CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 1, January – April 2024 8 AFRICA categorised according to the World Health Organisation’s nutrition/BMI guidelines and defined as a person’s weight in kilograms divided by the square of the person’s height in metres. Below 18.5 kg/m2 was defined as underweight, 18.5–24.9 kg/m2 as normal, 25.0–29.9 kg/m2 as pre-obesity, 30.0–39.9 kg/m2 as obese and above 40 kg/m2 as severe obesity. The study participants were divided into four groups; healthy volunteers (HV) (n = 29), patients with concomitant disease (type 2 diabetes mellitus and hypertension) but normal BMI (Nd) (n = 23), obese patients without concomitant disease (OB) (n = 29), and obese patients with concomitant disease (OBd) (n = 29). The eligibility criteria for healthy volunteers were male or female, aged 18–70 years with no abnormalities in the physical examination and no chronic or acute diseases (not on any chronic medication). The eligibility criteria for the study patients were male or female, aged 18–70 years, with type 2 diabetes and with or without hypertension, with a BMI ≤ 25 kg/m2 and on metformin as monotherapy or metformin plus sulfonylurea as a dual combination therapy plus hypertensive therapy (enalapril 10 mg and/or hydrochlorothiazide 12.5 mg) if needed. The obese patients were not on any medications used to treat hyperlipidaemia. No additional medication (and no withholding of medication) was given to the patients with diabetes or other concomitant diseases. The exclusion criteria were patients with type 1 diabetes mellitus, a history of ketoacidosis, current treatment with all types of insulin, patients acutely ill or unstable, and patients with poorly controlled concomitant chronic diseases, such as systolic blood pressure (SBP) ≥ 160 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg. Sample size calculations were based on estimation of the difference in PWV between any two groups. With a sample size of 26 per group, a two-sided t-test at the 5% level would have 80% power to detect a difference of 2 m/s (7–9) in PWV between any two groups, assuming a common standard deviation of 2.5 m/s. Sample size calculation was done on Query Advanced (Statistical Solution Ltd, Cortc, Ireland), version 8.1.1.0. Questionnaires were completed, and vital signs, BMI and fasting glucose levels were measured. After overnight fasting, venous blood was collected via vacupunture and determination of glycated haemoglobin (HbA1c) levels and lipid profiles was done by the National Health Laboratory Services, which is a South African National Accreditation System (SANAS) accredited laboratory. The National Health Laboratories Services handbook on standard operating procedures, version 1, active from 6 March 2015, and document number GPQ0064, was used as a guideline to ensure correct and consistent sample collection and handling. Other variables such as smoking and alcohol consumption were recorded. Validity was maintained by strict adherence to the inclusion and exclusion criteria. The AtCor SphygmoCor®, used for measuring PWV and Aix, was operated by a trained, dedicated user. All of the apparatus used in the laboratory investigations were acquired from reputable suppliers and the procedures were conducted according to the manufacturer’s protocol. PWV and Aix were assessed non-invasively using the AtCor SphygmoCor® system (AtCor Medical, Inc, Sydney, Australia). Electrocardiogram-gated carotid and femoral waveforms were recorded using applanation tonometry. Carotid–femoral path length was measured as the difference between the surface distance joining (1) the suprasternal notch, the umbilicus and the femoral pulse, and (2) the suprasternal notch and the carotid pulse. The carotid–femoral transit time was estimated in eight to 10 sequential femoral and carotid wave forms as the average time difference between the onset of the femoral and carotid waveforms. PWV was calculated as the carotid–femoral path length divided by the carotid–femoral transit time as expressed in metres per second.9 Aix was measured by pulse-wave analysis (PWA). Radial artery waves were recorded non-invasively by applanation tonometry. Twenty waves were captured and PWA was used to derive a central aortic pulse wave and haemodynamic measures by a generalised validated mathematical transfer function. Aix measurements were standardised to a pulse rate of 75 beats per min and expressed as a percentage (%).12 Assessment of arterial elasticity by determination of PWV and Aix was done in the obese black patients. Statistical analysis All statistical analyses were done on SAS (SAS Institute Inc, Carey, NC, USA). Continuous variables are summarised as mean values and standard deviations. Mean values of the demographic variables were compared between the four test groups by analysis of variance (ANOVA) followed by pairwise t-test comparison. Median values for both PWV and Aix were calculated. Linear regression analysis was performed with PWV and Aix @75 as outcomes (dependent) variables and the demographic variables as predictors (independent) variables. Results Of the 110 study participants, 29 were healthy volunteers aged 37.2 ± 10 years, 23 patients were non-obese with concomitant disease (type 2 diabetes mellitus and hypertension), aged 58.8 ± 8.4 years, 29 patients were obese without concomitant disease, aged 44.2 ± 14.6 years, and 29 patients were obese with concomitant disease, aged 53.1 ± 9 years. The clinical and haemodynamic characteristics of the study participants are shown in Table 1. The average BMI was 24.82 ± 1.9 kg/m2 for the HV group, 24.7 ± 2.4 kg/m2 for the Nd group, 35.4 ± 4.2 kg/m2 for the OB group and 35.4 ± 4.9 kg/m2 for the OBd group. All the participants in the OBd and Nd groups additionally had type 2 diabetes mellitus, and 65.2% of the Nd group and 75.9% of OBd group had concomitant hypertension (Table 1). The mean PWV levels were statistically significantly different in the obese group with and without concomitant disease. The PWV in the OB group (7.9 ± 2.9 m/s) and in the OBd group (9.2 ± 4.4 m/s) were, respectively, 19.7 and 33.3% higher (p < 0.05) than in the HV group (6.6 ± 2.1 m/s). The risk of CVD in the obese patient without additional disease was 50.7% higher. The presence of concomitant disease (type 2 diabetes mellitus and hypertension) in addition to obesity increased arterial stiffness further by 11.4% and therefore further increased the risk of CVD by 35.1%. Aix was higher in the OBd and Nd groups by 8.2 and 16.5%, respectively, however the increase was not statistically significant. Aix was directly correlated with age, heart rate and aortic SBP. Interestingly, Aix did not differ significantly in the OB group when compared to the HV group (Table 1).
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