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.
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. DE-CMR enables in-vivo study of infarct pattern within the LV - papillary muscle complex.
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.
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 1.5-fold 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 co-dominant coronary anatomy and was associated with larger angiographic jeopardy score (20.8±6.0 vs. 15.8±5.9, p=0.007). In contrast, only 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).
PMI is common following STEMI, with PMI extent paralleling infarct transmurality and contractile dysfunction within the adjacent LV wall. Current findings dispute the notion of papillary muscles as end-organ structures particularly susceptible to impaired perfusion, instead supporting the concept that papillary muscles and adjacent LV myocardium are similarly vulnerable to jeopardized arterial supply.
K23 HL102249-01, Lantheus Medical Imaging, Doris Duke Clinical Scientist Development Award (Jonathan W. Weinsaft, MD).