Abstract 15889: The Role of Physical Deconditioning in Distinguishing Hypertrophic Cardiomyopathy From Athlete's Heart

Abstract

Background: Vigorous systematic physical training can result in increased left ventricular wall thickness (LVWT) (i.e., “athlete’s heart”) which can be challenging to differentiate diagnostically from mild non-obstructive hypertrophic cardiomyopathy (HCM). The efficacy of a deconditioning strategy to observe changes in LVWT using cardiovascular magnetic resonance (CMR) that would support a diagnosis of athlete’s heart vs. HCM is not well established. Methods: We identified 9 highly trained patients involved in various organized sports who were referred to the Tufts Medical Center HCM center with a maximal LVWT in a diagnostic “gray area” of 13-15 mm. Maximal LVWT and other clinical and imaging variables were compared at baseline and following > 3 months of deconditioning from athletic training. A clinically relevant change in maximal LVWT at the end of athletic deconditioning was defined as a decrease of ≥2 mm, consistent with “athlete’s heart”. Imaging studies were interpreted blinded to study time period. Results: Among the 9 patients (23.1 ± 12.3 years old; 100% male), 4 demonstrated a ≥ 2 mm decrease in maximal LVWT (range: 2 mm to 3 mm) to ≤ 12 mm in 3 patients and 13 mm in one patient, with an average decrease of 2.3 mm. Among these 4 patients, LV and LA size also decreased (217.3 ± 31.5 ml to 208.9 ± 16.8 ml; and 55.4 ± 10.0 mm to 51.7 ± 9.1 mm, respectively), and there was no late gadolinium enhancement, pathogenic sarcomere mutation, or family history of HCM. Parameters of diastolic function were normal prior to deconditioning. After deconditioning evaluation and significant change in LVWT, these 4 patients were judged to not have a clinical diagnosis of HCM. The remaining 5 patients had a non-significant change in maximal LVWT after deconditioning of 0.2 mm, with maximal LVWT remaining ≥ 13 mm, and no change in LV or LA cavity size (p>0.2 for each). After deconditioning, these 5 patients were judged to have a clinical diagnosis of HCM. In the 9 patients that underwent a period of deconditioning, there was an average heart rate increase of 6.33. Conclusion: In athletes with maximal LVWT within the “gray zone” (13-15 mm) of overlap with HCM, athletic deconditioning using CMR to detect changes in maximal LVWT can aid in the differential diagnosis and inform management decisions.