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Biomedical subjects

M Ejiri

Publications and source records attributed to M Ejiri.

10 recordsLinked to original sources

Relationship between the preexistent coronary collateral circulation and successful intracoronary thrombolysis for acute myocardial infarction.

The purpose of this study was to evaluate whether the existence of coronary collateral circulation influences recanalization rates of intracoronary thrombolysis. The study population consisted of 85 consecutive patients undergoing intracoronary thrombolysis within 6 hours after the onset of the first acute myocardial infarction, all of whom had a complete occlusion of the infarct-related coronary artery. Intracoronary thrombolysis with high-dose urokinase (960,000 IU) was attempted at a rate of 24,000 IU/min. Of 18 patients (group A) who had good angiographic collateral circulation to the area perfused by the infarct-related coronary artery, the obstructed artery was recanalized to a residual luminal diameter stenosis of less than or equal to 90% (successful recanalization) in only five (28%). In contrast, of 67 patients (group B) with poor or no collateral circulation, recanalization was successful in 40 (60%) (p less than 0.05). Antegrade flow of infarct-related arteries was observed following thrombolysis in 12 (67%) of 18 group A patients and in 56 (84%) of 67 group B patients (p = NS). It was concluded that (1) the presence of collaterals correlates with the presence of high-grade stenosis; (2) the presence of collaterals correlates with the presence of high-grade stenosis; (2) the presence of collaterals is inversely related to the efficacy of thrombolytic therapy; and (3) the difference in successful recanalization rates observed between the two groups probably reflects the impact of underlying stenosis severity on the effectiveness of lytic therapy.

Adult

The sensitivity of intracoronary injection of acetylcholine in inducing coronary spasm differs in patients with stable and unstable angina.

In an attempt to clarify the role of coronary artery spasm in the pathogenesis of unstable angina, acetylcholine (20 and 50 micrograms) was injected directly into the coronary arteries of 19 patients with unstable effort angina (group 1), 30 patients with unstable spontaneous angina (group 2), and 15 patients with stable effort angina due to coronary artery organic stenosis (greater than or equal to 75%) (group 3). Coronary spasm was defined as severe vasoconstriction (greater than or equal to 90% of luminal diameter) with chest pain and/or ischemic ST-segment changes. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in 19 patients (100%) of group 1 and 28 (93%) of group 2 but only 3 (20%) of group 3 (p less than 0.01). When acetylcholine was injected into the left and right coronary arteries separately, multivessel spasm (spasm of both coronary arteries) was induced in 5 of 12 (42%) patients of group 1 and in 9 of 23 (39%) patients of group 2. In contrast, intracoronary acetylcholine did not cause multivessel coronary spasm in any of 15 patients of group 3 (0%). These results suggest that coronary arteries in patients with unstable effort angina as well as spontaneous angina are susceptible to spasm and that coronary artery spasm may be responsible at least in part for the genesis of attacks in these patients.

Acetylcholine

Biphasic changes (initial increase and late decrease) in coronary sinus venous oxygen saturation during anginal attacks induced by intracoronary acetylcholine in patients with variant angina.

In order to evaluate the effects of intracoronary acetylcholine on coronary resistance vessels, oxygen saturation in coronary sinus blood was continuously measured to compare its dynamic changes during intracoronary injection of acetylcholine in both patients with variant angina and control subjects. Group 1 consisted of 6 patients without coronary artery disease. Group 2 consisted of 10 patients with variant angina and spasm in the left anterior descending coronary artery. A fiberoptic reflection oximetry system was used for the continuous measurement of coronary sinus venous oxygen saturation. Acetylcholine (20 micrograms) was injected directly into the left coronary artery over 30 s. In the group 1 patients, coronary sinus venous oxygen saturation was increased from 39 +/- 2% (mean +/- SEM) to 54 +/- 3% at 30 s, continuously climbed to 70 +/- 3% at 60 s and then gradually decreased to 53 +/- 5% at 120 s after the initiation of intracoronary injection of acetylcholine. In contrast, in the group 2 patients, coronary sinus venous oxygen saturation was transiently increased from 39 +/- 2% to 56 +/- 4% at 30 s, reversed, decreased to 52 +/- 4% at 60 s and then rapidly decreased to 36 +/- 3% at 120 s with the onset of chest pain associated with electrocardiographic ischemic changes. Coronary arteriography during attacks demonstrated a total or subtotal occlusion of the left anterior descending coronary artery due to severe spasm in all of the 10 patients. The extent of increases in coronary sinus venous oxygen saturation at 30 s after acetylcholine injection was not significantly different between the two groups (group 1: 15 +/- 4%, group 2: 17 +/- 3%). Heart rate, blood pressure and rate-pressure product were essentially unchanged at 30 s after intracoronary injection of acetylcholine in both groups. These data suggest that in control adult humans, coronary blood flow was increased through dilatation of resistance vessels by acetylcholine, while in patients with variant angina, coronary blood flow was transiently increased by dilatation of resistance vessels, after which it was suddenly decreased by spasm of an epicardial artery induced by this agent. Relaxant responses to acetylcholine of coronary resistance vessels appear to be preserved well in patients with variant angina.

Acetylcholine

Adult respiratory distress syndrome in a patient with uncomplicated acute myocardial infarction.

A 53-year-old woman was admitted with a diagnosis of acute extensive anterior myocardial infarction. Pulmonary capillary wedge pressure was 17 mmHg, and cardiac index 2.4 l/min.m2. The patient was successfully treated with diuretics and nitrates but on the fifth hospital day moist rales were noted over the entire lung field. A chest roentgenogram showed diffuse bilateral pulmonary infiltration with unchanged cardiac silhouette. Arterial oxygen partial pressure was reduced to 45 mmHg under 3 liters of nasal oxygen inhalation. Pulmonary capillary wedge pressure was 8 mmHg. Diffuse infiltration was not ameliorated by intravenous injection of diuretics. The diagnosis of adult respiratory distress syndrome was finally established by successful treatment with steroids.

Electrocardiography

Usefulness of intracoronary injection of acetylcholine as a provocative test for coronary artery spasm in patients with vasospastic angina.

In order to examine both the sensitivity and specificity of coronary artery spasm induced by intracoronary injection of acetylcholine in patients with vasospastic angina, incremental doses of acetylcholine (20, 30, and 50 micrograms) were injected directly into each coronary artery in 21 patients with variant angina (group A), in 28 patients with other types of vasospastic angina (group B), and in 20 patients without any significant coronary artery disease (group C). Coronary artery spasm was defined as severe vasoconstriction (greater than or equal to 90% of reduction in luminal diameter) with chest pain and/or ischemic changes in the electrocardiogram. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in 20 patients (95%) of group A, in 27 patients (96%) of group B, and in only 2 patients (10%) of group C. The low dose of acetylcholine (20 micrograms) induced coronary spasm more frequently in group A patients (81%) than in group B patients (43%) (P less than 0.05). ST-segment elevation associated with anginal attacks was significantly (P less than 0.05) more frequent in group A (71%) than in group B (39%). When acetylcholine was injected separately into the left and right coronary arteries, spasm of both coronary arteries was observed in 7 out of 14 of group A (50%), in 8 out of 22 of group B (36%), and in none of the 20 of group C. We concluded that intracoronary injection of acetylcholine is a sensitive and reliable method for the induction of coronary spasm in patients with vasospastic angina as well as in those with variant angina.

Acetylcholine

Importance of coronary collateral circulation for increased treadmill exercise capacity by nitrates in patients with stable effort angina pectoris.

The purpose of this study was to elucidate the mechanism that induces an improvement in exercise capacity by nitrates in patients with stable effort angina pectoris. The study population was composed of 19 patients: group A, 10 patients with chronic stable effort angina who had a well-developed coronary collateral circulation to the potentially ischemic region; group B, 9 patients with chronic stable effort angina who had no collateral circulation to the jeopardized myocardium. Treadmill exercise was performed according to the standard Bruce protocol with and without pretreatment with orally administered 10 mg isosorbide dinitrate. Percent increases (mean +/- SE) in exercise duration were not significantly different between groups A and B (25 +/- 6 vs. 14 +/- 6%). Percent increases in the maximal rate-pressure product tended to be greater in group A than in group B (27 +/- 6 vs. 10 +/- 6%). Percent increases in the rate-pressure product at the onset of angina pectoris were significantly greater in group A than in group B (37 +/- 7 vs. 7 +/- 6%; p less than 0.01). Percent increases in the rate-pressure product at 0.1 mV S-T segment depression were also significantly greater in group A than in group B (26 +/- 6 vs. 1 +/- 5%; p less than 0.01). These results suggest that isosorbide dinitrate dilates epicardial collateral vessels with smooth muscle layers, but fails to dilate the coronary arteries with significant organic stenoses.

Angina Pectoris

Significance of collateral circulation in reversible left ventricular asynergy by nitroglycerin in patients with relatively recent myocardial infarction.

To evaluate the functional role of coronary collateral circulation in reversible asynergy of the left ventricle, cineventriculography was performed before and after the administration of sublingual nitroglycerin in 19 patients with complete occlusion of the proximal part of the left anterior descending coronary artery. In nine patients who had significant collateral circulation to the infarct-related coronary artery (group A), there was significant improvement in both the left ventricular ejection fraction (53% to 60%, p less than 0.05) and regional wall motion in the infarct zone (8% to 18%, p less than 0.01 in the anterolateral area) with administration of nitroglycerin. In contrast, in the remaining 10 patients without significant collateral perfusion (group B), there were no detectable changes in either global function (49% versus 50%) or regional wall motion (6% versus 8% in the anterolateral area) before and after nitroglycerin. Changes in heart rate and left ventricular peak systolic and end-diastolic pressures with nitroglycerin were comparable in both groups. These results suggest that angiographically demonstrable collaterals preserve viable myocardium, which can improve its contraction when the supply-demand relationship is favorably affected because of increased collateral flow and/or more favorable loading conditions produced by nitroglycerin.

Cineradiography

Comparative sensitivity of intracoronary injection of acetylcholine for the induction of coronary spasm in patients with various types of angina pectoris.

To elucidate the possible contribution of coronary artery spasm to the pathogenesis of angina pectoris, coronary arterial responses to intracoronary injection of acetylcholine were examined in patients with various types of angina pectoris. Coronary artery spasm with chest pain and/or electrocardiographic ischemic changes was angiographically demonstrated in 50 (85%) of 59 patients with angina pectoris. The sensitivity for coronary spasm was 92% (24 of 26) in patients with rest angina, 100% (16 of 16) in patients with both rest and effort angina, and 59% (10 of 17) in patients with effort angina, while it was only 6% (1 of 16) in patients without coronary artery disease. When patients with effort angina were subdivided according to the variability of anginal threshold for exertional angina, the sensitivity for coronary spasm was as high as 90% (9 out of 10) in patients with variable-threshold angina. In contrast, coronary spasm was less frequently (p less than 0.05) induced in patients with fixed-threshold angina (1 of 7, 14%). These results suggest that coronary arteries in patients with angina pectoris are quite susceptible to acetylcholine except in those patients with stable exercise tolerance or anginal threshold. Thus coronary artery spasm appears to play a significant role for the pathogenesis of angina pectoris in a large proportion of patients with effort angina as well as in patients with rest angina.

Acetylcholine

Development of collateral circulation after acute myocardial infarction: its role in preserving left ventricular function.

The present study evaluated the effects of coronary collateral circulation developing after acute myocardial infarction on global and regional left ventricular function during the chronic stage. The study group consisted of 16 patients with initial myocardial infarction having total occlusion of the proximal left anterior descending coronary artery. To eliminate the effects of collateral circulation existing at the onset of infarction, patients with pre-infarction angina were excluded from this study. The patients were categorized in two groups depending on the extent of their collateral circulation (collateral index: CI 0-3): group A--patients with significant collateral circulation (CI = 2 or 3) to the infarct-related coronary artery; group B--patients without significant collateral circulation (CI = 0 or 1). Their heart rate, left ventricular peak systolic and end-diastolic pressures and cardiac index were similar in the two groups. The left ventricular end-systolic volume index in the group B was significantly greater than that in the group A (60 +/- 21 ml/m2 vs 34 +/- 9 ml/m2, p less than 0.05). Left ventricular ejection fraction in the group A was significantly greater than that of the group B (55 +/- 9% vs 39 +/- 15%, p less than 0.05), and a significant difference was observed in the percentage of segment shortening in the infarct area between the groups A and B (10.8 +/- 9.2% vs -0.2 +/- 5.4%, p less than 0.01). It was concluded that coronary collateral circulation which develops after acute myocardial infarction exerts beneficial effects on global and regional left ventricular function during the chronic stage.

Adult

[Significance of collateral circulation in reversible asynergy].

The functional role of collateral circulation in reversible asynergy of the left ventricle was evaluated. Cineventriculograms were obtained before and after the administration of sublingual nitroglycerin (0.3 mg) in 19 patients with complete occlusion of the proximal portion of the left anterior descending coronary artery. In nine patients with well-developed collateral circulation, both left ventricular ejection fraction and regional wall motion were significantly improved by nitroglycerin. By contrast, in 10 patients without significant collateral circulation, there were no detectable changes in both global and regional wall motions before and after nitroglycerin. The left ventricular hemodynamic changes caused by nitroglycerin were comparable in both groups. These findings support the view that the improvement in asynergy caused by nitroglycerin appears to depend mainly on the extent of collateral circulation, rather than on decreases in both preload and afterload.

Aged