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Exercise-induced systolic dysfunction in patients with non-obstructive hypertrophic cardiomyopathy and mutations in the cardiac troponin genes
  1. Kenji Sakata (kenjis{at}yu.incl.ne.jp)
  1. Kanazawa University, Japan
    1. Hidekazu Ino
    1. Kanazawa University, Japan
      1. Noboru Fujino
      1. Kanazawa University, Japan
        1. Mitsuru Nagata
        1. Kanazawa University, Japan
          1. Katsuharu Uchiyama
          1. Kanazawa University, Japan
            1. Kenshi Hayashi
            1. Kanazawa University, Japan
              1. Tetsuo Konno
              1. Kanazawa University, Japan
                1. Masaru Inoue
                1. Kanazawa University, Japan
                  1. Hiromasa Kato
                  1. Kanazawa University, Japan
                    1. Yuichiro Sakamoto
                    1. Kanazawa University, Japan
                      1. Toshinari Tsubokawa
                      1. Kanazawa University, Japan
                        1. Masakazu Yamagishi
                        1. Kanazawa University, Japan

                          Abstract

                          Objectives 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 2 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 2 groups. The differences from baseline to peak exercise of the LV end-diastolic volume decreased similarly in the 2 groups. In contrast, the difference of the LV end-systolic volume in group A increased significantly compared with group B (p = 0.0031). Consequently, the difference of LVEF in group A decreased significantly in contrast with group B (p = 0.0025). Additionally, the changes in LVEF and stroke volume decreased significantly more in group A than in group B (p = 0.0017 and 0.0042, respectively).

                          Conclusions These results suggest that HCM patients with cardiac troponin gene mutations may display exercise-induced LV systolic dysfunction more frequently than HCM patients without this abnormality.

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