The Adverse Effects of Wealth on Cardiovascular Health: A Scientific Statement of the International College of Cardiology.

Background and Aims: Increase in economic status may be associated with increased consumption of Western type of foods and sedentary behaviour. In the present review, we discuss that increase in wealth may be associated with adverse effects on health behaviour Study Design and Methods: Internet search and discussion with colleagues. Results: Review of studies indicate that with increase in wealth, there is increased consumption of high fat, ready prepared foods and decrease in physical activity in most of the countries resulting in obesity and metabolic syndrome, leading to cardiovascular diseases (CVDs) and other chronic conditions. Many experts during the United Nations High Level Meeting in Sept 2011, misinterpreted the WHO estimates and proposed that, of total deaths, 22·4 million arise in the poorest countries, and 13.7 million in high-income and upper-middle-income countries and therefore poverty may be the major cause of deaths due to non-communicable diseases (NCDs). A recent study shows that 57.0 % of deaths in adults (aged 25-64 years) were due to CVDs and other chronic diseases, 25.5% due to communicable diseases and 15.9% due to injury and accidents. The deaths due to NCDs were highly prevalent among higher social classes compared to lower social classes who had greater deaths due to communicable diseases. It is interesting to know from new data from United States, that there is ‘Wealth’ without cardiovascular health in America. The whole world is likely to have the same scenario in the near future. Conclusions: Increase in wealth may be associated with altered health behaviour; greater consumption of unhealthy foods, tobacco consumption, mental load and sedentary behaviour resulting in increased risk of deaths due to CVDs and other chronic diseases which may change with knowledge about health education. Wealth may cause extension in life by buying of expensive drug therapy, intervention and surgery which are known to add income and employment in the west.

How brain influences neuro-cardiovascular dysfunction.

Mechanisms that may explain the association between brain-heart connection leading to abnormal heart rate variability (HRV) and blood pressure variability (BVP) resulting into increased morbidity and mortality due to cardiovascular diseases (CVD), are reviewed. Medline search till December, 2001 and articles published in various national and international journals were reviewed. Experts working in the field were also consulted. There is compelling evidence that saturated and total fat and sedentary behaviour can enhance sympathetic activity and increase the secretion of catecholamine, cortisol and serotonin, whereas omega-3 fatty acid supplementation may enhance parasympathetic activity and increase the secretion of acetylcholine in the hippocampus. While increased sympathetic activity has adverse effects on HRV and BPV, increased parasympathetic activity has beneficial effects and can directly inhibit sympathetic tone. A large body of evidence is available demonstrating that abnormal HRV measured over a 24-hour period, or for 7 days, provides information on the risk of subsequent death in subjects with and without heart disease. Meditation, beta blockers, ACE inhibitors, n-3 fatty acids, trimetazidine and oestrogen may have a beneficial influence on HRV. However, no definite and specific therapy is currently available to improve the prognosis for patients with abnormal HRV and blood pressure variability (BPV). Low HRV has been most commonly associated with a risk of arrhythmias and arrhythmic death, unstable angina, myocardial infarction, progression of heart failure and atherosclerosis. There is a need to develop a consensus on the measure of HRV for clinical purposes and whether 7-day record is necessary and practical. New analysis methods based on nonlinear dynamics may be more useful in risk stratification. More precise insight into the patho-physiological link between HRV and nutrition may be applied to clinical practice and used to direct therapy for prevention of disease risk.

Coenzyme Q in cardiovascular disease.

Coenzyme Q10 or ubiquinone normally present in many plant and animal cells is an antioxidant. Coenzyme Q10 deficiency has been observed in patients with congestive heart failure, angina pectoris, coronary artery disease, cardiomyopathy, hypertension, mitral valve prolapse and after coronary revascularization. Coenzyme Q10 is involved in the synthesis of ATP and hence is useful in preventing cellular damage during ischaemia-reperfusion injury. The clinical benefits are mainly due to its ability to improve energy production, antioxidant activity, and membrane stabilizing properties. Several studies showed that coenzyme Q could be useful in patients with congestive heart failure, angina pectoris, cardiomyopathy, coronary artery disease and in the preservation of myocardium. Coenzyme Q10 is normally present in the low density lipoprotein cholesterol fraction and inhibits its oxidation. It can also regenerate vitamin E. Coenzyme Q10 is known for producing minor gastrointestinal discomfort and elevation in SGOT and LDH when used.

Cardiovascular manifestations of aluminium phosphide intoxication.

Aluminium phosphide (ALP) a major suicidal agent in the developing countries is freely available as grain fumigant. It is highly toxic to lungs, heart and blood vessels causing pulmonary oedema, shock and arrhythmias. There is massive focal myocardial damage resulting in raised cardiac enzymes. Clinical manifestations were nausea and vomiting (32), dyspnoea and palpitations (25 each), cyanosis (12), hypotension (12) and shock (15). Cardiac arrhythmias were present in 28 cases and hypermagnesaemia in 13 patients. Mean serum magnesium level (1.95 +/- 0.2O, mEq/L) was significantly raised compared to mean magnesium level in control subjects (1.62 +/- 0.23 mEq/L). Hypermagnesaemia occurs due to myocardial and liver damage. Out of 32 cases studied, 22 died 18 within 24 hours of ALP ingestion. Thirty two cases of ALP were studied.