Papillary muscle infarction in relation to left ventricular infarct distribution and transmurality - assessment by delayed enhancement cardiac magnetic resonance imaging

Abstract

Summary This study used delayed enhancement CMR (DE-CMR) and invasive angiography to evaluate relationships between papillary muscle and left ventricular (LV) chamber wall infarction following ST segment elevation MI (STEMI). Results demonstrate that papillary muscle infarction (PMI) parallels infarct transmurality and contractile dysfunction within the adjacent LV wall. Background Papillary muscles and myocardium within the adjacent LV wall constitute two components of the mitral valve apparatus. Prior studies have demonstrated variable papillary arterial supply, and the relationship between PMI and overall LV infarct pattern is unknown. DECMR enables in-vivo study of infarct pattern within the LV - papillary muscle complex. Methods Patients with initial STEMI were enrolled in a prospective imaging registry. CMR (1.5T) was performed within 6 weeks (27±8 days) post-STEMI. Cine-CMR (SSFP) was used to assess LV wall motion (17 segment model, 5 point per-segment score) DE-CMR (IR-GRE, acquired 10-30 minutes post gadolinium [0.2 mmol/kg]) was used to assess infarct morphology: PMI was graded for location and extent (partial or complete, stratified by >50% papillary hyperenhancement); LV infarction was quantified based on global size and regional transmurality (17 segment, 5 point per-segment score). Invasive coronary angiograms were read blinded to CMR. Results 153 patients were studied, among whom 30% had PMI (74% posteromedial/37% anterolateral; 11% bilateral). Overall LV infarct size on DE-CMR was larger among patients with PMI (p=0.01). PMI strongly related to LV infarct distribution (Table 1), with prevalence increased 3-fold among patients with lateral wall, and over 1.5fold with inferior wall infarction on DE-CMR (p≤0.01). Angiography findings paralleled DE-CMR, with over a 2-fold increase in PMI with right coronary artery (RCA) or left circumflex (LCX) culprit vessel infarction (p<0.01). Among patients with RCA infarcts, PMI exclusively occurred (100%) in the setting of right or codominant coronary anatomy and was associated with larger angiographic jeopardy score (20.8±6.0 vs. 15.8 ±5.9, p=0.007). In contrast ,o nly one-third (36%) with PMI and LCX infarcts were left or co-dominant, with similar jeopardy scores between patients with and without PMI (19.4±9.8 vs. 15.3±11.6, p=0.45). Regarding extent, PMI was partial (≤50% hyperenhancement) in 76% of cases. PMI extent paralleled infarct transmurality in adjacent LV segments (Figure 1), with similar results when regional wall motion score was used as a surrogate for LV injury (all p<0.001). Additionally, there was a stepwise increase in LV lateral wall infarct size (% myocardium) among patients with bilateral PMI (12.8 ±4.2%) compared to those with isolated (3.5±4.2%) or absent PMI (0.8±2.0%) (p<0.001 for trend).