Why the study?
Does the presence of cardiac troponin gene mutations worsen exercise-induced LV systolic dysfunction in patients with non-obstructive hypertrophic cardiomyopathy?
Does the presence of cardiac troponin gene mutations worsen exercise-induced LV systolic dysfunction in patients with non-obstructive hypertrophic cardiomyopathy?
HCM patients with cardiac troponin gene mutations exhibit more pronounced exercise-induced LV systolic dysfunction compared to those without these mutations.
Troponin mutations may mark higher-risk non-obstructive HCM for exercise dysfunction; hypothesis-generating and needs prospective validation.
OBJECTIVES: The aim of this study was to investigate left ventricular (LV) function reserve in hypertrophic cardiomyopathy (HCM) patients with and without cardiac troponin gene mutations before transition to the dilated phase. METHODS: LV ejection fraction (EF) was continuously evaluated in 52 patients with non-obstructive HCM during supine ergometer exercise using radionuclide ventricular function monitoring with a cadmium telluride detector (VEST). On the basis of genetic analysis, patients were divided into two groups: 10 with cardiac troponin gene mutations (group A) and 42 without these gene mutations (group B). RESULTS: Exercise duration, peak exercise load, and heart rate during exercise did not differ between the two groups. The differences from baseline to peak exercise ofthe LV end-diastolic volume decreased similarly in the twogroups. In contrast, the difference of the LV end-systolicvolume in group A increased significantly compared withgroup B (17.7% (SD 12.7%) vs 3.4% (SD 13.2%);p=0.0031). Consequently, the difference of LVEF ingroup A decreased significantly in contrast with group B(-14.1% (SD 11.1%) vs -1.2% (SD 11.7%); p=0.0025).Additionally, the changes in LVEF and stroke volumedecreased significantly more in group A than in group B(-22.2% (SD 18.6%) vs -1.1% (SD 17.8%); p=0.0017and -12.9% (SD 21.7%) vs 12.3% (SD 24.4%);p=0.0042, respectively). CONCLUSIONS: These results suggest that HCM patientswith cardiac troponin gene mutations may displayexercise-induced LV systolic dysfunction more frequentlythan HCM patients without this abnormality
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Sakata et al. (2007) studied this question.
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