Obese patients who took fenfluramine and phentermine, dexfenfluramine alone, or dexfenfluramine and phentermine had a significantly higher prevalence of cardiac valvular insufficiency than a matched group of control subjects.

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Pulmonary pulse wave transit time (pPTT), defined as the time for the systolic pressure pulse wave to travel from the pulmonary valve to the pulmonary veins, has been reported to be reduced in pulmonary arterial hypertension (PAH); however, the underlying mechanism of reduced pPTT is unknown. Here, we investigate the hypothesis that abbreviated pPTT in PAH results from impaired right ventricular-pulmonary artery (RV-PA) coupling. We quantified pPTT using pulsed-wave Doppler ultrasound from 10 healthy age-and sexmatched controls and 36 patients with PAH. pPTT was reduced in patients with PAH compared with controls. Univariate analysis revealed the following significant predictors of reduced pPTT: age, right ventricular fractional area change (RV FAC), tricuspid annular plane excursion (TAPSE), pulmonary arterial pressures (PAP), diastolic pulmonary gradient, transpulmonary gradient, pulmonary vascular resistance, and RV-PA coupling (defined as RV FAC/mean PAP or TAPSE/mean PAP). Although the correlations between pPTT and invasive markers of pulmonary vascular disease were modest, RV FAC (r = 0.64, P < 0.0001), TAPSE (r = 0.67, P < 0.0001), and RV-PA coupling (RV FAC/mean PAP: r = 0.72, P < 0.0001; TAPSE/mean PAP: r = 0.74, P < 0.0001) had the strongest relationships with pPTT. On multivariable analysis, only RV FAC, TAPSE, and RV-PA coupling were independent predictors of pPTT. We conclude that shortening of pPTT in patients with PAH results from altered RV-PA coupling, probably occurring as a result of reduced pulmonary arterial compliance. Thus, pPTT allows noninvasive determination of the status of both the pulmonary vasculature and the response of the RV in patients with PAH, thereby allowing monitoring of disease progression and regression.Keywords: pulse wave velocity, right ventricular-pulmonary artery coupling, echocardiography. Pulmonary arterial hypertension (PAH) is a lethal disease, characterized by pathological pulmonary vascular remodeling, that leads to elevated pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR), decreased pulmonary arterial compliance, and eventual right ventricular failure and death.1,2 Growing evidence suggests that pulmonary arterial compliance plays a critical role in the pathogenesis of PAH and right ventricular failure. 3 Decreased pulmonary arterial compliance causes premature reflection of waves from the distal pulmonary vasculature, leading to increased pulsatile right ventricular afterload and altered right ventricular-pulmonary artery (RV-PA) coupling. 3-5 Both loss of pulmonary arterial compliance and impaired RV-PA coupling are clinically important, because they are associated with increased mortality in patients with pulmonary hypertension. 6-11Pulse wave velocity, defined as the velocity of pressure waves traveling through the arterial system, correlates inversely with arterial compliance in the systemic circulation.12 With decreasing compliance, pulse wave velocity increases, and the time taken by the pressure wave to travel between...

Background: The relationship of routine postoperative troponin I (TnI) monitoring in kidney transplant recipients and in-hospital myocardial infarction (MI) is not known. Methods: This observational study evaluated the prevalence of abnormal postoperative TnI (Ortho Clinical Diagnostics assay) in 376 consecutive kidney or kidney/pancreas transplant recipients. In-hospital MI was adjudicated using the universal definition. Rates of death and coronary revascularizations at 1 year were studied. Logistic regression analysis was performed to identify independent predictors of abnormal TnI. Results: Ninety-five (25%) recipients had abnormal TnI (>0.04 ng/ml) following transplantation. Abnormal TnI levels were more common in older (mean age: 52.2 ± 13.4 vs. 48.3 ± 13.2 years, p = 0.01), diabetic (57.9 vs. 45.6%, p = 0.04), and prior coronary artery disease (31.6 vs. 20.3%, p = 0.02) patients. In-hospital MI occurred in 6 patients (1.6%). All subsequent in-hospital cardiovascular events occurred in the abnormal postoperative TnI group; most in those with TnI levels >1 ng/ml. Previous coronary artery disease was the only independent predictor of a postoperative TnI level >1 ng/ml in multivariate analysis (odds ratio 4.61, 95% confidence interval 1.49–14.32). At 1 year there was no significant difference in death (3.2 vs. 1.8%, p = 0.42) and borderline significant difference in coronary revascularization (5.3 vs. 1.4%, p = 0.049) in abnormal versus normal TnI groups. Conclusions: In-hospital MI was infrequent, but abnormal TnI highly prevalent following renal transplantation. Normal TnI levels following renal transplantation had a high negative predictive value in excluding patients likely to develop subsequent postoperative MI. The role of a higher TnI cut-off for screening for postoperative MI in high-risk subgroups deserves future prospective evaluation.

Abstracts S357occasional development of LV-failure in PAH patients after bLTx. The creation of an ASD to relief RV pressure overload may offer a training period for the LV prior to bLTx and thereby avoiding the development of LV-failure. ( 995)Purpose: Diagnosis and assessment of therapeutic response in pulmonary hypertension (PH) are largely determined invasively using right heart catheterization, as there are few noninvasive methods available. Recently, reduced echocardiographically-calculated pulmonary pulsewave transit time (pPTT) was documented in PH patients, but the determinants were not elucidated. Here, we investigated the hypothesis that abbreviated pPTT is a non-invasive marker of intrinsic pulmonary vascular disease in PH. Methods: We retrospectively analyzed echocardiograms from ten healthy control and 62 PH patients to quantify pPTT, the time needed for the pressure pulse wave to travel from the pulmonary valve to the pulmonary veins. Univariate and multivariate analysis was performed to define predictors of pPTT. Finally, we determined whether right ventricular (RV) size and function were associated with pPTT. Results: We observed a significant reduction in pPTT in PH patients when compared to normal controls. Univariate analysis revealed diabetes, hemoglobin, serum creatinine, RV size and function, diastolic pulmonary gradient (DPG), transpulmonary gradient (TPG), and pulmonary vascular resistance (PVR) as significant predictors of pPTT. After correcting for age and gender, the association between pPTT and hemoglobin, serum creatinine, RV function, DPG, and PVR remained significant. Correlational analysis revealed inverse relationships between pPTT and DPG, TPG, and PVR, and the relationships between pPTT and DPG and TPG were stronger in the WHO Group 1 patients. Finally, pPTT was shortest in patients with severe RV dilation and dysfunction. Conclusion: Our results suggest pPTT is a noninvasive marker of intrinsic pulmonary vascular disease in PH.