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Biomedical subjects

S Koyanagi

Publications and source records attributed to S Koyanagi.

At least 73 records · Page 4Linked to original sources
PubMed1991

Clinical characteristics of patients with dilated cardiomyopathy and bradyarrhythmias.

The clinical characteristics of patients with dilated cardiomyopathy and bradyarrhythmias were studied. Among 50 patients with dilated cardiomyopathy, 6 had bradyarrhythmias. Among these patients were one with sinus bradycardia, one with atrial fibrillation and slow ventricular responses and sick sinus syndrome (SSS), one with SSS with advanced AV block, and 3 with advanced AV block. The average age at the onset of their cardiac symptoms (60.3 +/- 12.1 years (mean +/- SD)) was significantly (p less than 0.01) higher than that of 43 patients without bradyarrhythmias (40.0 +/- 17.6). The left ventricular diastolic dimension and ejection fraction were similar among patients with and without bradyarrhythmias. In 31 follow-up patients without bradyarrhythmias, 8 (25.8%) died of cardiac causes; whereas, in 5 patients with bradyarrhythmias, 4 had been implanted with pacemakers and 3 (60.0%) died of cardiac causes. Furthermore, the age at the onset of cardiac symptoms in patients with any kind of conduction disturbance, except tachyarrhythmia, was 50.4 +/- 16.5 years (n = 25), which was significantly higher (p less than 0.02) than that of patients without conduction disturbances (37.7 +/- 19.3 years, n = 23). We concluded that bradyarrhythmias are not rare complications in patients with dilated cardiomyopathy, and the mortality rate tends to be higher in patients with bradyarrhythmias than in those without them. Furthermore, the risks of conduction disturbances and bradyarrhythmias were higher in the elderly patients.

Adult↗
PubMed1990

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.

Angina Pectoris, Variant↗
PubMed1990

Familial dilated cardiomyopathy complicated by left ventricular aneurysm.

Two siblings presented with symptoms of left ventricular dysfunction and ventricular arrhythmias. Echocardiography and left ventriculography revealed dilatation, diffuse hypokinesis and apical aneurysm of the left ventricle in both cases. Myocardial infarction was unlikely by history and examinations. We diagnosed them as cases of familial dilated cardiomyopathy complicated by left ventricular aneurysm.

Arrhythmias, Cardiac↗
PubMed1989

Increased fibrinopeptide A during anginal attacks in patients with variant angina.

It is not known whether coronary vasospasm is associated with coronary thrombosis. In this study, plasma levels of fibrinopeptide A during anginal attacks in 24 patients with variant angina were examined. A hyperventilation test was used to induce angina. Hyperventilation induced angina and ST segment elevation (AST: 0.32 +/- 0.14 mV, p less than 0.01) in eight patients with variant angina. Fibrinopeptide A increased from 0.75 +/- 0.27 at control to 7.8 +/- 4.4 ng/ml (p less than 0.01) during anginal attacks in these eight patients. In addition, four patients had spontaneous attacks of angina; they also had elevated levels of fibrinopeptide A during attacks (from 2.0 +/- 1.2 at control to 21.9 +/- 18.0 ng/ml [p less than 0.01] during attacks). Hyperventilation did not induce either angina or ST segment elevation in 12 of the patients with variant angina. Fibrinopeptide A levels did not change with hyperventilation in these patients. To determine whether elevated plasma levels of fibrinopeptide A were associated with angina, the plasma levels of fibrinopeptide A were examined during exercise-induced angina in seven additional patients with stable effort angina. They all developed angina with treadmill exercise; however, plasma fibrinopeptide A did not change. Therefore, only the patients with variant angina demonstrated elevated levels of fibrinopeptide A during anginal attacks. These findings suggest that coronary vasospasm associated with myocardial ischemia may induce stasis of blood, resulting in fibrinogen-fibrin conversion in the coronary vessels.

Angina Pectoris, Variant↗
PubMed1989

Homogeneous distribution and pressure dependent reduction of coronary blood flow in right ventricular free wall during coronary hypoperfusion in anaesthetised open chest dogs.

Relationship of coronary perfusion pressure with total and regional myocardial blood flow in right ventricular free wall was studied in 10 anaesthetised open chest dogs. The right coronary artery was perfused by an autoperfusion system from the carotid artery. Total coronary blood flow into the perfused area was measured by an extracorporeal electromagnetic flow probe. Critical perfusion pressure of the right coronary artery, defined as the lowest pressure level below which the regional wall motion deteriorated, was 39(SEM1) mm Hg. Reactive hyperaemia was noted at 60(2) mm Hg, a level well above the critical perfusion pressure. There was an inverse linear relation between the level of reactive hyperaemia and perfusion pressure. Regional myocardial blood flow was measured by a tracer microsphere technique at control condition, just above and below the critical perfusion pressures and during coronary occlusion. This correlated closely with values obtained by an electromagnetic flow probe (r = 0.94, p less than 0.001) and both values were dependent on the level of perfusion pressure. Endocardial to epicardial flow ratio remained at unity at any level of coronary perfusion pressure. Thus the level of coronary perfusion pressure was a major determinant of the regional myocardial blood flow into the right coronary artery, and autoregulation of the regional myocardial blood flow was not apparent across the wall, despite the presence of a reactive hyperaemia.

Anesthesia, General↗
PubMed1989

Clinical characteristics of sudden cardiac death in patients with vasospastic angina.

Of 383 patients with vasospastic angina who were followed for a period of 3.2 +/- 0.1 years, 9 (2%) died suddenly from cardiac causes. Calcium antagonists had been given to 98% of our patients. Only one patient who died suddenly had a fixed coronary stenosis of 75% or greater. Eight of the 9 patients showed ST segment elevation during anginal attack at rest, and 3 patients showed ST segment elevation at both anterior and inferior leads. Sudden death occurred in 6 of 41 patients (12.5%) who were documented to have multivessel coronary spasm, but in only 3 of 342 patients (1%) who had single vessel spasm (p less than 0.01). Serious arrhythmia occurred during anginal episode in 3 of 9 patients who died suddenly (53%) and in 52 of 374 who did not (14%). These results suggest that the frequency of sudden cardiac death was rather low in Japanese patients with vasospastic angina. The risk of sudden death was increased in patients with multivessel spasm and serious arrhythmia during anginal attacks but not these with fixed coronary stenosis.

Adult↗
PubMed1988

The usefulness of equilibrium radionuclide ventriculography in the diagnosis of arrhythmogenic right ventricular dysplasia and a report of cases of a familial occurrence.

Arrhythmogenic right ventricular dysplasia (ARVD) is a recently identified clinical entity and its diagnosis rests on documentation of ventricular tachycardia (VT) of right ventricular origin and morphologic changes of the right ventricle. However, the diagnosis of ARVD is difficult noninvasively and often requires angiography. The usefulness of equilibrium radionuclide ventriculography as a noninvasive method for the diagnosis of ARVD has not been fully evaluated. We performed equilibrium radionuclide ventriculography in 7 patients with ARVD, 10 normal subjects and 9 patients with dilated cardiomyopathy (DCM). The right ventricular ejection fraction (EF) in patients with ARVD (25 +/- 8%, mean +/- SD) was lower (p less than 0.001) than that in normal subjects (56 +/- 7%) but was not significantly different from that in patients with DCM (32 +/- 10%). The left ventricular EF in patients with ARVD (57 +/- 12%) was lower (p less than 0.05) than that in normal subjects (70 +/- 7%), but higher (p less than 0.001) than that in patients with DCM (27 +/- 7%). These findings suggest that ARVD is a specific form of DCM which predominantly affects the right ventricle and that equilibrium radionuclide ventriculography may be a useful noninvasive method for the diagnosis of this disorder. In addition, we present a family in which 3 of 6 siblings were affected by ARVD, suggesting that some genetic factors may be involved in the etiology of this disorder.

Adolescent↗
PubMed1987

Relative importance of hypertension after coronary occlusion in chronic hypertensive dogs with LVH.

We have shown that there was a 50% increase in infarct size and a threefold increase in the incidence of sudden death following coronary occlusion in dogs with hypertension and left ventricular hypertrophy (LVH). To further investigate this problem, we separated the effects of hypertension from those of LVH by decreasing arterial pressure either by renal anastomosis or intravenous administration of nitroprusside in dogs with chronic renal hypertension and LVH. In 123 conscious dogs, the circumflex coronary artery was acutely occluded. Hemodynamics were monitored, myocardial perfusion was measured with labeled microspheres, the risk area was defined by postmortem angiography, and infarct size was determined pathologically 48 h after occlusion. The incidence of sudden death following acute coronary occlusion decreased dramatically in dogs with LVH if the arterial pressure was decreased with either nitroprusside or renal anastomosis. In addition, if arterial pressure was decreased with nitroprusside or renal anastomosis, infarct size in dogs with LVH was not augmented. In conclusion, normotension induced by renal anastomosis or nitroprusside returned infarct size and the incidence of sudden death in dogs with chronic hypertension and LVH toward control values. Thus it is likely that hypertension, as opposed to LVH, is the critical factor responsible for the increase in infarct size and the high incidence of sudden death observed in dogs with hypertension and LVH following sudden coronary occlusion.

Animals↗
PubMed1987

A case of primary dissecting aneurysm of the coronary artery.

A 37-year-old woman was admitted with an acute anterior myocardial infarction. Coronary arteriography revealed a dissecting aneurysm of the left main coronary artery. The patient died from perioperative myocardial infarction following aortocoronary bypass surgery on the 102nd hospital day. Histologic sections of the aneurysm revealed that granulation tissue had replaced the aneurysm, suggesting spontaneous healing of the dissecting aneurysm.

Adult↗
PubMed1987

Alterations in the coronary circulation in hypertrophied ventricles.

During the past decade our understanding of the complex interaction between cardiac muscle and coronary vascular growth has increased substantially. Some types of cardiac hypertrophy, for example, left ventricular hypertrophy secondary to hyperthyroidism, are associated with increased coronary vascular growth. However, in most animal preparations of hypertrophy and in several clinical types of hypertrophy of the left and/or right ventricles, pathologic cardiac enlargement impairs the ability of the coronary circulation to allow normal increases and perfusion in response to intense dilator stimuli. In general, clinical studies have demonstrated far more profound abnormalities than studies in experimental animals. These observations provide a plausible explanation of why patients with hypertrophied ventricles often exhibit signs and symptoms of myocardial ischemia in the absence of coronary obstructive disease. The recent observation that experimentally produced left ventricular hypertrophy secondary to renal hypertension augments infarct size and the incidence of sudden lethal arrhythmias has additional implications relevant to the interaction between cardiac hypertrophy and myocardial perfusion. Although coronary reserve is impaired in many types of pathologic hypertrophy, the anatomic or biochemical basis for these observations remains elusive.

Animals↗
PubMed1986

Augmented cardiopulmonary baroreflex control of forearm vascular resistance in young athletes.

The aim of this study was to examine the effect of exercise training on reflex control of vascular resistance in human males. Forearm vascular responses to lower body negative pressure (LBNP) at -10 and -40 mm Hg were compared between highly trained young athletes (21.5 +/- 0.5 years old, n = 14) and age-matched nonathletes (20.7 +/- 0.5 years old, n = 16). Resting heart rate was lower in athletes than in nonathletes. Resting blood pressure, central venous pressure, forearm blood flow, and forearm vascular resistance were not different between the two groups. The magnitude of reflex forearm vasoconstriction in response to LBNP at -10 mm Hg, which decreased central venous pressure but did not alter blood pressure or heart rate, was greater in athletes than in nonathletes. The slope of the regression line relating changes in central venous pressure and forearm vascular resistance was steeper in athletes than in nonathletes. Vasoconstrictive responses to intraarterially administered norepinephrine and angiotensin II did not differ between athletes and nonathletes. These results suggest that the tonic inhibitory influence of the cardiopulmonary receptors is augmented in athletes. This augmentation may contribute to some of cardiovascular and endocrine adaptations that occur with exercise training.

Adult↗
PubMed1986

Transmural distribution of myocardial infarction: difference between the right and left ventricles in a canine model.

The evolution of myocardial infarction 24 hours after ligating both the right coronary artery and the obtuse marginal branch of the left circumflex coronary artery was examined in 33 anesthetized dogs. Postmortem coronary angiography and a tracer microsphere technique were used to determine risk areas and their collateral blood flows, respectively. The mean weight of the risk areas was 11.3 +/- 0.5 g (mean +/- SEM) in the right ventricle and 10.5 +/- 0.9 g in the left ventricle (NS). The weight of infarcted tissue was 5.7 +/- 0.7 g in the right ventricle and 5.2 +/- 0.9 g in the left ventricle (NS). In both ventricles, infarct weight was linearly related to risk area size, and the percent of risk area necrosis was inversely correlated with the extent of collateral flow at 24 hours of coronary ligation, defined as the mean myocardial blood flow inside the central risk area. Ratios of infarct to risk area between the subendocardial and subepicardial layers were 0.76 +/- 0.06 and 0.28 +/- 0.05 in the right and left ventricles, respectively (p less than 0.01, between ventricles, n = 31), which coincided well with subendocardial-to-subepicardial-flow ratios at 24 hours, ie, 0.86 +/- 0.04 in the right ventricle and 0.32 +/- 0.06 in the left ventricle (p less than 0.01). The regional distribution of myocardial infarction correlated well with flow distribution inside the risk area; the slope of these relations was similar between the subendocardium and subepicardium in the right ventricle, whereas in the left ventricle it was larger in the subendocardium than in the subepicardium. Thus, in the dog, the inherent change in the regional distribution of coronary collateral blood flow is an important modifier in the evolution of myocardial infarction, especially in the left ventricle.

Angiography↗
PubMed1986

Wall motion abnormalities in Q wave and non-Q wave myocardial infarction in isolated left anterior descending coronary artery disease.

Although the frequencies of transmural involvements of Q wave and non-Q wave myocardial infarction (MI) are similar, their clinical features are different in many aspects. In the present study, the wall motion abnormalities of 34 patients with Q wave MI and eight patients with non-Q wave MI, all with isolated left anterior descending artery (LAD) lesion, were compared using left ventriculography and two-dimensional echocardiography. This study clearly demonstrated that the severity and distribution of asynergy were significantly greater in patients with Q wave MI than in those with non-Q wave MI. Akinesis or dyskinesis was observed in all 34 patients (100%) (151 of 544 segments) with Q wave MI, and in four of eight patients (50%) (eight of 128 segments) with non-Q wave MI (p less than 0.05). Apical aneurysm occurred exclusively in patients with Q wave MI. In non-Q wave MI, asynergy was localized at the papillary muscle level or the apex. At the chordal level, asynergy was observed in only one of eight cases with non-Q wave MI, and in 24 of 34 cases with Q wave MI (p less than 0.05). These results suggest that the infarct size may be smaller in non-Q wave MI than in Q wave MI in patients with isolated LAD lesion.

Echocardiography↗
PubMed1985

Myocardial infarct size threshold for two-dimensional echocardiographic detection: sensitivity of systolic wall thickening and endocardial motion abnormalities in small versus large infarcts.

This study evaluated the ability of 2-dimensional echocardiography to detect myocardial infarcts of varying sizes. Echocardiography was performed in 29 closed-chest, conscious dogs 2 days after circumflex coronary artery occlusion, and the ultrasonic recordings were analyzed for regional abnormalities in either wall thickening or endocardial motion. Acute myocardial infarct (AMI) size and extent were assessed by morphologic examination. In 5 dogs, coronary occlusion failed to produce AMI; in these dogs wall thickening analysis showed no abnormalities (100% specificity), and endocardial motion analysis yielded 1 false-positive result (80% specificity). In 24 dogs an AMI developed; infarcts larger than 18% of left ventricular mass uniformly resulted in echocardiographically detectable contraction abnormalities. When the AMI was small (1 to 6% of left ventricular mass) and primarily subendocardial, the sensitivity of echocardiography was poor: Only 3 of 10 of the dogs with a small AMI had abnormalities by wall thickening, and only 1 of 10 by endocardial motion. Thus, in this canine model of AMI, 2-dimensional echocardiography was insensitive to small, subendocardial AMI. If this is so in humans as well, it is a potential limitation of the clinical use of echocardiography in the detection of AMI.

Animals↗
PubMed1985

Detection of different blood flow patterns in the true and false lumina with aortic root dissection by pulsed Doppler echocardiography.

We report a 53-year-old man with aortic dissection, in whom pulsed Doppler echocardiography showed two different flow patterns within the dilated aorta. Although two-dimensional echocardiography has been successful in making the diagnosis of aortic root dissection, several conditions producing false positives have also been noted. Simultaneous recording of pulsed Doppler echocardiography may be useful to provide additional diagnostic clues in selected cases.

Aortic Dissection↗
PubMed1985

Role of afterload in determining regional right ventricular performance during coronary underperfusion in dogs.

The relationship between coronary perfusion pressure and regional myocardial performance of the right ventricular free wall was studied, in the presence or absence of right ventricular hypertension in 13 open-chest dogs. The right coronary artery was perfused through a shunt from a carotid artery. Regional systolic shortening of the right ventricular free wall was measured by means of a sonomicrometric technique at various levels of coronary perfusion pressure. Regional shortening was insensitive to coronary perfusion pressure or flow when it was above 31 mm Hg or 0.27 ml/min per g. Once coronary perfusion was below this critical level, regional shortening in both base to apex and circumferential orientations decreased linearly, depending on the degree of perfusion pressure. Despite the presence of a monoexponential relationship between coronary perfusion pressure or flow and regional shortening, a direct linear relation between perfusion pressure and flow was consistently noted, with or without pulmonary artery banding, suggesting that there is limited autoregulation of right coronary flow. The critical perfusion pressure for maintaining regional myocardial function of the right ventricle was highly dependent on the level of right ventricular systolic pressure (r = 0.64 - 0.72, P less than 0.05). Thus, right ventricular systolic pressure was one of the important determinants of regional wall motion during coronary underperfusion.

Animals↗