HEAL (Heart Evaluation of Arrhythmia and Lipomatosis) Study

PURPOSE We aim to conduct a prospective observational study to test the central hypothesis that myocardial LM begins early after STEMI, as a response to myocardial hemorrhage and reperfusion injury, and determines future susceptibility to malignant arrhythmia. Study participants will be 175 (allowing for 25 dropouts) men and women 2 months since percutaneous intervention (PCI) for acute STEMI at 3 hospitals within the University of Pennsylvania Health System (UPHS), recruited over the first 2.5 years of the proposed funding period. All patients will undergo CMR with functional cine, fat/water separation, LGE sequences, and quantitative susceptibility mapping (QSM), at baseline, and at 1- and 2-years follow-up. We anticipate that at least 150 patients with complete data (allowing for 25 dropouts from the total 175 recruitment plan) will be eligible for all aims. The specific aims of the proposal are:

Aim 1. To define the yearly incidence and volume of LM and cardiac remodeling, and their association with clinical factors, among patients with prior MI and PCI. The progression of LM and its association with clinical factors following PCI for STEMI remain undefined. We hypothesize that LM incidence occurs early post STEMI and that its progression is associated with time since reperfusion. We will utilize mixed-effects longitudinal modeling strategies to describe the progression of LM and LGE volume on fat/water separation and LGE imaging following MI. We will then estimate the extent to which the 2-year change in LM is associated with time since reperfusion and clinical factors including sex, biomarkers, and co-morbidities. Aim 2. To examine the association of LM evolution with infarct size and reperfusion injury. Early animal data suggests that hemorrhage in the MI zone results in apoptosis, and iron recycling, ultimately leading to LM.15 We hypothesize that the extent of LM is associated with reperfusion injury following PCI for STEMI. We will use mixed effects longitudinal models with time dependent LM volume on fat/water separation as the dependent variable, and extent of infarct on LGE and myocardial hemorrhage on QSM imaging as independent variables to define the association of LM evolution with the initial extent of reperfusion injury. Aim 3. To examine the association of sustained VT, appropriate ICD therapy, or sudden death with the evolution of viable corridors traversing LM. The longitudinal association of malignant arrhythmia with LM evolution remains unknown. We hypothesize that LM precedes and predicts the incidence of VT following MI. We will use Cox proportional hazards models with time to sustained VT, appropriate ICD therapy, or sudden death as the dependent variable, and the time dependent number of viable corridors traversing through LM as the primary independent variable. Aim 1 - The primary dependent variable will be LM volume, derived from fat/water separation imaging as a time dependent variable. Aim 2 - The primary dependent variable will be time-dependent LM volume, derived from fat/water separation imaging. Aim 3 - The primary dependent variable will be time to first sustained VT from ICD systems, sustained VT, sudden death or last follow-up Aim 1 - Secondary dependent variables will be time dependent: i. Fibrosis volume, ii. LVEF, iii. LVEDV, and iv. LV volume from functional cine images. Aim 2 - Secondary dependent variables will be time dependent: i. Fibrosis volume, ii. LVEF, iii. LVEDV, and iv. LV volume from functional cine images. Aim 3 N/A

You may be eligible for this study if you meet the following criteria:

• Conditions: Medical Research
• Age: 99 years or below
• Gender: All