Assessment of left ventricular systolic function in patients with iron deficiency anemia by three-dimensional speckle-tracking echocardiography

Abstract

Objective:The present study aimed to evaluate left ventricular (LV) systolic function in patients with iron deficiency anemia (IDA) by 3-dimensional speckle-tracking echocardiography (3DSTE).Methods:Participants were grouped by hemoglobin (Hb) levels in order to study the effect of anemia on cardiac function. Group A included 40 healthy volunteers. Eighty-three patients who were diagnosed with IDA were divided into 2 groups according to the Hb level. Group B (Hb 9 g/dL) included 44 patients, while group C (Hb 6–9 g/dL) included 39 patients. Left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular mass index (LVMI), and left ventricular ejection fraction (LVEF) were calculated by real-time 3-dimensional echocardiography (RT3D). Left ventricular global longitudinal strain (GLS), global area strain (GAS), global radial strain (GRS), and global circumferential strain (GCS) were obtained by 3DSTE.Results:LVMI, LVEDV and LVESV of group C increased and GCS, GRS, GLS, and GAS of group C decreased compared with those of groups A and B (all p<0.05). GAS and GLS decreased significantly compared with other parameters (both p<0.01).Conclusion:LV remodeling and LV systolic dysfunction occurred in patients when the hemoglobin level was in the range of 6–9 g/dL. 3DSTE can evaluate LV systolic function in patients with IDA, and GAS and GLS are more sensitive than other parameters.

Anemia and iron deficiency in heart failure: a review of echocardiographic features

“…Anemia leads to tissue hypoxia, which activates compensatory mechanisms such as increased cardiac output (by increasing stroke volume through cardiac contractility increase, as well as a blood viscosity decrease that leads to an increase in venous return and thus higher cardiac preload, and to a decrease in vascular peripheral resistances and thus lower cardiac afterload) . These hemodynamic changes cause an increase in left ventricular end‐diastolic volume (LVEDV), left ventricular end‐systolic volume (LVESV), left ventricular end‐diastolic diameter (LVEDD), and left ventricular end‐systolic diameter (LVESD), all proportional to the severity of anemia.…”

“…Anemia can lead to myocardial remodeling, with increasing absolute or indexed values of myocardial mass and the thickness of the interventricular septum and left ventricular posterior wall . Moreover, in patients with chronic kidney disease, the prevalence of ventricular hypertrophy can be higher in those with anemia, independently of arterial hypertension .…”

“…This bias can help explain the disparate results among studies. Several studies found no differences in systolic function between patients with and without anemia, but others found worse systolic function in patients with anemia . Moreover, different studies used different techniques to measure myocardial contractility (eg, left ventricular systolic time interval ratio or left ventricular pre‐ejection period in impedance cardiography), further confounding efforts to compare results …”

“…Speckle tracking can detect early ventricular systolic impairment in patients with anemia and may help demonstrate improved contractility after iron therapy. Anemic patients have decreased longitudinal peak strain in basal, mid, and apical segments of the left ventricle as well as decreased global longitudinal strain, global radial area, and global circumferential strain in the left ventricle. Moreover, some studies have shown that iron treatment is associated with improvement of the lateral systolic strain rate, although no changes in LVEF could be detected …”

“…57,58 Other studies have suggested that the main cause of changes in load conditions is anemia, not iron deficiency, because iron deficiency without anemia does not change indexed LVEDV, indexed LVESV, indexed stroke volume, or cardiac index. 59 Anemia can lead to myocardial remodeling, with increasing absolute or indexed values of myocardial mass 51,52,54 and the thickness of the interventricular septum and left ventricular posterior wall. 51,54 Moreover, in patients with chronic kidney disease, the prevalence of ventricular hypertrophy can be higher in those with anemia, independently of arterial hypertension.…”