ANGINA PECTORIS. angina pectoris is a symptom of myocardial ischemia in the absence of infarction
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1 Pharmacology Ezra Levy, Pharm.D. ANGINA PECTORIS A. Definition angina pectoris is a symptom of myocardial ischemia in the absence of infarction angina usually implies severe chest pain or discomfort during strenuous exercise, but it may develop unexpectedly with little or no exertion some patients describe a pressure sensation or heaviness instead of pain B. Types of Angina 1. Chronic Stable Angina (Exertional Angina) angina that is reproducible with a certain level of physical activity usually due to atherosclerosis or narrowing of coronary arteries relieved by rest or nitroglycerin (NTG) 2. Unstable or Crescendo Angina change in angina characterized by increased intensity, frequency, or duration of symptoms usually due to atherosclerosis 3. Prinzmetal or Variant Angina (Vasospastic Angina) occurs in patients without coronary heart disease and is due to a spasm of the coronary artery that decreases myocardial blood flow vasospastic angina may occur at rest 4. Mixed Angina when coronary vasospasm occurs at the site of a fixed atherosclerotic plaque, mixed angina results
2 2 C. General Management 1. Goal of Therapy relieve or prevent symptoms, and prevent myocardial ischemia and death 2. Lifestyle Alterations in chronic stable angina, alterations of lifestyle including avoidance of stresses known to precipitate an attack 3. Sublingual (SL) Nitroglycerin (NTG) and Aspirin (ASA) prophylactic NTG before known inciting events (e.g., exercise, coitus) also helps minimize the number of symptomatic episodes ASA provides antiplatelet protection against thromboembolic events 4. Frequent or Recurrent Angina recurrent angina is best treated with chronic scheduled drug therapy: (a) nitrates (b) beta blockers (c) calcium channel blockers combination therapy may be required in advanced disease D. Pharmacologic Agents 1. Nitrates a. Mechanisms of Action nitrates work by 2 mechanisms: (1) dilation of epicardial coronary vessels (1) venodilation (to decrease preload and ventricular filling pressures)
3 3 Nitrates (continued) b. Short-Acting Nitrates (e.g., SL NTG and translingual NTG spray) primarily used for immediate prophylaxis or to abort an acute attack c. Longer-Acting Nitrates used either alone or in combination with other drugs to decrease incidence of anginal attacks d. Commonly Prescribed Organic Nitrates Nitrates Dosage Form Duration Onset Usual Dosage SHORT-ACTING NTG SL min 1-3 min mg NTG Translingual spray min 2-4 min 0.4 mg/spray NTG IV 3-5 min 1-2 min initially 5 mcg/min (increase Q3-5min until pain is relieved or hypotension or hypotension occurs) LONG-ACTING NTG SR capsule 4-8 hrs 30 min mg Q8H NTG Topical ointment 4-8 hrs 30 min ½ - 2 inch Q4-6H NTG Transdermal patch 4-8 hrs 30 min mg Q24H NTG Transmucosal 3-6 hrs 2-5 min 1-3 mg Q3-5H ISDN SL 2-4 hrs 2-5 min mg Q2-4H (isosorbide Chewable 2-4 hrs 2-5 min 5-10 mg Q2-4H dinitrate) Oral 2-6 hrs min 5-60 mg Q4-6H SR 4-8 hrs min mg Q6-8H ISMO Oral 3-6 hrs min 20 mg BID (am & (isosorbide midday) mononitrate) Imdur Oral 8-12 hrs min mg QD (isosorbide mononitrate extended release)
4 4 Nitrates (continued) e. Transdermal NTG transdermal patches are available in a variety of delivery systems, but they all appear to be equally effective in releasing the drug in a reliable manner over a 24-hour period patients may prefer one-system over another based on comfort, aesthetics, and adhesiveness contact dermatitis has been reported with transdermal patches with the first few applications, exercise tolerance and anti-anginal protection may last for 24 hours after a single morning application; but continued use is associated with the development of tachyphylaxis resulting in only a 4-18 hour duration of effect dosage regimens should maintain a nitrate-free interval (i.e., at bedtime) examples: Nitro-Dur 0.1 mg/hr (2.5 mg/day) Transderm-Nitro 0.2 mg/hr (5 mg/day) Minitran 0.3 mg/hr (7.5 mg/day) Nitrodisc 0.4 mg/hr (10 mg/day) 2. Beta Adrenergic Blocking Agents a. Mechanism of Action beta blockers reduce myocardial oxygen demand by decreasing catecholamine-mediated increases in heart rate (HR), contractility, and blood pressure (BP) b. Indications beta blockers are especially indicated in patients with concurrent hypertension (HTN), arrhythmias, or vascular headaches beta blockers should be used with caution in patients with heart failure, COPD, asthma, or peripheral vascular disorders c. Cautions patients should be cautioned that abrupt withdrawal may lead to a rebound increase in underlying cardiac disease and possibly an increased risk of myocardial infarction or sudden death
5 5 3. Calcium Channel Blockers a. Mechanism of Action calcium channel blockers inhibit calcium influx into cells! decrease myocardial and vascular smooth muscle contraction! decrease myocardial oxygen consumption! decrease in anginal attacks dilation of large coronary arteries and relief of vasospasm is the basis for their use in vasospastic angina calcium channel blockers also produce peripheral arterial vasodilation and decrease workload (i.e., afterload) on the heart calcium channel blockers possess mild negative inotropic properties (especially, verapamil) similar to those of beta blockers b. Indications calcium channel blockers have an additive benefit in patients with: hypertension, supraventricular tachycardia (SVT), peripheral vascular disorders (e.g., Reynauds disease), and chronic migraine c. Cautions calcium channel blockers, notably verapamil, should be used with caution in patients with CHF
Anginal pain is a result of an imbalance between myocardial oxygen supply and demand. Pharmacological management is aimed at prevention of myocardial
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