateral-dependent myocardial region provides an opportunity to assess the effect of nitroglycerin on coronary collateral function during exercise. Stress thallium-201 computed tomography was performed in seven patients with effort angina and no history of myocardial infarction, both before and after nitroglycerin (0.3 mg). All patients had single-vessel disease with total or subtotal (99% with delay) occlusion of proximal left anterior descending coronary artery and well-developed collaterals. The pressure-rate product, mean blood pressure, and heart rate at peak exercise did not differ before and after nitroglycerin. The size of the perfusion defect and the severity of ischemia during exercise estimated by quantitative analysis of thallium-201 single photon emission computed tomography were significantly less after nitroglycerin administration (extent score: 23 +/- 17 vs 7 +/- 9, p less than 0.01; severity score: 20 +/- 22 vs 3 +/- 4, p less than 0.05). The pressure-rate products at peak exercise did not differ before and after nitroglycerin, which suggested that the reduction in perfusion defect size was unlikely to be the result of decreased myocardial oxygen consumption. These results suggest that nitroglycerin improved coronary collateral function during exercise and thus prevented exercise-induced myocardial ischemia.

Exercise-induced silent myocardial ischemia in patients with vasospastic angina

UNLABELLED To clarify the incidence and clinical characteristics of exercise-induced myocardial ischemia in patients with vasospastic angina, we performed exercise thallium computed tomography in 25 patients who had no significant coronary artery stenosis greater than 70%. Coronary artery spasm was documented by coronary angiography in all patients. Eleven patients (44%) developed exercise-induced perfusion defects, but only four of them had anginal pain (36%). Diltiazem (90 mg, administered orally) prevented the development of exercise-induced perfusion defects in all patients. Multivessel coronary spasm was documented by coronary angiography in 11 patients, and nine of them (82%) showed exercise-induced perfusion defects (p less than 0.05). CONCLUSION (1) Exercise-induced myocardial ischemia was demonstrated in 44% of patients who had vasospastic angina without fixed coronary stenosis, and 64% of them were asymptomatic. (2) Patients with multivessel spasm had a greater prevalence of exercise-induced myocardial ischemia than those with single-vessel spasm.

Age-Related Decreases in Cardiac Receptor Control of Forearm Vascular Resistance in Humans

We examined 1) the relationship between the magnitudes of reflex forearm vasoconstriction during lower body negative pressure (LBNP) at -10 mmHg and ages in 59 subjects whose ages ranged from 24 to 77 years old, and 2) the slopes of the regression lines relating changes in forearm vascular resistance and those in central venous pressure in the three age-groups; those younger than 35 years old (n = 15), those between 35 and 55 years old (n = 12) and those older than 55 years old (n = 12). Forearm blood flow was measured using a strain gauge plethysmograph and forearm vascular resistance was calculated from forearm blood flow and mean blood pressure. There was a significant negative correlation (r = -0.512, p less than 0.01) between age and the magnitude of reflex forearm vasoconstriction during LBNP at -10 mmHg. The slope of the regression line in the old age-group was less (p less than 0.05) than that in the young or middle age-group. Forearm vascular responses to the cold pressor test did not differ among the three age-groups. These results suggest that cardiac receptor control of forearm vascular resistance decreases with aging in humans.

Primary Cardiac Neurilemoma

A 50-year-old woman was admitted to our hospital for a close examination of a pericardial effusion. Five months before admission, she began experiencing episodes of exertional dyspnea and orthopnea. At the hospital she attended at that time, she was diagnosed as having a large pericardial effusion and was treated with pericardial drainage. On admission to our hospital, her chest x-ray films showed marked cardiac enlargement. An echocardiographic examination and cardiac magnetic resonance imaging (Fig 1 …

Tissue edema and loss of tracer microspheres in infarcted myocardium

SummaryMicrosphere loss from the ischemic myocardium was studied in a canine model after 2 and 7 days coronary occlusion. 10 million tracer microspheres (TM) of 7–10 μm diameter were injected into the left atrium before and 15 minutes after left anterior descending coronary artery (LAD) occlusion. To determine the tissue water content, dried tissue weight was measured after desiccation. TM content in the nonoccluded left circumflex coronary artery (LCX) area was unchanged before and after coronary occlusion. In the infarcted area, microsphere loss was maximum at the low flow endocardial region averaging 27% and 42% in 2 and 7 days occlusion, respectively. An inverse linear correlation between TM loss and regional blood flow in 2 (r=−0.82, p<0.05) and 7 (r=−0.96, p<0.01) days coronary occlusion was noted. Water content was increased in the ischemic endocardium by 4.1 and 5.7% in 2 and 7 days occlusion, thus approximately 17% of TM loss was attributed to tissue edema. These results suggest that there is an ischemia-dependent reduction of TM in the ischemic myocardium and that microsphere migration participates in the major part of TM loss. Thus flow measurements by TM may be invalid when this compound is injected during the active phase of microsphere migration or during water content alterations.

Linear relationship between perfusion area and infarct size

SummaryThe purpose of this study was to develop a technique measuring the perfusion area of the coronary artery preocclusively and to study the relationship between the perfusion are aand infarct size.125I tracer microspheres were selectively injected into the left circumflex coronary artery (LCX) preocclusively, and then the LCX was ligated 48 hours later the heart was removed, rapidly frozen, and 50-μ transverse sections were obtained from base, middle and apex of the canine left ventricle, and used for autoradiography to measure perfusion area and for tetrazolium staining to measure infarct size. Dogs were divided into 2 groups: group 1 in which the main trunk of the LCX was occluded to produce large infarct (n=10) and group 2 in which the distal branch of the LCX was occluded to produce small infarct (n=10). There was a linear correlation between the perfused and infarcted area regardless of a size or location of the perfusion area involved. These results indicate that the extent of infarction is directly proportional to the perfusion area and is not altered by the location in the ventricle.

Constriction of the epicardial coronary artery induced by α-adrenergic stimulation

SummaryEffects of alpha adrenergic stimulation on diameter change of the epicardial coronary artery were studied in in-situ canine heart. The diameter of the left circumflex coronary artery (LCX) was continuously measured by 10 MHz PZT crystals applied to the external wall of the LCX. Aortic pressure was measured using high fidelity catheter-tip manometer.Enhanced activity of alpha adrenergic receptor by humoral and/or somatic nerve stimulations caused a reduction of the LCX diameter despite of the systemic pressure rise.