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Lifelong Left Ventricular Remodeling of Hypertrophic Cardiomyopathy Caused by a Founder Frameshift Deletion Mutation in the Cardiac Myosin-Binding Protein C Gene Among Japanese

Toru Kubo, MD^_*, Hiroaki Kitaoka, MD, PhD^_*, Makoto Okawa, MD^_*, Yoshihisa Matsumura, MD, PhD^_*, Nobuhiko Hitomi, MD^_*, Naohito Yamasaki, MD^_*, Takashi Furuno, MD^_*, Jun Takata, MD, PhD^_*, Masanori Nishinaga, MD, PhD^_*, Akinori Kimura, MD, PhD and Yoshinori L. Doi, MD, PhD, FACC^_*,_*

^_* Department of Medicine and Geriatrics, Kochi Medical School, Kochi, Japan
Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan

View larger version (25K): [in a new window]   Figure 1 (A to G) Pedigree of families H007, H008, H011, H015, H027, H034, H037, H041, H047, H048, H061, H067, H074, H086, and H090. The genotypic status and phenotypic status of subjects are indicated.

View larger version (18K): [in a new window]   Figure 2 Longitudinal echocardiographic changes in 39 genotype-positive individuals during the follow-up period. (A) Changes in left ventricular end-diastolic diameter (LVEDD). (B) Changes in ejection fraction (EF). (C) Changes in maximum left ventricular wall thickness (MLVWT).