Treatment of Angina and CAD -Adje Flashcards
age more likely to get ischemic heart disease with coronary heart disease?
65 or older
-higher risk in american Indians/Alaska natives
normal myocardium
- extracts more O2 than any other organ in the body
- get angina pectoris if O2 supply does not meet demand*
- ischemic heart disease with decreasing O2 carrying capacity or blood supply
- adenosine hypothesis = relaxation of smooth muscle vascular and coronary arteries
endothelial factors produced in normal myocardium**
- NO* produces nitroglycerin –> relaxes vascular smooth muscle decreasing coronary artery resistance
- vascular smooth muscle contains alpha/beta receptors that lead to vasoconstriction/dilation*
- antithrombotic action
most common cause of myocardial ischemia**
atherosclerosis***
-narrows the vessels
-in ACS (unstable angina and NSTEMI) –> disrupt atherosclerotic plaque –> platelet aggregation and thrombus formation
reversible vs. irreversible myocardial damage*
- angina –> reversible from stenosis or spasm
- MI –> irreversible from complete coronary occlusion (permanent)
stable angina
- predictable transient discomfort in the chest**
- worse with exertion, better with rest
- nitroglycerin helps
unstable angina
- similar to stable angina
- occurs at rest, lasts for >10 min
- more severe/frequent discomfort
- NOT relieved by nitroglycerin**
- troponins NEG**, unlike NSTEMI
Prinzmetal angina
- spasm with no atherosclerotic lesions*
- occurs at rest
- RELIEVED by nitroglycerin*
-can have silent ischemia (no discomfort) –> common in diabetic neuropathy
modifiable risk factors***
Tobacco smoking Hypertension Diabetes mellitus High total and LDL cholesterol Low HDL cholesterol Obesity (central abdominal) Lack of physical activity
-dyslipidemia with obesity and diabetes –> can give HMG-CoA reductase inhibitors (statins)
non-modifiable risk factors***
Aging
Gender
Ethnic background
Family history of premature coronary heart disease
statins**
-powerful treatment on atherosclerosis and ischemic heart disease
EKG findings
- ST segment depression, T wave flattening or inversion
- ST segment elevation with transmural ischemia
- may be normal in chronic cases
- Q waves show previous MI
stress testing
- exercise with EKG
- duration is symptom limited (85% of max predictive HR for age/sex)
- stop with ST depression 2mm or drop in SBP >10
- + if ST segment depression is >0.1 mV below baseline lasting longer than 0.08 sec - pharmacologic
- for peripheral vascular or MSK disease, exertional dyspnea, or deconditioning
when do you use a CT to examine the heart?
- detect atherosclerotic plaque changes –> calcification
- use Agatston score to measure Ca2+ level
indications for coronary arteriography***
- chronic stable angina with severe symptoms and being considered for PCI or CABG
- to confirm/rule out IHD
- angina pectoris after surviving cardiac arrest
- ischemia with evidence of ventricular dysfunction on other testing
- risk of coronary events with severe ischemia signs on other testing
- people with high risk jobs or someone about to undergo high risk surgery
what is the preferred cardiac biomarker for myocyte necrosis?
-troponin** - more sensitive and specific than CK-MB
nitroglycerin mechanism of action***
-drug of choice for acute angina pectoris (short acting)
- MOA: nitrates relax smooth muscle relieving ischemia in 2 ways
1. vasodilate veins –> decrease venous return –> decrease LVEDV (preload) relieving wall stress –> less O2 consumption –> relieve ischemia
2. vasodilate coronary arteries –> increases coronary blood flow –> increase O2 supply - good in coronary vasospasm
long term treatment to prevent recurrent acute angina attack
- long acting nitrates
- beta blockers***- reduce cardiac O2 demand by blocking beta1,2 receptors
- block beta1 –> decrease ventricular contraction and HR –> less O2 demand - Ca2+ channel blockers - vasodilators/reduce contractility
- ranolazine
treatment to prevent acute cardiac ischemia
- antiplatelet therapy –> aspirin (help stabilize plaque), clopidogrel
- lipid regulating therapy –> HMG-CoA reductase ihibitors (statins) (also stabilize plaque)
- ACE inhibitors
mechanical revascularization
- PCI
- balloon-tipped catheter - CABG
- vein graft –> great saphenous vein
- artery graft –> internal mammary aka internal thoracic artery
when are coronary arteries getting perfused?**
during DIASTOLE
-less perfusion during rapid ejection period
