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A hub-and-spoke model in South India improved STEMI care through greater use of PCI and may improve 1-year mortality. This model may serve as an example for developing STEMI systems of care in other low- to middle-income countries.

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Background:Catestatin is emerging as a novel regulator of cardiovascular/metabolic functions. Results: We discovered a common amino acid substitution variant of catestatin that caused profound changes in plasma catecholamines, glucose, and lipid levels. Conclusion: Naturally occurring variants of catestatin peptide seem to alter the risk for metabolic syndrome. Significance: These findings provide new insights into the mechanism of metabolic diseases in humans.

The prevalence of coronary artery disease and STelevation myocardial infarction (STEMI) are increasing in India. Although recent publications have focused on improving preventive measures in developing countries, less attention has been placed on the acute management of STEMI. Recent policy changes in India have provided new opportunities to address existing barriers but require greater investment and support in the coming years.Coronary artery disease (CAD) is currently the most common, non-infectious disease in India and will affect over 65 million of its people by the year 2015. 1 One of the gravest complications of CAD is ST-elevation myocardial infarction (STEMI), a lifethreatening medical emergency that results from a sudden, occlusive thrombus in the coronary artery. When STEMI patients are treated promptly with reperfusion therapy, significant reductions in mortality and morbidity are possible. 2 3 Unfortunately, the overall use and quality of acute reperfusion therapy in India lags significantly behind North America and Europe.In this paper, we discuss the current state of STEMI care in India and argue for greater investment in acute reperfusion therapy. Although recent publications have focused appropriately on improving preventive measures for CAD in India, 4e6 less attention has been placed on the acute management of STEMI, or in particular, how 'systems of care' approaches, popularised in North America and Europe, may be implemented. 7 8 We specifically highlight recent policy changes that provide new opportunities to address existing barriers and briefly describe a 'real-world' example of a STEMI systems of care programme initiated in the southern Indian state of Tamilnadu.

All three modes of diuretic therapies can be practiced with no difference in worsening of renal function and electrolyte levels. Bolus dose administration with its rapid volume loss and shorter hospital stay might be a more effective diuretic strategy.

With effective hospital strategies, the DTB time of 90 min can be achieved in majority of patients. The chief delay in DTB time in this study was due to a delay in obtaining consent and financial reasons.

Catestatin (CST), an endogenous anti-hypertensive/anti-adrenergic peptide, is a novel regulator of cardiovascular physiology. Here, we report case-control studies in two geographically/ethnically-distinct Indian populations (n≈4000) that showed association of the naturally-occurring human CST-Gly364Ser variant with increased risk for hypertension (age-adjusted odds ratios: 1.483, p=0.009 and 2.951, p=0.005). Consistently, 364Ser allele carriers displayed elevated systolic (up to ~8 mmHg, p=0.004) and diastolic (up to ~6 mmHg, p=0.001) blood pressure. The variant allele was also found to be in linkage disequilibrium with other functional SNPs in the CHGA promoter and nearby coding region. Functional characterization of the Gly364Ser variant was carried out using cellular/molecular biological experiments (viz. peptide-receptor binding assays, nitric oxide [NO], phospho extracellular regulated kinase [ERK] and phospho endothelial nitric oxide synthase [eNOS] estimations) and computational approaches (molecular dynamics simulations for structural analysis of wild-type [CST-WT] and variant [CST-364Ser] peptides, and docking of peptide/ligand with beta-adrenergic receptors [ADRB1/2]). CST-WT and CST-364Ser peptides differed profoundly in their secondary structures and showed differential interactions with ADRB2; while CST-WT displaced the ligand bound to ADRB2, CST-364Ser failed to do the same. Furthermore, CST-WT significantly inhibited ADRB2-stimulated ERK activation suggesting an antagonistic role on ADRB2 unlike CST-364Ser. Consequently, CST-WT was more potent in NO production in human-umbilical-vein-endothelial-cells as compared to CST-364Ser. This NO producing ability of CST-WT was abrogated by ADRB2 antagonist ICI 118551. In conclusion, CST-364Ser allele enhanced the risk for hypertension in human populations, possibly via diminished endothelial NO production due to altered interactions of CST-364Ser peptide with ADRB2 as compared to CST-WT.