Myocardial Infarction (MI) Complications
Cardiogenic shock: One of the life-threatening complications of STEMI is cardiogenic shock during which hypotension is present from low cardiac output.
This results in end-organ hypoperfusion and potentially multi-system organ failure and can be fatal. Revascularization by PCI or CABG is recommended in this setting (see SHOCK trial). Hemodynamic support may be needed using intraaortic balloon counterpulsation (IABP or balloon pump) and when severe left ventricular assist device insertion (LVAD).
Left ventricular aneurysm: A left ventricular aneurysm can form after a STEMI. Most commonly, the apex of the heart is involved however, the inferior wall can form an aneurysm as well. The four main concerns in patients with left ventricular aneurysm are:
1. Heart failure: The portion of the heart that contains the aneurysm is not contractile and is frequently “dyskinetic”. This results in overall decrease in heart function and the development of congestive heart failure.
2. Left ventricular thrombus formation: When blood stagnates in any area of the body, there is a risk of platelet aggregation and thrombus formation. The aneurysmal portion of the LV is no different. Embolization of left ventricular thrombi can lead to embolic stroke or other systemic embolisms.
3. Ventricular tachycardia: The scar within the left ventricular aneurysm is a focus for ventricular arrhythmias which can lead to sudden cardiac death.
4. Angina pectoris: The aneurysmal tissue can still cause symptoms of angina, even if revascularized.
An LV aneurysm can be diagnosed on ECG when there is persistent ST segment elevation occurring 6 weeks after a known transmural MI (usually anterior). Without knowing the persons past medical history, the ECG changes of an aneurysm may mimic an acute ST segment elevation MI. With an anterior or apical aneurysm, the persistent ST elevation is in lead V1 and V2. In an inferior aneurysm it would be in lead II, III and aVF. The only way to be sure of an LV aneurysm diagnosis on an ECG (not from an acute MI) is to have the patient’s history of a prior heart attack and cardiac imaging to document the presence of an aneurysm.
There is a surgical procedure during which the surgeon resects the aneurysm and uses a Dacron patch. This is called the “Dor procedure” or the EVCPP (endoventricular circular patch plasty). This procedure is indicated when medical therapy fails to control or acceptably improve the above mentioned complications/symptoms from the left ventricular aneurysm.
Ventricular arrhythmia: The most common cause of pre-hospital death during STEMI is ventricular fibrillation. The widespread availability of automated external defibrillators (AED) has been of benefit in this situation. Ventricular tachycardia commonly occurs as well during and after STEMI and can be life-threatening. Treatment includes amiodarone and/or lidocaine. See the ventricular tachycardia review for more detail and multiple ECG examples.
An accelerated idioventricular rhythm is a common post-STEMI rhythm and is also termed “slow ventricular tachycardia” since it meets morphology criteria for VT, however has a heart rate < 100. This is a benign, hemodynamically stable rhythm and no treatment is necessary. See the idioventricular rhythms review for more detail and multiple ECG examples
The prophylactic administration of lidocaine to suppress premature ventricular contractions or prevent ventricular tachycardia/fibrillation is not recommended. Likewise, the CAST trial demonstrated increased mortality using encainide, flecainide and moricizine to suppress premature ventricular contractions after an acute coronary syndrome.
Atrial fibrillation: Atrial fibrillation is not a common complication of STEMI, however it can occur when atrial infarction occurs (as indicated by PR depression on the ECG). Rapid control of heart rates is crucial to limit the extent of ischemia. Recall that oxygen demand increases as heart rate increases. Emergent cardioversion and amiodarone therapy is frequently needed in the setting of atrial fibrillation and STEMI.
Ventricular septal defect: When infarction of the interventricular septum occurs, this area can thin with the remodeling process and on occasion, a complete defect between the right and left ventricles can develop. This results in left to right shunting of blood and can be life-threatening when acute. A holosystolic murmur at the left lower sternal border occurs. Right heart catheterization will show an “oxygen step-up” between the right atrium and right ventricle (since oxygenated blood will be present in the right ventricle).
The ventricles are good at adapting to hemodynamic stress when gradually introduced, as in worsening aortic regurgitation, however when acute, ventricular failure and shock occurs as is present with acute VSD formation. Emergency surgical repair is warranted in this setting. Without surgical intervention, the mortality rate is > 90%. Fortunately, with the early revascularization techniques now employed (PCI), VSD formation is less common.
Acute mitral regurgitation: Acute severe mitral regurgitation is a life-threatening disorder. Papillary muscle rupture after acute myocardial infarction can occur as a complication of an inferior MI (right coronary artery supply) since the posteromedial papillary muscle is the most likely to rupture.
There are two papillary muscles that comprise part of the complex anatomy of the mitral valve. The anterolateral papillary muscle receives dual blood supply from the left anterior descending coronary artery and the left circumflex coronary artery in most individuals while the posteromedial papillary muscle receives its sole blood supply from the right coronary artery. Complete infarction of the posteromedial papillary muscle can occur during an inferior MI while only partial or no damage will be done to the anterolateral papillary muscle during an anterior (left anterior descending) or lateral (circumflex) infarction since there is dual blood supply to this papillary muscle. Thus, the posteromedial papillary muscle is the most likely to rupture.
Emergent surgical repair or replacement of the mitral valve is indicated. Mortality approaches 100% if not surgically fixed. As a bridge to surgery, intraaortic balloon counterpulsation can be helpful hemodynamically to reduce afterload and lessen the mitral regurgitation. Right heart catheterization will show prominent “V waves” in the pulmonary capillary wedge pressure tracing.
Left ventricular thrombus: After myocardial infarctions (especially anteriorly), the myocardial stunning that occurs can result in blood pooling toward the akinetic segment (frequently the cardiac apex) resulting in thrombus formation. Embolization of this thrombus can cause a stroke. There is no good data in regards to prevention of left ventricular thrombi, however the ACC/AHA guidelines give a class I, level of evidence B recommendation to warfarin therapy for 3 months when there is a cardiac source of embolus suspected after a myocardial infarction.
Left ventricular free wall rupture: This is a fatal complication of myocardial infarction and occurs when thinning of the left ventricular free wall occurs as a part of remodeling. A complete defect results in blood from the left ventricle filling the pericardium. This usually occurs rapidly resulting in cardiac tamponade, pulseless electrical activity (PEA) and death. Treatment is emergent surgical repair.
Right heart catheterization will show increased right heart pressures and decreased left heart pressures with inspiration. Also, the diastolic pressures are elevated and equal. Normally, the pericardium can expand as the heart fills, however with cardiac tamponade from a large pericardial effusion or constrictive pericarditis, this is not able to occur. As a person inspires, venous return is increased to the right heart and the interventricular septum bulges to the left impairing left ventricular filling, reducing left heart cardiac output and thus decreasing systemic pressure (increasing the “pulsus paradoxus”). As a person exhales, right ventricular filling decreases and the left heart fills causing the interventricular septum to bulge to the right impairing right ventricular filling. The diastolic pressures are elevated and equal since every cardiac chamber pressure influences the other considering the heart is not able to expand as mentioned above.
Right ventricular infarction: This can occur simultaneously with an inferior STEMI since the right coronary artery supplies the right ventricle. Acute right ventricular failure can occur leading to hypotension and cardiogenic shock. Since the right ventricle is not able to contract, the cardiac hemodynamics become “preload dependant”. If preload is high enough, blood can be “forced” through the right heart. Nitrates decrease preload by venodilation and can cause profound hypotension in the setting of right ventricular infarction. The treatment of choice is IV fluids to help increase preload. A right-sided ECG will show ST elevation and should be done in all inferior STEMI patients.
Aortic dissection: During ascending aortic dissection, the right coronary ostium may be involved causing an inferior STEMI. This is relatively uncommon, however must be recognized quickly as surgical intervention is crucial for survival.
Systolic heart failure: The left ventricular systolic dysfunction can results after STEMI can cause chronic systolic congestive heart failure (see review on Congestive Heart Failure - Systolic).
No-reflow: When coronary angiography is performed late after symptom onset during STEMI, there is a risk of “no-reflow” or “microvascular obstruction”. This results in significant decrease in forward blood flow in the coronary circulation despite the major vessel remaining patent. Since the distal, smaller vascular bed is occluded with thrombus, there is no circulatory channel for the blood to leave the coronary arteries. Catheter-based thrombus aspiration (thrombectomy) can help prevent no-reflow, although data is limited. More aggressive use of glycoprotein IIb/IIIa inhibitors may help as well, although again data is limited. The presence of no-reflow does predict worse outcomes after STEMI.
Dressler’s Syndrome: Dressler’s syndrome (a.k.a. post-myocardial infarction syndrome) is an autoimmune phenomenon that can occur after myocardial infarction and manifests 2-3 weeks later as pericarditis and a pericardial effusion. The diagnosis is clinical and based on ECG changes of pericarditis. Treatment includes aspirin and colchicine to decrease inflammation. Anticoagulation should be avoided in order to prevent hemorrhage into the pericardium and cardiac tamponade.
Pregnancy: ST elevation myocardial infarction is rare during pregnancy however can occur. Atherosclerotic plaque rupture in those with typical risk factors is the most common etiology. Spontaneous coronary dissection risk is increased during pregnancy as well. Percutaneous coronary intervention is the primary treatment option as thrombolytics and glycoprotein IIb/IIIa inhibitors are contraindicated during pregnancy.
Mimicking STEMI: Many disorders can mimic STEMI in both the symptomatic presentation and the ECG findings. Remember STEMI is an acute coronary syndrome which implies an unstable atherosclerotic plaque and thrombosis. Other disorders that can cause anginal symptoms and ischemic ST elevation on the ECG, but are not from atherosclerotic plaque rupture include: Coronary spasm, aortic dissection, vasculitis, Takotsubo cardiomyopathy (stress-induced cardiomyopathy), radiation therapy, coronary embolus, non-cardiac chest pain with chronic ECG changes (LBBB or LVH), myocarditis, cocaine use, trauma or cardiac contusion, and congenital coronary anomalies.
Non-steroidal anti-inflammatory drugs (NSAIDs): These agents (ibuprofen, naproxen, rofecoxib) have many negative effects on the heart during and after STEMI. They can interfere with the beneficial actions of aspirin, increase the risk of myocardial infarction (COX-2 selective inhibitors), exacerbate heart failure, and increase blood pressure. These drugs should be discontinued immediately when STEMI is diagnosed.
Glucose control: Tight control of blood sugar levels has become the standard of care during acute coronary syndromes. There is currently insufficient data to support a reduction in morbidity or mortality with more intensive control (insulin drips) at this time.