Ischaemic heart disease and stroke are among the most common causes of death and disability in the world. The Indian subcontinent (including India, Pakistan, Bangladesh, Sri Lanka, and Nepal) has among the highest rates of cardiovascular disease (CVD) globally. Previous reports have highlighted the high CVD rates among South Asian immigrants living in Western countries, but the enormous CVD burden within the Indian subcontinent itself has been underemphasized. In this review, we discuss the existing data on the prevalence of CVD and its risk factors in the Indian subcontinent. We also review recent evidence indicating that the burden of coronary heart disease in the Indian subcontinent is largely explained on the basis of traditional risk factors, which challenges the common thinking that South Asian ethnicity per se is a strong independent risk factor for coronary heart disease. Finally, we suggest measures to implement in policy, capacity building, and research to address the CVD epidemic in the Indian subcontinent.

Cerebral malaria is the most common cause of non-traumatic encephalopathy in the world. The mainstay of therapy is either quinine or artemisinin, both of which are effective antimalarials. The clinical picture of cerebral malaria may persist or even become worse in spite of the clearance of parasites from blood. The death rate is unacceptably high even with effective antimalarials in tertiary care hospitals. The mortality increases in presence of multi organ failure (renal failure, jaundice, respiratory distress, severe anaemia, lactic acidosis, etc.). The pathogenesis of cerebral malaria is multifactorial and includes clogging, sequestration, rosette formation, release of cytokines, cerebral oedema, increased intracranial hypertension, etc. Attempts are made to use adjuvant therapy which will act through alternate mechanisms and address one or more of the pathogenetic processes. In this review, we have discussed the role of corticosteroids, pentoxifylline, desferrioxamine, mannitol and newer agents in the treatment of cerebral malaria. Though the literature on adjuvant therapy in cerebral malaria is large enough, there are a number of shortcomings in the clinical trials, many being open and non randomized or of very small sample size. Further research is of utmost importance through large multicentric, double-blind controlled trials to show the efficacy of any of these drugs.

Nicotine is one of many substances that may be acquired through active and passive smoking of tobacco. In man, nicotine is commonly consumed via smoking cigarettes, cigars or pipes. The addictive liability and pharmacological effects of smoking are primarily mediated by the major tobacco alkaloid nicotine. High stress jobs favour repeated smoking and further reinforce addictive behaviours. There are elevated serum cadmium and lead levels in smokers resulting in glomerular dysfunction. Nephropathies are accelerated by nicotine with an increased incidence of microalbuminuria progressing to proteinuria, followed by type-1 diabetes mellitus induced renal failure. Cigarette smoke-induced renal damage is due, at least in part, to activation of the sympathetic nervous system resulting in an elevation in blood pressure. Ethanol, nicotine, or concurrent intake significantly increases lipid peroxidation in liver, and decreased superoxide dismutase activity and increased catalase activity in the kidney. This review describes the effects of nicotine, smoking, smoke extracts and other tobacco constituents on renal and cardiovascular functions, and associated effects on the nervous system. Both active and passive smoking is toxic to renal function.