Chlamydia pneumoniae and anti-infective therapy: their role in the pathogenesis and treatment of coronary artery disease.

Cardiovascular disease remains the most common cause of death in the United States; however, conventional cardiovascular risk factors fail to explain completely the pathogenesis of atherosclerosis and coronary artery disease. There has been recent interest in the association between Chlamydia pneumoniae and the risk of development or progression of atherosclerotic disease. This association has become evident through serologic, pathologic, and animal-based models and, more recently, through limited trials of antichlamydial antibiotics in humans. Whether C. pneumoniae is a causative agent or "innocent bystander" or whether antibiotic therapy has any role in the treatment of cardiovascular disease remains to be determined.

Oral angiotensin-converting-enzyme inhibitors.

The pharmacology, pharmacokinetics, clinical uses, adverse effects, drug interactions, dosage, cost, and therapeutic interchange of oral angiotension-converting-enzyme (ACE) inhibitors are reviewed. ACE inhibitors attenuate the formation of angiotension II and may lead to the accumulation of kinins. Although the hypotensive effects of many ACE inhibitors may persist for 24 hours, some patients require more than one dose per day to achieve adequate control. These agents accumulate in patients with renal or hepatic dysfunction, but it is unclear whether dosage adjustments are necessary. ACE inhibitors are effective against mild to moderate hypertension; for severe hypertension, additional anti-hypertensive agents may be necessary. Other conditions in which ACE inhibitors have shown efficacy include congestive heart failure, myocardial infarction, left ventricular dysfunction, left ventricular hypertrophy, chronic renal insufficiency, insulin sensitivity, and coronary artery disease. The most common adverse effect is a persistent nonproductive cough. Angioedema, fetal and neonatal morbidity and mortality, acute renal failure, and hyperkalemia may also occur. ACE inhibitors may interact with diuretics, lithium, nonsteroidal anti-inflammatory drugs, oral hypoglycemic agents, and some other drugs. ACE inhibitor therapy should be initiated with low doses that may then be slowly adjusted upward. Many of the agents have similar costs for lower and higher dosages. The only significant differences among the ACE inhibitors are the time of onset of hypotensive effects, time to peak effect, and duration of effect. Each formulary should include, at least, captopril and one intermediate-acting and one long-acting ACE inhibitor.