Reduced flow in the left ventricle after anterior acute myocardial infarction: a case control study using 4D flow MRI [post]

2019 unpublished
Acute myocardial infarction (AMI) alters left ventricular (LV) hemodynamics, resulting in decreased global LV ejection fraction and global LV kinetic energy. We hypothesize that anterior AMI effects localized alterations in LV flow and developed a regional approach to analyze these local changes with 4D flow MRI. Methods: 4D flow cardiac magnetic resonance (CMR) data was compared between 12 anterior AMI patients (11 males; 66±12yo; prospectively acquired in 2016-2017) and 19 healthy volunteers
more » ... healthy volunteers (10 males; 40±16yo; retrospective from 2010-2011 study). The LV cavity was contoured on short axis cine steady-state free procession CMR and partitioned into three regions: base, mid-ventricle, and apex. 4D flow data was registered to the short axis segmentation. Peak systolic and diastolic through-plane flows were compared region-by-region between groups using linear models of flow with age, sex, and heart rate as covariates. Results: Peak systolic flow was reduced in anterior AMI subjects compared to controls in the LV mid-ventricle (fitted reduction = 3.9 L/min; P=0.01) and apex (fitted reduction = 1.4 L/min; P=0.02). Peak diastolic flow was also lower in anterior AMI subjects compared to controls in the apex (fitted reduction = 2.4 L/min; P=0.01). Conclusions: A regional method to analyze 4D LV flow data was applied in anterior AMI patients and controls. Anterior AMI patients had reduced regional flow relative to controls. Background Acute myocardial infarction (AMI) is widespread [1] and has high mortality and morbidity [2]. AMI alters left ventricular (LV) hemodynamics, resulting in increased left ventricular volumes and decreased left ventricular ejection fraction (LVEF) -both powerful prognostic indicators post-AMI [3]. A common complication of AMI is left ventricular thrombus (LVT) -a causal substrate for stroke [4] . In a prospective study of 201 AMI patients, LVT were identified in 8% of all subjects and in 15% of those with anterior infarctions using cardiac magnetic resonance (CMR) within 30 days of infarction, with all thrombi located in the LV apex [5] . The pathogenesis of LVT is caused by a combination of blood stasis, endothelial injury and hypercoagulability, often referred to as Virchow's triad [6] . Velocity-sensitive imaging offers the opportunity to investigate blood stasis in the post-AMI left ventricle, shedding light on the mechanisms behind high rates of LVT. Several studies to date have
doi:10.21203/rs.2.10741/v2 fatcat:7zk4ficlpnb7pllylfhapm3q7e