Management of Stable Angina - Current Guidelines: A Critical Appraisal.

Guidelines provide recommendations to improve patient outcomes, but many of the recommendations made for treating patients with stable angina are opinion based rather than evidence based. Risk stratification to predict patients at an increased risk of myocardial infarction (MI) and sudden ischemic death, and selection of patients for possible revascularization, is based on expert opinion. Randomized trials have compared optimal medical therapy to revascularization, after the coronary anatomy was known, and yet routine coronary angiography to exclude left main disease is not recommended. What exactly is optimal antianginal treatment varies considerably from one country's guideline recommendations to another. None of the antianginal drugs reduce mortality or MI and these drugs are equally effective in treating angina pectoris; and yet beta-blockers and calcium channel blockers are recommended as first line therapy. Double and triple therapy with different classes of antianginal drugs is also expert opinion based rather than evidence based. Recommendations to reduce the incidence of MI and sudden death are appropriate; however the use of a potent, high dose statin, is recommended by AHA/ACC and NICE guidelines for all patients with ischemic heart disease, while the European guidelines recommend a target LDL goal in patients with coronary artery disease (CAD). Management of patients with stable angina pectoris with normal coronary arteries remains ambiguous. This short review critically appraises the recommendations for managing patients with stable angina pectoris.

The risk of cardiovascular side effects with anti-anginal drugs.

INTRODUCTION: Angina pectoris is a common presenting symptom of underlying coronary artery disease or reduced coronary flow reserve. Patients with angina have impaired quality of life; and need to be treated optimally with antianginal drugs to control symptoms and improve exercise performance. A wide range of antianginal medications are approved for the treatment of angina, and often more than one class of antianginal drugs are used to adequately control the symptoms. This expert opinion highlights the likely cardiac adverse effects of available antianginal drugs, and how to minimize these in individual patients and especially during combination treatment. Areas covered: All approved antianginal drugs, including the older and newly approved medications with different mechanism of action to the older drugs as well as some of the unapproved herbal medications. The safety profiles and potential cardiac side effects of these medications when used as monotherapy or as combination therapy are discussed and highlighted. Expert opinion: Because of the different cardiac safety profiles and possible side effects, we recommend selection of initial drug or adjustment of therapy based on the resting heart rate; blood pressure, hemodynamic status; and resting left ventricular function, concomitant medications and any associated comorbidities.

Comparison of effects of nisoldipine-extended release and amlodipine in patients with systemic hypertension and chronic stable angina pectoris.

The efficacy and safety of nisoldipine-extended release (ER) and amlodipine were compared in a 6-week multicenter, randomized, double-blind, double-dummy, parallel group, titration-to-effect trial in patients with stage 1 to 2 systemic hypertension (90 to 109 mm Hg diastolic blood pressure [BP]) and chronic stable angina pectoris. After a 3-week placebo run-in period, patients (n = 120) were randomly assigned to active treatment with either nisoldipine-ER (20 to 40 mg) or amlodipine (5 to 10 mg) once daily, titrated as necessary after 2 weeks to achieve diastolic BP <90 mm Hg. After 6 weeks, the mean reduction in systolic/diastolic BP from baseline was 15/13 mm Hg with nisoldipine-ER and 13/11 mm Hg with amlodipine (p = NS/p = NS). Both drugs resulted in similar BP responder rates (diastolic BP <90 mm Hg in 87% of patients who received nisoldipine-ER and 78% of patients on amlodipine, p = NS) and anti-ischemic responder rates (increasing exercise time >20% in 20% and 27%, respectively [p = NS], and increasing exercise time >60 seconds in 32% and 29% of patients, respectively [p = NS]. Also, after 6 weeks of active therapy, there was a similar mean increase in total exercise duration (23 seconds in the nisoldipine-ER group and 21 seconds in the amlodipine group, p = NS). Neither drug increased heart rate and both decreased frequency of anginal episodes. Adverse events were infrequent, and typically were vasodilator-related effects (including headache and peripheral edema) that occurred with somewhat higher incidence in the nisoldipine-ER group. Thus, nisoldipine-ER and amlodipine provided comparable antihypertensive and anti-ischemic efficacy, and both were generally well tolerated.