Band 100, Heft s11

More than 5 million Americans visit hospital emergency departments each year with the complaint of chest pain. Two million patients are admitted to hospitals because of chest pain, but the diagnosis of coronary heart disease is confirmed in only one fourth of them. Acute coronary syndrome represents a clinical syndrome that includes unstable angina, non-Q-wave myocardial infarction and Q-wave myocardial infarction. The goal of management of patients with acute coronary syndrome is to rapidly recognize and manage their cardiac ischemic event, define the risk of myocardial ischemia and recurrent cardiac events, and minimize unnecessary risk to the patient. These decisions can all be made by the use of standard clinical descriptors that include chest pain, the electrocardiogram, and biochemical markers of myocardial injury during and after an acute ischemic episode.

Acute coronary syndromes are a major public health problem and the leading cause of death in the western world. Acute coronary syndromes consist of unstable angina pectoris, non-ST-segment-elevation myocardial infarction, and ST-segment-elevation myocardial infarction. These diseases represent a continuum of increasing severity and are pathophysiologically linked to intracoronary thrombus formation that is nonocclusive, transiently occlusive, or completely occlusive, respectively. Antiplatelet treatment with aspirin is the cornerstone of treatment for all acute coronary syndromes. Newer intravenous antiplatelet agents reduce 30-day mortality and myocardial infarction in unstable angina and non-ST-segment-elevation myocardial infarction. Adenosine diphosphate antagonist antiplatelet agents have an ill-defined role in the treatment of acute coronary syndromes. Fibrinolytic therapy has been shown to reduce mortality in ST-segment-elevation myocardial infarction but may pose a hazard in other acute coronary syndromes.

When evaluating a patient with known coronary artery disease or a patient with hypercholesterolemia without overt clinical symptoms of coronary artery disease or other vascular disease, it is helpful to understand the vascular biology behind primary and secondary prevention. This article reviews the progression of the atherosclerotic plaque, endothelial function, and the impact of current modes of therapy.

The past 10 years have seen dramatic changes in how we treat deep vein thrombosis (DVT). A decade ago, we would treat patients for 5 days with intravenous heparin and then start warfarin sodium therapy and continue administering both anticoagulants for another 5 to 7 days. In the early 1990s, we started warfarin therapy at the same time heparin was begun and decreased the hospital stay from 10 to 14 days to 5 to 7 days. With the development of low-molecular-weight heparin and the approval for use as outpatient treatment, patients are now spending 1 to 2 days in the hospital, and many times, they are not admitted. A case scenario (in italics) is integrated into this review to illustrate the cost-effective application of an evidence-based approach.

Diagnosis and management of carotid arterial occlusive disease and its ensuing comorbid illnesses have been the focus of extensive debate during the past two decades. The development of sophisticated ultrasound technology has enabled us to objectively define the severity of carotid stenosis in regions commonly accountable for stroke. Results from several well-designed prospective randomized trials have enhanced our understanding of the epidemiology of this disease and have guided our judgment with regard to aggressive diagnosis and intervention. As clinicians, we have been charged to address underlying risk factors, including hyperlipidemia and smoking abuse, as well as concomitant coronary, renal, and lower extremity artery disease. Carotid endarterectomy coupled with optimal medical management is superior to medical management alone in asymptomatic patients with high-grade carotid stenosis (> 70% diameter reduction) and recently has been shown to have value for symptomatic patients with stenosis of 50% to 69%.