7/27/2019 case 13 MI

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CASE 13: MYOCARDIAL INFARCTION (MI)

ETIOLOGY

- Blockage of blood flow in a coronary artery Lack of O2 and variousmetabolites to an area of myocardium

- Predisposing factors: Genetic and other factors

HISTORY AND PHYSICAL EXAMINATION- 46 y/o, male- Severe retrosternal pain of 1 hour duration, profuse sweating

- Smoker heavily previously advised with vegetarian diet and restrictedsalt intake

- Heredofamilial disease: father died of heart attack at age 52, one of twosiblings had MI at age 49

- Medications:o HMG-CoA reductase inhibitor

o combination of ACE inhibitor and thiazide diuretic (for

moderate hypertension)o aspirin (81mg/day)

- Vital signs:o BP = 150/90

o HR = 60

- No evidence of cardiac fai lure

- Treatment: M ORPHINE relief of pain and coronary dilating effect transfer to CCU (continuous ECG monitoring)

LABORATORY FINDINGS

- Initial ECG = ST segment elevation and other changes in certain leads

anterior transmural left ventricular infarction- Cardiac biomarker: 8 fold Elevation of Troponin T levels 6H after

admission- Total cholesterol = <5.17 mmol/L (normal)- LDL/HDL cholesterol ratio = 4:1 (normal)- Triacylglycerols = 1.5mmol/L (normal <2.26mmol/L)

Various proteins and enzymes released from infracted tissue at

different rates different half lives in circulation:o Myoglobin

o MB isozyme of creatine kinase

o Aspartate aminotransferase

o Alanine aminotransferase

o Heart muscle isozyme of lactate dehydrogenase

TREATMENT

- Tissue plasminogen activator (t-PA) IV- Chest pain disappeared after 12H- Discharged improved after 7 days- Discharge instructions:

o Continue meds

o Cardiac rehab

o STOP smoking

DISCUSSION

Myocardial infarction- Caused by occlusive thrombus lying in close proximity to an unstable

atherosclerotic plaque which has often ruptured recently

- Rupture of plaque generates thrombus- Major aims of treatment:

o Prevent death from cardiac arrhythmia by drugs and limit size

of infarction

o T-PA given up to 12 hours of onset of symptoms althoughpreferably sooner

o Percutaneous coronary intervention (PCI)  

percutaneous transluminal coronary angioplasty (PTCA) withor without stent

- Normal metabolism of myocardium: aerobic  ATP derived fromoxidative phosphorylation

Atherosclerosis- Patchy plaques in the intima of medium and large arteries- Risk factors:

o Age

o Family history

o Male sex

o High levels of LDL

o Low levels of HDL

o Hypertension

o DM

o smoking

Endothelial dysfunction- Important in genesis of atherosclerosis- Platelets & fibrin deposit on luminal aspect and monoclonally derived

smooth muscles present in medial layer of artery grow into intimal lesion

attracted by growth factors released by macrophages and platelets(e.g .platelet derived growth factor)

- Plasma lipoproteins, glycosaminoglycans, collagen, calcium 

accumulate in a lesion FATTY STREAK  intimal plaque  

inflammation and hemorrhage into the plaque rupture of its surface

and exposure of underlying constituents to blood adherence of platelet

to exposed collagen THROMBUS 

- Oxidized LDL in lesions encourages recruitment of macrophages

(inflammatory cells ) stimulates release of growth factors 

- Inflammation key factor in atherosclerosis accumulation ofmacrophages and lymphocytes

- C – reactive protein: elevated reflection of chronic inflammation

- Precise metabolic changes that commit a cell to dying  understudy: depletion of ATP, activation of intracellular phospholipases(damage to cellular membranes), activation of proteases, accumulation ofintracellular Ca

Development of atherosclerosis (usually polygenic)↓plaque rupture↓formation of large thrombus in a coronary artery (occlusion 90% of vessel wall)↓deprivation of blood supply (ischemia ) to an area of the myocardium andcompromised oxygen supply of affected area↓shift to anaerobic glycolysis (decreased synthesis of ATP [only 1/10 th of ATPproduced by oxidative phosphorylation], depletion of adenine nucleotide pool)↓increased NADH due to inactive terminal electron transport chain; due to lack of

oxygen↓accumulation of lactic acid and other metabolites in myocardial muscle, causingincreased cellular osmolarity [↑ intracellular oncotic pressure] and altered membranepermeability [cell swelling]

↓decreased pH in heart muscle cells [severe acidosis]

↓increasingly inefficient contraction of heart muscle

↓cessation of contraction↓activation of membrane phospholipases, degradation of proteins by proteases, influxof Ca↓death of affected area of heart muscle