Heart failure with reduced ejection fraction and atrial fibrillation: a Sub-Saharan African perspective

Abstract

Cardiovascular diseases are a well-established cause of death in high-income countries. In the last 20 years, Sub-Saharan Africa (SSA) has seen one of the sharpest increases in cardiovascular disease-related mortality, superseding that of infectious diseases, including HIV/AIDS, in South Africa. This increase is evidenced by a growing burden of heart failure and atrial fibrillation (AF) risk factors. AF is a common comorbidity of heart failure with reduced ejection fraction (HFrEF), which predisposes to an increased risk of stroke, rehospitalizations, and mortality compared with patients in sinus rhythm. AF had the largest relative increase in cardiovascular disease burden between 1990 and 2010 in SSA and the second highest (106.4%) increase in disability-adjusted life-years (DALY) between 1990 and 2017. Over the last decade, significant advancements in the management of both HFrEF and AF have emerged. However, managing HFrEF/AF remains a clinical challenge for physicians, compounded by the suboptimal efficacy of guideline-mandated pharmacotherapy in this group of patients. There may be an essential role for racial differences and genetic influence on therapeutic outcomes of HFrEF/AF patients, further complicating our overall understanding of the disease and its pathophysiology. In SSA, the lack of accurate and up-to-date epidemiological data on this subgroup of patients presents a challenge in our quest to prevent and reduce adverse outcomes. This narrative review provides a contemporary overview of the epidemiology of HFrEF/AF in SSA. We highlight important differences in the demographic and aetiological profile and the management of this subpopulation, emphasizing what is currently known and, more importantly, what is still unknown about HFrEF/AF in SSA.

Keywords: Atrial fibrillation; Heart failure with reduced ejection fraction (HFrEF); Sub-Saharan Africa.

Figure 1

The effects of atrial fibrillation (AF) on heart failure with reduced ejection fraction (HFrEF). AF significantly impairs the quality of life and increases the risk of stroke, rehospitalization, and mortality in patients with HFrEF. AF is both a cause and a result of HFrEF with both entities sharing independent risk factors. Genetic polymorphisms in the beta‐adrenergic receptor may modulate beta‐blocker efficacy in patients with HFrEF/AF.

Figure 2

Genotype‐dependent efficacy of beta‐blockers in heart failure with reduced ejection fraction/atrial fibrillation (HFrEF/AF). Grey: HFrEF pathways where the efficacy of beta‐blockers are genotype independent. Navy blue: HFrEF pathways where the efficacy of beta‐blockers are genotype dependent. In sinus rhythm patients, there is dose‐dependent mortality benefit and reduction in new‐onset AF in patients with the gain of function Arg389Arg variant. In patients with HFrEF/AF, the Arg389Arg variant was unresponsive to the rate‐lowering effects of non‐selective beta‐blockers.