Thrombosis and thrombolysis in unstable angina (original) (raw)
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Effects of thrombolytic therapy in unstable angina: Clinical and angiographic results
Journal of the American College of Cardiology, 1988
The incidence of intracc ronary thrombus and the effects of thrombolytic therapy were studied in 41 patients with unstable angina . AH patients underwent coronary angiography 2 to 69 h (mean 19) after their last attack of chest pain. Immediately after angiography, 21 patients received iatracoronary streptokinase (250,000 III in 45 min) and were retrospectively analyzed . Twenty patients received intravenous recombinant tissue-type plasminogen activator (art-PA) (100 mg to 3 h) and were involved in a prospective study .
Comparison of Complete and Incomplete Revascularization by Coronary Angioplasty for Unstable Angina
Journal of Interventional Cardiology, 1988
When a "culprit lesion" can be identifed in a patient with unstable angina, it may be possible to achieve clinical improvement with incomplete revascularization. We analyzed actuarial survival free of an event (severe angina, myocardial infarction, coronary artery bypass graft, or death) at 6, 12, 18, and 24 months in 83 patients with multivessel disease and unstable angina who had undergone successful percutaneous transluminal coronary angioplasty (PTCA); revascularization was complete in 31 patients and incomplete in 52. Event-free survival in 85 patients with single-vessel disease and unstable angina who had undergone successful PTCA also was analyzed. Event-free survival at 24 months was worse in the multivessel disease patients than in the single-vessel disease patients (62% vs 85%; P = 0.001). Multivessel disease patients with complete revascularization had the same event-free survival CIS those with incomplete revascularization (63% vs 61%; P NS). Diagnostic angiograms revealed thrombus or an irregular ulcerated lesion in 42 of the multivessel disease patients. The event-free survival of these 42 patients was not direrent from that of the multivessel disease patients as a whole (64% vs 60%; P NS). We conclude that in patients with multivessel disease and unstable angina the event-free survival after PTCA is poorer than in patients with singlevessel disease and unstable angina. In the former patients, event-free survival does not necessarily depend on the completeness of revascularization. The outcome of patients who have intracoronary thrombus or an irregular ulcerated lesion resembles the outcome of patients who lack these findings. (J Interven Cardiol: 1988: 1: 1) percutaneous transluminal coronary angioplasty, incomplete revascularization, unstable angina, culprit lesion
Unstable angina—prospective and randomized study of its evolution, with and without surgery
The American Journal of Cardiology, 1974
A prospective and randomized study of 142 patients was undertaken to evaluate medical or surgical treatment in patients with unstable angina. The condition of each patient was classified according to one of three categories: intermediate syndrome (44 patients); progressive angina with and wfhout previous infarction (53 patients); and postinfarction angina (14 patients). Of the 142 patients, 31 were excluded on the basis of specific criteria. A detailed research protocol, which included early blind random choice of medical or surgical therapy, was foilowed.
… International Journal of …, 1994
Patients with unstable angina, refractory to intensive medical therapy, are at high risk for developing thrombotic complications, such as recurrent ischemia, myocardial infarction and coronary occlusion during coronary angioplasty. As both platelet aggregation and/or thrombus formation play an important role in this ongoing ischemic process, a monoclonal platelet GPIIb/IIIa receptor antibody (c7E3) or thrombolytic therapy (alteplase) might be able to modify the clinical course and underlying coronary lesion morphology. To evaluate whether alteplase or c7E3 could influence the incidence of complications, we randomized 36 and 60 patients, respectively to alteplase or placebo, or c7E3 or placebo. All patients exhibited dynamic ECG changes and recurrent pain attacks, despite maximal tolerated medical therapy. Patients were randomized in both studies after initial angiography had demonstrated a culprit lesion amenable for angioplasty. After study drug infusion quantitative angiography was repeated and angioplasty performed. Recurrent ischemia during study drug infusion occured in 5, 6, 9 and 16 patients from the alteplase, placebo, c7E3 and placebo group, respectively. Major events defined as death, myocardial infarction or urgent intervention occurred in 7, 3, 1 and 7 patients, respectively. Two patients died: one in the alteplase group and one in the placebo group from the c7E3 study. The first patient due to retroperitoneal hemorrhage, the second as a result of recurrent infarction. Qualitative angiography showed resolution of clots in the c7E3 group only, while the same group of patients showed in 20% an improvement in TIMI flow grade, without deterioration in any patient from this group. Quantitative angiography showed a significant improvement in percentage diameter stenosis in the c7E3 group, which was not observed in all three other groups, although differences between groups were not significant. Alteplase infusion in patients with refractory unstable angina did not change the clinical course, nor the coronary morphology, c7E3 on the other hand, both improved the clinical course and the coronary lesion morphology and rheology in the same category of patients.
Unstable angina: Natural history and determinants of prognosis
The American Journal of Cardiology, 1981
One hundred one patients with unstable angina were treated conservatively without the routine use of beta receptor blocking agents, calcium antagonist drugs, anticoagulant agents or nitrates. Only two patients underwent arteriography and coronary arterial bypass surgery during hospitalization and one patient during the 1st year of follow-up study. The 28 day mortality rate was 4 percent and the total 1 year cardiac mortality rate 10 percent. Two patients died from carcinoma. The incidence rate of nonfatal myocardiai infarction was g percent during the first 28 days and a further 3 percent for the 1st year. These resufts compare favorably with the immediate and 1 year prognosts reported from other studies using different treatment procedures, including modem intensive drug treatment and coronary arterial bypass surgery. Various factors studied during the acute stage of unstable angina were assessed in an effort to predict the immediate and tong-term outcome. Only persistence of pain after admission to the hospital was found a significant indicator of an adverse prognosis.
Regular review: Treatment possibilities for unstable angina
BMJ, 2000
Unstable angina is frequently encountered by general practitioners and cardiovascular specialists. In the United States, of the 2.5 million patients admitted to hospital every year with suspected acute coronary syndromes, 1.5 million have unstable angina. The rest have myocardial infarction with or without ST elevation. 1 Earlier published literature classified acute ischaemic episodes as unstable angina and either non-Q wave or Q wave infarction. As Q wave and non-Q wave infarctions can only be definitely distinguished by electrocardiography several days after the clinical event, the classification does not help with emergency patients. Moreover, the prognostic value of Q wave versus non-Q wave infarction classification is limited. 2 A new nosological scheme has derived from the need to rapidly assess patients at presentation so that powerful new treatments can be appropriately selected. All acute presentations suggesting acute coronary syndromes can be further divided into infarction with ST elevation (possibly including patients with new bundle branch blocks) and infarction without ST elevation and unstable angina combined. The distinction between the last two conditions can be reliably made by measuring serum markers. This classification makes sense because early thrombolytic treatment saves the lives of patients with infarction with ST elevation but has no beneficial, and probably some deleterious, effect in those with infarction without ST elevation or unstable angina. Moreover, the therapeutic approaches in the last two conditions are similar. 3 Hence we consider unstable angina and infarction without ST elevation as a single entity, especially regarding treatment. Figure 1 shows a plan for assessment and classification of suspected acute coronary syndrome. Methods We extracted data from the personal collection of journal articles of the authors and from Medline whenever necessary. We also obtained information from review articles on different subtopics. Pathophysiology of unstable angina Braunwald described unstable angina as a syndrome with five mutually non-exclusive causes; thrombosis, mechanical obstruction, dynamic obstruction (spasm of microvasculature and macrovasculature), inflammation or infection, and increased oxygen demand. 4 Unstable angina occurs from the interplay of these factors, with thrombosis and mechanical obstruction usually dominating. Transient or subtotal obstruction due to a platelet rich "white clot" over a fissured atherosclerotic plaque is considered causal in most episodes of unstable angina. This differs from the fibrin rich "red clot" associated with total coronary occlusion in infarction with ST elevation. In contrast to the Braunwald model, European investigators have advocated a central role for inflammation in unstable angina. 5 6 Increased concentrations of acute inflammatory markers, such as C reactive protein, are more often found in unstable angina than in chronic stable angina. Also, an increased concentration of C reactive protein at admission among patients with unstable angina has been correlated with worse outcomes both in hospital and after one year. 7-9 Several authors have shown varying associations of different subpopulations of T lymphocytes, granulocytes, macrophages, and cytokines with unstable angina. 5 6 Although the role of inflamma-Chest pressure, pain, or both, or angina equivalent Acute coronary syndrome Evaluation of initial electrocardiogram Early reperfusion strategy Evaluation of serum markers Evaluation after 48 hours Management strategy for unstable angina or infarction without ST elevation Non-cardiac cause ST elevation absent ST elevation present Unstable angina Infarction without ST elevation Infarction with ST elevation Unstable angina Non-Q wave infarction Q wave infarction Fig 1 Assessment and classification of suspected acute coronary syndrome
Management Strategies for a Better Outcome in Unstable Coronary Artery Disease
Clinical Cardiology, 1998
Unstable coronary artery disease is a term encompassing both unstable angina and non-Q-wave (non-ST-segment elevation) myocardial infarction. Patients with these conditions are at risk of early progression to acute myocardial infarction and death. Thus, management of these conditions must aim to reduce long-term mortality and morbidity. Risk stratification is crucial for the identification of patients whose risk of early progression is high; they may require coronary angiography and (if suitable) either percutaneous transluminal coronary angioplasty or coronary artery bypass surgery. No single variable can accurately predict risk, but considerable data are emerging to show that biochemical markers of myocardial injury, such as troponin-T and troponin-I, are valuable in combination with electrocardiographic findings and clinical features. Routine early invasive procedures (coronary angiography with or without revascularization) have not yet been shown to have any significant advantage over conservative regimens for the majority of patients. Antiplatelet, anticoagulant, and anti-ischemic agents remain the mainstay of treatment in the acute phase. New agents, such as glycoprotein IIbAIIa receptor inhibitors and low-molecular-weight hep-arins, as well as antithrombins and Factor Xa inhibitors add to the treatments currently available. Thrombolytic agents are contraindicated in the absence of ST-segment elevation. After clinical stabilization, ongoing assessment should include exercise testing for all patients who are able; other imaging techniques should be used for patients unable to exercise. A profile indicating a high risk of future events is an indication for elective angiography and consideration for revascularization.
Current Management of Unstable Angina
American Journal of Cardiovascular Drugs, 2002
Patients presenting with unstable angina pectoris or non-Q-wave myocardial infarction (MI), if treated inadequately, are at a high risk of MI and subsequent mortality. The use of intravenous small molecule glycoprotein IIb/IIIa inhibitors along with standard therapeutic management options improves outcome. Since the publication of the Thrombolysis in Myocardial Ischemia IIIB, Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) and Fragmin and Fast Revascularization during InStability in Coronary artery disease II (FRISC II) studies, there is great debate about the advantages of following an early 'invasive' treatment option with coronary angiography and revascularization after initial medical therapy compared with the 'conservative' approach, where angiography is reserved for those who remain symptomatic. The Treat angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy-Thrombolysis in Myocardial Infarction 18 (TACTICS-TIMI 18) study has helped to resolve some of the controversies since it was designed with more current medical (early and routine use of tirofiban) and revascularization (use of stents during percutaneous coronary interventions) options as part of the invasive treatment protocol. This study indicated that an early invasive strategy in risk stratified patients combined with early use of tirofiban with standard medical therapy significantly improves outcome and appears well tolerated.
Unstable angina: Comparison of medical and surgical management
The American Journal of Cardiology, 1977
Medical versus surgical treatment of unstable angina was compared in a prospective nonrandomized study of 119 patients. Acute transient ST-T wave changes were present during chest pain in all patients. Acute infarction was excluded by serialelectrocardiograms and enzyme studies. All patients admitted to the coronary care unit from 1970 to 1975 who fulfilled the entry criteria were included in the study. The starting point for data evaluation was 5 days after hospital admission. Characteristics at entry were similar in 66 medically treated patients and 52 patients who had coronary bypass vein graft surgery. During a mean follow-up period of 23 months in 66 medically treated patients with unstable angina the incidence rate of nonfatal myocardial infarction was 17 percent and the total mortality rate 21 percent compared with respective rates of 19 percent and 5.8 percent in 52 surgically treated patients. In the surgical group 8 patients (15 percent) had a perioperative infarction and only 2 (4 percent) had a late infarction; one patient (2 percent) died at operation. Symptomatic improvement was observed more frequently in the surgically treated group. Sixty percent of surgically treated patients were free of angina compared with 21 percent of medically treated patients. Eight medically treated patients (12 percent) required late surgical treatment for persistent severe angina despite optimal medical management.
Primary Stable Microvascular Angina: A Long-Term Clinical Follow-Up Study
Circulation, 2017
P revious studies of patients with primary stable microvascular angina showed excellent prognosis despite frequent recurrence of symptoms. 1,2 Recent large studies challenged this view, however, reporting a sizeable rate of major adverse cardiovascular events (MACE) in patients with stable angina and no obstructive coronary artery disease. 3,4 To get further insight into this clinical controversy, we performed longterm follow-up of a rather large population of patients with microvascular angina. We included in this study all patients with primary stable microvascular angina who participated in clinical investigations performed at our institute between 1991 and 2011. All patients had exercise-induced angina, positive exercise stress test, angiographically normal coronary arteries, and no other relevant cardiac or systemic disease. 5 In suspected cases, coronary spasm was excluded by ergonovine test. Patients were carefully characterized for cardiovascular risk factors and symptoms. All patients gave their informed consent to participate in the study, which was approved by our institutional review board. Follow-up was done by clinical visits or structured telephone interview. In the case of death, its cause was established from interview of patient's relatives and, when necessary, clinical records and death certificates. Clinical events included total, cardiovascular, and cardiac death, nonfatal acute myocardial infarction or unstable angina, coronary revascularization, other major cardiovascular events (stroke, transient ischemic attack, pulmonary embolism, etc), emergency room access, hospital admission, and repeat coronary angiography. Finally, patients were asked to report whether their symptoms improved, remained unchanged, or worsened over time. Data were also analyzed to identify predictors of the following clinical end points: (1) total mortality, (2) MACE (cardiovascular death, acute myocardial infarction, coronary revascularization), (3) emergency room access for angina, and (4) lack of symptom improvement. The association of variables with end points was tested by univariable and multivariable Cox regression analysis. Variables showing 2-sided P<0.1 at univariable analysis were included in multivariable models. Data were analyzed with SPSS 21.0 (SPSS Italia). The multivariable association of variables with end points is reported as hazard ratio (HR) with 95% confidence interval (CI). Basal clinical data of patients and follow-up results are summarized in the Table. The population included 250 patients. Vital state was ascertained for 240 patients (96%). At a median follow-up of 16.0 years (interquartile interval, 12-21), total, cardiovascular, and coronary mortality were 10.8%, 3.75%, and 0.83%, respectively (annual rates, 0.68%, 0.23%, and 0.05%, respectively). Among 207 patients with appropriate data, MACE occurred in 17.9% (1.12% per year). Sixty-five of these patients (31.4%) underwent ≥1 new coronary angiograms, and obstructive stenoses were found in 11 patients (5.3%) who underwent coronary revascularization (percutaneous in 9, surgical in 1, both in 1).