Key result
Non-severe Plasmodium vivax malaria linked to ~5-point lower LVEF versus healthy controls.
Why the study?
Cardiovascular changes in patients with the non-severe form of Plasmodium vivax malaria had been poorly addressed, motivating an evaluation of cardiac structure, function, and serum markers of cardiovascular injury.
Does non-severe Plasmodium vivax malaria cause alterations in cardiac structure, function, and serum markers of cardiovascular injury compared to healthy controls?
Case-Control (n=51)
No
Does non-severe Plasmodium vivax malaria cause alterations in cardiac structure, function, and serum markers of cardiovascular injury compared to healthy controls?
Provides the first clinical evidence that even non-severe Plasmodium vivax malaria causes subclinical, largely reversible left and right ventricular dysfunction, increased pulmonary vascular resistance, and elevated myocardial injury biomarkers.
Non-severe P. vivax malaria was associated with subclinical biventricular dysfunction; hypothesis-generating and requires prospective confirmation before clinical adoption.
BACKGROUND: malaria has been poorly addressed. The aim of this study was to evaluate cardiac structures and function, and serum markers of cardiovascular injury in patients with the non-severe form of vivax malaria in Manaus, Amazonas State, Brazil. METHODS AND RESULTS: We prospectively evaluated 26 patients with vivax malaria in an outpatient referral hospital and compared results with a control group of 25 gender- and age-matched healthy individuals. Patients underwent clinical evaluation, laboratory tests, and transthoracic echocardiography at first evaluation (day zero, D0) and seven days (D7) after malaria diagnosis. At D0 echocardiography showed higher left ventricular (LV) systolic diameter (28.8 ± 2.82 vs 30.9 ± 4.03 mm; p = 0.037) and LV diastolic volume (82.4 ± 12.3 vs 93.8 ± 25.9 ml; p = 0.05), and lower LV ejection fraction (Teicholz method: 73.2 ± 6.59 vs 68.4 ± 4.87%; p = 0.004) in patients compared to controls. Right ventricle (RV) fractional area change (54.7 ± 5.11 vs 50.5 ± 6.71%; p = 0.014) was lower, and RV myocardial performance index (0.21 ± 0.07 vs 0.33 ± 0.19; p = 0.007), and pulmonary vascular resistance (1.13 ± 0.25 vs 1.32 ± 0.26 Woods unit; p = 0.012) were higher in patients than controls. Patients presented higher serum levels of unconjugated bilirubin (0.24 ± 0.15 vs 1.30 ± 0.89 mg/dL; p < 0.001), soluble vascular cell adhesion molecule-1 (sVCAM-1; 453 ± 143 vs 1983 ± 880 ng/mL; p < 0.001), N-terminal prohormone brain natriuretic peptide (0.59 ± 0.86 vs 1.08 ± 0.81 pg/mL; p = 0.045), and troponin T (861 ± 338 vs 1037 ± 264 pg/mL; p = 0.045), and lower levels of plasma nitrite (13.42 ± 8.15 vs 8.98 ± 3.97 μM; p = 0.016) than controls. Most alterations had reversed by D7. CONCLUSION: malaria present subclinical reversible cardiovascular changes.
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Filho et al. (2016) conducted a case-control in Non-severe Plasmodium vivax malaria (n=51). Non-severe Plasmodium vivax malaria infection vs. Age- and gender-matched healthy individuals testing negative for malaria was evaluated on Left ventricular ejection fraction (Teicholz method) at day 0 (p=0.004). Non-severe Plasmodium vivax malaria patients had lower left ventricular ejection fraction (68.4% vs 73.2%, p=0.004) and right ventricular fractional area change (50.5% vs 54.7%, p=0.014) than controls.
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