Clinical Consequences of Myocardial Infarction
A) Short Term
i. Cardiac Arrest; accounts for most acute deaths complicating myocardial infarction and is due to ventricular fibrillation. Treatment is immediate defibrillation. Understanding that, this one of the most lethal complications of acute MI led to the introduction of ICU monitoring for acute MI patients. This risk is usually seen during the first 24 hours of an MI. While VF arrest within the first 48 hours of an MI does not portend an adverse long-term prognosis, VF arrest beyond the first 48 hours does, and reflects extensive myocardial injury and poor underlying myocardial function. It also predicts a high future likelihood of recurrence of VF arrest.
ii. Congestive Heart Failure; A consequence of a sizeable myocardial infarction (> 25% cardiac muscle). The single most important determinant of prognosis after an acute STEMI. Carries a poor prognosis.
iii. Cardiogenic Shock; Seen when > 40% of myocardial muscle is injured. Marked by hypotension, poor peripheral perfusion and drop in urine output. Portends a very poor prognosis (50%-60% mortality) and is the cause of death in 60% of STEMI. Systolic BP < 80 mmHg, high filling pressure > 18 mmHg, and low cardiac index < 1.8L/min/M2). May also be the consequence of ruptured papillary muscle or interventricular septum.
iv. Rupture; Into the pericardial space resulting in immediate death due to pericardial tamponade. Usually complicating anterior or lateral wall MIs and in older individuals.
v. Pseudoaneurysm; A pseudoaneurysm is a confined free wall rupture held up by clot formation. Once identified it should be surgically corrected urgently. The difference between a pseudoaneurysm and a true aneurysm is that the wall of a true aneurysm contains myocardial tissue whereas the wall of a pseudoaneurysm is composed of clot and pericardial tissue.
A) Short Term
i. Cardiac Arrest; accounts for most acute deaths complicating myocardial infarction and is due to ventricular fibrillation. Treatment is immediate defibrillation. Understanding that, this one of the most lethal complications of acute MI led to the introduction of ICU monitoring for acute MI patients. This risk is usually seen during the first 24 hours of an MI. While VF arrest within the first 48 hours of an MI does not portend an adverse long-term prognosis, VF arrest beyond the first 48 hours does, and reflects extensive myocardial injury and poor underlying myocardial function. It also predicts a high future likelihood of recurrence of VF arrest.
ii. Congestive Heart Failure; A consequence of a sizeable myocardial infarction (> 25% cardiac muscle). The single most important determinant of prognosis after an acute STEMI. Carries a poor prognosis.
iii. Cardiogenic Shock; Seen when > 40% of myocardial muscle is injured. Marked by hypotension, poor peripheral perfusion and drop in urine output. Portends a very poor prognosis (50%-60% mortality) and is the cause of death in 60% of STEMI. Systolic BP < 80 mmHg, high filling pressure > 18 mmHg, and low cardiac index < 1.8L/min/M2). May also be the consequence of ruptured papillary muscle or interventricular septum.
iv. Rupture; Into the pericardial space resulting in immediate death due to pericardial tamponade. Usually complicating anterior or lateral wall MIs and in older individuals.
v. Pseudoaneurysm; A pseudoaneurysm is a confined free wall rupture held up by clot formation. Once identified it should be surgically corrected urgently. The difference between a pseudoaneurysm and a true aneurysm is that the wall of a true aneurysm contains myocardial tissue whereas the wall of a pseudoaneurysm is composed of clot and pericardial tissue.
vi. Ruptured Papillary Muscle; Resulting in acute mitral regurgitation. Seen more commonly after an inferior myocardialinfarction. Requiresurgent surgical repair.
vii. Ruptured Interventricular Septum; Usually after an acute anterior wall MI. Results in heart failure and requires urgent surgical therapy
viii. Aneurysm formation; This is an intermediate-term complication of a myocardial infarction. When a segment of myocardium becomes sluggish in its contraction secondary to a myocardial infarction it is described as hypokinetic. When the segment does not contract it is akinetic. When it bulges outward during systole; dyskinetic. This segment is aneurysmal and can lead to clot formation and ventricular arrhythmias.
B) Long Term
i. Heart failure; Coronary artery disease is the commonest cause of congestive heart failure in the Western economies
ii. Sudden cardiac death; Due to ventricular arrhythmias
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