Late Complications of Myocardial Infarction

           Postinfarction complication rates have fallen dramatically since the advent of early reperfusion strategies. Nevertherles, many patients (large infarction, silent infarction, late presentation, delayed or incomplete reperfusion) remain at high-risk for life-threatening late complications of myocardial infarction. The role of an urgent beside echocardiogram for a rapid diagnosis cannot be overemphasized. The mnemonic "FEAR A MI" is a logical way to remember and respect these potentially life-threatening complication while caring for a patient in the ICU, as demontrated below:

a. FAILURE: Left Ventricledysfunction is the single most powerful predictor of survival following a myocardial infarction. Clinical symptoms of heart failure are more likely in patients with large infarction, advanced age, and/or diabetes.

b. EFFFUSION and TAMPONADE: Post-Myocard Infarction effusion are rarely life-threatening. However, if tamponade physiology is present, consider hemorthagic effusion from a ventrucalar rupture.

c. ARRHYTMIA: Infarction-spesific arrhytmia include the following
1. Accelerated Idioventricular Rhythm (AIVR) is considered a "reperfusion rhythm" as it is often seen immedietly after a successful reperfusion. No treatment is warranted for this arryhtmia when it is combined with clinical scenario of reperfussion
2. Vebtricular Tachycardia (VT) is often the terminal rhythm in the peri-infarc time period and is associated with increased mortality when it occurs in the first, 48 hours of hospitalization. Aggresive restoration of sinus rhythm is achieved through the use of antiaryhtmia medications (amiodarone, lidocaine) and/or sychronized DC cardioversion. Because Hypokalemia and hypomagnesemia have been associated with the development of sustained ventricular tachycardia, it is reasonable to correct electrolyte levels in the setting of an infarction. In contrast, non-sustained ventricular tachycardia (NSVT) is not associated with an increased risk of death during the index hospitalization or over the first year infarction.
3. Myocardial Infarction can cause a block at any level of the conduction system. In general, proximal (AV nodal) conduction disease is associated with an infarct of the right coronary artery (RCA). This causes a transient AV block and often does not warrant immediate temporary pacemaker palcement. One exception is AV block in the setting of Right Ventricular Infarction, where restoration of AV synchrony can improve RV filling and thus cardiac output. Distal (infranodal) conduction disease is frequently associated with a left anterior descending (LAD/septal infarct and is longer lasting and life-threatening. Immediare pacing efforts should be pursued.

d. RUPTURE: The clinical presentation of Ventricular rupture is often striking and life-threatening. The rupture can be in the ventricular free wall, ventricular septum, or papilllary muscle. A clinical suspicion and the timely use of echocardiography and pulmonary artery (PA) catheter are essential for prompt diagnosis of this serious complication, which generally requires emergent surgival consultation.

e. ANEURYSM: True Left Ventricular (LV) Aneurysm complicate less than 5% of Acute Infarctions but are associated with considerably lower survival rate. The characteristic ECG findings LV aneurysm are Q waves with persistent ST Elevetion, though the diagnosis is best confirmed with a non invasive imaging study. Apseudoaneurysm, distinct from an aneurysm, can be thought of as a "contained rupture". It is most often seen with an inferior infarction and treatment is emergent surgery. Both surgical and medical treatments carry a very high mortality.

f. MYOCARDIAL INFARCTION: The complaint of chest pain after myocardial infarction may represent reccurent ischemia from incomplete revascularization. Ischemia recurs in 20%-30% of patients receiving thrombolytic therapy and up to 10% of patients after percutane revascularization. Serial cardiac biomakers and ECG can help identify at-risk patients. Normally, antianginal medications (nitrates, beta blocker) can control symptoms. Reinfarction due to stent trombosis usually has a dramatic presentation with severe anginal pain refractory to medical therapy and envloving ST elevations on ECG. These findings warrant additional prompt revascularization efforts.