A Multicenter Evaluation of the Impact of Therapies on Deep Learning-based Electrocardiographic Hypertrophic Cardiomyopathy Markers.

Background: Artificial intelligence-enhanced electrocardiography (AI-ECG) can identify hypertrophic cardiomyopathy (HCM) on 12-lead ECGs and offers a novel way to monitor treatment response. While the surgical or percutaneous reduction of the interventricular septum (SRT) represented initial HCM therapies, mavacamten offers an oral alternative. Objective: To evaluate biological response to SRT and mavacamten. Methods: We applied an AI-ECG model for HCM detection to ECG images from patients who underwent SRT across three sites: Yale New Haven Health System (YNHHS), Cleveland Clinic Foundation (CCF), and Atlantic Health System (AHS); and to ECG images from patients receiving mavacamten at YNHHS. Results: A total of 70 patients underwent SRT at YNHHS, 100 at CCF, and 145 at AHS. At YNHHS, there was no significant change in the AI-ECG HCM score before versus after SRT (pre-SRT: median 0.55 [IQR 0.24-0.77] vs post-SRT: 0.59 [0.40-0.75]). The AI-ECG HCM scores also did not improve post SRT at CCF (0.61 [0.32-0.79] vs 0.69 [0.52-0.79]) and AHS (0.52 [0.35-0.69] vs 0.61 [0.49-0.70]). Among 36 YNHHS patients on mavacamten therapy, the median AI-ECG score before starting mavacamten was 0.41 (0.22-0.77), which decreased significantly to 0.28 (0.11-0.50, p <0.001 by Wilcoxon signed-rank test) at the end of a median follow-up period of 237 days. Conclusions: The lack of improvement in AI-based HCM score with SRT, in contrast to a significant decrease with mavacamten, suggests the potential role of AI-ECG for serial monitoring of pathophysiological improvement in HCM at the point-of-care using ECG images.

Exercise After Acute Myocarditis: When and How to Return to Sports.

Myocarditis is an inflammatory disease of the myocardium secondary to infectious and noninfectious insults. The most feared consequence of myocarditis is sudden cardiac death owing to electrical instability and arrhythmia. Typical presenting symptoms include chest pain, dyspnea, palpitations and/or heart failure. Diagnosis is usually made with history, electrocardiogram, biomarkers, echocardiogram, and cardiac MRI (CMR). Application of the Lake Louise criteria to CMR results can help identify cases of myocarditis. Treatment is usually supportive with medical therapy, and patients are recommended to abstain from exercise for 3 to 6 months. Exercise restrictions may be lifted after normalization on follow-up testing.

Exercise recommendations for patients with hypertrophic cardiomyopathy.

Individuals with hypertrophic cardiomyopathy (HCM) have historically been advised to limit exercise and sports participation to mild-intensity activities due to concerns for sudden cardiac arrest (SCA). However, more contemporary data have shown SCA is rare in patients with HCM and emerging data is shifting towards support for the safety of exercise in this patient population. Recent guidelines endorse exercise in patients with HCM after a comprehensive evaluation and shared-decision making with an expert provider.

Exercise After Acute Myocarditis: When and How to Return to Sports.

Myocarditis is an inflammatory disease of the myocardium secondary to infectious and noninfectious insults. The most feared consequence of myocarditis is sudden cardiac death owing to electrical instability and arrhythmia. Typical presenting symptoms include chest pain, dyspnea, palpitations and/or heart failure. Diagnosis is usually made with history, electrocardiogram, biomarkers, echocardiogram, and cardiac MRI (CMR). Application of the Lake Louise criteria to CMR results can help identify cases of myocarditis. Treatment is usually supportive with medical therapy, and patients are recommended to abstain from exercise for 3 to 6 months. Exercise restrictions may be lifted after normalization on follow-up testing.

Cardiac structure and function in elite female athletes: A systematic review and meta-analysis.

We conducted a meta-analysis to synthesize the best available evidence comparing cardiac biventricular structure and function using cardiac magnetic resonance imaging (CMR) and transthoracic echocardiography (TTE) in elite female athletes and healthy controls (HC). Chronic exposure to exercise may induce cardiac chamber enlargement as a means to augment stroke volume, a condition known as the "athlete's heart." These changes have not been clearly characterized in female athletes. Multiple databases were searched from inception to June 18, 2019. Outcomes of interest included left ventricular (LV) and right ventricular (RV) dimensional, volumetric, mass, and functional assessments in female athletes. Most values were indexed to body surface area. The final search yielded 22 studies, including 1000 female athletes from endurance, strength, and mixed athletic disciplines. CMR-derived LV end-diastolic volume (LVEDV) and RV end-diastolic volume (RVEDV) were greater in endurance athletes (EA) versus HC (17.0% and 18.5%, respectively; both p < 0.001). Similarly, TTE-derived LVEDV and RVEDV were greater in EA versus HC (16.8% and 28.0%, respectively; both p < 0.001). Both LVEF and RVEF were lower in EA versus HC, with the most pronounced difference observed in RVEF via TTE (9%) (p < 0.001). LV stroke volume was greater in EA versus HC via both CMR (18.5%) and TTE (13.2%) (both p < 0.05). Few studies reported data for the mixed athlete (MA) population and even fewer studies reported data for strength athletes (SA), therefore a limited analysis was performed on MA and no analysis was performed on SA. This evidence-synthesis review demonstrates the RV may be more susceptible to ventricular enlargement. General changes in LV and RV structure and function in female EA mirrored changes observed in male counterparts. Further studies are needed to determine if potential adverse outcomes occur secondary to these changes.

Subaortic Membrane Papillary Fibroelastoma.

A 61-year-old male presented for an annual exam and received a transthoracic echocardiogram (TTE) which revealed a mobile mass arising from a subaortic membrane. Further investigations with a transesophageal echocardiogram (TEE) and cardiac computerized tomography angiography (CTA) confirmed the presence of a mobile 9 mm × 3 mm mass on a subaortic membrane. Cardiothoracic surgery was performed with an open operation removing the mass and subaortic membrane. Upon visual inspection, the mass was likened to a sea anemone and immunohistochemical staining performed pathologically confirmed the diagnosis of cardiac papillary fibroelastoma. This case represents the first reported example of a cardiac papillary fibroelastoma (PFE) arising from a subaortic membrane. Although PFEs are benign cardiac tumors, proper identification and consideration for excision of these lesions may be indicated to prevent thromboembolic complications.

Eosinophillic Myocarditis Secondary to Metastatic Melanoma.

Eosinophilic myocarditis is a rare form of myocarditis that may manifest from cancer-mediated inflammation. A case of eosinophilic myocarditis secondary to metastatic melanoma is described; metastatic melanoma can cause a T helper type 2 lymphocyte-mediated increase in circulating levels of interleukin-5, which is known to stimulate eosinophil proliferation resulting in myocardial inflammation and fibrosis. Cardiac imaging with transesophageal echocardiography revealed a large immobile left ventricular apical thrombus. Cardiac MRI was then performed and revealed enhancing fibrosis along the endocardial surface. © RSNA, 2019 Supplemental material is available for this article.

Eosinophillic Myocarditis Secondary to Metastatic Melanoma.

Eosinophilic myocarditis is a rare form of myocarditis that may manifest from cancer-mediated inflammation. A case of eosinophilic myocarditis secondary to metastatic melanoma is described; metastatic melanoma can cause a T helper type 2 lymphocyte-mediated increase in circulating levels of interleukin-5, which is known to stimulate eosinophil proliferation resulting in myocardial inflammation and fibrosis. Cardiac imaging with transesophageal echocardiography revealed a large immobile left ventricular apical thrombus. Cardiac MRI was then performed and revealed enhancing fibrosis along the endocardial surface. © RSNA, 2019 Supplemental material is available for this article.