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what does the left main coronary artery supply
intraventricular septum and anterior wall of left ventricle
what does the circumflex artery supply
posterolateral left ventricle and anterolateral papillary muscle
what does the right coronary artery supply
right ventricle
what does the posterior descending artery supply
posterior and inferior walls of left ventricle
ischemic heart disease
imbalance between myocardial oxygen supply vs demand; caused mostly by atherosclerotic lesions in epicardial coronary arteries and microvascular disease
non-obstructive triggers of ischemic heart disease
increased demand - left ventricular hypertrophy (LVH), increased preload/afterload, tachycardia
decreased supply - anemia, hypoxia, hypotension, vasospams
clinical manifestations of ischemic heart disease
angina (stable, variant, unstable), dyspnea, myocardial infarction, sudden death, chronic ischemic heart disease
symptoms of angina
substernal/precordial chest discomfort, “something sitting on my chest”, can radiate (shoulders, neck, jaw, epigastric)
associated symptoms: dyspnea, nausea, diaphoresis
stable angina
associated with activity, dissipates with rest
printzmetal angina
younger patients, transient vasospam, associated with stimulant drug use (cocaine)
causes: hyperreactivity, ANS dysfunction, endothelial dysfunction, allergy
unstable angina
at rest or increasing in frequency, disruption of plaque, needs urgent intervention
sudden cardiac death
unexpected death, no symptoms or <24 hours after onset of symptoms
causes: coronary artery disease (most common), congenital heart disease in younger patients
mechanism: arrhythmia
chronic ischemic heart disease
ischemic cardiomyopathy, progressive CHF from cumulative ischemic injury, often seen post-MI
Pathogenesis of myocardial infarction
acute plaque change → exposure of contents → platelet activation/microthrombi → vasospasm → coagulation cascade → vessel occlusion
time is muscle - outcome depends on duration, location, severity, collaterals
reversible MI
minutes, decreases contractility, cell swelling, glycogen depletion
irreversible MI
greater than 20-30 minutes of severe ischemia, leads to necrosis
myocardial necrosis
begins subendocardium and progresses transmural; necrosis half thickness in 2-3 hrs and fully transmural by 6 hours; initial sign: membrane disruption and protein leak (biomarkers)
complications of MI
contractile dysfunction: LV failure, RV failure
arrhythmias: bradycardia, AFib, AV block, VFib, ventricular tachycardia
rupture: free wall, septum, papillary muscle
ventricular aneurysm: late complication, leads to thrombus, arrhythmia, HF
mural thrombus: embolic risk
papillary muscle dysfunction
chronic ischemic cardiomyopathy
STEMI
MI from ST elevation, transmural, full thickness of myocardium
NSTEMI
MI from ST depression, subendocardial, partial thickness
type 1 NSTEMI
classic MI due to obstruction
type 2 NSTEMI
from supply-demand mismatch without obstructive lesion
Biomarkers used for MI diagnosis
EKG, troponin (gold standard), CK-MB
best practice for diagnosis of MI
troponin and EKG
troponin
increased 2-4 hours, lasts 7-12 days, sensitive and specific; trend in NSTEMI, false highs in CKD
CK-MB
rises in 4-6 hours, peaks 16-30 hours, not used clinically; false positives in skeletal muscle injury, post-op, hypothyroid, marathoners, chronic renal failure
emergency department tools in risk assessment of MI
HEART score (most common), ED-ACS (sensitive, not specific), TIMI (older, not used)
Long-term tools in risk assessment of MI
Framingham, QRISK, ACC/AHA pooled equations
ACC/AHA 2013 Statin Guidelines
4 groups benefiting most: 1. clinical ASCVD 2. LDL >190 3. age 40-75 with diabetes and LDL 70-189 4. age 40-75 with LDL 70-189 and ASCVD risk >7.5%
total cholesterol
LDL + HDL + (TG/5)
low density lipoprotein (LDL)
bad cholesterol, target of statins; lipoprotein(a) = higher CAD risk
high density lipoprotein (HDL)
good cholesterol; increases with exercise, smoking cessation, omega-3, red wine, purple fruits, weight loss
Triglycerides (TG)
part of lipid panel