Chapter 21 Marini Acute Coronary Syndromes

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CHAPTER 21 • Acute Coronary Syndromes

a 24-hours mortality rate near 70%. MR typically occurs 2 to 10 days after posterior or inferior MI and should be suspected in any patient with MI develop- ing a new murmur (often at the cardiac apex). The murmur of MR is often unimpressive; there- fore, a high degree of suspicion should be maintained anytime a patient rapidly develops symptoms of left ventricular failure, especially when normal systolic function seems preserved. Regurgitant flow is great- est after papillary muscle rupture and less intense when dysfunction is caused by ischemia without structural damage. The diagnosis may be confirmed by echocardiography or pulmonary artery catheter- ization. Echocardiography (especially transesopha- geal studies) may reveal a hyperdynamic (unloaded) LV and flail mitral leaflet. (The surface echocar- diogram may fail to detect small valvular defects.) Doppler studies may demonstrate the regurgitant left atrial jet. Invasive monitoring is indicated in almost all patients with MI who develop a new mur- mur, particularly if pulmonary congestion is present. Although pulmonary artery pressure tracings usually reveal large V waves produced by retrograde flow of blood across an incompetent mitral valve, V waves are much more sensitive than specific. VSD, mitral stenosis, or severe heart failure occasionally mimics MR by producing large V waves. The primary objective in treating acute MR is to reduce left ventricular impedance (afterload). For stable patients with mild MR, LV afterload reduc- tion may be sufficient. However, when florid pul- monary edema follows papillary muscle rupture, vasodilators (nitroprusside, nicardipine, or NTG) and intra-aortic balloon pumping should be fol- lowed immediately by surgery. Ventricular Septal Defect The ventricular septum ruptures in approximately 2% of all MIs. Predisposing factors for postinfarc- tion VSD include an anterior–septal MI, hyper- tension, female gender, advanced age, and first infarction. VSD-related, left-to-right shunting reduces effective output and causes pulmonary edema. The anterior portion of the interventricular septum is supplied predominantly by a single vessel (the LAD), whereas the posterior portion is fed col- laterally by several sources. Therefore, postinfarc- tion VSD usually is a consequence of an anterior MI that involves the LAD. Conversely, VSD develop- ing after a (true) posterior MI is a marker of diffuse multivessel disease and carries a worse prognosis.

For most patients, physical examination reveals biventricular heart failure and a new murmur. The new murmur usually is loud, harsh, holosystolic, and of maximal intensity at the left lower sternal bor- der. An accompanying thrill is common. Pulmonary artery catheterization demonstrates a step-up in hemoglobin saturation between the right atrium and pulmonary artery (usually >10%). Diagnosis also can be made by left heart catheterization dem- onstrating movement of contrast from the LV to the RV. Hemodynamic compromise and magnitude of the left-to-right shunt parallel the size of the defect. Echocardiography may demonstrate a VSD, par- ticularly if Doppler techniques and transesophageal imaging are used. A “bubble” echocardiogram (with agitated saline or optisonic contrast) occasionally shows bidirectional ventricular flow. Therapy for a VSD depends on systemic and pulmonary capillary wedge pressures. Hypotensive patients with a low wedge pressure should receive fluids initially. If the blood pressure is maintained adequately and the wedge pressure is lower than 18 mm Hg, semielective surgical repair should be undertaken. Vasodilators may be useful if blood pressure remains adequate despite a low cardiac out- put and an elevated wedge pressure. If the patient is hypotensive with a high wedge pressure, temporary support by balloon pumping, inotropes, and vasodi- lators should precede immediate surgical correction. An increasingly sophisticated array of inter- ventional devices (e.g., Amplatzer [Abbott Vascular, Santa Clara CA, USA], CardioSEAL [NMTMedical, Boston MA, USA]) is now available for percutaneous closure of a VSD. This alternative is an attractive alternative to surgery, especially in the most severely ill patients, for whom the surgical risk remains intimidatingly high. Historically, the outcome of post-MI VSD has been very poor, with mortality mounting to approxi- mately 90% at 2 months. However, the long-term results in patients undergoing successful early repair are excellent. Therefore, surgical repair at the earliest possible time after hemodynamic stabiliza- tion is desirable. Free Wall Rupture Almost invariably, rupture of the ventricular free wall proves rapidly fatal, as the patient succumbs to tamponade physiology. Although unusual (inci- dence between 2% and 8%), ventricular rupture occurs more commonly than either papillary muscle