Cardiovascular disease remains the leading cause of mortality worldwide and contributes substantially to the rising non-communicable disease burden in sub-Saharan Africa (SSA), where it now co-exists with the long-standing burden of communicable, maternal, and nutritional disorders [1]. Although atherosclerosis-driven ischaemic heart disease historically appeared less common in SSA than in high-income countries, the Global Burden of Diseases 2010 analysis highlighted that CVDs in this region are uniquely distributed—about half are non-atherosclerotic—and that the deaths from CVD occur at substantially younger ages than elsewhere in the world [2]. A ten-year hospital survey in Kinshasa reported that CVD accounted for 31% of medical admissions and 35% of in-hospital deaths, with stroke being the predominant contributor to cardiovascular mortality [3]. In a national-level analysis covering the DRC, the prevalence of hypertension rose rapidly over a five-year period (15.1%) and CVDs and diabetes respectively accounted for 20.4% and 5.4% of mortality, yet health facilities were generally not prepared to manage these conditions [4]. These signals indicate a pressing need for evidence-based lipid management strategies tailored to Central African populations.

Dyslipidemia is a well-established, causally related driver of atherosclerotic cardiovascular disease. The 2019 European Society of Cardiology and European Atherosclerosis Society guidelines eliminated the older “LDL-C hypothesis” in favour of an established causal relationship, lowering LDL-C goals to <55 mg/dL for very high-risk patients, <70 mg/dL for high-risk patients, and <100 mg/dL for moderate-risk patients [5][6]. Pharmacological management in these guidelines recommends high-intensity statins up to the highest tolerated dose as first-line therapy, with ezetimibe and, where needed, PCSK9 inhibitors as add-on agents when targets are not achieved [7]-[9]. Despite the strength of these recommendations, international observational data show that LDL-C goal attainment remains poor: in the International Cholesterol Management Practice Study covering 18 countries outside Western Europe, including several in Africa and the Middle East, only 32.1% of very high-risk patients on stable lipid-lowering therapy achieved their LDL-C target [10][11].

Among the statins, rosuvastatin offers favourable pharmacological characteristics: high affinity for HMG-CoA reductase due to additional binding interactions, relative hydrophilicity, selective hepatic uptake, low CYP3A4 metabolism, and a long half-life [12]-[14]. Rosuvastatin 10 - 40 mg reduces LDL-C by 52% - 63%, increases HDL-C by up to 14%, and reduces triglycerides by up to 28%, with 10% - 20% additional LDL-C reduction compared with atorvastatin across equivalent dose ranges [12][13][15]. Landmark trials such as JUPITER established that rosuvastatin 20 mg reduced major cardiovascular events by 44% (HR 0.56, 95% CI 0.46 - 0.69) and all-cause mortality by 20% (HR 0.80, 95% CI 0.67 - 0.97) in apparently healthy individuals with elevated high-sensitivity C-reactive protein [16][17]. Subsequent real-world studies from Asia, including a multicentre Indian study of rosuvastatin plus ezetimibe (mean LDL-C reductions of 92 - 100 mg/dL across statin-intensity strata) and a retrospective Nepalese study (mean LDL-C reduction of 63.4 mg/dL with rosuvastatin 10 mg, with only 3.03% adverse events), have confirmed consistent efficacy and tolerability in routine practice [18][19].

However, SSA populations remain under-represented in such evidence. Because of pharmacogenomic differences in transporters and metabolising enzymes (ABCG2, SLCO1B1, CYP2C9, APOE, and HMG-CoR) between African and Caucasian or Asian populations, the efficacy, dose-response relationship, and safety profile of rosuvastatin cannot always be extrapolated from non-African trials [20]. Real-world evidence from the Democratic Republic of the Congo is therefore essential to inform local treatment decisions, identify barriers to adherence, and contextualise international guideline recommendations.

The PEARL study was designed to address this gap. Its primary objective was to document the real-world usage pattern of rosuvastatin in DRC patients with dyslipidemia. Secondary objectives were to quantify within-patient changes in lipid parameters, assess anthropometric and blood-pressure trends, describe treatment adherence and persistence, and catalogue adverse events.

The PEARL study contributes one of the first multicentre, real-world evidence datasets on rosuvastatin use in the DRC, addressing a critical evidence gap given the rising cardiovascular and metabolic disease burden in Central Africa [1][3]. The demographic profile of the cohort—predominantly middle-aged, with a female majority and a high prevalence of cardiometabolic risk factors—mirrors the broader epidemiological transition described in DRC mortality data, where cardiovascular and metabolic causes together accounted for roughly a quarter of all deaths even within health facilities not optimally equipped for NCD care [3].

Figure 3.Global assessment of efficacy and safety of treatment by physician.

The headline finding of PEARL is that rosuvastatin (Roshal^TM), prescribed at predominantly moderate (10 mg) intensities, achieved clinically and statistically meaningful reductions in LDL-C, total cholesterol, and triglycerides within a single follow-up cycle. The overall LDL-C reductions by dose (−9.22% at 5 mg, −25.29% at 10 mg, and −18.81% at 20 mg) align with the pharmacological profile of rosuvastatin reported in dose-ranging and comparator studies, in which 10 - 40 mg of rosuvastatin lowers LDL-C by roughly 50% - 63%—here attenuated because of the relatively short follow-up window and the inclusion of dose groups with small sample sizes [12]-[15]. The pattern across dose groups is broadly consistent with reviews noting that rosuvastatin allows greater proportions of patients to attain LDL-C targets earlier than other statins, reducing the need for up-titration [12][14]. The total-cholesterol reduction of 15.70% and the triglyceride reduction of 15.64% further confirm the pleiotropic action of rosuvastatin on multiple lipid fractions, mirroring the JUPITER trial—in which rosuvastatin 20 mg reduced LDL-C by 50%, hs-CRP by 37%, and triglycerides by 17% within 12 months—and the consistent efficacy observed in retrospective multicenter studies, such as a 63.4 mg/dL mean LDL-C reduction with rosuvastatin 10 mg in a Nepalese cohort (95% CI 43.0 - 83.8, p < 0.001) [16][17][19].

The PEARL efficacy findings concur with those reported in landmark trials and intensive-care cohorts. In head-to-head real-world comparisons in Bangladesh, rosuvastatin 5 mg produced a larger LDL-C reduction than atorvastatin 10 mg (135.6 → 95.3 mg/dL vs. 140.7 → 110.4 mg/dL, p = 0.027) with fewer adverse events [21]. An Indian multicentre study of rosuvastatin plus ezetimibe in statin-pretreated patients reported mean LDL-C reductions of 92 - 100 mg/dL across low-, moderate-, and high-intensity baseline statin strata [18]. The within-dose reductions in the PEARL study were statistically significant for LDL-C at every dose (5 mg p = 0.006; 10 mg p = 0.023; 20 mg p = 0.002), confirming a real within-group lipid-lowering effect at each dose even in this lower-resource setting. However, because the reduction observed at 20 mg (−18.81%) was smaller than that at 10 mg (−25.29%), these unadjusted within-group comparisons should not be interpreted as evidence of a dose-response relationship; they more plausibly reflect confounding by baseline risk, baseline LDL-C, and prescribing indication (e.g., higher doses being preferentially prescribed to patients with more severe or difficult-to-control dyslipidemia).

The HDL-C and triglyceride patterns observed in PEARL are also coherent with international evidence. The triglyceride reduction of 15.64% overall, and the dose-stratified reductions of −25.51 mg/dL (10 mg) and −35.22 mg/dL (20 mg), fall within the 10% - 28% range described for rosuvastatin [13][14]. This is clinically meaningful in a Central African cohort in which mixed dyslipidemia and metabolic syndrome are increasingly common and in which triglyceride-rich lipoprotein remnants are emerging as additional targets of therapy [7].

The mean reductions observed in systolic (−19.35 mmHg) and diastolic (−10.73 mmHg) blood pressure likely reflect concomitant antihypertensive therapy rather than a direct statin effect—although statin-induced improvements in endothelial function may contribute a small independent component, as suggested in reviews of statin pleiotropy [15]. The high proportion of patients achieving medium (57.52%) or high (37.58%) adherence, with only 4.90% classified as poor, indicates that rosuvastatin was well accepted and integrated into the daily routine of this DRC cohort. This is encouraging given international data showing that long-term adherence to lipid-lowering therapy declines over months and years, with worse persistence typically observed among women and among patients on multiple agents in real-world German and Australian cohorts [22][23]. In sub-Saharan Africa, undertreatment remains the larger problem: ACE sub-analysis showed that more than three-quarters of eligible outpatients in the region are not on any statin therapy, including two-thirds of those with prior coronary artery disease, cerebrovascular disease, peripheral arterial disease or diabetes [11]. The relatively high adherence observed in PEARL may be attributable to once-daily rosuvastatin dosing (no major CYP3A4 drug-to-drug interactions, allowing safe co-prescription with antihypertensives and antidiabetics) and to the simplicity of long-term adherence messaging in the participating centres.

The overall AE rate of 2.8% in PEARL is consistent with—and slightly lower than—rates reported elsewhere. In the Korean ROSulord^® study, rosuvastatin showed favourable safety with infrequent adverse drug reactions in real-world use [24]; a retrospective multicentre study from Nepal reported AEs in only 3.03% of patients [19]; and the HILL-India rosuvastatin-ezetimibe combination study described rosuvastatin-based therapy as well tolerated across dose strata [18]. The PEARL safety profile—predominantly mild, with no severe AEs and no AE-related deaths—is consistent with the safety profile established for rosuvastatin in larger phase III/IV programmes [12][13][17].

The PEARL study has several limitations that should be considered when interpreting the findings. First, this was a single-country study conducted in the Democratic Republic of Congo, which may limit the generalizability of the findings to other African populations with different demographic profiles, healthcare systems, and genetic backgrounds. The non-interventional, observational design with no control group limits the ability to establish causality or to compare rosuvastatin with other lipid-lowering therapies or placebo. The absence of long-term outcome data, such as major adverse cardiovascular events, hospitalizations, or mortality, precludes assessment of the clinical impact of the observed lipid improvements.

In this prospective, multicentre, real-world PEARL cohort from the Democratic Republic of the Congo, rosuvastatin (Roshal^TM)—predominantly prescribed at 10 mg—produced clinically and statistically significant reductions in LDL-C, total cholesterol, and triglycerides across all dose groups, accompanied by modest improvements in blood pressure and weight. The drug was well tolerated: only 2.8% of patients experienced an adverse event, none of which were severe, and adherence was predominantly medium-to-high. These findings support the integration of rosuvastatin into routine CVD prevention pathways in the DRC and provide locally relevant evidence that complements international trial data and guideline recommendations.

Author Contributions

Dr. Tresor Mude & Dr. Raymond Dinaouz conceived and designed the study. Dr. Tresor Mude & Dr. Raymond Dinaouz collected and analyzed the data. Dr. Tresor Mude & Dr. Raymond Dinaouz prepared the original manuscript draft. Dr. Tresor Mude & Dr. Raymond Dinaouz critically reviewed and edited the manuscript. Dr. Tresor Mude & Dr. Raymond Dinaouz supervised the study. All authors reviewed and approved the final manuscript.