Abstract

Cardiovascular system involvement in patients with Plasmodium vivax 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. 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. Patients with non-severe Plasmodium vivax malaria present subclinical reversible cardiovascular changes.

Abstract

Aortic valve stenosis (AS) is characterized by chronic left ventricular pressure overload, leading to left ventricular hypertrophy (LVH). We assessed correlations in left ventricular volumes and function between echocardiography and quantitative gated SPECT (QGS) in patients with AS. The study population consisted of 28 patients with AS defined as a peak velocity of > 3.0 m/s and 28 age- and sex-matched control subjects. Patients with AS had a peak pressure gradient of 73.4 ± 24.5 mm Hg and a larger LVM index compared to control subjects (115.5 ± 29.2 g/m2 vs 78.3 ± 12.1 g/m2, p < 0.01). There were good correlations in end-diastolic volume and end-systolic volume between echocardiography and QGS in patients with AS as well as control subjects. Bland–Altman plot for end-systolic volume showed a significant negative slope of − 0.51 in patients with AS. There was a good correlation in ejection fraction between the 2 methods in patients with AS as well as control subjects. However, Bland–Altman plots showed significant negative slopes of − 0.40 in patients with AS and − 0.74 in control subjects. Our data suggested that QGS was a useful method for assessing left ventricular volumes and function even in patients with AS. Cardiologists should recognize its specific characteristics.