Showing papers on "Acute coronary syndrome published in 1996"
TL;DR: Serum levels of ICAM-1 were elevated in patients with acute coronary syndrome within 24 h, while the E-selectin levels did not change significantly, suggesting that adhesion molecule may play an important role in the postrolling process of leukocyte-endothelial cell interaction in acute coronary Syndrome.
71 citations
40 citations
TL;DR: Cardiac troponin T(TnT) measured in 35 patients with unstable angina and in 40 patients undergoing coronary reperfusion therapy for acute myocardial infarction indicated that persistent release of TnT reflects progressive irreversibleMyocardial damage in unstable angINA and indicates a risk of future cardiac events.
Abstract: The present study measured cardiac troponin T(TnT) for the pathophysiological analysis of evolving ischemic myocardial injury in 35 patients with unstable angina (3: Class IB, 32: Class IIIB) and in 40 patients undergoing coronary reperfusion therapy for acute myocardial infarction. Serum TnT, creatine kinase (CK), CKMB, myoglobin (Mb), and myosin light chain 1 (MLC1) were measured every 2-24 h for 10 days after admission to the CCU. In patients with unstable angina, positive test results were detected in 65.7% for TnT, 20% for CK, 37.1% for CKMB, 60.9% for Mb, and 26% for MLC1. Of the 23 patients with positive TnT, 12 (52.2%) had cardiac events. Of the 12 patients with negative TnT, 11 (91.6%) were event-free. All of the patients who developed cardiac events showed a persistent (n = 10) or delayed elevation (n = 2) pattern 28-120 h beforehand. The sensitivity for predicting cardiac events was 92.3% for TnT, 80% for Mb, 53.8% for CKMB, and 50% for MLC1. In patients with acute myocardial infarction, TnT release kinetics showed 2 peaks after coronary reperfusion therapy. TnT values at the 1st peak significantly correlated with maximum CKMB (r = 0.70, p < 0.05) and early-stage left ventricular wall motion score (r = 0.60, p < 0.05), while 2nd-peak TnT values significantly correlated with maximum MLC1 (r = 0.59, p < 0.05), the T1-SPECT score (r = 0.78, p < 0.05) and left ventricular ejection fraction (r = -0.74, p < 0.05) in the convalescent stage. The 2nd/1st-peak TnT ratio significantly correlated with the nQ/nST elevation index (ratio of the number of leads developing abnormal Q-wave 1 week after the onset to the number of leads showing ST elevation of more than 1 mm at admission) (r = 0.63, p < 0.05) in patients with anterior myocardial infarction. These data indicate that persistent release of TnT reflects progressive irreversible myocardial damage in unstable angina and indicates a risk of future cardiac events. In acute myocardial infarction, the 2nd/1st-peak TnT ratio in patients undergoing coronary reperfusion therapy may be useful for the quantitative evaluation of myocardial salvage.
25 citations
TL;DR: Long-term therapy would appear to be beneficial, at least in high-risk patients, in the light of increasing evidence that the underlying lesion in acute coronary syndromes resolves over a period of weeks or months.
Abstract: Standard heparin, low molecular weight heparin and aspirin are at present the only antithrombotic agents of proven value in the initial treatment of patients with an acute coronary syndrome. The combined use of aspirin and one of the heparins for at least 6 days should be considered for all such patients. With their high bio availability after subcutaneous injection and prolonged half-life, low molecular weight heparins simplify short-term treatment in the acute phase and enable long-term therapy to be maintained on an outpatient basis without the need for repeated laboratory monitoring of anticoagulant effects. Such long-term therapy would appear to be beneficial, at least in high-risk patients, in the light of increasing evidence that the underlying lesion in acute coronary syndromes resolves over a period of weeks or months.
22 citations
01 Jan 1996
TL;DR: Patients with intractable angina percutaneous and surgical revascularization are available with high initial success and good long-term prognosis, and recent observations indicate that it is not the severity of stenosis (plaque volume) that determines the outcome; it is the type of stenotic condition and the extent of collateral development.
Abstract: Coronary atherosclerosis without thrombosis is generally a benign disease that is asymptomatic or presents as chronic stable angina. The great majority of patients can be treated pharmacologically, and in those with intractable angina percutaneous and surgical revascularization are available with high initial success and good long-term prognosis. The acute manifestations of coronary atherosclerosis — unstable angina, acute myocardial infarction, or sudden cardiac death — share a common pathophysiologic phenomena: coronary thrombosis. This life threatening complication usually occurs at the site of plaque fissure or rupture. Several studies have shown that plaque rupture plays a key role in the pathophysiology of acute coronary syndromes [1]. Recent observations indicate that it is not the severity of stenosis (plaque volume) that determines the outcome; it is the type of stenosis (plaque composition) and the extent of collateral development [2].
7 citations
TL;DR: Though these lipoprotein abnormalities would not play a trigger role in acute coronary syndrome, they are characteristic of the lipid profile of patients with coronary artery disease.
5 citations
TL;DR: In patients with atherosclerotic heart diseases, angina pectoris is a significant risk predictor, but anti-ischemic intervention should be considered even in patients in whom the major problem is heart failure or arrhythmias, especially during episodes with elevated sympathetic activity.
Abstract: Angina pectoris is a significant risk predictor in patients with atherosclerotic heart disease. The major complications are myocardial infarction, heart failure, and arrhythmias. Plaque rupture turns stable angina pectoris into acute coronary syndrome by provoking platelet aggregation and thereby thrombus formation. Verapamil significantly inhibits platelet aggregation and thrombus formation, which may be one of several reasons for the protective effect of verapamil on reinfarction in patients recovering from myocardial infarction. Ischemia may lead to left ventricular dilation and diastolic dysfunction, and thereby heart failure. In postinfarction patients intervention with verapamil significantly reduced the use of diuretics compared with placebo, indicating that anti-ischemic intervention may prevent heart failure. Ventricular arrhythmias are significantly associated with arrhythmic as well as non-arrhythmic death. The lack of preferential association of ventricular arrhythmias with arrhythmic death rather than nonarrhythmic death may imply that arrhythmias are provoked by ischemia. Antiarrhythmic intervention in postinfarction patients significantly increases death and arrhythmic events compared with placebo, especially in patients with residual ischemia. This may be due to a significant slowing of conduction during ischemia in patients treated with antiarrhythmic agents. In animal studies anti-ischemic agents prevent or suppress ventricular arrhythmias during ischemia, whereas traditional antiarrhythmic drugs have no effect or even worsen the arrhythmias, especially during episodes with elevated sympathetic activity. Verapamil significantly reduces plasma norepinephrine levels and the norepinephrine release during ischemia, whereby ventricular arrhythmias may be prevented. Also, supraventricular arrhythmias are significantly associated with myocardial ischemia and are prevented by verapamil. In patients with atherosclerotic heart diseases, angina pectoris is a significant risk predictor, but anti-ischemic intervention should be considered even in patients in whom the major problem is heart failure or arrhythmias.
4 citations
Journal Article•
3 citations
TL;DR: It is concluded that 25 mg of transdermal NTG tape dilates coronary arteries and is applicable for acute coronary syndrome, with few complications.
Abstract: We analyzed the acute, direct effects of nitroglycerin (NTG) tape on the coronary arteries and hemodynamics in 38 patients who underwent coronary angiography. The diameters of the 3 main coronary arteries were compared among the angiograms obtained at baseline, 15 minutes following transdermal administration of 10 mg (8 patients) or 25 mg (30 patients) of NTG (Millisrol tape®), and after intracoronary injection of 2.5 mg isosorbide dinitrate (ISDN). Only the left main trunk and proximal portion of the left anterior descending artery dilated after 10 mg of transdermal NTG administration (p < 0.05). However, every measured coronary segment (segments 1-8, 11, and 13) dilated (p < 0.05) after 25 mg of NTG. Systemic blood pressure decreased slightly but significantly from 150 ± 22 to 147 ± 21 mmHg during the study, with no change in heart rate. Left ventricular end-diastolic pressure decreased significantly from 16 ± 7 to 14 ± 5 mmHg. We conclude that 25 mg of transdermal NTG tape dilates coronary arteries and is applicable for acute coronary syndrome, with few complications.
2 citations
Journal Article•
TL;DR: Encouraging results are gained from experience with high effective direct inhibitors of thrombin and antagonists of glycoprotein IIb/IIIa and it seems that they soon will find justification in the therapy of arterial thrombosis.
Abstract: Thrombotic occlusion of coronary arteries is the reason of most acute coronary syndromes. A significant role in their prevention and therapy is taken by antiplatelet therapy. Acute coronary syndrome justifies also the use of anticoagulation therapy, name by heparin. The adjuvant therapy by means of heparin in thrombolysis seems to be necessary especially when alteplase (t-PA) is used. Peroral anticoagulants represent a further therapeutical procedure in patients with coronary ischaemia. Regarding the increased risk of bleeding, the cost and difficulties coinciding with therapy by cumarine derivates, the antiplatelet therapy is currently preferred. Cumarine derivates, however, should be used in patients with simultaneous atrial fibrillation, venous thromboembolism and it should be considered in patients with heart failure and pre-thrombotic states. Studies aimed at the assessment of the role of low-molecular heparin in acute coronary ischaemia currently take place. Encouraging results are gained from experience with high effective direct inhibitors of thrombin (e.g. hirudin) and antagonists of glycoprotein IIb/IIIa. It seems that they soon will find justification in the therapy of arterial thrombosis. Interesting field of the research is represented by the studies which compare low doses of acetylosalicylic acid with low doses of cumarine derivates. (Ref. 43.)
1 citations
01 Jan 1996
TL;DR: It is assumed that therapeutic interventions aimed at lowering the lipid and/or macrophage pools stored in the plaque may “stabilize” the plaque and, hence, reduce the incidence of plaque rupture.
Abstract: Rupture of coronary atherosclerotic plaque and subsequent formation of an occlusive intracoronary thrombus have been recognized as the major events precipitating acute coronary syndromes and, therefore, represent the main foci of preventive strategies [1–6]. The vulnerable plaque — i.e., the one which is most prone to rupture and cause unstable angina, myocardial infarction, or sudden cardiac death — is smaller in size [7], richer in lipids [1,2], and more infiltrated with macrophages [2,3,8–10] than the stable, fibromuscular plaque. Therefore, it is assumed that therapeutic interventions aimed at lowering the lipid and/or macrophage pools stored in the plaque may “stabilize” the plaque and, hence, reduce the incidence of plaque rupture [2,4–6]. Indeed, cholesterol-lowering trials have yielded a significant reduction in acute cardiac events [11–18]. Since thrombus formation is another important factor in the conversion of chronic to acute coronary events, antithrombotic therapies may further prevent acute coronary syndromes by altering the consequences of plaque rupture [4].
01 Jan 1996
TL;DR: In general, acute myocardial infarction is associated with larger and more persistent thrombus than is unstable angina, and the amount and duration of intracoronaryThrombus play a major pathophysiologic role in acute ischemic syndromes.
Abstract: The most frequently recognized cause of ischemic syndromes is atherosclerotic disease. Atherosclerotic lesions in the coronary tree may cause stable syndromes of ischemia by means of direct luminal arterial narrowing (stable lesions) or unstable ischemic syndromes by inducing acute intraluminal thrombus formation (unstable lesions). Rupture of the surface of an atherosclerotic plaque with subsequent exposure of thrombogenic plaque components to flowing blood is the key event to initiate thrombosis within coronary arteries. Clinical consequences of intracoronary thrombus depend on many factors such as the degree and acuteness of blood flow obstruction, the duration of decreased perfusion and the relative myocardial oxygen demand at the time of atherosclerotic plaque rupture. Therefore, the amount and duration of intracoronary thrombus play a major pathophysiologic role in acute ischemic syndromes. In general, acute myocardial infarction is associated with larger and more persistent thrombus than is unstable angina. Superimposed vasospasm and presence of adequate collateral circulation may also contribute to determine the clinical outcome of the ischemic insult.
TL;DR: Information is summarized on ongoing and planned clinical trials in acute coronary syndrome from the Registry of Multicenter Clinical Trials.
Abstract: This report summarises information on ongoing and planned clinical trials in acute coronary syndrome. Information for the report is extracted and summarised from the Registry of Multicenter Clinical Trials, produced on behalf of the Council on Thrombosis and Haemostasis of the International Society and Federation of Cardiology and the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis.