A retrospective, descriptive, and analytical study was conducted at the Epidemic Treatment Center (ETC) of Saint-Louis CHR over 21 months (March 2020 to December 2021).

The population consisted of all patients hospitalized at the ETC with a positive PCR test for SARS-CoV-2 and having at least one pre-existing cardiovascular pathology. Pre-existing cardiovascular pathology was defined as having documented cardiovascular risk factors (hypertension defined as systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mmHg or current antihypertensive treatment; diabetes mellitus defined as fasting glucose ≥ 1.26 g/L or HbA1c ≥ 6.5% or current antidiabetic treatment; obesity defined as BMI ≥ 30 kg/m²) or established cardiovascular disease (documented coronary artery disease, heart failure, valvular heart disease, arrhythmias, or peripheral arterial disease).

Incomplete medical records or those without cardiovascular evaluation were excluded. From the initial pool of 450 hospitalized COVID-19 patients, 353 were excluded: 97 patients met the inclusion criteria of having documented cardiovascular pathology with complete medical records and cardiovascular evaluation.

Data were collected from ETC and laboratory registers using a pre-established form. Variables collected included:

Sociodemographic: age, sex, origin.

Clinical: cardiovascular risk factor, functional signs at admission, clinical form of COVID-19 (asymptomatic, moderate, severe according to WHO COVID-19 Clinical Management: Living Guidance, version dated 25 January 2021).

Biological: glycemia, creatininemia, CRP, lipid profile (total cholesterol, HDL, LDL, triglycerides), troponin.

Evolution: hospitalization duration, outcome (recovery or death).

Data were analyzed using SPSS version 25. Qualitative variables are expressed as frequencies and percentages, and quantitative variables as means ± standard deviation. Chi-square (or Fisher’s exact) tests and Student’s t-test were used for comparisons. A p-value < 0.05 was considered significant.

Data anonymity and confidentiality were strictly respected. The study was approved by the Saint-Louis CHR administration.

Among 450 patients hospitalized for COVID-19, 97 (21.6%) presented cardiovascular pathology. Table 1 presents their sociodemographic and clinical characteristics.

The most frequently reported symptoms at admission were cough (48.5%), dyspnea (46.4%), fatigue (43.3%), and fever (39.2%).

In terms of laboratory findings, nearly 40% of patients had hyperglycemia and renal function was impaired in 24% of cases. Table 2 summarizes measured biological parameters and prevalence of abnormalities among patients.

Among the 97 patients, 7 died, representing a fatality rate of 7.2%. This fatality is associated with factors such as advanced age, severity of clinical condition and elevated CRP, among others. Table 3 presents factors significantly associated with death in univariate analysis.

The multivariate analysis was not performed due to the limited sample size in the death group (n = 7), which provides insufficient statistical power for a stable multivariable regression model. A minimum of 10 events per predictor variable is generally recommended to avoid overfitting and ensure reliable coefficient estimates.

The advanced age, confirmed as a major mortality risk factor, is consistent across COVID-19 literature [10] [11] . Recent meta-analyses have demonstrated that each decade increase in age is associated with a 2-3-fold increase in mortality risk [12] . This reflects physiological frailty, immunosenescence, and higher comorbidity burden. In sub-Saharan Africa, where the median age is lower than developed countries, the relatively younger cardiovascular population may partially explain our lower mortality rates compared to Western studies [13] .

The marked CRP elevation in deceased patients is the most significant marker in our analysis. This result corroborates numerous studies indicating that cytokine storm and hyper-inflammatory state are major drivers of COVID-19 severity and mortality [14] [15] . Recent research has established specific CRP thresholds (>100 mg/L) as strong predictors of severe outcomes and mortality [16] [17] . The extreme CRP elevation (192 mg/L) in our deceased patients aligns with this evidence. Furthermore, longitudinal studies have shown that persistent CRP elevation rather than peak values may be more predictive of adverse outcomes [18] .

The troponin elevation, a marker of myocardial injury, was strongly associated with death. This can be explained by several mechanisms: direct viral myocardial lesion via ACE2 receptor, aggravation of underlying ischemic heart disease by hypoxia and stress, or inflammatory myocarditis [5] [6] [19] . Recent studies have demonstrated that cardiac injury occurs in 20% - 30% of COVID-19 patients and is associated with 3-5-fold increased mortality risk [20] [21] . The SARS-CoV-2 virus directly infects cardiomyocytes through ACE2 receptors, leading to myocarditis, arrhythmias, and heart failure [22] . Additionally, the hypercoagulable state induced by COVID-19 increases myocardial infarction risk through coronary thrombosis [23] .

Renal function impairment (elevated creatinine) is another well-established poor prognostic factor. It may result from dehydration, pre-existing nephropathy, drug nephrotoxicity, or virus-related glomerulonephritis [24] . Recent data suggest that acute kidney injury occurs in 5% - 15% of hospitalized COVID-19 patients and is associated with significantly higher mortality [25] [26] . The kidney expresses high levels of ACE2 receptors, making it vulnerable to direct viral injury. Additionally, systemic inflammation, hypoxia, and hypercoagulability contribute to acute kidney injury in COVID-19 [27] .

The association between low HDL-cholesterol levels and mortality is particularly intriguing. HDL possesses anti-inflammatory and antioxidant properties. Its decrease during acute inflammatory syndrome is well-known and could contribute to worsening SARS-CoV-2-induced endotheliopathy and vascular dysfunction [28] . Recent research has revealed that COVID-19 significantly alters lipid metabolism, with marked decreases in HDL-cholesterol levels correlating with disease severity [29] [30] . This phenomenon is linked to impaired reverse cholesterol transport, which may contribute to endothelial dysfunction and thrombosis risk in COVID-19 patients [31] .

The increased vulnerability of cardiovascular patients to severe COVID-19 involves multiple pathophysiological mechanisms beyond those identified in our study. The renin-angiotensin-aldosterone system (RAAS) plays a central role, as ACE2 downregulation by SARS-CoV-2 leads to unopposed angiotensin II activity, promoting inflammation, vasoconstriction, and thrombosis [32] [33] . Endothelial dysfunction, a hallmark of cardiovascular disease, is exacerbated by COVID-19 through direct viral invasion and inflammatory mediators, leading to increased vascular permeability, coagulopathy, and organ dysfunction [34] [35] .

Our findings contribute to the growing body of evidence from sub-Saharan Africa, where COVID-19 outcomes in cardiovascular patients may differ from high-income countries due to younger population demographics, different genetic factors, and varying healthcare systems [36] [37] . Recent systematic reviews have shown that while cardiovascular comorbidities remain significant risk factors across all populations, case fatality rates in sub-Saharan Africa are generally lower than reported in Europe and North America [38] [39] .

The identified prognostic factors: age, inflammatory state (CRP), myocardial injury (troponin), renal dysfunction, and lipid profile disturbances are accessible indicators that should alert clinicians and guide intensive, multidisciplinary management. Recent clinical practice guidelines recommend systematic cardiac biomarker monitoring in COVID-19 patients with cardiovascular comorbidities [40] [41] . Risk stratification tools incorporating these parameters have been developed and validated for predicting severe outcomes in COVID-19 patients with cardiovascular disease [42] [43] .

This study has several limitations, including its retrospective and single-center design, small sample size in the death group limiting multivariate analysis power, and absence of data on certain examinations (chest CT, systematic ECG). Additionally, we lacked data on specific cardiovascular medications (ACE inhibitors, ARBs, statins) that may influence COVID-19 outcomes. The study period (March 2020-December 2021) also spans different pandemic phases with varying dominant viral variants, which could influence outcomes.