Antianginal Drugs Flashcards
Coronary Artery Disease: Causes
Atherosclerosis Coronary artery vasospasm - Variant or prinxmetals angina - Serotonin, histamine, and endothelium-derived factors all implicated Emboli Congenital coronary artery abnormalities
Angina: Pathphysiology
Condition of intermittent, relative myocardial ischemia accompanied by pain in the chest
Inability of coronary arteries to supply sufficient oxygenated blood to heart muscle
Angina Risk factors
Hyperlipemia Elevated BP Cigarette smoking ECG abnormalities Diabetes mellitus Hyperthyroidism Anxiety Psychosocial problems Caffeine Medications
Goal of Drug Therapy for Angina
Correcting inadequacy of myocardial oxygenation
Increasing delivery of oxygen to ischemic areas by dilation of coronary arteries
How do you correct oxygen inadequacy
Reduce HR, contractility, afterload and/or preload
Limitations of coronary vasodilators
Physical limits imposed by plaques
Vasculature in ischemic areas may already be maximally dilated
“Coronary steal”
- Blood diverted away from ischemic areas by dilating healthier vessels
Vasodilators still useful in treating angina precipitated by coronary spasm
Classification of Angina
Stable angina (Type 1) Vasospastic angina (Type 2) Unstable angina (Type 3)
Signs of Type 1 angina
Usually atherosclerosis without rupture of atheroma
No thrombosis
Exertion, cold, stress, emotion or eating increases myocardial demand
Responds positively to rest and/or nitroglycerin
Treatment of Stable angina
Decrease cardiac load (pre/after), increase blood flow
Type 2 symptoms
Caused by transient vasospasm of the coronary vessels
Usually associated with underlying atheromas without rupture of atheroma
No thrombosis
Occurs at rest, during REM sleep
Responds positively to nitroglycerin
Vasospastic angina treatment
Decrease vasospasm of coronary vessels
Type 3 symptoms
Caused by recurrent episodes of small platelet clots at the site of a ruptured atherosclerotic plaque
Can precipitate local vasospasm
Change in character, frequency, and duration
Requires vigorous therapy as it signals the imminent occurrence of a MI
Unstable angina treatment
Inhibit platelet aggregation and thrombus formation, decrease cardiac load, and vasodilate coronary arteries
Function of Organic Nitrates (Nitrovasodilators)
Reduction in preload
Decrease cardiac oxygen demand by dilating veins and decreasing venous return
Direct relaxation of smooth muscles, particularly vascular smooth muscle of veins
Produces a decrease in venous return
- Results in a decreased ventricular end-diastolic volume and decreased CO
- Decreased ventricular wall tension associated with decreased myocardial O2 requirement
Effect of NTG in Stable Angina
An alternative hypothesis proposed for nitroglycerin action suggests that these drugs produce specific redistribution of coronary blood flow by dilating intra-arterial anastomosis
- Total coronary blood flow and coronary vascular resistance remain fixed or decreased
Antianginal effect of nitrates is due to decreased oxygen demand associated decreased venous return and subsequent decrease in intracardiac volume-> decreased wall tension-> decreased cardiac work