South Africa has recently been rated as one of the countries with the highest hypertension prevalence rates, with alcohol abuse being one of the most significant contributors to hypertension, especially in black Africans. Prospective data from the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study revealed that more than two-thirds of black participants met the criteria for hypertension, whilst only 39% of the white African participants were classified as hypertensive.
Additionally, alcohol consumption and dependence are greater in the SABPA black cohort, due to its utilization as a possible coping strategy in a psycho-socially demanding environment. The metabolism and tolerance of alcohol also vastly differ between black and white individuals from South Africa, due to the inherent genetic differences in two of the enzymes responsible for alcohol metabolism. Studies have concluded that, in blacks, alcohol is very rapidly and effectively metabolized – with little to no lingering effects on the liver itself. Numerous studies have drawn similar conclusions and state that blacks display a higher rate of alcohol metabolism and tolerance, compared to whites.
We explored the detrimental effect of excessive alcohol consumption on the cardiovascular system between ethnicities using ethnic-specific cut-points for the alcohol-consumption marker gamma-glutamyl transferase (γGT), to determine the association between the degree of alcohol consumption and risk markers pertaining to cardiac perfusion, electrical, and structural alterations in a South African bi-ethnic cohort.
The electrocardiogram (ECG) is the most basic tool for assessing hypertrophy of the left ventricle (LVH) in hypertensive subjects. This hypertrophy occurs due to the increased contractile force that has to be generated by the cardiac muscle to overcome the increased resistance posed by hypertensive vasculature. The corrected QT (QTc) interval represents the flow of electrical current through the ventricles and its prolongation is associated with arrhythmias, oxygen deficits, and LVH. Our findings noted that an increased QTc was associated with excessive alcohol consumption, indicating delayed electrical conductance, possibly due to increased stress on the cardiac muscle.
Another cardiac stress marker, amino-terminal pro-brain natriuretic peptide (NT-proBNP), is produced by the cardiac cells as the heart fills with blood, as it promotes vasodilation in the peripheral vasculature, readying the systemic arteries and veins to receive blood. We found that elevated levels of NT-proBNP associated with pre-clinical hemodynamic and structural modifications, similar to those leading to heart failure, arrhythmias, and LVH. These elevated levels of NT-proBNP indicated an increased cardiovascular disease risk in our Black cohort exclusively. Increased levels of NT-proBNP, present in Black high alcohol consumers, might be a hemodynamic attempt to alleviate the increased peripheral resistance and cardiac workload.
Our results showed that alcohol-consumption related to alterations in cardiac perfusion, electrical activity, and structure in a South African, bi-ethnic population. Overall, we demonstrated that ischemia and structural modifications were associated with both QTc prolongation and increased NT-proBNP levels, predominantly in Black excessive alcohol consumers. These cardiac modifications and hemodynamic alterations might increase their risk for cardiovascular disease development.
These findings are described in the article QTc prolongations, increased NT-proBNP and pre-clinical myocardial wall remodelling in excessive alcohol consumers: The SABPA study, recently published in the journal Alcohol. This work was conducted by Annemarie Wentzel, Leoné Malan, JD Scheepers and Nico T Malan from the Hypertension in Africa Research Team (HART) from the North-West University, South Africa.
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