pathophysiology of myocardial infarction

Types and pathophysiology of myocardial infarction

1. PATHOPHYSIOLOGY OF MYOCARDIAL INFRACTION By :- VIKAS AAGRAHARI Pharm-d 4th yr

2. INTRODUCTION: Myocardial infarction is an irreversible injury to a part of the heart or myocardial tissue that results from ischemia and hypoxia finally necrosis of particular cells.  Usually this is because one of the coronary arteries that supplies blood to the heart develops a blockage due to an unstable buildup of atherosclerotic plaques and other blood cells.   Myocardial infarction is one of the leading killer in the United States.  This is called Acute MI if it is sudden and serious.  64% of cases does not have chest pain or other symptoms.  This is called Silent myocardial infarction.

3. TYPES OF MI:

4. TYPES OF MI 2007 consensus document classifies MI into five main types:  Type 1 – spontaneous MI related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection  Type 2 – MI secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension  Type 3 – sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by new ST elevation,  Type 4 – associated with coronary angioplasty or stents:           Type 4a – MI associated with Percutaneous coronary intervention (PCI)    Type 4b – MI associated with stent thrombosis as documented by angiography or at autopsy  Type 5 – MI associated with CABG (Coronary Artery Bypass Graft)

5. SYMPTOMS:

6. RISK FACTORS: Cardiovascular disease Old age Tobacco smoking  High blood levels of LDL, low levels of HDL, Diabetes High blood pressure Lack of physical activity Obesity Chronic kidney disease Excessive alcohol consumption Use of Cocaine and Amphetamines

7. pATHOPHYSIOLOGY:  The pathophysiology of acute myocardial infarction is complex. Loss of viable myocardium impairs cardiac function, which can lead to reduced cardiac output, if damage is severe, cause cardiogenic shock. Infarction is tissue death caused by ischemia. AMI occurs when localized myocardial ischemia causes the development of a defined region of necrosis. A collagen scar forms in the necrosis place. Apoptosis also plays a role in the process of tissue damage subsequent to MI. As a result, the patient's heart will be permanently damaged. Ischemia can cause arrhythmias and conduction blocks that can further impair function and become life-threatening in some cases. Reduced cardiac output and arterial pressure can elicit baroreceptors, that lead to activation of sympathetic nerves and the RAAS.

8. MECHANISMS AND CONSEQUENCES OF PLAQUE RUPTURE:  Coronary plaques which are prone to rupture are typically small and nonobstructive, with a large lipid-rich core covered by a thin fibrous cap. Activated macrophages and T-lymphocytes localized at the site of plaque rupture are thought to release metalloproteases and cytokines which weaken the fibrous cap, rendering it liable to tear due to the stress exerted by the blood flow. Plaque rupture reveals subendothelial collagen, which serves as a site of platelet adhesion, activation and aggregation.

9. The resulting deficit of antithrombotic factors such as Thrombomodulin and Prostacyclin enhances thrombus formation. Platelet-derived factors (e.g. TXA2, 5-HT) to cause vasoconstriction. This may promote the development of local vasospasm, which worsens coronary occlusion. Sudden death and acute coronary syndrome is peaking at 9 a.m. and 11 p.m.  Increased levels of Catecholamines at this time resulting in increased platelet aggregability, vascular tone, heart rate and blood pressure, which may trigger plaque rupture and thrombosis. Increased physical and mental stress can also cause MI and sudden death, supporting a role for increases in catecholamines in MI pathophysiology.

10. The degree of coronary occlusion and myocardial damage caused by plaque rupture probably depends on systemic catecholamine levels, as well as local factors such as plaque location and morphology, the depth of plaque rupture, and the extent to which coronary vasoconstriction occurs.  Severe and prolonged ischemia produces a region of necrosis spanning the entire thickness of the myocardial wall (STEMI).  Less severe and protracted ischemia (NSTEMI)can arise when:  1. Coronary occlusion is followed by spontaneous reperfusion.         2. The infarct-related artery is not completely occluded.  3. The oxygen demand in the affected zone of myocardium is smaller.

11. DIAGNOSIS:   ECG - differentiate between two types of myocardial infarctions.  Blood tests are Troponin and Creatine kinase (CK-MB). 

12. TREATMENT:  Aspirin - which prevents further blood from clotting, chest pain.  Nitroglycerin – Vasodilator.  STEMI is treated by reperfusion therapy, angioplasty (arteries are pushed open) Thrombolytics.  People who have multiple blockages of their coronary arteries, particularly if they also have diabetes, treated with CABG).