M. Pego

Exercise‐Induced Pulmonary Hypertension in Scleroderma Patients: A Common Finding but with Elusive Pathophysiology

Background: The etiology of exercise‐induced pulmonary hypertension (exPH) in systemic sclerosis (SSc) remains a complex task, as both left ventricle (LV) diastolic dysfunction and pulmonary vascular disease can contribute to its development. We determined the incidence of exPH in SSc and examined the association between pulmonary artery systolic pressure (PASP) and tissue Doppler‐derived indexes of pulmonary capillary wedge pressure (PCWP). Methods: Thirty‐eight patients with SSc were studied, using a cycloergometer protocol; 10 were excluded due to resting PH or absence of tricuspid regurgitation (TR); TR and mitral E‐wave velocities, LV outflow tract time‐velocity integral and LV septal E′‐wave were measured before and in peak exercise to calculate cardiac output (CO), PCWP and pulmonary vascular resistance (PVR). Results: Mean age of diagnosis was 57.9 ± 8.9 years. At a mean workload of 64 ± 29 Watts, 48% of patients increased PASP ≥ 50 mmHg. PCWP, assessed by the E/e′ ratio, did not change significantly during exercise (10.2 ± 3.1–10.0 ± 5.1; P = NS). Only 3 patients had elevations of the E/e′ ratio ≥ 13 during exercise; 2 of them had an exercise PASP ≥ 50 mmHg, yielding a proportion of exPH due to elevated LV filling pressures of 2/11 (18%). Patients with exPH had lower DLCO and had more frequently the diffuse SSc. Conclusion: The elevation of PASP during exercise in most patients of this cohort seems to be related to a reduced pulmonary vascular reserve, and not to an increase in PCWP. Further studies are warranted to determine the therapeutic, as well as prognostic implications of these findings.

Externalized biventricular implantable cardioverter-defibrillator

A 52-year-old man presented to the emergency department with externalization of a biventricular implantable cardioverter defibrillator (Figure 1). He had been admitted six months earlier with a fistula surrounding the device but left the hospital against medical advice before treatment. At admission to the emergency room his heart rate was 105 beats/min and his blood pressure was 122/96 mmHg. Cardiac auscultation revealed a systolic murmur at the apex; there were no breath sounds at the right lung base and lower limb edema was observed.

A case of cardiogenic shock with preserved ejection function.

http://dx.doi.org/10.1016/j.rce.2015.08.006 0014-2565/© 2015 Elsevier España, S.L.U. y Sociedad Española de Medic Her temperature was 36.8 ◦C, heart rate 60 beats/min nd blood pressure 85/50 mmHg; a large tongue and juguar venous distention were evident; vesicular murmur was bolished at both lung bases; and palpable cervical lymhadenopathy was present. The electrocardiogram showed first degree atrioventricular block, left bundle branch lock morphology and low QRS voltage (Fig. 1). A coronary ngiography was immediately performed and coronary diease was excluded. The patient was admitted to the intensive care unit.

Lowering Pulmonary Wedge Pressure after Heart Transplant: Pulmonary Compliance and Resistance Effect

Background Right ventricular (RV) afterload is an important risk factor for post-heart transplantation (HTx) mortality, and it results from the interaction between pulmonary vascular resistance (PVR) and pulmonary compliance (CPA). Their product, the RC time, is believed to be constant. An exception is observed in pulmonary hypertension because of elevated left ventricular (LV) filling pressures. Objective Using HTx as a model for chronic lowering of LV filling pressures, our aim was to assess the variations in RV afterload components after transplantation. Methods We retrospectively studied 159 patients with right heart catheterization before and after HTx. The effect of Htx on hemodynamic variables was assessed. Results Most of the patients were male (76%), and the mean age was 53 ± 12 years. HTx had a significant effect on the hemodynamics, with normalization of the LV and RV filling pressures and a significant increase in cardiac output and heart rate (HR). The PVR decreased by 56% and CPA increased by 86%. The RC time did not change significantly, instead of increasing secondary to pulmonary wedge pressure (PWP) normalization after HTx as expected. The expected increase in RC time with PWP lowering was offset by the increase in HR (because of autonomic denervation of the heart). This effect was independent from the decrease of PWP. Conclusions The RC time remained unchanged after HTx, notwithstanding the fact that pulmonary capillary wedge pressure significantly decreased. An increased HR may have an important effect on RC time and RV afterload. Studying these interactions may be of value to the assessment of HTx candidates and explaining early RV failure after HTx.

Platelet size deviation width measured at hospital admission predicts in-hospital mortality and all cause mortality at follow up after discharge in acute pulmonary embolism

Introduction: Platelet distribution width (PDW) directly measures the variability in platelet size and it has been postulated that large platelets may be an indi- cator of platelet activation. No data has been reported so far about the impact of this index on prognosis of acute pulmonary embolism (APE). Thus, the aim of this study was to assess the impact of PDW measured at hospital admission on both in-hospital and after discharge prognosis in patients with APE diagnosed by multislice computed tomography (MSCT).nnMethods and population: Retrospective, observational study that included all patients with APE diagnosed by MSCT during emergency room (ER) stay in the year of 2010. Blood tests, including PDW, were obtained at hospital admission. The primary endpoint was in-hospital death of all causes. The secondary endpoint was all-cause death at follow-up. A receiver operating characteristics (ROC) curve was used to test PDW as a predictor of the primary endpoint and to obtain the best cut-off point. Then we transformed PDW into a categorical variable with 2 groups and conducted a univariate regression analysis to test the strength of prediction. We then performed analysis for the secondary endpoint, testing the cutoff in a Cox regression model.nnResults: Between January and December 2010, 218 patients were diagnosed APE by MSCT (age 73±16 years, 102 males). For the outcome in-hospital mortality, area under the curve (AUC) was 0,741 (p≤ 0,001). We considered the best cut off point to be 17,55 (sensitivity 68%, specificity 78%). In the univariate regression analysis, a PDW higher than 17,55 was found to be strongly associated to worse outcome [odds ratio (OR) 7,212; 95% confidence interval (CI) 2,852–18,233; p≤0,001)]. For the outcome all cause mortality at follow up after discharge, AUC was 0,623 (p=0,01). A 17,45 cut off point was found to predict the secondary endpoint with a sensitivity of 48% and a specificity of 73%. In a Cox regression analysis, a value higher than the cut-off was associated with lower event-free survival (hazard ratio (HR) 2,52; 95% CI 1,46-4,35; p≤0,001).nnConclusion: PDW is a predictor of both in-hospital mortality and all cause mortality at follow-up after APE.