Ischemic Heart Disease Flashcards
What syndromes are associated with ischemic heart disease?
Homocystinuria and hyperuricemia
What is the formula for myocardial oxygen supply?
MvO2 = CBF * (CaO2 - CvO2) where CaO2 = 1.34 * Hb * SaO2 + 0.003 * PaO2
What is normal coronary blood flow? Myocardial oxygen consumption?
CBF = 0.7 - 1 mL/min/g of cardiac tissue; MvO2 = 0.1 mL/min/g of cardiac tissue
What is the autoregulation range of coronary blood flow?
40 - 140 mmHg (vasodilation at the low end and vasoconstriction at the high end)
What happens to the autoregulation range of coronary blood flow with stress?
The range gets smaller since the HR, SBP, and contractility goes up
How much oxygen does the myocardium extract at rest?
70-80% of oxygen
What is coronary flow reserve?
The heart’s ability to increase coronary blood flow above baseline; the ratio of maximum coronary blood flow to baseline coronary blood flow
What factors reduce coronary flow reserve?
Tachycardia + increased preload (increase in compressive resistance to diastolic perfusion) + anything that increases baseline CBF (i.e. increase O2 consumption, anemia, hypoxia)
How do you calculate total coronary resistance?
Add the resistances in series: R1 (large epicardial arteries with minimal resistance) + R2 (small arteries and arterioles) + R3 (extravascular compressive resistance that is mainly based on systolic contraction)
Why is the subendocardium primarily perfused in diastole?
Systolic contraction of the LV increases resistance in the coronary beds (increases R3)
When is the subepicardium perfused?
Throughout the cardiac cycle since in systole, the subepicardial pressure is equal to pleural pressures (unlike the subendocardium which is only perfused during diastole)
What happens with beta1 innervation? Beta2? Alpha1?
Beta1 = increased contractility and myocardial oxygen consumption leading to vasodilation; Beta2 = direct vasodilation; Alpha1 = direct vasoconstriction
What local mediators are present in the coronary vasculature to help with vasodilation?
Nitric oxide + endothelium-dependent hyperpolarizing factor (EDHF) + prostacyclin
How does nitric oxide help with vasodilation? What does oxidative stress do to it?
cGMP-mediated pathway which causes vasodilation; oxidative stress inactivates NO via a superoxide (doesn’t allow for vasodilation)
How does Endothelium-dependent hyperpolarizing factor (EDHF) cause vasodilation?
Responds to bradykinin and shear stress -> hyperpolarization of vascular smooth muscle -> vasodilation
How does prostacyclin help with vasodilation?
Gets produced from arachidonic acid by COX -> vasodilation
What does endothelin do in the coronary vasculature?
Slow-acting vasoconstrictor
What do platelets release to cause effects at the coronary vasculature?
Serotonin (vasoconstriction) + ADP (vasodilation due to NO production) + vWF + fibronectin + thrombospondin + PDGR (proliferation of smooth muscle after vessel damage)
What contributes to myocardial work?
External work (moving stroke volume against an arterial pressure) + Internal work (potential energy)
What is myocardial work efficiency?
External work / O2 consumption
What happens when you have plaque rupture in the coronary vessels?
Thrombogenic subendothelial substrates leads to platelet adherence (GP1b binds vWF and GPIIb/IIIa binds vWF/fibrinogen/fibronectin) -> this leads to platelet activation (epi, collagen, and thrombin bind platelets leading to activation of phospholipase C and phospholipase A2 -> activates thromboxane A2 (platelet aggregation and vasoconstriction) + prostacyclin (vasodilation))
What are angina equivalents and who are these symptoms more common in?
Mid-epigastric discomfort + dyspnea + exercise intolerance + fatigue; more often seen in women, older adults, and diabetics
What are the cutoffs for ST-depression and elevations?
ST-depression: >/= 0.5mm; STEMI: >/= 1mm in multiple leads
Does a normal ECG rule out ACS?
No
When can you see an elevated troponin if it isn’t ACS?
Renal disease, sepsis, COVID-19, infection, PE, stroke
What is a Bruce protocol?
The protocol for stress echoes
What is myocardial flow reserve?
The ratio of maximum blood flow to resting blood flow; this is the equivalent to coronary flow reserve
What does it mean if you have attenuation artifact on nuclear myocardial perfusion study?
Depicts a fixed perfusion defect but has normal wall motion movement on echo
What does it mean if you have scar tissue noted on nuclear myocardial perfusion study?
Fixed defects in perfusion with abnormal wall motion on echo
What does it mean if you have ischemia noted on nuclear myocardial perfusion study?
Reversible defects in perfusion with normal or abnormal wall motion
What are contraindications to nuclear studies?
Contraindication to vasodilators + bronchospastic disease + use of dipyridamole-containing meds + use of methylxanthines + hypersensitivity to adenosine or regadenoson
What are the indications for cardiac cath?
Stable ischemic heart disease with negative non-invasive studies but high suspicion for disease + unstable angina + STEMI
What are the AHA/ACC classifications of lesions for cath?
Type A (<10mm, <45 degree, little/no calcification, not totally occluded), Type B (10-20mm, 45-90 degree, totally occlusion <3 mon, ostial lesion), Type C (>20mm, >90 degree, total occlusion > 3mon, degenerated vein graft)
What is silent ischemia and how frequent is it seen?
Ischemia 2/2 autonomic neuropathy; seen in 1/3 of patients with chronic stable angina
What is Type 1 ischemia?
Acute coronary syndrome
What is Type 2 ischemia?
Demand ischemia (tachycardia is most common cause of this)
How long should you be on dual antiplatelet therapy after DES or BMS?
DES: 6 months; BMS: 1 month; If it is 2/2 ACS, then it should be for 12 months
Does LVH increase or decrease myocardial wall stress?
Decreases since there is increased wall thickness and more tissue to take the pressure
What plasma protein levels decrease with STEMI? What plasma proteins are increased?
Anticoagulant factors (i.e. Protein C, Antithrombin, and alpha-2 macroglobulin); Procoagulant factors are increased (fibrinogen, factor VIII, vWF, alpha-1 antitrypsin)
What determines right or left dominance in coronary anatomy?
If the PDA comes off the RCA, it is right dominant; if the PDA comes off the LCX, it is left dominant
What major branches come off the LCX? LAD?
LAD = diagonals and septal perforators; LCX = obtuse marginal
When is CABG preferred over PCI?
Left main disease or left main equivalent (>70% stenosis between proximal LAD and LCX) + triple vessel disease + proximal LAD stenosis
What is stunned myocardium? How long does it take for function to return?
Viable myocardium with contractile dysfunction; usually seen after brief periods of ischemia with transient myocardial dysfunction; responds well to inotropes; restoration of function in hours to weeks
What is hibernating myocardium?
Reversible, chronic contractile dysfunction in areas that receive enough blood flow for viability (but not full flow); function can be partially or fully restored after reperfusion (takes weeks to months)
What is necrotic myocardium?
Fibrotic or scarred myocardium; tissue is no longer viable even after revascularization
How do you test for myocardial viability?
Via viability testing; Dobutamine stress echo, SPECT, PET
What is the preferred intervention in single-vessel disease? Two-vessel disease? Three-vessel disease?
Single vessel = DES; Two vessel = PCI with DES, if LAD involved, CABG; Three vessel = CABG
What is the second most important graft after the LAD to use?
Radial artery
