Stable CAD Flashcards
Clinical expression of stable ischemic heart disease reflects a…
imbalance between myocardial demand and supply of/for O2.
Myocardial Oxygen Supply based on
Blood O2 content (Hgb level and O2 sat)
Coronary Flow
What determines coronary flow
Directly related to perfusion pressure and indirectly related to vascular resistance.
Perfusion pressure
Coronary flow during diastole. Minimum diastolic pressure of 60-65 mmHg needed to ensure flow.
Conditions that reduce coronary flow
Things that lower diastolic pressure like aortic regurgitation or hypotension. Also if LVEDP is higher than normal (aortic regurg), gradient between aorta and LV is decreased and blood won’t flow.
What controls coronary vascular resistance?
Vascular tone and degree of coronary stenosis.
Most important mediator of vascular tone?
Adenosine – which is produced during hypoxemia and causes vessels to dilate causing increased coronary blood flow.
Do coronary vessels have alpha and beta receptors?
yes! B2 receptors
Endothelium dependent vasodilators
ACh, serotonin, shear stress. These things cause endothelium to release NO which causes vascular smooth muscle relaxation and increased blood flow. These things increase eNOS to create NO from L-arg. NO diffuses and promotes activity of GC, which increases cGMP, which causes vasodilation.
Endothelium dependent vasoconstrictors
Thrombin, ang II, epinephrine. Cause endothelin I to be released from endothelial cells which is a potent vasoconstrictor.
Normal, endothelium INdependent effect of ACh? ACh with normal/abnormal endothelium
Vasoconstrictor. But when given in the setting of normal endothelium, vascular smooth muscles dilate. However, in abnormal endothelium (increased number of risk factors) ACh causes vasoconstriction again.
Relationship between wall stress and myocardial oxygen demand
Increased wall stress (due to pressure/volume overload), increased myocardial demand. Wall stress = Pxr / 2h
What is worse, a thicker plaque causing lumen obstruction, or a longer plaque?
Thicker plaque. R = L / r^4
Relationship between stenosis and coronary flow at rest and during exertion.
During exertion, Coronary flow is maximal until about 70% stenosis. Before 70%, endothelial cells are able to compensate.
During rest, coronary flow is normal until about 93% occlusion. This is unstable angina.
What happens in endothelial cell dysfunction?
Release of endothelium-dependent vasodilators is impaired due to shear stress or other stimuli. Vasoconstricting effects of catecholemines predominate.
Loss of antithrombotic effect too, so thrombosis is more likely.
Are problems with coronary arteries worse in macro or microvasculature?
Microvasculature. There’s so much that can’t be seen on angiogram.
Non atherosclerotic myocardial ischemia caused by?
Reduced O2 supply (aortic regurg – decrease in diastole, decrease in perfusion pressure), acute blood loss
Increased O2 demand (tachyarrhythmias like afib, hypertensive crisis which causes increased wall stress, severe aortic stenosis)
What are the sequellae of ischemia?
Myocyte necrosis
Myocyte stunning
Myocyte hibernation
Myocyte necrosis
Irreversible cell death. Can be detected by EKG by presence of Q wave, and by cardiac imaging.
Stunned myocardium
Systolic dysfunction after transient ischemia – not necrosis. Function gradually recovers.
Hibernating myocardium
Chronic ventricular dysfunction due to chronic multivessel CAD. Need to revascularize to restore function, but function can be restored.
Stable angina
Retrosternal chest discomfort caused by exertion or emotional stress (increase BP increase contract, increase demand for O2)
Unstable angina
New-onset severe angina or increase in severity/frequency of previously stable symptoms. Plaque rupture leads to thrombosis reducing myocardial oxygen supply
Prinzmetal
Variant angina. Episodes of coronary spasm reducing oxygen supply. Tends to occur at rest.
Syndrome X
Chest pain, positive stress test, but normal coronary arteries. Pain.
Thought to be caused by microvascular dysfunction.
Silent ischemia
Ischemia that occurs without clinical symptoms.
Duration of stable angina
Few minutes. Happens for years
Quality of stable angina
Various presentations. Burning, pressure, tightness, heaviness
Differential for chronic stable angina
Pericarditis (sxs worse with dep inspiration or positional changes)
GI (reflux, peptic ulcer disease)
MSK (costochondritis)
ECG finding for ischemia
St segment depression
ECG finding for infarction
ST segment elevation
Is ECG normal for stable angina?
50% of the time
How else to test for angina?
Stress test. Look at EKG, do nuclear perfusion imaging
Angiography limitation
Only shows lumen. Not able to assess atherosclerosis in vascular wall.
Nitrates
Used for treatment of sxs in angina. Causes venodilation and reduction in LV volume, which lowers wall stress and myocardial oxygen demand.
Also vasodilates the coronary arteries, but this is less relevant because endothelial cells are already trying to maximally dilate.
No long term effect on survival
B-blockers for angina
Reduce myocardial oxygen demand by slowing HR and decreasing force of contraction.
Also increases duration of diastole, so can increase oxygen supply to myocardium.
Mortality benefit in patients with heart failure and MI.
CCB types
Dihydropyridines and non-dihydropyridines
Dihydropyridines and function
Amplodipine, nifedipine.
Vasodilate (decrease preload AND afterload) and decrease myocardial oxygen demand by reducing wall stress
Non-dihydropyridines
Diltiazem, verapimil
Cardiac suppressants, reduce HR and contractility. Lower oxygen demand.
Careful when combining with B blockers.
Ranazoline
Decreases anginal frequency, improves exercise tolerance, but unsure how. Maybe decreases diastolic dysfunction.
Aspirin for angina
Reduces risk of thrombotic complication by inhibiting platelet aggregation.
Clopidigrel (thienopyridine)
Inhibitors of platelet P2Y12 receptor. Antithrombotic, more powerful than aspirin. Don’t combine them.
HMG-CoA reductase therapy
Statins. Lower risk for death/mi in patients with CAD. Give to all high risk patients.
Ace inhibitor for CAD
Reduce cardiac events like LV dysfunction, post MI.
Revascularization for CAD
Can be accomplished by stenting and/or coronary artery bypass graft.
Bare metal stents vs Drug eluting stents
Pros and cons
Bare metal stents cause intima proliferation around the stent, which is antithrombotic, but can result in restenosis.
Drug eluting stents inhibit restenosis, but increases the risk for thrombosis. Necessitates the use of long term dual antiplatelet therapy.
What did the courage trial reveal?
No reduction in death or MI with upfront PCI in addition to medical therapy.
So medical therapy first, then PCI.
Venous vs arterial bypass grafts
Venous graphs aren’t as durable.
Arterial grafts have 90% patency at 10 years.
Is CABG or PCI better?
CABG mostly. Better for sicker patients.
