Nifedipine and metoprolol in suspected unstable angina. Unstable angina pectoris.
Explore the source record for details and available documents.
Adrenergic beta-Antagonists↗
SEARCH · PubMed Health
Results for “Angina, Unstable”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Diagnosing and managing unstable angina. Unstable Angina Guideline Panel. Agency for Health Care Policy and Research.
Explore the source record for details and available documents.
Angina, Unstable↗
Calcium antagonists for Prinzmetal's variant angina, unstable angina and silent myocardial ischemia: therapeutic tool and probe for identification of pathophysiologic mechanisms.
The calcium antagonists provide a unique tool to reduce myocardial oxygen demand and prevent increases in coronary vasomotor tone. For patients with Prinzmetal's variant angina, diltiazem, nifedipine and verapamil are extremely effective in preventing episodes of coronary vasospasm and symptoms of ischemia. Unstable angina pectoris is a more complex pathophysiologic syndrome with episodes of ischemia due to increases in coronary vasomotor tone, intermittent platelet aggregation or alterations in the underlying atherosclerotic plaque. Each of the calcium antagonists is effective as monotherapy in decreasing the frequency of angina at rest. Nifedipine is the only calcium antagonist that has been studied in a combination regimen with beta blockers and nitrates for patients with unstable angina, and control of angina is better with the combination regimen than with either form of therapy alone. Although symptoms of myocardial ischemia in unstable angina are reduced by calcium antagonists, these agents do not seem to decrease the incidence of adverse outcomes. Antiplatelet therapy appears to improve morbidity and mortality in patients with unstable angina, suggesting that thrombus formation may play a central role in that disorder. Episodes of silent or asymptomatic myocardial ischemia, identified by ST-segment monitoring, occur in a variety of disorders of coronary disease. Among patients with Prinzmetal's variant angina and unstable angina, episodes of silent ischemia appear to be as frequent as episodes of angina and the calcium antagonists are effective in decreasing episodes of ischemia regardless of the presence or absence of symptoms. Persisting episodes of silent ischemia among patients with unstable angina despite maximal medical therapy identify patients at high risk for an early unfavorable outcome. Among patients with stable exertional angina, episodes of silent ischemia may be up to 5 times as frequent as episodes of angina, and may be due to increases in coronary vasomotor tone, transient platelet aggregation or increases in myocardial oxygen demand. Preliminary experience suggests that calcium antagonists and beta blockers are effective in decreasing episodes of silent ischemia in patients with stable exertional angina and that a combination regimen may be more effective than either form of therapy alone.
Angina Pectoris↗
Autoantibodies against oxidized low density lipoproteins in patients with stable angina, unstable angina or peripheral vascular disease; pathophysiological implications.
BACKGROUND: Antibody antioxidized low density lipoproteins (oxLDL) might play a role both in atherogenesis and in the pathogenesis of acute coronary syndromes. METHODS AND RESULTS: Antibody titres to oxLDL and levels of C-reactive protein were compared in unstable angina, stable angina or peripheral artery disease. Antibody titres to LDL oxidated by CuSO(4)for 2, 4 and 18 h (Cu-oxLDL-Ab(2-4-18)) or by peroxidase (HRP-oxLDL-Ab) were assessed by ELISA. Cu-oxLDL-Ab(2-4-18)were consistently higher in peripheral artery disease than in unstable angina (P<0.001, P<0.001, P=0.01, respectively) or in stable angina (P<0.001, P=0.01, P=ns) but similar in unstable and stable angina. Accordingly, HRP-oxLDL-Ab were higher in peripheral artery disease than in unstable angina (P<0.001) or stable angina (P=0.04) but similar in unstable and stable angina. The number of arterial stenoses was higher in peripheral artery disease than unstable and stable angina (P<0.01). Cu-oxLDL-Ab and HRP-oxLDL-Ab correlated with the severity of atherosclerosis (P<0.01, R=0.4;P=0.02, R=0.3 respectively). Conversely, C-reactive protein levels were higher in unstable than in stable angina (P<0.001) or in peripheral artery disease (P<0.03) but similar in stable angina and peripheral artery disease and did not correlate with the severity of atherosclerosis. CONCLUSION: The autoimmune response to oxLDL is likely to play an important role in atherogenesis but not in precipitating acute coronary syndromes.
Aged↗
Comparison of the histopathology of culprit lesions in chronic stable angina, unstable angina, and myocardial infarction.
BACKGROUND: The etiology of unstable angina (UA) and myocardial infarction (MI) both involve rupture of an atherosclerotic plaque in a coronary artery. It has been suggested that the two syndromes differ because MI results if a red occlusive permanent thrombus occurs and UA occurs only if a nonocclusive platelet (white) thrombus occurs. HYPOTHESIS: The purpose of this study was to determine the differences between coronary lesion pathology in MI and UA and compare them with lesions of chronic stable angina (CSA). METHODS: We reviewed the pathologic specimens of culprit lesions obtained by directional coronary atherectomy in 27 patients with MI, 29 patients with UA, and 16 patients with CSA. RESULTS: The incidence of ruptured plaque was high and identical in patients with MI (77.8%), and UA (75.8%), and significantly lower in patients with CSA (25.0%) (p < 0.001). Similarly, the incidence of red thrombus was the same in MI (92.6%) and UA (82.7%), and significantly less in CSA (p < 0.001). CONCLUSIONS: The underlying pathophysiology of both UA and MI appears to be the same, with red thrombus playing an important role in both syndromes. The only difference is in the degree of occlusiveness of the red thrombus on the ruptured plaque and whether the occlusion is transient (UA) or persistent (MI). The balance between thrombosis and endogenous clot lysis determines which syndrome occurs. Lytic therapy is not effective in UA, probably because the clot is not occlusive or because endogenous lysis has already achieved the degree of coronary opening that eventuates from tissue plasminogen activator or streptokinase administration. Prompt catheterization and revascularization may be as indicated in patients with MI if there remains viable myocardium as in patients with UA.
Aged↗
A review of nitrate therapy in stable angina, variant angina, unstable angina and myocardial infarction.
Explore the source record for details and available documents.
Angina Pectoris↗
[The role of inflammation in the pathogenesis and prognosis of unstable angina].
Unstable angina is a clinical syndrome which results from the unstabilization of the coronary atherosclerothic plaque, leading to its ulceration or rupture and to the formation of superimposed thrombus. The mechanism underlying plaque unstabilization is a subject of intense basic research. In the last few years, new knowledge has emerged that relates inflammation in the atherosclerothic lesion with its gradual growth and development, as well as with its sudden transformation into a complicated plaque causing unstable angina or myocardial infarction. In this article we will review the evidence that links inflammation with the pathogenesis of unstable angina and its prognosis.
Angina, Unstable↗
Initial and late results of coronary angioplasty for early postinfarction unstable angina.
Unstable angina that occurs in the early postinfarction period is associated with an increased incidence of unfavorable cardiac events despite aggressive medical therapy. We examined the results of coronary angioplasty in 47 consecutive patients with postinfarction unstable angina who were referred for the procedure 12.9 +/- 7 days following myocardial infarction, 14 of which were Q wave and 33 of which were non-Q-wave. Coronary angioplasty was performed on a total of 55 arteries with a mean predilatation stenosis of 95 +/- 8%. These included 46 infarct-related arteries and nine noninfarct arteries. Double-vessel angioplasty was performed in eight patients. Successful coronary angioplasty (greater than 30% reduction of predilatation stenosis) was achieved in 43 patients (91%), with a mean residual stenosis of 33 +/- 28%. There was one in-hospital death, one patient required emergency bypass surgery, and two patients had early reocclusion resulting in myocardial infarctions. The 39 patients who had successful angioplasty procedures and who were discharged from the hospital without an unfavorable outcome were followed for 16.3 +/- 7 months, and repeat coronary angioplasty was required in five patients from 45 to 105 days after the initial procedure. Two patients had subsequent elective bypass surgery, one had a recurrent myocardial infarction, and one patient had a noncardiac death. For selected patients with suitable coronary anatomy, coronary angioplasty appears to offer an efficacious therapeutic option for early postinfarction unstable angina.
Adult↗
Medical versus surgical treatment of unstable angina.
Unstable angina is an important symptom of coronary artery disease. Two general clinical presentations may occur: (1) stable angina with a recent increase in severity or angina of recent onset, or (2) acute coronary insufficiency or angina at rest with chest pain resembling that of acute infarction. The risk of death or infarction is greater in patients who have recurrent chest pain and ST-T wave abnormalities despite hospital treatment. In patients without electrocardiographic or serum enzyme evidence of a completed infarct, coronary arteriography and bypass graft surgery can be performed with an acceptably low mortality rate. Surgical treatment provides better symptomatic relief than medical management in many patients, but the significant incidence of perioperative infarction makes it difficult to determine if surgery prevents infarction. Some studies indicate that surgery improves survival in subgroups, but data from large scale randomized studies will be needed to answer this question securely. Patients with disease of the left main coronary artery should probably have surgical treatment. Medical treatment will relieve symptoms in most patients with unstable angina and on a long-term basis may obviate the need for surgery. A preliminary period of intensive medical treatment before surgery may be advantageous since there is little evidence that survival rates are improved by treating unstable angina as an acute surgical emergency.
Acute Disease↗
[Treatment of unstable angina].
Unstable angina generally is a serious condition which often requires hospital treatment. In this review article, we shall describe our therapeutic approach to unstable angina. It is almost identical worldwide. This attitude is based on the evidence provided by well controlled clinical trials. It is therefore a good example of Evidence-Based Medicine.
Angina, Unstable↗
[Clinical aspects and classification of unstable angina].
Unstable angina pectoris is a clinical syndrome with multiple underlying pathophysiologic mechanisms. This presentation is concerned with primary angina pectoris exclusively. In the majority of cases a rupture of an atherosclerotic plaque and an intracoronary thrombus are responsible for instable angina. The practitioner's role is to identify those patients who will develop complications with the aid of clinical parameters. Prinzmetal's angina is also instable, occurs at rest and leads to ST-segment elevation. It is most likely due to coronary spasm, developing in disease-free and atherosclerotic coronary segments alike. This variant of unstable angina is treated most successfully with calcium antagonists. The recognition of the responsible pathophysiologic mechanism permits adjustment of treatment of every patient taking into consideration the seriousness of his prognosis.
Angina Pectoris, Variant↗
Management of unstable angina.
Unstable angina is a common condition that presents a challenge to physicians because of its complex pathophysiology, and because of the high incidence of associated death and myocardial infarction. This article summarizes key strategies that can be employed in managing unstable angina and describes their interaction with the mechanisms that underpin the condition.
Adrenergic beta-Antagonists↗
-New perspectives in therapy of unstable angina-.
Unstable angina is a critical phase of coronary heart disease with high risk of myocardial infarction and death. Recently, major advances have been made concerning therapeutic management and risk stratification. PATHOGENETIC MECHANISMS: Plaque rupture followed by local thrombus formation is the underlying mechanism for the majority of patients with unstable angina. The process that leads to plaque rupture is a complex sequence of events which includes local inflammatory activity. Rapid progression and vasospasm play a pathogenetic role only in a few patients. NEW THERAPEUTIC STRATEGIES: Pain relief is frequently successfully achieved by intravenous nitrates combined with betablockers. Calciumantagonists may be added, if angina persists. Prognostic improvement is achieved by platelet inhibitors, like acetylsalicylic acid or ticlopidine. In patients with persisting angina at rest platelet inhibitors should be combined with high-dose heparin. Thrombolytics have no advantage and should not be given without electrocardiographic evidence of myocardial infarction. The potential additional benefit of new glycoprotein IIb/IIIa receptor inhibitors or more potent anti-thrombins, like hirudin or hirulog, need to be further evaluated in larger trials. THERAPY CONTROL: The detection of minor myocardial cell injury by measurements of new cardiac markers like troponin T is associated with an unfavourable outcome. Troponin T may therefore serve as parameter for risk stratification in emergency rooms and control therapeutic regimens.
Angina, Unstable↗
[Nitrates in unstable angina].
Unstable angina is an acute coronary syndrome between stable angina and myocardial infarction, with different clinical and laboratory features. Angiographically, these patients are more likely to have progression of coronary artery disease, vasospastic phenomena and intracoronary thrombus. Sudden plaque rupture, thrombus formation and the occlusion of an epicardial coronary vessel seem to be the underlying pathological mechanism. Patients with unstable angina are at an increased risk of major complications, especially fatal and nonfatal myocardial infarction, justifying an aggressive therapy in an Intensive Coronary Care Unit with beta-blockers, calcium antagonists and, in particular, nitrates, usually in association. The use of antiplatelet agents, namely aspirin, has been proved to be beneficial significantly reducing the risk of death and myocardial infarction. On the other hand, heparin and thrombolytic therapy are still a matter of some controversy, although the former is largely used in the acute phase. Coronary angiography should be done in all patients refractory to medical treatment to allow further management of the underlying coronary lesions by PTCA or coronary bypass surgery. However, some authors have advised a more aggressive attitude, performing the revascularization in an early phase. Randomized studies have shown that, with surgery, only patients with reduced left ventricular function may improve with the procedure, having a better two-year survival rate. Concerning PTCA, although the complication rate is somewhat higher than in the elective procedure, the probability of late infarction and death is significantly reduced in patients in which there was initial success.
Angina, Unstable↗
Soluble P-selectin is a marker of plaque destabilization in unstable angina.
Unstable coronary syndromes usually involve platelet activation and thrombus formation at the site of atherosclerotic plaque. P-selectin in platelets and endothelial cells mediates adhesive interaction with leucocytes to form thrombi. The aim of this study was to asses the level of soluble P-selectin (CD62P) as a non invasive marker of coronary plaque destabilization in unstable angina (U.A.). Serum samples were collected from 23 male patients with UA, 20 male patients with stable angina (SA) and 13 healthy controls. Soluble P-selectin (sP-selectin) level was measured by ELISA technique. The mean sP-selectin level was significantly higher in patients with UA (87.6+/-30.10 ng/ml) than SA (36.2 +/-13.8 ng/ml) and control subjects (16.7+/-8.6 ng/ml). In conclusion, s-Pslectin level could be used as a marker of plaque destabilization in unstable angina.
Adult↗
Unstable angina.
Unstable angina can manifest as an array of symptom complexes. In some patients, medical therapy will stabilize the episodes of angina, and only predismissal exercise testing or angiography (or both) will be necessary. At the other end of the spectrum are patients with rest angina or multiple episodes of silent ischemia who are refractory to medical therapy and experience undetected microinfarction. Most of these patients require immediate catheterization and subsequent intervention with intra-aortic balloon pulsation, percutaneous transluminal coronary angioplasty, or coronary artery bypass grafting. An entire spectrum of manifestations exists between these two extremes. One challenge during the 1990s will be better stratification of patients with unstable angina so that safe, efficient, cost-effective treatment strategies can be appropriately applied to all patients.
Angina Pectoris↗
Management of unstable angina.
Unstable angina (defined as attacks that are increasingly frequent and/or prolonged, that occur at rest, or are brought on by trivial provocation) is one of the commonest reasons for emergency admission to hospitals in the UK. Even with appropriate treatment, the risk of myocardial infarction (MI) or death may be as high as 10% in the first 6 weeks after its development. The mechanisms underlying unstable angina, and the role of the alternative treatments that are available, are better understood than when we reviewed the topic 8 years ago. Here we reappraise the management of this important condition.
Angina, Unstable↗
Glycoprotein IIb/IIIa receptor antagonists for the treatment of unstable angina.
Unstable angina and non-Q-wave myocardial infarction, part of the acute coronary syndromes, are characterized by coronary arterial plaque rupture and endovascular thrombus formation. Plaque rupture leads to exposure of subendothelial components such as collagen and fibronectin, and these substances are known to cause platelet activation, aggregation, and initiation of the coagulation cascade. Aspirin and heparin have been used as therapeutic mainstays for acute coronary syndromes, acting as antiplatelet and antithrombin agents, respectively. Despite treatment with this conventional anticoagulant strategy and antianginal drugs, substantial morbidity and mortality continue to be associated with unstable angina and non-Q-wave myocardial infarction. Specific antagonists of the platelet glycoprotein IIb/IIIa inhibitor have proved effective in substantially reducing ischemic events following percutaneous coronary revascularization, and several trials using these agents in acute coronary syndromes are now completed. Compared to patients receiving standard therapy (aspirin and heparin), platelet IIb/IIIa antagonists have further reduced the incidence of major ischemic events. Ongoing studies are addressing the optimal extent and duration of platelet inhibition in patients with acute coronary syndromes.
Abciximab↗