title: Relation of functional and morphological changes in mitochondria to myocardial contractile and relaxation reserves in asymptomatic to mildly symptomatic patients with hypertrophic cardiomyopathy.
abstract: OBJECTIVE
  To examine the relation between mitochondrial dysfunction and myocardial contractile and relaxation reserves in hypertrophic cardiomyopathy (HCM).
  
  
  RESULTS
  Thirty HCM patients (LVEF >or=60%) underwent biventricular cardiac catheterization analysis both at rest and during atrial pacing as well as myocardial (99m)Tc-sestamibi scintigraphy at rest to calculate washout rate. Endomyocardial biopsy specimens were obtained for quantitative mRNA analysis and electron microscopy. The HCM patients were divided into two groups-group A: normal force-frequency relation and a pressure half-time (T(1/2)) of <30 ms (n = 15); group B: abnormal force-frequency relation or T(1/2) of >or=30 ms (n = 15). The (99m)Tc-sestamibi washout rate was significantly correlated with T(1/2) for all patients (r = 0.74, P < 0.01) and was also significantly greater in group B (29.2 +/- 6.3%) than in group A (19.3 +/- 3.1%). The abundance of mRNAs for mitochondrial electron transport-related enzymes was significantly higher in group A than in group B. Mitochondria showed a greater variation in size and were more disorganized in group B than in group A.
  
  
  CONCLUSIONS
  Mitochondria showed functional impairment and morphological disorganization in the left ventricle of HCM patients without baseline systolic dysfunction. These mitochondrial changes were associated with impaired myocardial contractile and relaxation reserves.
authors.affiliation: Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
authors.forename: Kazumasa
authors.initials: K
authors.lastname: Unno
authors.forename: Satoshi
authors.initials: S
authors.lastname: Isobe
authors.forename: Hideo
authors.initials: H
authors.lastname: Izawa
authors.forename: Xian Wu
authors.initials: XW
authors.lastname: Cheng
authors.forename: Masakazu
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Akihiro
authors.initials: A
authors.lastname: Hirashiki
authors.forename: Takashi
authors.initials: T
authors.lastname: Yamada
authors.forename: Ken
authors.initials: K
authors.lastname: Harada
authors.forename: Satoru
authors.initials: S
authors.lastname: Ohshima
authors.forename: Akiko
authors.initials: A
authors.lastname: Noda
authors.forename: Kohzo
authors.initials: K
authors.lastname: Nagata
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Kato
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Yokota
authors.forename: Toyoaki
authors.initials: T
authors.lastname: Murohara
mesh_terms: D006328:Cardiac Catheterization; D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008929:Mitochondria, Heart / Q000000981:diagnostic imaging / Q000473:pathology / Q000502:physiology*; D009200:Myocardial Contraction / Q000502:physiology*; D055414:Myocardial Perfusion Imaging / Q000379:methods; D012146:Rest / Q000502:physiology; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*