Acute Myocardial Infarction

Introduction

1.25 million MI’s in the US every year

30% of patients die before reaching the hospital
another 10% die in the hospital
yet another 10% die within a year of their first MI
and 4% die per year following the first year of survival

Early diagnosis and treatment are key!

Coronary Syndromes

Stable angina – an occluded coronary artery that doesn’t allow enough blood flow in for exercise but is fine at rest

Unstable angina – an ongoing process that leads to Þ MI – necrosis and death of tissue

Plaque rupture Þ exposed collagen Þ activated platelets release TXA₂ Þ vasospasm and platelet aggregation Þ thrombus Þ obstruction of coronary blood flow.

Evidence of platelet involvement

(1) ASA and IIb IIIa inhibitors stop the process of thrombus formation

(2) Ý [TXA₂] measured during MI’s

(3) thrombolysis works

Diagnosis of Mis

History – Chest pain (like an elephant sitting on the chest), however can have silent ischemia

Cardiac Enzymes – enzymes released into the blood during the death of myocytes

Myoglobin – nonspecific marker of muscle injury appears first within 2 hours

Troponin – cardiac-specific isoenzymes of TnI and TnT are detectable next, 3 hours after the onset of chest pain

CK-MB – cardiac-specific creatine kinase starts to rise 4 - 8 hours after infarction

LDH – LDH₁ is the most cardiac specific of the 5 isoenzymes of LDH. A LDH₁/LDH₂ ratio > 1.0 is indicative of myocardial necrosis. Serum levels of LDH peak 3-5 days after an acute MI.

EKG Changes in MI

Complications of MI

CHF – diastolic dysfunction because the heart becomes stiffer

Cardiogenic shock – ischemia Þ impaired contractility Þ ß CO Þ ß BP Þ ß coronary perfusion

90% mortality of patients in Cardiogenic shock. Only treatment that makes an impact is Angioplasty

must get the coronary artery open!

RV infarction – ß ß BP, ß CO, Ý Ý venous pressure. Treatment is fluids to maintain BP and therefore CO

Arrhythmias – the MOST COMMON CAUSE OF DEATH IN MI, V tach and V fib are the biggies, but any other arrhythmia could happen. CCU’s monitor patients to quickly shock them out of V Fib.

Heart Block – if the infarction involves the conduction tissue a heart block may result

Aneurysm – the weak, damaged wall may balloon out during systole

Ruptured septum – leading to communication between the ventricles

Ruptured papillary muscles – results in mitral regurgitation

Ruptured free wall – death from cardiac tamponade

Thrombus – stasis leads to thrombus formation, which can result in stroke. Treatment is anti-coagulation.