||The paucity of data concerning the etiology and development of coronary heart disease (CHD) and its risk factors prompted this case-control study. The prevalence of CHD and its accompanying CHD-risk factors among black people from Africa during the twentieth century is covered in the literature review. Differences between developed and developings countries and the possible role of multivariate analyses for the recognition of CHD are addressed. The aims and objectives follow the discussion of the literature review. Between 1982 and 1986 we identified 89 black South African patients with CHD, according to > 2 criteria of the World Health Organization (WHO) for CHD. The diagnosis of underlying coronary artery disease (CAD) was confirmed using coronary angiography, and/or necropsy until 1994. Exercise-radionuclide imaging was also used to confirm manifestations of underlying CHD. A control group of 356 black people living in the same study area and with no evidence of underlying CHD (< 2 WHO criteria or no CHD signs/symptoms along with negative and/or questionable exercise-induced/stress electrocardiography) were also selected. The two study groups were stratified according to age, sex and ethnicity. Using Stata Corp 2001 statistical software release 7, and a multiple logistic regression procedure three models with large surfaces under the Receiver Operator Characteristic (ROC)-curve (0,9331, 0,9350 and 0,9592) were built, for the recognition of CHD in black people. According to the Odds Ratios [95% Confidence Interval] the family history (FH) of myocardial infarction (MI; FHMI): 11,55 [2,63; 50,76]; >Gr II retinopathy (KWB): 8,18 [2,45; 27,26]; left ventricular hypertrophy (LVH): 7,13 [3,08; 16,55]; total cholesterol (TC): 6,4 [2,14; 19,09]; peripheral vascular disease (PVD): 3,72 [1,3; 9,99]; renal target organ damage: 3,41 [1,49; 7,78]; family history of hypertension (FHHT): 2,12 [0,89; 5,01]; and personal history of type 2 diabetes mellitus (NIDDM-II): 2,09 [0,65; 6,57] contributed significantly to the development of CHD in urban black people. From the comparisons between the models it can be concluded that the life-long exposure to lifestyle-related CHD risk factors (hypertension, NIDDM-II and elevated cholesterol levels), which were poorly controlled, along with genetic factors (FHMI and FHHT), lead to the development of CHD and target organ damage. It was accompanied by environmental factors such as poor socio-economic background and extended exposutre to urbanisation. The high prevalence rates of the known CHD risk factors resembled those of African American people with confirmed CHD. The Framingham absolute score for selected risk factor categories gave credibility to the risk factor status of both CHD patients as well as the control group. This is the first South-African study confirming the link between atherosclerotic CHD and the traditional CHD risk factors. A separate substudy using age- and sex-adjusted standardised mortality rates (MR) for CHD (ICDC 410-414) for the total white and black South African populations between 1970 and 1980 revealed a possible changing trend. The decline in white CHD MR in the younger age groups contrasts with those of black people. The observed (O) relative to the expected (E) CHD MR exceeded the 100% mark in the younger age groups. This observation is in agreement with the cumulative incidence rate (3,41) with a 95% confidence interval [2,51; 6,53] of this study relative to the study by Seftel et al. (1965-1968). Shortcomings in the reporting of CHD MR and the datasets, as well as inaccurate vital statistics, provide additional evidence of CHD mortality and morbidity in South African black people. The suggestion of a changing trend remains unsure. The two profiles of CHD in South African black people, 30-40 years apart, form the platform for proposed cardiovascular research in African black people. The study concludes with recommendations leveled at the National Department of Health for the treatment and prevention of CHD in South African black people.