Echocardiographic evaluation of cardiac involvement in myeloproliferative disorders

Abstract EN

C events are common cause of death in patients with myeloproliferative disorders (MPD) especially those with cardiac involvement.

In previous studies, cardiac involvement, including coronary arterial thrombosis, myocardial infarction, pulmonary hypertension (PHT), asymptomatic pericardial effusion, cardiac tamponade, intractable cardiac failure due to intraventricular thrombosis, and stenosis of aortic, mitral valves, even requiring surgical treatment had been reported in MPD This cohort study was carried out in three Iraqi teaching hospitals for Medicine including Al-Kadhimyya Teachginmg Hospital, Al-Yarmook Teaching Hospital (including National haematology Centre) and Merjan Teaching hospital in Babylon.

The study groups were 26 patients (mean age female and male) with MPD and 30 age-matched healthy controls.

MPD group included sixteen cases chronic phase chronic myelogenous leukemia (CML), two idiopathic myelofibrosis (MF), seven polycythemia vera and one essential thrombocythemia .

History regarding thrombotic and bleeding complications, examination and lab investigations are evaluated for these patients and transthoracic echocardiographic study was done for them and for the control subjects.

The results are compared by statistical methods.

Mitral regurgitations were present in 9 patients (34.6%) and two controls (6.7%) (P < 0.05).

Aortic regurgitation were present in 3 patients (11.5%) and no control (0.00%) (p < 0.05%).

Rates of regurgitations of other valves were not different in-between MPD subgroups and control (P>0.05).

The rates of annular calcifications and valvular thickening were not different between MPD and control groups.

Pulmonary hypertension (PHT) was not detected in patients or control.

Measurements of ejection fraction, fractional shortening of left ventricle, E/A ratio and aortic root dimension are significantly different between MPD and control (P<0.05).

Left atrial dimension of patients with MPD was larger than controls (P>0.05).

Left atrial dimension was the largest in PV (P<0.005).

End-diastolic diameter of left ventricle, opening of aortic valve and left atrial dimension were larger in patients with thromboembolic events than patients without thromboembolic events (P<0.05).

Measurements of ejection fraction and fractional shortening of left ventricle were lower in MPD groups than control (P<0.05 and <0.005) respectively.

The rates of all other echocardiographic parameters were not significantly different related to existence of thromboembolic events (P>0.05).

This study showed that valvular lesions were more prevalent in MPD.

Erythrocytosis was more important than thrombocytosis in relation to cardiac parameters which related to thromboembolic events.

Further evaluation of the cardiac changes in MPD subgroups with extended studies including trans-esophageal echocardiography, right-heart catheterization and longer follow-up periods would be appropriate