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At least 1,153 records · Page 64Linked to original sources
PubMed1988

Platelet activation in angina at rest. Evidence by paired measurement of plasma beta-thromboglobulin and platelet factor 4.

Indexes of in vivo platelet activation, beta-thromboglobulin and platelet factor 4 were measured in triplicate in plasma from venous blood of 69 patients with proven ischaemic heart disease (IHD), discarding samples with a ratio of the plasma concentrations of the two proteins less than 2.6, in order to rule out sampling artifacts. Compared with 60 control volunteers, differences were not significant [for beta-thromboglobulin controls (ng ml-1, mean +/- SD) 27.8-8.6, ischaemic patients 32.3 +/- 17.1; for platelet factor 4 controls 4.3 +/- 1.4, ischaemic patients 5.9 +/- 5.7]. However, when patients were stratified according to disease activity (Group I--patients without spontaneous ischaemic episodes at rest during 4 days of continuous electrocardiographic monitoring; Group II--patients with less than 1 ischaemic episode/day; Group III--patients with greater than 1 episode/day), these indexes were increased in 'active' patients (for beta-thromboglobulin, in Group II--32.4 +/- 10.5 ng ml-1, P less than 0.05 vs. Group I; in Group III--42.6 +/- 14.6 ng ml-1, P less than 0.01 vs. Group I, P less than 0.05 vs. control. Platelet factor 4 was increased only in Group III--8.9 +/- 7.2 ng ml-1, P less than 0.05 vs. control). Beta-thromboglobulin and platelet factor 4 were 25.0 +/- 6.7 ng ml-1 and 4.9 +/- 4.8 ng ml-1, respectively, in Group I (P = NS vs. control). A relationship with the number of spontaneous ischaemic episodes at rest was confirmed by linear regression analysis (in Group III patients for beta-thromboglobulin: r = 0.76, P less than 0.01, and for platelet factor 4 r = 0.62, P less than 0.01). Levels were not elevated in patients with previous myocardial infarction without ischaemia at rest and/or patients with stable angina, and were not influenced by the occurrence of a positive exercise stress test. Coronary angiograms of ischaemic patients were analyzed to assess the extent and severity of atherosclerotic involvement: for both extent and severity, involvement was similar in the three groups. These data support the hypothesis of the occurrence of platelet activation in patients with spontaneous angina at rest, but not in other subsets of IHD patients, and establish the possibility of detecting in vivo platelet activation in IHD by means of such circulating markers.

Adult↗
PubMed1999

Beware of the heart: the multiple picture of cardiac involvement in myositis.

A 42-yr-old woman with dermatomyositis had two myocardial infarctions, episodes of acute chest pain and an acute lung oedema. These events were initially misinterpreted as atherosclerotic ischaemic heart disease accompanying the autoimmune disease. The lack of improvement of cardiac symptoms with anti-ischaemic and immunosuppressive drugs indicated other mechanisms. Intracoronary drug provocation as well as myocardial biopsy revealed a coincidence of small-vessel disease and vasospastic angina as a cause for the severe cardiac symptoms. After initiating therapy with high doses of calcium channel blockers, marked improvement of cardiac symptoms occurred. In the pathogenesis of cardiac involvement in dermatomyositis, two different mechanisms should be considered: inflammatory processes due to dermatomyositis and vasoconstriction caused by an impaired regulation of vascular tone, such as abnormal vessel reactivity or disturbed neuropeptide release. Signs of this generalized vasopathy are Raynaud's phenomenon, Prinzmetal's angina and small-vessel disease, which can coincide. In patients with severe cardiac symptoms and autoimmune diseases, Prinzmetal's angina should be excluded by intracoronary drug provocation using acetylcholine.

Angina Pectoris, Variant↗
PubMedDate not supplied

Discrepancy between early and late electrocardiographic indices of myocardial ischemic involvement in a patient with acute myocardial infarction.

A patient with acute myocardial infarction is described who showed marked ST-segment elevation in the ECG early in the course of his illness. Electrocardiograms at discharge, clinical course, myocardial scintigraphy and enzyme levels were suggestive of myocardial necrosis less extensive than expected from the magnitude and extent of intial ischemic injury by ECG. The factors which could have contributed to the modification of natural course of ECG evolution in this case are discussed.

Acute Disease↗
PubMed1989

Different vasomotor action of nifedipine on dynamic coronary obstructions and therapeutic response in effort and prinzmetal angina.

Variations induced by nifedipine (10 mg sublingually) in the residual lumen diameter of significant (greater than 50%) coronary lesions were assessed angiographically in 58 patients with effort angina (group 1) and in 19 patients with Prinzmetal angina (group 2). A relationship was sought between these acute variations of the stenotic lumen and the clinical response to treatment with the same drug (20 mg four times daily). Treatment efficacy was evaluated with exercise testing in group 1 and Holter monitoring in group 2. In group 1 the residual segment of stenotic diameter showed an increase, decrease, or no change with the calcium antagonist. Nifedipine failed to improve 40% of the cases (21% unchanged and 19% worsened) in group 1. In the same group of patients, the responses to exercise tests were dissociated from the acute vasomotor pattern. Changes in the pressure-rate product also did not explain the clinical results. In group 2 the majority of lesions had compliant portions, which invariably reacted to nifedipine with dilatation. All patients with the Prinzmetal form had relief of the anginal episodes with treatment. These data suggest that the therapeutic efficacy of nifedipine in classic effort angina probably is the net result of influences on the myocardial oxygen consumption and supply, and the acute coronary vasomotor pattern does not allow to predict the clinical response. Stenotic lesions in the Prinzmetal form possess a distinct sensitivity to the relaxant action of calcium channel blockade, which reasonably explains the highly positive response to treatment.

Adult↗
PubMed1996

Calcium-channel blockers in ischemic heart disease.

Recent reports add to a growing body of evidence that short-acting calcium-channel blockers, whether used for hypertension, unstable angina, or acute myocardial infarction, may have unfavorable effects. Short-acting nifedipine has no role in acute myocardial infarction, and the United States Food and Drug Administration has recently issued a warning discouraging its use in hypertension and unstable angina. Other short-acting calcium antagonists such as diltiazem and verapamil may have associated adverse effects as well, although the evidence is not as definitive. What effect sustained-release preparations and newer calcium antagonists have on the clinical endpoints of myocardial infarction and death is not known, and large prospective randomized clinical trials with these medications, some of which are underway, are needed to address these issues. Until that time, only medications with clearly documented efficacy and safety should be used for first-line therapy for hypertension, unstable angina, and acute myocardial infarction.

Angina Pectoris↗
PubMed1999

Enhancement of constrictor response of spastic coronary arteries to acetylcholine but not to phenylephrine in patients with coronary spastic angina.

This study examined the direct response of smooth muscle of coronary spasm sites to alpha1-adrenergic stimulation in patients with coronary spastic angina. Phenylephrine (1 microM in the coronary circulation, for 5 min), a stimulator of alpha1-adrenoreceptors, was directly infused into coronary arteries with spasm in 10 patients with coronary spastic angina and into normal coronary arteries in 10 control patients. The luminal diameter of epicardial coronary arteries was determined by computer-assisted quantitative angiography. The constrictor response to intracoronary injection of acetylcholine (ACh; 50 microg) was greater in spastic arteries than in control arteries (decrease from baseline, 48+/-2% vs. 12+/-2%, respectively; p<0.001). ACh (50 or 100 microg) induced coronary spasm associated with myocardial ischemia in all of patients with coronary spastic angina but not in any control patients. On the other hand, phenylephrine infusion did not induce coronary spasm in any of patients with coronary spastic angina or in control subjects. The constrictor response to phenylephrine infusion was comparable between spasm and control coronary arteries (decrease from baseline, 11+/-2% vs. 9+/-2%, respectively; p = NS). The results indicate that smooth muscle of spastic coronary arteries does not exhibit enhancement of constrictor response to direct stimulation of alpha1-adrenoreceptor on coronary smooth muscle. There may be receptor-specific enhancement of constrictor response to agonists in smooth muscle of spastic coronary arteries in patients with coronary spastic angina.

Acetylcholine↗
PubMed1985

Calcium antagonists in patients with cardiovascular disease. Current perspectives.

Since their introduction in the United States about 4 years ago, the calcium antagonists have achieved an important place in the medical therapy of several cardiovascular disease entities. These pharmacologic agents differ markedly in their clinical utility. Verapamil is extremely effective in patients with supraventricular tachyarrhythmias, hypertrophic cardiomyopathy, and the various anginal syndromes, but it appears to be ineffective or possibly even deleterious in those with pulmonary hypertension, congestive heart failure of any cause, and Raynaud's phenomenon or disease. Nifedipine exerts a powerful vasodilatory effect and, as a result, is efficacious in individuals with systemic or pulmonary hypertension, congestive heart failure, and Raynaud's phenomenon or disease. It is also beneficial in patients with various kinds of angina, especially when it is administered concomitantly with a beta-adrenergic blocker. It is totally ineffective as an antiarrhythmic agent. Diltiazem is an effective antianginal agent and may be beneficial as an antiarrhythmic agent, but it is largely untested in patients with systemic or pulmonary hypertension, Raynaud's disease, and hypertrophic cardiomyopathy. A thorough understanding of each drug's hemodynamic and electrophysiologic effects allows the practicing physician to prescribe them skillfully and safely.

Angina Pectoris↗
PubMed1978

Coronary artery spasm in a patient with unstable angina pectoris.

A 32-year-old male with the clinical syndrome of unstable angina is presented. During cardiac catheterization and coronary cineangiography, the coronary arteries were found to be free of atherosclerosis, but segmental spasm of the right coronary artery was observed. Spasm was reproduced, but to a milder degree, upon the administration of ergonovine maleate intravenously. The patient was discharged on a regimen of oral nylidrin HCL, with symptomatic improvement.

Adult↗
PubMed1994

Facilitation of coronary spasm by propranolol in Prinzmetal's angina: fact or unproven extrapolation?

BACKGROUND: Alpha-adrenergic activation enhances coronary vascular tone; beta-blockade leaves alpha-adrenergic vasoconstriction unopposed. Whether beta-adrenergic blockade facilitates coronary spasm in patients with Prinzmetal's angina is unknown. METHODS: Using quantitative angiography, we evaluated the response of normal and narrowed coronary arteries to intravenous propranolol, a cold pressor test (an alpha-stimulus), and the combination of the two in 15 patients with Prinzmetal's (group 1) and in 19 with classic (group 2) angina. From measurements of heart rate, systemic and pulmonary arterial pressures, and left and right ventricular ejection times, we derived the tension-time index per minute as a measure of the oxygen need (O2 demand) of the whole heart. RESULTS: In group 1, cold invariably constricted normal and diseased vessels, and in two patients elicited spasm at sites of significant lesions; these changes did not correlate with those in O2 demand. In group 2, the vasomotor reaction of normal and narrowed vessels in response to cold correlated with the modifications in O2 demand. After propranolol administration, (1) in normal vessels in both groups, the baseline luminal diameter varied in parallel with the changes in myocardial O2 demand; (2) narrowings in group 1 patients invariably dilated and in group 2 the caliber varied according to changes in O2 demand; (3) during cold stimulation, luminal narrowing in group 1 varied in parallel with O2 demand, and, in group 2, vessels were uniformly constricted. CONCLUSION: These results do not support the facilitation of coronary spasm by propranolol in Prinzmetal's angina and support the hypothesis that the contractility of coronary vessels in patients with this form of angina is different from that in the classic form.

Adult↗
PubMed2000

Clandestine ischemia in patients with vasospastic angina.

BACKGROUND: Coronary vasospasms generally occur at rest, but can also be triggered by physical exercise. Anginal pain and ST-segment elevation may be seen during exercise-stress tests. ST-segment depression, due to nonocclusive vasospasms, has also been found to occur. When the result of a test is positive, scintigraphy usually reveals perfusion defects. True silent or clandestine ischemia (normal result of exercise test with perfusion defects) in these patients is very uncommon. OBJECTIVE: To stress the need for suspecting occurrence of coronary vasospasms in order to perform a proper diagnosis. METHODS: Eight patients with angina were selected for this study. They had negative results of exercise tests with perfusion defects detected by thallium-201 tomography, normal coronary arteries and vasospasms. Maximal exercise-stress tests with thallium-201 tomography were performed. Sizes of perfusion defects were quantified by examining polar maps. Coronary angiography and then an intracoronary ergonovine test were performed for each patient. RESULTS: Significant defects were seen in territory of the right coronary artery, the left anterior descending artery, or both. Lung:heart ratio was normal in every case. The coronary arteries were normal and vasospasms were elicited with ergonovine in all the patients. Correspondence between the location of perfusion defects and angiographic spasms was generally observed. After treatment with calcium antagonists and nitrates all of them improved and defects detected by thallium tomography were no longer found when tests were repeated. CONCLUSIONS: Some patients with vasospastic angina may have normal results of exercise-stress tests and reversible perfusion defects detectable by scintigraphy. This finding must lead one to perform coronary angiography without administration of nitroglycerine beforehand and an ergonovine test if the coronary arteries are normal.

Adult↗
PubMed2004

Changing characteristics of patients with vasospastic angina in the era of new calcium channel blockers.

In the 1980s, clinical characteristics and long-term prognosis of patients with vasospastic angina (VSA) were investigated; however, they remain to be updated after the introduction of new calcium channel blockers, benidipine and amlodipine, in 1990s. Our patient cohort registered 726 patients with VSA from January 1980 to December 2002. Before and after 1990, 138 and 527 patients were respectively entered in this study with a follow-up rate of 92%. Most of the patients were treated with calcium channel blockers, while benidipine and amlodipine were used in 28% and 21% of them only after 1990. Survival without cardiovascular events (96% versus 96%) at 5 years remained good before and after 1990. The presence of significant coronary stenosis had a negative prognostic impact both before and after 1990, whereas after 1990, diabetes mellitus, smoking, and a history of myocardial infarction became more influential. Among the calcium channel blockers, benidipine showed a better prognosis. These results suggest that in the era of new calcium channel blockers, the prognosis of patients with VSA remains good with more prognostic impact of diabetes mellitus, smoking, and a history of myocardial infarction and that benidipine might have some better prognostic effects.

Administration, Sublingual↗
PubMed1985

Role of coronary spasm in different anginal syndromes.

Angina pectoris is a clinical syndrome caused by transient myocardial ischaemia due to an imbalance between myocardial oxygen demand and supply. It is now evident that coronary artery spasm plays an important role in the pathogenesis of various forms of angina pectoris. Angina pectoris that is mainly caused by coronary artery spasm (coronary spastic angina) has one or more of the following characteristics: 1) the attack occurs at rest, 2) the attack is associated with ST-segment elevation in the ECG, 3) the attack has a variable exercise threshold, and 4) the attack is suppressed by Ca-antagonists but not by beta-adrenergic blocking agents. On the other hand, angina pectoris that is caused by increased myocardial oxygen demand in the presence of severe and extensive organic stenosis (organic angina) has the following characteristics: 1) the attack is induced by constant amount of exertion irrespective of hour and day and is relieved by rest, 2) the attack is associated with ST-segment depression in the ECG, and 3) the attack is suppressed by beta-adrenergic blocking agents, which decrease myocardial oxygen demand.

Angina Pectoris↗
PubMed1987

Vasospastic angina: control of disease activity and efficacy of drug treatment using the prolonged hyperventilation test.

Sixteen consecutive patients with vasospastic angina underwent a control provocation test in the coronary care unit or the cardiac catheterization laboratory in order to evaluate the disease activity and the efficacy of long-term calcium antagonist treatment. In patients without angina at rest, the prolonged hyperventilation test was negative in 10/10 patients on calcium antagonist treatment (group A + B) and in 4/5 patients without medication (group C). The test was positive in 1/1 patient with angina at rest without medication (group D). However, the test provoked vasospastic angina in 1/5 patients who were asymptomatic without medication. In both the latter patients the prolonged hyperventilation test became negative after the restart of calcium antagonist treatment. During a mean follow-up period of 18 months (range 16-19) after the control hyperventilation test, no relapse of angina at rest, arrhythmias, syncopes, deaths or myocardial infarctions were registered. Thus, a negative test is compatible with low disease activity and/or efficacy of calcium antagonist treatment. Further, the test may reveal a subclinical tendency to coronary artery spasm.

Adult↗
PubMed1985

Prevention of vasospastic angina with nicardipine.

Anti-ischaemic effects and safety of nicardipine were assessed in 14 patients with vasospastic angina using a placebo comparison, cross-over design study for 8-13 weeks. The average daily dose of nicardipine for optimal angina prevention was 84 mg (range 40-160 mg). Nicardipine administration, as compared with placebo, significantly reduced anginal frequency and nitroglycerin consumption during the single- and double-blind phases of the study. Nicardipine appears to be effective in the prevention of vasospastic angina and not to cause major adverse effects.

Angina Pectoris, Variant↗