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At least 919 records · Page 51Linked to original sources
PubMed1981

Platelet activation in clinical coronary artery disease and spasm.

Current concepts of atherogenesis, based on animal models, suggest a role for platelets in the development of atherosclerotic lesions, possibly through the release of alpha granule constituents. Platelets may also contribute to the development of vascular spasm through thromboxane A2 production. Platelet activation in the coronary circulation in patients with coronary artery disease (CAD) should occur if these hypotheses apply clinically. We measured aortic and coronary sinus plasma levels of the platelet alpha granule constituent beta-thromboglobulin (B-TG) and thromboxane B2 (TX B2) by radioimmunoassay in 15 patients with severe atherosclerotic CAD, seven patients with angiographically normal coronaries, and five patients undergoing evaluation for coronary artery spasm (CAS). Compared with the controls, CAD patients had significantly greater transmyocardial release of B-TG (11.1 +/- 8.1 ng/ml, mean +/- SEM vs 62.5 17.2, p less than 0.05 by rank sum test); TX B2 gradients showed a similar trend but the difference was not statistically significant (-0.08 +/- 0.03 ng/ml vs 0.22 +/- 0.02, 0.05 less than p less than 0.10). Three of the five patients studied developed CAS which was associated with acute elevation in coronary sinus TX B2; the two non-CAS patients with drug provocation had undetectable coronary sinus TX B2. We conclude that abnormal platelet activation takes place in the coronary circulation of CAD patients, and that production of acute myocardial ischemia by CAS occurs with increased coronary sinus TX B2.

Angina Pectoris↗
PubMed1981

Intracoronary thrombus in syndromes of unstable myocardial ischemia.

The association of coronary thrombosis and transmural myocardial infarction is well documented. We have recently observed apparent intracoronary thrombi in patients with unstable myocardial ischemia without transmural infarction. To assess the frequency and angiographic characteristics of intracoronary defects consistent with thrombi, we reviewed the angiograms of all patients undergoing catheterization within 1 month of the onset of unstable angina or the intermediate coronary syndrome. Of 129 such patients, eight (6.2%) had nonoccluding, hazy, or nonopacified intracoronary filling defects consistent with thrombus in angiographically well-opacified vessels. All defects were just distal to a significant (80% to 99%) coronary stenosis. In each instance the thrombus-involved vessel supplied a myocardial segment referable to the electrocardiographically defined area of ischemia. Support for the theory that the intracoronary defects were thrombi includes three patients with enlargement of the filling defects, who underwent repeat angiography within 7 days, and two patients with embolization of defect fragments. Furthermore these defects were angiographically similar to poststenotic intraluminal defects seen transiently in some patients after partial intracoronary streptokinase recanalization. In conclusion, we have observed, angiographically, intracoronary filling defects consistent with thrombus in some patients with unstable myocardial ischemia.

Adult↗
PubMed1981

Clinical course of patients following the demonstration of coronary artery spasm by angiography.

The clinical course of 25 patients was determined during an average of 2.7 years following the angiographic demonstration of coronary artery spasm (CAS). Seventeen patients received medical treatment after the demonstration of coronary spasm and six patients had cardiac surgery. Twenty-three patients were living and two patients had died at the time of follow-up. Twenty-one of the 23 surviving patients has either no chest pain or markedly reduced symptoms. However, the demonstration of CAS by angiography was associated with a high incidence of subsequent cardiac complications, which included myocardial infarct (four patients), cardiac arrest (four patients), and death (two patients). We concluded from this study that after the demonstration of CAS by angiography: (1) the clinical course was variable, with most patients (21 of 25 patients, 84%) having improvement of symptoms at the time of follow-up; (2) major cardiac complications were frequent (11 out of 25 patients, 44%) and; (3) although clinical and coronary angiographic features were of limited use in predicting major cardiac complications, most of the patients who had an uncomplicated course (11 of 14 patients, 79%) had either less than 50% fixed coronary artery luminal diameter narrowing (CAN) or coronary artery bypass graft operations, the majority of patients with less than 50% CAN (8 of 11 patients, 73%) had no major cardiac complications, and myocardial infarction or death usually occurred during periods of increased angina pectoris.

Adult↗
PubMed1982

Nifedipine therapy in angina pectoris: evaluation of safety and side effects.

Nifedipine, a calcium-channel blocker, differs in structure and mode of action not only from the nitrates and beta blockers but also from the other well-known calcium-channel blockers. These differences have important implications for the treatment of angina pectoris. Our clinical experience over a period of 6 years with all types of angina patients--mostly those with chronic stable angina but also those with Prinzmetal's and unstable angina-corroborates the efficacy reports published in the world literature. Although the safety profile of nifedipine has been generally regarded as favorable, a few reports of clinically significant adverse effects in specific patient groups have appeared in the literature. In order to provide a more comprehensive assessment of safety, the records of over 3000 patients treated with nifedipine in open and controlled multiple-dose studies were tabulated and analyzed. Of special concern were patients with clinically significant adverse experiences, patients with a concomitant diagnosis of congestive heart failure (CHF), patients who were being treated concurrently with beta blockers, and patients who had been taking nifedipine for more than 6 months. Results of this analysis confirm that nifedipine can be safely administered to a broad spectrum of angina patients, including those with a concomitant diagnosis of CHF and those receiving concurrent therapy with beta-blocking agents.

Adrenergic beta-Antagonists↗
PubMed1982

Inpatient treatment of unstable angina: clinical perspective and sequential management.

In the last decade, increasing information has become available to the effect that an increase in coronary artery tone and coronary artery spasm play an important role in patients with various ischemic heart disease syndromes. Coronary spasm may be superimposed on a coronary vessel already severely obstructed by atherosclerosis. Conversely, spasm may occur in an artery that is only minimally involved with atherosclerosis. The majority of patients studied in the United States with both stable and unstable angina pectoris have underlying severe organic obstructive coronary artery disease. There has now emerged a considerable amount of information from several centers showing that the calcium-channel blockers or calcium-flux antagonists are highly effective in the treatment of stable and unstable angina pectoris. This report focuses on the uses and limitations of one of these agents, nifedipine, in patients with unstable angina and provides a sequential approach to their management.

Angina Pectoris↗
PubMed1982

Vasospastic ischemic mechanism of frequent asymptomatic transient ST-T changes during continuous electrocardiographic monitoring in selected unstable angina patients.

Asymptomatic episodes of ST segment and/or T wave changes are often reported during Holter monitoring in patients with angina pectoris. However, the interpretation of such changes is debated relative to silent myocardial ischemia. We studied 11 patients admitted to the CCU because of frequent episodes of unstable anginal attacks who had undergone repeated periods of Holter monitoring, characterized by predominantly occurring asymptomatic episodes of ST segment and/or T wave changes associated with less frequent typical anginal attacks. In a total of 89 days of Holter monitoring, the patients evidenced 520 episodes of transient ECG changes including 180 of ST elevation, 73 of ST depression, and 267 of T wave alterations. Only 12% of episodes were symptomatic. Coronary injection during asymptomatic ST-T changes was performed in eight patients. In six it was possible to document spontaneous coronary spasm. In seven patients ergonovine administration induced anginal pain, ST-T changes, and coronary spasm. In all patients the anginal attacks completely disappeared with medical treatment and the asymptomatic episodes were abolished in six and reduced in four. Our findings support the hypothesis that in certain selected unstable anginal patients, transient asymptomatic ECG changes are caused by acute myocardial ischemia.

Angina Pectoris↗
PubMed1983

Serial thallium-201 imaging at rest in patients with unstable and stable angina pectoris: relationship of myocardial perfusion at rest to presenting clinical syndrome.

In order to determine whether there are differences in myocardial perfusion at rest among patients with various unstable and stable angina syndromes, serial thallium-201 imaging was performed at rest in 19 patients presenting with rapidly worsening exertional angina (unstable angina, group A), 12 patients with rest angina alone without exertional symptoms (unstable angina, group B), and 34 patients with chronic stable angina. No patient had an episode of angina within 4 hours of study. Nineteen of 19 (100%) patients in group A demonstrated transient defects compared to only 3 of 12 (25%) patients in group B (p less than 0.0001) and 4 of 34 (12%) stable angina patients (p less than 0.0001). The majority of zones demonstrating transient defects in group A were associated with hypokinesis of the corresponding left ventriculogram segment without associated ECG evidence of previous infarction. There were no significant differences in the frequency of persistent thallium defects, severity of angiographic coronary artery disease, or frequency of regional wall motion abnormalities of myocardial segments supplied by stenotic coronary arteries among the three groups of patients. Transient defects have been shown to reflect reduction in regional coronary blood flow to viable myocardium. Therefore, we conclude that regional resting hypoperfusion of viable myocardium is far more common in patients with exertional unstable angina symptoms than in patients with rest angina alone or chronic stable angina.

Angina Pectoris↗
PubMed1983

Myocardial infarction in patients with coronary artery spasm demonstrated by angiography.

Twelve cases of myocardial infarction (MI) were documented in 11 of 39 patients who had coronary artery spasm (CAS) that was observed by angiography either before MI (3 patients), after MI (5 patients), or both before and after MI (3 patients). MI corresponded in location to sites of ECG changes of myocardial ischemia during spontaneous angina pectoris in 7 of 7 patients and to the region of myocardium supplied by the vessel in which CAS was observed by angiography in each patient. MI occurred in the distribution of the right coronary artery in 8 patients and of the left coronary artery in 4 patients. Of 12 vessels that supplied infarcted regions of myocardium, 7 vessels had greater than or equal to 50% diameter fixed coronary artery narrowing (CAN), but the remaining 5 vessels had minimal (10%) or no fixed CAN. In those patients who were studied after MI, coronary angiography demonstrated that only 3 of 9 vessels in the distribution of infarcted regions of myocardium were completely occluded. Clinical follow-up for an average of 1.3 years after MI showed that 7 patients continued to have chest pain, 2 patients were asymptomatic, and 2 patients died suddenly 9 weeks and 1 year, respectively, after MI. Therefore, among our patients with CAS demonstrated by angiography, MIs (1) were frequent (28%), (2) occurred in the distribution of observed coronary spasm, (3) were frequently (5 of 12 arteries) in the distribution of vessels having minimal or no fixed narrowing, and (4) were often (6 of 9 arteries) in the distribution of vessels that were demonstrated to be patient after MI.

Adult↗
PubMed1984

Transient changes in left ventricular mechanics during attacks of Prinzmetal's angina: an M-mode echocardiographic study.

M-mode echocardiograms were recorded in 12 patients with Prinzmetal's angina during 29 episodes of transient myocardial ischemia at rest (18 spontaneous and 11 ergonovine-induced). At peak ST segment elevation a regional mechanical impairment was observed in the interventricular septum during 23 episodes of angina and in the posterior wall during six episodes. In the 18 spontaneous episodes the left ventricular ischemic wall, when compared to the basal state, was found to have a significant reduction in motion (-76.3 +/- 9.1%) (mean +/- SEM), in diastolic thickness (-11.7 +/- 2.5%), and in percent systolic thickening (-88.0 +/- 5.6%). Increase in left ventricular end-diastolic diameter (+13.1 +/- 2.1%) and decrease in percent fractional shortening (-38.1 +/- 3.7%) were also observed. When ST segment was back to the isoelectric line, a transient overshoot in regional left ventricular function was observed. In induced episodes statistically significant changes could be detected by M-mode echocardiography even before appearance of ST segment elevation and anginal pain. No significant difference was found in type or degree of mechanical impairment between induced and spontaneous episodes. Therefore, in patients with Prinzmetal's angina: (1) M-mode echocardiography allows detection of mechanical changes due to transient myocardial ischemia; and (2) mechanical impairment occurs earlier than clinical (pain) and electrocardiographic (ST segment elevation) signs of transmural ischemia.

Adult↗
PubMed1984

Transient changes in left ventricular mechanics during attacks of Prinzmetal angina: a two-dimensional echocardiographic study.

Fifty-five ischemic attacks at rest with ST segment elevation were recorded by two-dimensional echocardiography (2DE) in 20 patients with Prinzmetal angina. Eighteen ischemic attacks were recorded starting from intravenous injection of ergonovine maleate while 37 spontaneous ischemic attacks were recorded from onset of either anginal pain or ECG changes or from the basal state. In each ischemic attack at least one of the following transient alterations was observed by 2DE during ST elevation: (1) Regional hypokinesia, akinesia, or dyskinesia; (2) "step sign," that is, a sharp demarcation between an akinetic or dyskinetic area and an adjacent normal or hypercontracting region; and (3) geometric changes in left ventricular shape, that is, globular appearance in diastole and hourglass silhouette in systole. Regional myocardial asynergy was detected earlier than onset of pain (which was not present in 21 [38%] ischemic episodes) or ST segment elevation on ECG, as documented in 40 ischemic episodes (16 induced and 24 spontaneous) in which echocardiographic monitoring was performed from basal state and carried on up to the appearance of ischemia. All described mechanical changes were fully reversible after pain subsided and ST segment was back to isoelectric, either spontaneously or with nitrates; furthermore, a contractile "rebound phenomenon" of the previously ischemic wall was observed in some episodes. In conclusion, these results outline a role for 2DE in detecting cardiac mechanical impairment due to transient myocardial ischemia with ST segment elevation in humans.

Adult↗