Mapping the emergence of heart disease in a black, urban population in Africa: The Heart of Soweto Study

Background: There is increasing evidence that many populations in the developing world are in epidemiologic transition with the subsequent emergence of more affluent disease states. The Heart of Soweto Study will systematically investigate the emergence of heart disease (HD) in a large urban population in South Africa. Methods: Part of the conurbation of Johannesburg, South Africa, Soweto is a predominantly Black African community of I million individuals. During an initial two year period, all individuals presenting to the local Baragwanath Hospital (3500 beds) with any form of HD will be studied. Demographic and diagnostic coding data in those with pre-established HD will form an abbreviated clinical registry of > 12,000 prevalent cases. Similarly, socio-demographic, clinical and diagnostic data (e.g. echocardiography and ECG) in newly diagnosed patients will form a more detailed clinical registry of > 5000 incident cases. Sub-studies of the relationship between HIV status and H D and the optimal management of chronic heart failure will also be performed. Results: These data will provide a unique insight into the causes and consequences of a broad spectrum of HD-related conditions in a developing world community in epidemiologic transition. Initially documented Population rates, in addition to detailed examinations of the underlying risk factors and causes of HD-related morbidity/mortality will provide an important platform for future stages of the study: a community-based, population screening program and culturally specific primary and secondary programs of care. Conclusion: There is an urgent need to systematically track the emergence of HD in the developing world. Initially involving more than 15,000 individuals, the unique Heart of Soweto Study has the potential to provide a wealth of information in this regard. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

Diabetic heart disease

Diabetes mellitus is responsible for a spectrum of cardiovascular disease. The best known complications arise from endothelial dysfunction, oxidation, inflammation, and vascular remodelling and contribute to atherogenesis. However, the effects on the heart also relate to concurrent hypertensive heart disease, as well as direct effects of diabetes on the myocardium. Diabetic heart disease, defined as myocardial disease in patients with diabetes that cannot be ascribed to hypertension, coronary artery disease, or other known cardiac disease, is reviewed.

Contribution of changes in risk factors to the decline of coronary heart disease mortality in Australia over three decades

BACKGROUND: Coronary heart disease has been a major cause of mortality in Australian adults, but the rate has declined by 83% from the 1968 peak by the year 2000. The study objective is to determine the contribution of changes in population risk factors - mean serum cholesterol and diastolic blood pressure and tobacco smoking prevalence - to the decline in coronary heart disease mortality in Australia over three decades. METHODS: Coronary heart disease deaths (International Classification of Disease-9, 410-414) and population by year, age group and sex were obtained from the Australian Bureau of Statistics. Risk factor levels were obtained from population surveys and estimated average annual changes by period were used to calculate average annual 'attributable' proportional declines in CHD mortality by period (age 35-64 years). RESULTS: Over the period 1968-2000, 74% of male decline and 81% of the female decline in coronary heart disease mortality rate was accounted for by the combined effect of reductions in the three risk factors. In males 36% of the decline was contributed by reductions in diastolic blood pressure, 22% by cholesterol and 16% by smoking. For females 56% was from diastolic blood pressure reduction, 20% from cholesterol and 5% from smoking. Effects of reductions in serum cholesterol on coronary heart disease mortality occurred mainly in the 1970s. Declines in diastolic blood pressure had effects on coronary heart disease mortality over the three decades, and declines in tobacco smoking had a significant effect in males in the 1980s. CONCLUSION: Most of the spectacular decline in coronary heart disease mortality over the last three decades in Australia can be ascribed to reductions in population risk factors from primary and secondary prevention.

Structural ambiguity of the Chinese version of the Hospital Anxiety and Depression Scale in patients with coronary heart disease

Background The Hospital Anxiety and Depression Scale (HADS) is a widely used screening tool designed as a case detector for clinically relevant anxiety and depression. Recent studies of the HADS in coronary heart disease (CHD) patients in European countries suggest it comprises three, rather than two, underlying sub-scale dimensions. The factor structure of the Chinese version of the HADS was evaluated in patients with CHD in mainland China. Methods Confirmatory factor analysis (CFA) was conducted on self-report HADS forms from 154 Chinese CHD patients. Results Little difference was observed in model fit between best performing three-factor and two-factor models. Conclusion The current observations are inconsistent with recent studies highlighting a dominant underlying tri-dimensional structure to the HADS in CHD patients. The Chinese version of the HADS may perform differently to European language versions of the instrument in patients with CHD.

The fraction of ischaemic heart disease and stroke attributable to smoking in the WHO Pacific and South-East Asian regions

Background: Tobacco will soon be the biggest cause of death worldwide, with the greatest burden being borne by low and middle-income countries where 8/10 smokers now live. Objective: This study aimed to quantify the direct burden of smoking for cardiovascular diseases (CVD) by calculating the population attributable fractions (PAF) for fatal ischaemic heart disease (IHD) and stroke (haemorrhagic and ischaemic) for all 38 countries in the World Health Organization Western Pacific and South East Asian regions. Design and subjects: Sex-specific prevalence of smoking was obtained from existing data. Estimates of the hazard ratio (HR) for IHD and stroke with smoking as an independent risk factor were obtained from the,600 000 adult subjects in the Asia Pacific Cohort Studies Collaboration (APCSC). HR estimates and prevalence were then used to calculate sex-specific PAF for IHD and stroke by country. Results: The prevalence of smoking in the 33 countries, for which relevant data could be obtained, ranged from 28-82% in males and from 1-65% in females. The fraction of IHD attributable to smoking ranged from 13-33% in males and from < 1-28% in females. The percentage of haemorrhagic stroke attributable to smoking ranged from 4-12% in males and from < 1-9% in females. Corresponding figures for ischaemic stroke were 11-27% in males and < 1-22% in females. Conclusions: Up to 30% of some cardiovascular fatalities can be attributed to smoking. This is likely an underestimate of the current burden of smoking on CVD, given that the smoking epidemic has developed further since many of the studies were conducted.

Association between glutathione S-transferase M1 and T1 and the risk for coronary heart disease (CHD)

Deficiency of Glutathione S-transferases (GST) M1 and T1 are associated with chronic diseases (e.g. lung cancer, MS) and could be one factor for the risk for CHD.We conducted a pros-pective case-control study in 93 pts. with angiographically proven CHD and 161 controls matched for age ±2y and gender (resulting in n=91 pairs, of which 18 were female). Genes coding for functional GST M1 and T1 were analysed acoording to previously published methods. The association between GST M1, T1 was tested using Fisher's exact test; logistic regression analysis was performed to control for HDL-cholesterol, diabetes smoking, diabetes, hypertension. 41% of cases were smokers, 25% had diabetes and 68% hypertension, corresponding figures for controls were 31%, 13% and 33%. Mean HDL-cholesterol levels were comparable (pts: 46±14 mg/dl, controls: 43± 19 mg/dl). There was no overall significant correlation between functional GST T1 and M1 genotypes and CHD, however, there seems to be an association between GST M1, HDL-cholesterol and CHD. Larger studies are needed to verify these data.