Lectures 18-19: Stable CAD Flashcards
Course of ischemic heart disease
Asymptomatic ischemia -> angina pectoris -> unstable angina -> myocardial infarction
Coronary flow occurs during…Minimum pressure?
Diastole; 60-65 mm Hg
What are two conditions that could lower diastolic pressure?
Hypotension or aortic regurgitation
Generally we don’t change pressure, but rather…
Resistance
What mediates vascular tone? (three classes)
Metabolic factors: adenosine*, acetate, hydrogen ions, CO2; Neural factors: NE –> alpha and beta receptors; Endothelium factors
Endothelial vasodilators and vasoconstriction. What dominates?
ACh, 5-HT, shear stress –> NO; thrombin, AII, Epi; healthy state = vasodilation, disease state = vasoconstriction
What can cause increased wall stress? How is this related to CAD?
Pressure/volume overload –> myocyte hypertrophy to normalize wall stress –> increased O2 demand of cardiac tissues
Besides enlarged myoctyes, what else can increase myocardial oxygen demand? (2)
Increased HR and contractility
Relationship between atherosclerotic plaques and CAD?
Reduce diameter of coronary arteries –> increased resistance
What is more important for increased resistance due to plaques…length of lesion or reduced diameter?
Reduced diameter (r^4)
What is the function of the coronary microvasculature? What happens in disease?
Modulates vasomotor tone; in disease, endothelium is impaired and vasodilation in response to needs does not occur
At rest, what level of stenosis is required for ischemia? How about exertion? What angina’s are associated with this? Why are these numbers so high?
~90% (unstable angina); ~70% (stable angina); flow is augmented by microvasculature
What are four ways that endothelial cell dysfunction can occur?
Release of endothelium-dependent vasodilators (prostacyclin/NO) may be impaired in response to normal stimuli (shear stress); Vasodilatory effects of local metabolites also blunted (i.e. adenosine); Vasoconstricting effects of catecholamines predominates; Loss of antithrombotic effect of endothelial cells in response to stimuli (ADP, serotonin, thromboxane) –> small thrombi
Two classes of non-atherosclerotic causes of ischemia and examples
Reduced O2 supply (aortic regurge, bleeding); Increased O2 demand (tachyarrhythmias, hypertensive crisis, severe aortic stenosis)
Impacts of ischemia (3)
Myocyte necrosis; stunned myocardium; hibernating myocardium
What is stunned myocardium
Transient systolic dysfunction after ischemic insult
What is hibernating myocardium
Chronic ventricular dysfunction due to multivessel CAD w/ reduced blood supply; revascularization treats this
Define stable angina
Retrosternal chest discomfort precipitated by exertion
Define unstable angina
New-onset severe angina or increased severity/frequency of stable symptoms
Define variant angina
Episodes of coronary spasm reduces O2 supply, occurs at rest
Define syndrome X. Treatment?
Chest pain but normal coronary arteries, due to microvasculature dysfunction; medically: cannot be treated surgically
Define silent ischemia. Treatment?
Ischemia w/out clinical symptoms; not sure if we should treat, currently addressed with ISCHEMIA trial
Stable angina: sensation
Pressure, tightness, heaviness, burning
Stable angina: duration
Few minutes
Stable angina: location
Diffuse, not focal
Stable angina: associated sxs
SOB, fatigue, nausea
Stable angina: precipitants
Exertion and emotional stress
Stable angina: frequency
Distinguishes from unstable
Systems on differential dx
Cardiac (spasm, pericarditis), GI, MSK
Stable angina: ECG
Typically normal, not of high value
What is one way to dx chronic stable angina?
Stress testing: make them exercise and then detect ischemia (ECG, echo, nuclear perfusion imaging)
Describe coronary angiography
Invasive procedure requiring contrast media for direct visualization of stenotic lesions; gold standard in dx of CAD
Describe nitrates: use, mechanism
Treatment of stable CAD; cause venodilation –> reduce LV volume –> reduce wall stress –> decrease mycoardial O2 demand
Side effects of nitrates
Lightheadedness, headache
T/F: Nitrates improve long-term survival
False
Describe beta-blockers use for stable CAD
Reduce mycardial O2 demand by decreasing HR and contractility
Side effects of beta-blockers (3)
Bronchospasm, bradycardia, impotence
T/F: Beta-blockers improve long-term survival
True
If a patient has had a prior MI, what do you give them?
Beta-blocker! Can extend life
DON’T give beta-blockers to these three groups
Patients in shock, patients with airway disease, diabetics (may mask reflexive tachycadia from hypoglycemia)
Ca2+ Channel Blockers…groups and effects
Dihydropyridines: vasodilating»_space; cardiac depression; nondihydropyridines: cadiac depressant»_space; vasodilating
Once again, vasodilating improves CAD how?
Decreases myocardial O2 demand by reducing wall stress
Should you combine Ca2+ blockers and beta-blockers?
NOPE: accentuate negative chronotropy/inotropy –> major bradycardia
What is ranolazine?
New drug to treat angina w/ unclear molecular mechanism
What does aspirin do?
Reduce risk of thrombotic complications by inhibition of platelet aggregation
What is another antiplatelet therapy?
Thienopyridine (Clopidogrel): inhibits platelet receptor
Why do we give a lipid lowering therapy? Quantity or quality of life? When do you give?
Lowers risk of death in patients at risk with established CAD (quantity); administer statin to patients with >7.5% risk of MI in 10 years
Why would ACE inhibitors be helpful for CAD?
Reduce cardiac events
Medical therapy for stable CAD (summary)
Quality: nitrate, beta-blocker, CCB, ranolazine; Quantity: aspirin, statin, beta-blocker, ACE-I
Two revascularization options
Stenting and coronary artery bypass grafting
What is a drug-eluting stent?
Stents coated with antiproliferative agent to inhibit restenosis but delays endothelializaion –> increased risk for thrombosis
Two types of grafts
Venous and arterial (very high patency)
What is the preferred strategy for complex patients (multivessel disease, left-main, diabetic)
Coronary artery bypass grafting
Advantages/disadvantages of PCI
Advantages: low procedural risk, minimal recuperation; Disadvantages: need dual antiplatelet therapy, higher rates of revascularization
Advantages/disadvantages of CABG
Advantages: complete revascularization, no need for long term DAPT, proven mortality benefit; Disadvantages: higher procedural risks, longer recuperation
