Acute Coronary Syndromes: Therapy with aspirin is recommended for all patients with acute myocardial ischemic syndromes unless contraindications for its use is present. None of the studies thus far have conclusively established evidence for a selective dose of aspirin. Until conclusive evidence exists, aspirin in doses of 81 mg (children's tablet) to 325 mg (adult tablet) are recommended. Ticlopidine may prove to be an attractive alternate choice in those who cannot take aspirin. According to the ACC/AHA task force recommendations, patients with acute myocardial infarction receiving thrombolytic therapy should receive both heparin and aspirin. Aspirin is to be administered in a dose of 160 mg daily. Heparin can be discontinued after 2 days if the patient's clinical course remains uncomplicated. Aspirin should be continued indefinitely. An alternative strategy in those who cannot take aspirin is to switch to warfarin before hospital discharge with a view toward long-term anticoagulant therapy. Secondary Prevention: Aspirin in a dose of 325 mg daily is recommended for all survivors of an acute myocardial infarction. No benefit derives from the addition of dipyridamole. The role of sulfinpyrazone remains undefined. Warfarin is an effective antithrombotic alternative to aspirin for secondary prevention after a myocardial infarction. However, aspirin is cheaper to administer and follow up when compared with warfarin. From available information, aspirin appears to be an adequate antithrombotic agent in patients who have near-normal left-ventricular function, the elderly, patients with coexisting cerebrovascular or peripheral vascular disease, and those with contraindications for anticoagulants. Warfarin should be preferred in high-risk patients with anterior or apical myocardial infarction, left-ventricular dysfunction with or without a mural thrombus, and those with associated atrial fibrillation. A randomized study assessing aspirin versus warfarin for secondary prevention after myocardial infarction is being initiated to determine the relative efficacy and safety of these drugs in secondary prevention after myocardial infarction.

Angina, Unstable↗

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Antithrombotic therapy in atrial fibrillation: a review of randomized trials with special reference to the Stroke Prevention in Atrial Fibrillation II (SPAF II) Trial.

Nonvalvular atrial fibrillation is common and is associated with a high risk of system embolism. Recently, several large randomized trials have been completed that have established the efficacy of antithrombotic therapy for both primary and secondary prevention of systemic thromboembolism with an acceptable rate of bleeding complications in these patients. This section of clinical trials review summarizes data from all published randomized trials of antithrombotic therapy in atrial fibrillation. The efficacy of aspirin versus warfarin is analyzed. The role of clinical and echo-cardiographic findings to stratify patients is also highlighted. The Stroke Prevention in Atrial Fibrillation II trial is discussed in detail.

Atrial Fibrillation↗

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Angiotensin-converting enzyme inhibition after acute myocardial infarction with special reference to the Fourth International Study of Infarct Survival (ISIS-4).

Role of ACE inhibitors in the management of asymptomatic or symptomatic left ventricular (LV) dysfunction after acute myocardial infarction (AMI) is well established. More recently, large clinical trials have evaluated the use of angiotensin-converting enzyme (ACE) inhibitors early after AMI, ie, within 24 hours of symptom onset. This concept has emerged with the understanding of pathophysiological changes occurring after AMI. Neurohormonal activation and ventricular remodelling after AMI form the basis of these changes, whereas the extent of LV dysfunction remains strongly predictive of poor outcome. The large clinical trials with mortality end point have shown modest benefit with early use of ACE inhibitors in an unselected population. However, the generalized use of ACE inhibitors remains controversial because of an overall small benefit. We review the pathophysiological changes occurring after AMI, the rationale for early use of ACE inhibitors, and the data available from the large clinical trials. We recommend consideration of early ACE inhibitor in all but the lowest risk patients. Clinical features of such a low-risk population would include small and nonanterior infarctions in patients less than 65 years of age and with LV ejection fractions greater than 50%. Objective assessment of LV function is warranted during hospitalization for AMI to appropriately select patients for ACE inhibitor therapy. Dosing should be started carefully to avoid hypotension and should be titrated to the goal of doses used in the large trials. Duration of therapy in patients at high risk for death or ventricular enlargement should be indefinite. Further large-scale secondary prevention trials with long-term treatment are underway to assess the effect of ACE inhibition on coronary disease progression and reinfarction.

Angiotensin-Converting Enzyme Inhibitors↗

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Role of antiarrhythmic agents after myocardial infarction with special reference to the EMIAT and CAMIAT trials of amiodarone. European Myocardial Infarct Amiodarone Trial. Canadian Amiodarone Myocardial Infarction Trial.

The role of antiarrhythmic agents in the post-MI patients has been investigated for several years. Recently, clinical trials have assessed the effects of amiodarone in the post-MI population. The Basel Antiarrhythmic Study of Infarct Survival (BASIS) trial showed a reduction in total mortality, sudden death, and life-threatening ventricular arrhythmias with amiodarone therapy. The European Myocardial Infarct Amiodarone Trial (EMIAT) did not show a mortality benefit, but amiodarone was associated with fewer antiarrhythmic deaths. The Canadian Amiodarone Myocardial Infarction Trial (CAMIAT) showed no significant impact on mortality, but arrhythmia deaths and resuscitated cardiac deaths were reduced. Amiodarone therapy after MI should be reserved for the treatment of symptomatic or sustained ventricular arrhythmias. The current data do not support routine use of amiodarone in all patients after MI.

Amiodarone↗

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Antiplatelet and anticoagulant therapy in the prevention of thromboemboli in chronic heart failure.

Thromboembolism is an important complication in patients with heart failure. Several recent clinical trials have established the efficacy of anticoagulant therapy in patients with heart failure and atrial fibrillation. There is renewed interest in examining the role of antiplatelet and anticoagulation therapy in patients with heart failure in sinus rhythm. There is a need to identify patients at risk for thromboembolism in heart failure. However, there are data to suggest that occult thromboembolic events may contribute to disease progression, ischemic events, and sudden cardiac death. This review summarizes the incidence, potential mechanism, and therapeutic approaches for management of thromboembolism in heart failure.

Anticoagulants↗

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Barrett's oesophagus and Helicobacter pylori.

In order to demonstrate the presence of Helicobacter pylori in the metaplastic epithelium of Barrett's oesophagus and to evaluate its possible association with this entity, we examined 29 cases of Barrett's oesophagus where concomitant antral biopsies were also available. These cases were compared with an equal number of age and sex matched controls of uncomplicated reflux oesophagitis. H. pylori was present in 11 of 29 cases of Barrett's oesophagus (38%). No increase in the frequency of H. pylori antral gastritis was found in patients of Barrett's oesophagus compared to the control group of uncomplicated reflux oesophagitis. The positivity of Barrett's oesophagus for H. pylori correlated with the presence of H. pylori antral gastritis (P < 0.05), although in two cases of H. pylori-positive Barrett's oesophagus antral biopsies were negative for H. pylori. No difference was found in the severity of inflammatory and dysplastic changes of H. pylori-positive and H. pylori-negative Barrett's oesophagus. Presence of H. pylori does not seem to alter the natural history of Barrett's oesophagus.

Adult↗

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Medical therapy of acute myocardial infarction: Part I. Role of thrombolytic and antithrombotic therapy.

Thrombolytic therapy has been established as a safe and effective therapeutic strategy in acute myocardial infarction (MI). Its efficacy is improved with early administration, although modest benefits can be demonstrated for up to 12 hours. Tissue plasminogen activator (TPA) appears to offer benefits over streptokinase when administered to patients who present within 4 hours, those with an anterior MI, and who are less than 75 years old. Age alone is not a contraindication for thrombolysis because the risk of bleeding complications in the elderly is outweighed by a significant improvement in mortality. One of the major limitations of thrombolytic therapy in acute MI is reocclusion. Use of adjunctive antithrombotic therapy can reduce the rate of reocclusion following successful thrombolysis. The beneficial role of aspirin is well established. Use of intravenous heparin in conjunction with streptokinase offers no clinical benefit. The efficacy of heparin when administered with other thrombolytic agents remains to be established. These issues and the role of newer antiplatelet and antithrombin agents are being examined in ongoing clinical trials. The objective of this review is to provide the information needed for careful and appropriate judgment in the use of thrombolytic agents and antithrombotic therapy. General principles are emphasized, and specific recommendations are included as guidelines.

Aged↗

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Medical therapy of acute myocardial infarction: Part II. The role of adjunctive medical therapy.

The second part of this review summarizes the role of other classes of pharmacological therapy in treatment of acute myocardial infarction (MI). The goals of pharmacological therapy are to alleviate symptoms, to stabilize hemodynamic status, and to prevent arrhythmias. These agents have been utilized primarily because of their ability to limit infarct size. Other beneficial properties may include their effects on neurohormonal activation, hemodynamics, and arrhythmias. In an individual patient, age, associated medical conditions, and hemodynamic status are important considerations in choosing a specific class of drug therapy. The beta-adrenergic blocking agents have modest effects on mortality, and they are useful when used alone and in combination with thrombolytic agents. Calcium antagonists have a limited role in acute MI. Diltiazem reduces the incidence of reinfarction in patients with non-Q MI. Oral nitrate therapy has not been shown to reduce mortality. Data from recent trials suggest that prophylactic administration of antiarrhthymic therapy is also not useful in acute MI. The role of angiotensin-converting enzyme inhibitors when administered in the acute phase of MI needs to be evaluated further. These agents are safe and well tolerated, and they offer greatest benefit when given in patients with left ventricular dysfunction.

Acute Disease↗