Epidemiological studies have demonstrated an association between low serum albumin levels and coronary heart disease and mortality. Nevertheless, the impact of a low serum albumin level during acute coronary syndrome has not yet been established. The aim of the present study was to investigate whether low serum albumin levels are associated with adverse outcomes in acute coronary syndrome. We enrolled 82 consecutive patients with acute coronary syndrome from whom venous blood for serum albumin measurement was drawn immediately upon hospital admission. Thirty-five patients had a low albumin level (hypoalbuminemia) and 47 had a normal albumin level (normoalbuminemia). In-hospital adverse outcomes (death, acute heart failure, cardiogenic shock, and reinfarction) were recorded during hospitalization in the intensive coronary care unit. The results of our study showed that the incidence of in-hospital adverse outcomes was 43%, with death occurring in 8 patients (10%). In-hospital adverse outcomes occurred more frequently in patients presenting with hypoalbuminemia, whereas mortality did not differ significantly. Univariate analysis showed that hypoalbuminemia was associated with a 2.8-fold greater risk of developing adverse outcomes. This risk was greater in the subgroup of NSTEACS (5.4-fold increased risk), but not in those with STEMI. Adjustment with other covariates revealed that hypoalbuminemia did not predict independently in-hospital adverse outcomes. It interacted with other predictors, especially Killip class II-IV, which was consistently an independent predictor of in-hospital adverse outcomes.

Backgrounds: The COngenital HeARt Disease in adult and Pulmonary Hypertension (COHARD-PH) registry is the first registry for congenital heart disease (CHD) and CHD-related pulmonary hypertension (PH) in adults in Indonesia. The study aims to describe the demographics, clinical presentation, and hemodynamics data of adult CHD and CHD-related PH in Indonesia. Methods: The COHARD-PH registry is a hospital-based, single-center, and prospective registry which includes adult patients with CHD and CHD-related PH. The patients were enrolled consecutively. For this study, we evaluated the registry patients from July 2012 until July 2019. The enrolled patients underwent clinical examination, electrocardiography, chest x-ray, 6-min walking test, laboratory measurement, and transthoracic and transesophageal echocardiography. Right heart catheterization was performed to measure hemodynamics and confirm the diagnosis of pulmonary artery hypertension (PAH). Results: We registered 1012 patients during the study. The majority were young, adult females. The majority of CHD was secundum ASD (73.4%). The main symptom was dyspnea on effort. The majority of patients (77.1%) had already developed signs of PH assessed by echocardiography. The Eisenmenger syndrome was encountered in 18.7% of the patients. Based on the right heart catheterization, 66.9% of patients had developed PAH. Patients with PAH were significantly older, had lower peripheral oxygen saturation, had lower 6-min walking distance, and higher NTproBNP. The NTproBNP level independently predicted the development of PAH among CHD. Conclusions: The COHARD-PH registry is the first Indonesian adult-CHD and CHD-related PH registry. The demographics, clinical presentation, and hemodynamics dataof this registry reflect the situation in developing countries which needs to be compared with similar registries from developed countries.

Endothelin-1 (ET-1) has been shown to be involved in human pulmonary fibrosis. However, recent clinical trials targeting the ET-1 pathway with ET-1 receptor antagonists failed to achieve beneficial outcomes. Another strategy opposing the actions of ET-1 involves the inhibition of endothelin-converting enzyme–1 (ECE-1). We hypothesize that ECE-1 inhibition exerts beneficial effects on pulmonary fibrosis. Pulmonary fibrosis was induced by instilling bleomycin intratracheally into ECE-1 heterozygous knockout mice (ECE-1+/−) and their wild-type control mice (ECE-1+/+). Lung inflammation and fibrosis were assessed on Days 7, 14, and 28 after bleomycin instillation. The activity of ECE-1 and the concentrations of its related peptides, ET-1, bradykinin, atrial natriuretic peptide (ANP), and calcitonin gene–related peptide (CGRP), were determined. ECE-1+/− mice demonstrated less lung inflammation and limited fibrosis compared with control mice. ECE-1 activity was half-reduced in ECE-1+/− mice, and this activity also altered ET-1 and CGRP concentrations, but not concentrations of bradykinin and ANP. ET-1 concentrations were found to be lower in ECE-1+/− mice after the development of fibrosis, in contrast to the unaltered concentrations during inflammation. Reduced ECE-1 activity resulted in higher CGRP concentrations, which altered the pathological functionality of the lung, indicating the activation of the CGRP pathway involving cyclic adenosine monophosphate (cAMP)/exchange protein directly activated by cAMP and cAMP/protein kinase A in ECE-1+/− mice. Bleomycin instillation on Day 14 induced the accumulation of M2 macrophages expressing CGRP receptors in ECE-1+/− mice. Our results emphasize that the in vivo ECE-1–mediated degradation of CGRP promotes the transition from lung inflammation to fibrosis. Further, our study identified M2 macrophages as the target cells of CGRP action during this transition.

Introduction: Activated platelets generate microparticles. Increased platelet microparticles occur in acute myocardial infarction (AMI) and contribute to intracoronary thrombosis and subsequent myocardial injury. This study aimed to investigate the impact of platelet microparticles on...