ischemic heart disease Flashcards
Ischemic heart disease
imbalancee between supply and demand for oxygen and nutrients and the removal of metabolites
Ischemia- insufficient blood flow
Hypoxia- insufficient oxygen
Ischemia worse than hypoxemia bc lack of perfusion prevents delivery of nutrients (w/ oxygen) and removal of metabolites
IHD epidemiology: preventative measures (directed against development of atherosclerosis- smoking cholesterol HTN lifestyle) meds and surgery
IHD pathogenesis
diminshed coronary blood flow relative to mycardial demand–> ischemia
Cause of IHD: >90% REDUCED CORONARY BLOOD FLOW (DUE TO ATHEROSCLEROSIS)- other causes lowered systolic BP, vasculitis, structural anomaly, severe HTN, diminished O2 in blood
Causes of decreased blood flow: fixed atherosclerotic narrowing, acute plaque change, thrombosis overlying ruptured plaque, vasospasm
Fixed obstruction
anatomic narrowing/ occlusion
narrowing of >70% causes symptomatic ischemia with exercise, >90% stenosis causes ischemia at rest
often multiple arteries are affected, most commonly first CMs of LAD, LCX, entire length of RCA
Effect modified by collaterals
Acute plaque change
unpredictable, abrupt conversion of stable plaque to an unstable atherothrombotic lesion that results in myocardial ischemia:
Rupture/fissures/ulcerations: exposes underlying throbogenic substances
Hemorrhage into atheroma: expands plaque and further narrows lumen
Results in acute coronary syndromes: acute MI, unstable angina, sudden cardiac death
influences contributing to acute plaque change
intinsic factors: structure and composition of plaque (large areas of foam cells/ lipid, thin fibrous cap, most dangerous lesions are the moderately stenotic, lipid rich atheromas, abundant inflammation, few smooth muscle cells, mechanical stress (at the junction of fibrous cap and adjacent normal wall))
Extrinsic factors: adrenergic stimulation (upon awakening, emotional)
Coronary thrombosis
partial or total, superimposed on a partially stenotic plaque
Critical to the pathogenesis of acute coronary syndromes
Total occlusion- acute transmural MI or sudden death
Incomplete occlusion (mural thrombus)- unstable angina, acute subendocardial infarct, sudden death, Emboli (into more distal coronary artery)
vasoconstriction
compromises lumen size and increases mechanical forces that contribute to plaque rupture
Leads to severe but transient reduction reduction in coronary blood flow
Stimulated by: adrenergic agonists in circulation, locally released platelet contents, endothelial dysfuncition–> impaired secretion of endothelial relaxing factors. Mediators released from mast cells
Clinical syndromes of IHD: angina pectoris
paroxysma and recurrent attacks of chest pain caused by transient myocardial ischemia, 15 s to 15 min
No cellular necrosis
Three patterns:
- Stable (produced by physical activity or emotional excitement, attributed to chronic stenosing coronary AS)
- Prinzmetal (due to coronary artery spasm, at rest)
- Unstable (occurs with progressively increasing frequency and progressively less effort, often at rest and of prolonged duration, induced by disruption of plaque with superimpsed partial thrombosis, prodrome of acute MI)
Clinical syndromes of IHD: myocardial infarction
Death of cardiac muscle due to ischemia, M>F
Risk factors: increasing age, predisposition to atherosclerosis (HTN, cigarettes, DM, increased cholesterol/lipid)
Pathogenesis: in 90%- acute plaque change resulting in thrombosis and occlusion of coronary artery
in 10% vasospasm, emboli or unexplained
Transmural: full thickness of ventricular wall, confined to distribution of one vessel, fixed coronary obstruction with superimposed acute plaque change and complete obstructive thrombosis
Subendocardial: necrosis limited to inner 1/3, may extend llaterally beyond perfusion of one vessel, fixed coronary obstruction with acute plaque change but with non occlusive thrombus or lysis of thrombus or HTN
MI Myocardial response
Loss of contractility (60s of ischemia, may precipitate acute heart failure), loss of blood supply–reversible damage in early stage, 20-40 minute–irreversible damage consisting of coagulative necrosis, early thrombotylitic therapy (3-4 hours)–reperfusion and limit size of of infarct, arrythmias (MI secondayr to ischemia/infarct–vFiv–> sudden death
Progression of necrosis starts from within epicardium
Morphology: LAD (most often),–> RCA–> LCA
MI gross morphology
<12 hours (not apparent, tetrazolium stain- pale areas 2-3 hours post occurence
12-24 hrs: dark red mottling (stagnant blood)
1-14 days: early sharply define yellow tan area, late yellow tan central, hyperemic border
2 weeks: gray white scar begins
MI histology
4-12 hrs: wavy fibers
12 hrs-7 days: coagulative necrosis becomes well established and ongoing, initially pyknotic nuclei (hyper eosinophilitc myocytes), followed by PMNs (max 1-3 days) loss of nuclei and striations, by 7 days, Macrophages at border
7-14 days: granulation tissue well established, collagen begins to deposit
> 14 days: progressively more collagen deposition, eventually dense fibrous scar
Acute MI reperfusion injury
Usually occurs after: thrombolysis, baloon angioplasty or bypass grafts
Reperfusion prevents necrosis if occurs within 20 mins
Pathology associated with reperfusion: Gross (hemorrhage into infarcted tissue)
micro: necrosis with contractile bands, due to influx of calcium
Oxygen ffree radicals released from leukocytes, microvascular injury causes hemorrhage and endothelial swelling that occludes capillaries (no flow), platelet and complent activation
MI clinical features and diagnosis
Chest pain (sever, crushing, substernal), radiation into left arm, neck jaw epigastrium, last several minutes to hrs, no relief by nitroglycerin or rest
Rapid weak pulse, diaphoresis, dyspnea due to pulmonary edema
10-15% w/o symptoms, ECG patterns, cardiac enzymes and CRP
Complication of MI: contractile dysfunction, cardiogenic shock pumpm failure, arrhythmia, myocardial rupture, pericarditis
