Endothelial dysfunction is a key triggering event in atherosclerosis. Following the entry of lipoproteins into the vessel wall, their rapid modification results in the generation of advanced glycation endproduct epitopes and subsequent infiltration of inflammatory cells. These inflammatory cells release receptor for advanced glycation endproduct (RAGE) ligands, specifically S100/calgranulins and high-mobility group box 1, which sustain vascular injury. Here, we demonstrate critical roles for RAGE and its ligands in vascular inflammation, endothelial dysfunction, and atherosclerotic plaque development in a mouse model of atherosclerosis, apoE -/-mice. Experiments in primary aortic endothelial cells isolated from mice and in cultured human aortic endothelial cells revealed the central role of JNK signaling in transducing the impact of RAGE ligands on inflammation. These data highlight unifying mechanisms whereby endothelial RAGE and its ligands mediate vascular and inflammatory stresses that culminate in atherosclerosis in the vulnerable vessel wall.

Aims Limited data on the uptake of guideline-directed medical therapies (GDMTs) and the mortality of acute decompensated HF (ADHF) patients are available from India. The National Heart Failure Registry (NHFR) aimed to assess clinical presentation, practice patterns, and the mortality of ADHF patients in India. Methods and resultsThe NHFR is a facility-based, multi-centre clinical registry of consecutive ADHF patients with prospective follow-up. Fifty three tertiary care hospitals in 21 states in India participated in the NHFR. All consecutive ADHF patients who satisfied the European Society of Cardiology criteria were enrolled in the registry. All-cause mortality at 90 days was the main outcome measure. In total, 10 851 consecutive patients were recruited (mean age: 59.9 years, 31% women). Ischaemic heart disease was the predominant aetiology for HF (72%), followed by dilated cardiomyopathy (18%). Isolated right HF was noted in 62 (0.6%) participants. In eligible HF patients, 47.5% received GDMT. The 90 day mortality was 14.2% (14.9% and 13.9% in women and men, respectively) with a re-admission rate of 8.4%. An inverse relationship between educational class based on years of education and 90 day mortality (high mortality in the lowest educational class) was observed in the study population. Patients with HF with reduced ejection fraction and HF with mildly reduced ejection fraction who did not receive GDMT experienced higher mortality (log-rank P < 0.001) than those who received GDMT. Baseline educational class, body mass index, New York Heart Association functional class, ejection fraction, dependent oedema, serum creatinine, QRS > 120 ms, atrial fibrillation, mitral regurgitation, haemoglobin levels, serum sodium, and GDMT independently predicted 90 day mortality. Conclusion One of seven ADHF patients in the NHFR died during the first 90 days of follow-up. One of two patients received GDMT. Adherence to GDMT improved survival in HF patients with reduced and mildly reduced ejection fractions. Our findings call for innovative quality improvement initiatives to improve the uptake of GDMT among HF patients in India.

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Pheochromocytoma patients can rarely have prolonged QT interval in the ECG. We report three cases of pheochromocytoma in females presenting with ventricular arrhythmia; two had torsades de pointes and a third patient had frequent VPCs and nonsustained ventricular tachycardia. All the patients were treated with surgical removal of the tumor with complete relief of symptoms and normalization of QT interval.