Inhibitors of the renin-angiotensin- aldosterone system should be provided as tolerated, and the indications for beta-blocker therapy should be evaluated con- tinuously throughout the hospital course. 9.3. RV Infarction RV infarction complicates the course of approximately one third of patients with inferior STEMI, is most often due to proximal occlusion of the right coronary artery, and is asso- ciated with a higher mortality risk. Evidence of RV involve- ment should be sought in all patients with inferior STEMI. The clinical triad of hypotension, clear lung fields, and elevated jugular venous pressure is characteristic. Demon- stration of 1-mm ST elevation in lead V1 and in right pre- cordial lead V4 R is the most sensitive ECG marker of RV Transthoracic echocardiography can be helpful in patients with initially nondiagnostic findings.467 Treat- ment includes maintenance of RV preload, reduction of RV afterload, inotropic support if needed, and immediate reper- Nitrates and diuretics should be avoided. Restora- tion of atrioventricular (AV) synchrony or cardioversion from AF may be needed. 9.4. Mechanical Complications Mechanical complications after STEMI have a bimodal, tem- poral distribution: Most occur in the first 24 hours, and the remainder present within the first week. The presence of a new systolic murmur indicates the possibility of either ventricle septal rupture or mitral regurgitation. Diagnosis usually can be established with transthoracic echocardiography. Surgical con- sultation should be obtained when a mechanical defect is sus- pected. Prompt repair (with or without CABG) is indicated in most cases. IABP can provide temporary circulatory support. 9.4.2. Mitral Regurgitation Mitral regurgitation after STEMI occurs via 1 of 2 mecha- nisms: papillary muscle rupture or postinfarction LV remod- eling with displacement of the papillary muscles, leaflet tethering, and annular dilatation. 