Complications
Arrhythmias (e.g., ventricular ectopy, atrial fibrillation, brady- or tachyarrhythmias, ventricular fibrillation [VF], or ventricular tachycardia [VT]) occur from injury to the cardiac conduction system. They may cause sudden death or induce cardiogenic shock.[150] Bradycardia is often seen in right-sided or posterior infarction.
The incidence of VF is <2%. The majority of VT/VF occurs within the first 48 hours after admission.[151]
Electrolyte abnormalities should be monitored and corrected. Cardioversion or antiarrhythmic therapy may be needed. In patients with heart block or symptomatic bradycardia, transcutaneous or transvenous pacing may be required.
CHF in the acute setting develops in about 8% of patients. It is most often secondary to compromised left ventricular function from a large ischemic event. Pump failure often results in pulmonary edema, hypotension, and oliguria.
CHF requires prompt diagnosis and aggressive stabilization to prevent progression to shock. Therapy includes diuresis, vasodilators, and staged pharmacotherapy (e.g., ACE inhibitors).
Develops in 4.5% of acute myocardial infarction (MI).[147] NSTEMI accounts for approximately 20% of cardiogenic shock complicating MI. Typically, it occurs after a massive MI or repeated ischemic events, and it is predominantly caused by left ventricular failure.[148] Median time to development is about 7 hours. Associated mortality is 70% to 80%, with an in-hospital mortality of 59%.[148][149]
Cardiogenic shock requires urgent percutaneous coronary intervention or CABG surgery if not already carried out. The patient needs intensive care and pressor support and may need intra-aortic balloon pump counterpulsation or other circulatory assist devices as a bridge toward definitive therapy.
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Occurs in 1% to 3% of all infarcts (STEMI more than NSTEMI), usually secondary to a weakened necrotic wall.[148] It is associated with CHF, right-sided heart failure, pulmonary edema, or cardiogenic shock. Glucocorticoid administration has been associated with slightly higher risk of rupture.
Prompt diagnosis is the key to treatment of ventricular rupture or aneurysm. Therapy includes management of complications (CHF or shock). Small ruptures can be managed without surgery. Larger ruptures need surgery but the timing of surgery is controversial.
Most often secondary to papillary muscle rupture or acute left ventricle dilation. Acute mitral regurgitation predominantly occurs after inferior infarction.
Complete papillary muscle ruptures need emergency surgical correction. Moderate to severe mitral regurgitation in association with left ventricular dysfunction is acutely managed as CHF.
Dressler syndrome is mediated by inflammatory byproducts and the formation of ischemic myocardium. Inflammation involves the pericardium and is treated with nonsteroidal anti-inflammatory drugs or colchicine (preferably colchicine as it may reduce the risk of recurrence). If hemodynamic compromise is present, pericardiocentesis or surgical intervention is required.
MI has been associated with an increased risk of VTE, particularly for pulmonary embolism.[152]
A risk factor for cardiovascular disease, but an acute cardiovascular event can also precipitate depression in patients without prior psychiatric conditions.[46] Data suggest that a combined psychosocial approach to the treatment of depression improves outcome in patients. Exercise combined with pharmacotherapy may be the most efficacious approach.[45]
Often precipitated by cessation of dual antiplatelet therapy. Occurs more frequently with drug-eluting stents.[138]
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