Acute Myocardial Infarction AMI Causes PATHOPHYSIOLOGY  Atherosclerosis and Etiology

• Acute coronary syndrome (ACS) may present as unstable angina (no ST segment elevation), or acute myocardial infarction. Acute myocardial infarction (AMI) implies irreversible damage to the myocardium.
• MI Causes usually occurs when an atheromatous plaque in a coronary artery ruptures, and the resulting clot obstructs the injured blood vessel

Acute Myocardial Infarction AMI Causes PATHOPHYSIOLOGY Atherosclerosis and Etiology

Causes Acute Myocardial Infarction Etiology:

• Proven risk factors for MI are tobacco use,
• high blood pressure, male sex, advanced age, obesity, physical inactivity
• diabetes mellitus, abnormal cholesterol levels,
• high blood pressure, male sex, advanced age, obesity, physical inactivity
• AMI may be associated with ST elevation or ST de­pression in the ECG.
• AMI With ST elevation is called STEMI (ST segment elevation MI) and AMI without ST segment elevation is called NSTEMI (Non ST seg­i]1ent elevation MI).
• In NSTEMI cardiac markers like troponins are normal (not elevated).
• In TEMI~ardc markers like  troponins are elevated.
• Q waves do not evolve in NSTEMI but Q waves are
• seen to evolve in STEMI. ~
• Mortalit is 30%. 25% die in 1st year after AMI

Acute Myocardial Infarction AMI Causes PATHOPHYSIOLOGY Atherosclerosis and Etiology

PATHOPHYSIOLOGY Causes of Acute Myocardial Infarction

I. Atherosclerosis

• Coronary arteries are narrowed by athero­sclerosis.
• Abrupt closure can occur by throm­botic occlusion.
• Very gradual narrowing leads to development of collaterals and therefore lesser incidence of MI.

Factors which precipitate thrombotic occlusion of coronary vessels are:

• Vascular injury (damage to endothelium of coro­naries)
• Vascular injury is precipitated by cigarette smoking, hypertension and hyperlipidemia.
• Fissuring of atherosclerotic plaque
• Rupture of atherosclerotic plaque
• Ulceration

Acute Myocardial Infarction Causes Thrombogenesis

• Atherosclerotic plaque with rich lipid core and thin @:>rous cap are very p..!:one to rupture.
• Iatelets are activated by: ADP
• Collagen Epinephrine  Serotonin.
• There is release of thromboxane A₂•

Thtrhromboxane A₂ is a potent

• vasoconstrictor which causes coronary spasm and precipitates total coro­nary oc~sion and infarctio’!.
• activated platelets are resistant to thrombolysis.
• Platelets also bring about a change in GP IIb / IIIa
• receptors which can now bind to 2 platelets at a time involving von Willebrand factor and fibrinogen.
• Prothrombin is converted to thrombin and fibrinogen to fibrin resulting in formation of clots.

II. Total Coronary occlusion resulting in Acute MI occurs due to :

• Presence of multiple risk factors
• Hypercoagulability
• Collagen vascular disease
• Cocaine abuse
• Intracardiac thrombi or masses leading to coronary embolization.

III. Other causes of Coronary occlusion are less important e.g. :

• Coronary embolism
• Congenital abnormalities
• Coronary spasm
• Systemic and inflammatory disease .