Chapter 21 Marini Acute Coronary Syndromes

466

SECTION II • Medical and Surgical Crises

rupture or VSD; 10% of MI deaths result from free wall rupture. Most myocardial ruptures are early events; half occur within 4 days and almost all occur within 2 weeks after AMI. Hypertension accentu- ates wall stress and contributes to muscle disruption at the border of the normal and infarcted tissue. Ventricular rupture is most likely in elderly patients with extensive transmural damage and little col- lateral flow. Late fibrinolysis may hasten the occur- rence of perforation. The clinical presentation of wall rupture usually is one of recurrent chest pain rapidly followed by neck vein distension, paradoxi- cal pulse, shock, and death. ECG may show recur- rent ST elevation or may not show any change at all. Differential diagnosis includes pericardial tampon- ade, tension pneumothorax, and massive muscle damage. Immediate thoracotomy must follow tem- porary stabilization with volume expansion, transfu- sion, and pericardiocentesis. Echocardiography may visualize a defect of the LV wall, free pericardial fluid, and diastolic right-sided cardiac collapse. Cardiac catheterization is not feasible for most patients and delays definitive surgical therapy, which is perhaps the only hope in many patients with this condition. Systemic Embolism The incidence of mural thrombi and arterial embo- lism may reach 30% in selected subsets of patients with MI. Large infarctions, particularly those involving the anterior and apical segments of the LV, predispose systemic embolism. Systemic embo- lism is less common now that many patients receive heparin and aspirin (with or without thrombolytic therapy) for AMI therapy. Patients with large infarc- tions, mural thrombi, or overtly dyskinetic segments on echocardiography should be anticoagulated, unless compelling contraindications exist. Role of ICD in Myocardial Infarction Patients who demonstrate sustained or nonsus- tained VT after the first 48 hours of AMI are at increased risk of SCD during and after discharge from hospital. Severe LV systolic dysfunction is also a marker of risk for SCD. An ICD device is implanted just like a pacemaker, and in fact, most of the currently available ICD models can also pace the heart for bradycardia. The ICD device monitors the rhythm, and if the patient goes into rapid VT, it is programmed to perform antitachycardia pacing, followed by delivery of DC shock if needed. If the

patient drops into VF, it will deliver a shock immedi- ately. The risk of SCD can be reduced significantly after revascularization and with use of adequate medical therapies ( β -blocker, antiplatelet agents [clopidogrel and aspirin], statins, ACEI, and pos- sibly also fish oils). The MADIT-1, MADIT-2, and MUSTT trials have helped form some guidelines for ICD implantation in post-MI patients. The following are the guidelines for use of an ICD device following an MI: 1. Resuscitated VT/VF arrest after the first 48 hours of an MI 2. LV ejection fraction less than 35%, nonsus- tained VT on monitor, and inducible, nonsup- pressible VT on EP study 3. LV ejection fraction less than 30% on echocar- diography 1 month after MI, especially if the QRS duration is greater than 0.12 second Incessant VT/VF episodes, those with class IV CHF, and those with other severe comorbid condi- tions (terminal cancer, lung, or liver disease) are con- sidered contraindications for the ICD. Those with ischemic cardiomyopathy should ideally undergo revascularization procedures first (if they are can- didates) and later be reevaluated for ICD. Patients who have suffered a large MI should undergo repeat echocardiography and possibly also 24- or 48-hours Holter monitoring 1 to 3 months after the event. SUGGESTED READINGS Bhatt DL, Hulot JS, Moliterno DJ, Harrington RA. Antiplatelet and anticoagulation therapy for acute coro- nary syndromes. Circ Res. 2014;114(12):1929-1943. Boudoulas KD, Triposciadis F, Geleris P, Boudoulas H. Coronary atherosclerosis: pathophysiologic basis for diagnosis and management. Prog Cardiovasc Dis. 2016;58(6):676-692. Chew DP, Scott IA, Cullen L, et al.; NHFA/CSANZ ACS Guideline 2016 Executive Working Group. National Heart Foundation of Australia & Cardiac Society of Australia and New Zealand: Australian clinical guide- lines for the management of acute coronary syndromes 2016. Heart Lung Circ. 2016;25(9):895-951. De Caterina R, Husted S, Wallentin L, et al. Oral antico- agulants in coronary heart disease (Section IV). Position paper of the ESC working group on thrombosis— Task force on anticoagulants in heart disease. Thromb Haemost. 2016;115(4):685-711. Gupta R, Munoz R. Evaluation and management of chest pain in the elderly. Emerg Med Clin North Am. 2016;34(3):523-542. Hollander JE, Than M, Mueller C. State-of-the-art evalu- ation of emergency department patients presenting with