Interplay of COVID-19 and cardiovascular diseases in Africa: an observational snapshot

Abstract

The COVID-19 pandemic, which started around December 2019 has, at present, resulted in over 450,000 deaths globally, and approximately 1% of these deaths have been reported in Africa. Despite the high prevalence of COVID-19 risk factors, namely: hypertension, diabetes, chronic pulmonary disease, cardiovascular diseases (CVDs) such as rheumatic heart disease, compromised immunity and obesity, low case fatality rates have been recorded in many parts of Africa so far. COVID-19 severity has previously been shown to be worse in patients with CVD and hypertension. We observed the severity of COVID-19 and mortality rates in Africa, and compared outcomes with prevalence of established risk factors (hypertension and CVD). We stratified data as per the United Nations' 5 African subregions. North African countries show a positive association between the risk factors and the mortality rates from COVID-19. However, we observed discordant patterns in the relationship between COVID-19, and either CVD or hypertension, in sub-Saharan African countries. In this paper, we also review the pathogenesis of SARS-CoV-2 infection and how it worsens CVD and postulate that the differences in modulation of the renin-angiotensin-aldosterone system (RAAS) axis which controls angiotensin-converting enzyme (ACE)/ACE2 balance may be an important determinant of COVID-19 outcomes in Africa.

Keywords: Africa; COVID-19; Cardiovascular diseases; Hypertension; RAAS; SARS-CoV-2.

Fig. 1

Clinical presentation of COVID-19 and SARS Cov-2 infection. a The clinical progression of COVID-19 occurs in four distinct phases that are characterised by various symptoms as shown Adapted from Oberfeld B et al. SnapShot: COVID-19. Cell. 2020;181(4):954- e1. b The organs in which ACE2 receptors are expressed include the eyes, respiratory airway tract, lung, heart, and small intestines. The respiratory tract is the primary site of ACE2 infection. c The infection cycle of SARS-CoV-2 is initiated when the virion attached to the hosts ACE2 receptor protein (1). Upon attachment, the virion then enters the cells via endocytosis (2) and the viral RNA is released in the host cells (3). Using the host cells’ protein synthesis machinery, new viral proteins are synthesized and assembled; therefore, allowing for multiplication. (4). The new viruses are then released from the host cell (5)

Fig. 2

Cardiotoxic effects of SAR Cov-2 infection. The cardiotoxic effects of SARS-CoV-2 may either be direct or indirect. SARS-CoV-2 may directly affect the heart through direct viral replication within the myocardium, thus resulting in myocardial damage. Alternatively, SARS-CoV-2 infection may indirectly induce myocardial inflammation which impairs cardiac function

Fig. 3

The overview of COVID19 mortality, CVD mortality burden, and hypertension prevalence in Africa. COVID19 cases in Africa show varied distribution across the continent (a). The insert shows that Africa had a relatively lower rise in cases. A map of Africa showing COVID-19 mortality rates* (b). Comparing the COVID-19 mortalities and hypertension, and CVD seemed directly proportional to COVID-19 mortality rates in North Africa. However, there seems to be discordant patterns with the rest of the continent (c). *COVID-19 Data as at 20 June 2020 sourced from https://ourworldindata.org/covid-testing#source-information-country-by-country

Fig. 4

Schematic summary of Renin-angiotensin system showing the main pathways associated with cardiovascular and immunology pathologies. Angiotensinogen (AGT) is cleaved by renin from the kidneys into angiotensin I (Ang I) which is then converted to Ang II by angiotensin converting (ACE), which is associated with most of the pathologies. Ang II is also hydrolyzed to a lesser extent by neutral endopeptidase (NEP) to Ang-(1–7). Further, Ang II is hydrolyzed to Ang III by aminopeptidase A which is later hydrolyzed to Ang IV by amino peptidase N. Ang I to a lesser extent is converted to Ang-(1–9) by angiotensin converting enzyme 2 (ACE2) which is further hydrolyzed to Ang-(1–7) by ACE. The major activity for ACE2 is hydrolyzing Ang II to Ang-(1–7) which associated with cell survival activities

Fig. 5

Schematic summary of the ACE/ACE2 axes balance in normotensive and hypertensive individuals and the role it plays in developing mild or severe ALI and ARDS upon SARS-CoV-2 infection. The proposed mechanism further demonstrates how the ACE/ACE2 axis may not be directly involved in hypertensive patients of African ancestry upon COVID-19 infection. ALI Acute Lung Injury, ARDS Acute Respiratory distress syndrome, IL-12 Interleukin 12, NO nitric oxide, TNF-a Tumor necrosis factor alpha, ACE and ACE2 Angiotensin Converting enzyme and angiotensin converting enzyme 2