Background-Although the recent surgical treatment of ischemic heart failure substudy reported that revascularization of viable myocardium did not improve survival, these results were limited by the viability imaging technique used and the lack of inducible ischemia information. We examined the relative impact of stress-rest rubidium-82/F-18 fluorodeoxyglucose positron emission tomography identified ischemia, scar, and hibernating myocardium on the survival benefit associated with revascularization in patients with systolic dysfunction. Methods and Results-The extent of perfusion defects and metabolism-perfusion mismatch was measured with an automated quantitative method in 648 consecutive patients (age, 65±12 years; 23% women; mean left ventricular ejection fraction, 31±12%) undergoing positron emission tomography. Follow-up time began at 92 days (to avoid waiting-time bias); deaths before 92 days were excluded from the analysis. During a mean follow-up of 2.8±1.2 years, 165 deaths (27.5%) occurred. Cox proportional hazards modeling was used to adjust for potential confounders, including a propensity score to adjust for nonrandomized treatment allocation. Early revascularization was performed within 92 days of positron emission tomography in 199 patients (33%). Hibernating myocardium, ischemic myocardium, and scarred myocardium were associated with all-cause death (P=0.0015, 0.0038, and 0.0010, respectively). An interaction between treatment and hibernating myocardium was present such that early revascularization in the setting of significant hibernating myocardium was associated with improved survival compared with medical therapy, especially when the extent of viability exceeded 10% of the myocardium. Conclusions-Among patients with ischemic cardiomyopathy, hibernating, but not ischemic, myocardium identifies which patients may accrue a survival benefit with revascularization versus medical therapy. (Circ Cardiovasc Imaging. 2013;6:363-372)

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Background Data comparing outcomes in heart failure ( HF ) across Asia are limited. We examined regional variation in mortality among patients with HF enrolled in the ASIAN ‐HF (Asian Sudden Cardiac Death in Heart Failure) registry with separate analyses for those with reduced ejection fraction ( EF ; <40%) versus preserved EF (≥50%). Methods and Results The ASIAN ‐ HF registry is a prospective longitudinal study. Participants with symptomatic HF were recruited from 46 secondary care centers in 3 Asian regions: South Asia (India), Southeast Asia (Thailand, Malaysia, Philippines, Indonesia, Singapore), and Northeast Asia (South Korea, Japan, Taiwan, Hong Kong, China). Overall, 6480 patients aged >18 years with symptomatic HF were recruited (mean age: 61.6±13.3 years; 27% women; 81% with HF and reduced r EF ). The primary outcome was 1‐year all‐cause mortality. Striking regional variations in baseline characteristics and outcomes were observed. Regardless of HF type, Southeast Asians had the highest burden of comorbidities, particularly diabetes mellitus and chronic kidney disease, despite being younger than Northeast Asian participants. One‐year, crude, all‐cause mortality for the whole population was 9.6%, higher in patients with HF and reduced EF (10.6%) than in those with HF and preserved EF (5.4%). One‐year, all‐cause mortality was significantly higher in Southeast Asian patients (13.0%), compared with South Asian (7.5%) and Northeast Asian patients (7.4%; P <0.001). Well‐known predictors of death accounted for only 44.2% of the variation in risk of mortality. Conclusions This first multinational prospective study shows that the outcomes in Asian patients with both HF and reduced or preserved EF are poor overall and worst in Southeast Asian patients. Region‐specific risk factors and gaps in guideline‐directed therapy should be addressed to potentially improve outcomes. Clinical Trial Registration URL : https://www.clinicaltrials.gov/ . Unique identifier: NCT 01633398.

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ECHOCARDIOGRAPHY IS THE USUAL INITIAL TEST IN DYSPNEIC PATIENTS, but its application to right ventricular (RV) analysis is challenging. RV evaluation involves 3 steps, starting with quantification of afterload and pre-load. RV afterload is assessed by measurement of pulmonary artery systolic pressure (PASP) from tricuspid regurgitation (TR) velocity and right atrial pressure; pulmonary regurgitation velocity can also be used to assess pulmonary artery (PA) diastolic and mean PA pressure. Estimation of pulmonary vascular resistance (PVR) is useful if RV function is impaired. The second step is to assess the mechanism and severity of TR. For quantification of RV performance, we usually use 1 conventional (tricuspid annular plane systolic excursion [TAPSE], fractional area change [FAC], or right ventricular index of myocardial performance [RIMP]) and 1 novel method (pulsed wave or color Doppler tissue imaging systolic velocity [s'], or strain imaging). RV volumes may be measured using 3-dimensional echocardiography (Fig. 1, Table 1).Case 1-RV dysfunction with increased PASP and PVR. When RV dysfunction occurs in the setting of left ventricular dysfunction and mitral regurgitation, it may be due to myocardial disease or pulmonary hypertension (PHT). The patient shown in Figure 2 has elevation of both PASP and PVR.There is severe TR with tricuspid annular dilatation (Fig. 3). Although RV parameters show that RV systolic function is impaired (Fig. 4), this is in the context of increased afterload and pre-load. Case 2-preserved RV systolic function with increased PASP and normal PVR.In patients with right heart failure and severe tricuspid regurgitation, the latter may be secondary from PHT or a primary valvular abnormality. Despite mild elevation of PASP to 44 mm Hg (Fig. 5), PVR was normal (1.3 Wood units). There is severe TR with apical displacement of the septal leaflet and coaptation point (Fig. 6). The RV is volume loaded but RV systolic function is normal (Fig. 7).Case 3-RV dysfunction with normal PASP and increased PVR. Reduced stroke volume caused by RV dysfunction may compromise the assessment of RV afterload. Increased PA resistance (Fig. 8) is not apparent from PASP because forward RV stroke volume is reduced by severe TR (Fig. 9) and RV dysfunction (Fig. 10).