AimsReactive pulmonary hypertension (PH) is a severe form of PH secondary to left-sided heart failure (HF). Given the structural and functional abnormalities in the pulmonary vasculature that occur in reactive PH, we hypothesized that pulmonary artery capacitance (PAC) may be profoundly affected, with implications for clinical outcome. Methods and resultsWe studied 393 HF patients of whom 124 (32%) were classified as having passive PH and 140 (36%) as having reactive PH, and 91 patients with pulmonary arterial hypertension (PAH). Mean PAC was highest in patients without PH (4.5 ± 2.1 mL/mmHg), followed by the passive PH group (2.8 ± 1.4 mL/mmHg) and was lowest in those with reactive PH (1.8 ± 0.7 mL/mmHg) (P = 0.0001). PAC and pulmonary vascular resistance (PVR) fitted well to a hyperbolic inverse relationship (PAC = 0.25/PVR, R 2 = 0.70), with reactive PH patients dispersed almost predominantly on the flat part of the curve where a reduction in PVR is associated with a small improvement in PAC. Elevated PCWP was associated with a significant lowering of PAC for any PVR (P = 0.036). During a median follow-up of 31 months, both reactive PH [hazard ratio (HR) 2.59, 95% confidence interval (CI) 1.14-4.46, P = 0.02] and reduced PAC (HR 0.72 per 1 mL/mmHg increase, 95% CI 0.59-0.88, P = 0.001) were independent predictors of mortality.

Hybrid SPECT/CTCA imaging results in improved specificity and PPV to detect hemodynamically significant coronary lesions in patients with chest pain. Single-photon emission computed tomography/CTCA might play a potentially important role in the noninvasive diagnosis of coronary artery disease and introduce an objective decision-making tool for assessing the need for interventions in each occluded vessel.

Background-In patients with heart failure, pulmonary hypertension (PH) predicts higher risk for morbidity and mortality.However, few data are available on the prognostic implications of reactive (precapillary) PH superimposed on passive (postcapillary) PH. Methods and Results-We performed a subgroup analysis of 242 patients with acute decompensated heart failure assigned to pulmonary artery catheter placement in the Vasodilation in the Management of Acute Congestive Heart Failure trial. Patients were classified into 3 groups, using the final (posttreatment) hemodynamic measurements: (1) no PH (mean pulmonary artery pressure Յ25 mm Hg; (2) passive PH (mean pulmonary artery pressure Ͼ25, pulmonary capillary wedge pressure Ͼ15 mm Hg, and pulmonary vascular resistance Յ3 Wood units); and (3) reactive PH (mean pulmonary artery pressure Ͼ25, pulmonary capillary wedge pressure Ͼ15 mm Hg, and pulmonary vascular resistance Ͼ3 Wood units). Fifty-eight patients were classified as normal mean pulmonary artery pressure, 124 with passive PH and 60 with reactive PH. During follow-up of 6 months, 5 (8.6%), 27 (21.8%), and 29 (48.3%) deaths occurred in patients without PH, patients with passive PH, and with reactive PH, respectively (PϽ0.0001). After multivariable adjustments, reactive PH remained an independent predictor of death, with an adjusted hazard ratio of 4.8 compared with patients without PH, and 2.8 compared with patients with passive PH (95% confidence interval, 1.7 to 4.7, Pϭ0.0001). Similar results were obtained when reactive PH was defined on the basis of transpulmonary gradient. Conclusions-Reactive PH is common among patients with acute decompensated heart failure after initial diuretic and vasodilator therapy. The adverse outcome associated with PH is predominantly due to increased mortality rates in the subgroup of patients with reactive PH. (Circ Heart Fail. 2011;4:644-650.)