Sean Wilson

Mitral Apparatus Assessment by Delayed Enhancement CMR: Relative Impact of Infarct Distribution on Mitral Regurgitation

OBJECTIVES This study sought to assess patterns and functional consequences of mitral apparatus infarction after acute myocardial infarction (AMI). BACKGROUND The mitral apparatus contains 2 myocardial components: papillary muscles and the adjacent left ventricular (LV) wall. Delayed-enhancement cardiac magnetic resonance (DE-CMR) enables in vivo study of inter-relationships and potential contributions of LV wall and papillary muscle infarction (PMI) to mitral regurgitation (MR). METHODS Multimodality imaging was performed: CMR was used to assess mitral geometry and infarct pattern, including 3D DE-CMR for PMI. Echocardiography was used to measure MR. Imaging occurred 27 ± 8 days after AMI (CMR, echocardiography within 1 day). RESULTS A total of 153 patients with first AMI were studied; PMI was present in 30% (n = 46 [72% posteromedial, 39% anterolateral]). When stratified by angiographic culprit vessel, PMI occurred in 65% of patients with left circumflex, 48% with right coronary, and only 14% of patients with left anterior descending infarctions (p <0.001). Patients with PMI had more advanced remodeling as measured by LV size and mitral annular diameter (p <0.05). Increased extent of PMI was accompanied by a stepwise increase in mean infarct transmurality within regional LV segments underlying each papillary muscle (p <0.001). Prevalence of lateral wall infarction was 3-fold higher among patients with PMI compared to patients without PMI (65% vs. 22%, p <0.001). Infarct distribution also impacted MR, with greater MR among patients with lateral wall infarction (p = 0.002). Conversely, MR severity did not differ on the basis of presence (p = 0.19) or extent (p = 0.12) of PMI, or by angiographic culprit vessel. In multivariable analysis, lateral wall infarct size (odds ratio 1.20/% LV myocardium [95% confidence interval: 1.05 to 1.39], p = 0.01) was independently associated with substantial (moderate or greater) MR even after controlling for mitral annular (odds ratio 1.22/mm [1.04 to 1.43], p = 0.01), and LV end-diastolic diameter (odds ratio 1.11/mm [0.99 to 1.23], p = 0.056). CONCLUSIONS Papillary muscle infarction is common after AMI, affecting nearly one-third of patients. Extent of PMI parallels adjacent LV wall injury, with lateral infarction-rather than PMI-associated with increased severity of post-AMI MR.

Meaningful Thresholds for the Volume-Outcome Relationship in Total Knee Arthroplasty.

BACKGROUND Increasing evidence supports the finding that patients undergoing a total knee arthroplasty with high-volume physicians and hospitals achieve better outcomes. Unfortunately, the existing definitions for high-volume surgeons and hospitals are highly variable and entirely arbitrary. The aim of this study was to identify a set of meaningful hospital and surgeon total knee arthroplasty volume thresholds. METHODS Using 289,976 patients undergoing primary total knee arthroplasty from an administrative database, we applied stratum-specific likelihood ratio (SSLR) analysis of a receiver operating characteristic (ROC) curve to generate sets of volume thresholds most predictive of adverse outcomes. The outcomes considered for surgeon volume included 90-day complication and 2-year revision. For hospital volume, we considered 90-day complications and 90-day mortality. RESULTS SSLR analysis of the ROC curves for 90-day complication and 2-year revision rates by surgeon volume identified four volume categories: 0 to 12, 13 to 59, 60 to 145, and ≥146 total knee arthroplasties per year. Complication rates decreased significantly (p < 0.05) in progressively higher-volume categories. Revision rates followed a similar pattern, but did not decrease between surgeons performing 60 to 145 arthroplasties per year and those performing ≥146 arthroplasties per year. SSLR analysis of 90-day complication and 90-day mortality rates by hospital volume also identified four volume categories: 0 to 89, 90 to 235, 236 to 644, and ≥645 total knee arthroplasties per year. Complication rates decreased significantly (p < 0.05) in progressively higher-volume categories, but the rates did not decrease between hospitals performing 236 to 644 arthroplasties per year and those performing ≥645 arthroplasties per year. Mortality rates for hospitals with ≥645 total knee arthroplasties per year were significantly lower (p < 0.05) than those below the threshold. CONCLUSIONS Our study supports the use of SSLR analysis of ROC curves for risk-based volume stratification in total knee arthroplasty volume-outcomes research. SSLR analysis established meaningful volume definitions for low, medium, high, and very high-volume total knee arthroplasty surgeons and hospitals. This should help patients, surgeons, hospitals, and policymakers to make decisions with regard to the optimal delivery of total knee arthroplasty. LEVEL OF EVIDENCE Therapeutic Level III. See Instructions for Authors for a complete description of levels of evidence.

Pulmonary hypertension and right ventricular dysfunction in left heart disease (group 2 pulmonary hypertension)

Group 2 pulmonary hypertension is most frequently caused by left heart disease, a heterogeneous set of disorders. These processes include left ventricular systolic dysfunction, left ventricular dysfunction with preserved ejection fraction and valvular (mitral and/or aortic) diseases. Left heart disease may cause passive backward transmission of pressure leading to elevated left atrial and pulmonary arterial pressures due to a myriad of processes. Increasingly, it has been recognized that some patients may develop pulmonary arterial pressure out of proportion from what is expected. This is believed to be due to increases in vasomotor tone and/or vascular remodeling. Over time patients may go on to develop progressive right ventricular dysfunction, a marker for poor prognosis. This review will explore the different characteristics of these conditions including the incidence, pathophysiology, clinical implications, prognosis and current state of available medical therapies.

Arthrodesis of the First Metatarsocuneiform Joint: A Comparative Cadaveric Study of External and Internal Fixation

UNLABELLED Arthrodesis of the first metatarsocuneiform joint for the treatment of severe hallux abductovalgus with or without hypermobility of the first ray has gained popularity in recent years. The purpose of the current study was to compare the strength of external fixation to internal fixation for arthrodesis of the first metatarsocuneiform joint in a cadaveric model. Ten pairs of fresh frozen lower extremity cadaver specimens were used, and randomly assigned to fixation at the first metatarsocuneiform joint with crossed cannulated screws or a monorail uniplanar external fixator. Test specimens were then loaded to failure, which was defined as 3 mm or more of displacement at the arthrodesis site. Because of complications encountered during testing, 4 pairs of specimens were excluded from the final results. In the remaining 12 specimens (6 pairs of cadaver limbs), the mean maximal load to failure was 2300.02 +/- 711.86 N for the external fixator and 1666.38 +/- 1072.75 N for the internal fixation construct, and although this difference was not statistically significant (P = .2557), it was likely to have been clinically significant since approximately 27.55% more force was required to disrupt the external fixation construct in comparison with the internal fixation construct. Given these findings, further research into the mechanical and clinical properties of internal and external fixation for first metatarsocuneiform joint arthrodesis is warranted. LEVEL OF CLINICAL EVIDENCE 5.

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

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).

A worrisome interventricular septum: more than meets the eye.

![Figure][1] [![Graphic][3] ][3][![Graphic][4] ][4][![Graphic][5] ][5][![Graphic][6] ][6] A 59-year-old woman with known enteropathy-associated T-cell lymphoma (EATL) presented with weakness and malaise. An electrocardiogram demonstrated sinus tachycardia, right bundle

Correction to: Patient and Surgeon Expectations Prior to Anterior Cruciate Ligament Reconstruction

The degree of author Hassan Ghomrawi was listed incorrectly in the original article. It is correct here.

ETIOLOGY AND DOWNSTREAM HEMODYNAMIC IMPACT OF PULMONARY HYPERTENSION IN PATIENTS UNDERGOING TRANSCATHETER AORTIC VALVE REPLACEMENT

Pulmonary hypertension (PH) is common among pts with pulmonary disease and aortic stenosis undergoing transcatheter aortic valve replacement (TAVR). The prevalence of pre- and postcapillary PH among TAVR pts and its impact upon hemodynamics are unknown. We compared changes in invasively determined

Mitral apparatus assessment by delayed enhancement CMR - relative impact of papillary muscle and left ventricular wall infarction on ischemic mitral regurgitation

Summary Lateral wall infarction on DE-CMR, independent of papillary muscle involvement, confers increased risk for ischemic mitral regurgitation. Background The mitral apparatus contains two myocardial components - papillary muscles and the adjacent left ventricular (LV) wall. Delayed enhancement CMR (DE-CMR) enables in-vivo study of potential contributions of LV wall and papillary muscle infarction (PMI) to MR. This study examined the relative impact of papillary muscle and LV wall infarction on mitral regurgitation (MR) following ST elevation MI (STEMI). Methods Multimodality imaging was prospectively performed among patients with first STEMI: DE-CMR (IR-GRE, acquired 10-30 minutes post gadolinium [0.2 mmol/kg]) was used to assess LV infarct pattern - including PMI (graded by location and extent - complete or partial, stratified using threshold of >50% papillary myocardium) and LV wall infarction (17 segment model, 5 point score/segment). Cine-CMR (SSFP) was analyzed for cardiac function and geometry - including LV chamber size, regional wall motion (5 point score/segment), and mitral annular diameter. Echocardiography (echo) was used to quantify MR (0-4+ grade) using established consensus criteria. Each imaging modality was read independently.