title: Myocardial oxygen consumption is unchanged but efficiency is reduced in patients with essential hypertension and left ventricular hypertrophy.
abstract: BACKGROUND
  Patients with hypertension and left ventricular hypertrophy (LVH) are prone to develop heart failure. We tested the hypothesis that compensatory LVH is associated with normalization of myocardial oxygen consumption and that this occurs at the expense of a decrease in the ratio between cardiac work and oxygen consumption (efficiency).
  
  
  RESULTS
  Nine hypertensive men with LVH (LVH+) (age 42+/-2 years), left ventricular mass index (LVMI) 161+/-8 g/m(2), blood pressure (BP) 145+/-16/88+/-10 mm Hg (mean+/-SD); 8 hypertensive men without LVH (LVH-) (age 39+/-5 years, LVMI 107+/-15 g/m(2), BP 140+/-15/90+/-11 mm Hg); and 10 normotensive men (CONT) were studied. Myocardial blood flow, oxygen consumption, and glucose uptake were measured during euglycemic hyperinsulinemia using PET techniques. LV dimensions, volumes, and workload were determined by echocardiography, and efficiency was calculated. Myocardial workload (2.5+/-0.8 versus 3.0+/-0.6 versus 2. 3+/-0.5 mm Hg. mL. min(-1). g(-1) for CONT versus LVH- versus LVH+; P<0.05, LVH- versus LVH+), myocardial blood flow (0.84+/-0.16 versus 1.06+/-0.22 versus 0.81+/-0.09 mL. g(-1). min, respectively; P<0.05, LVH- versus other groups) and oxygen consumption (0.09+/-0.02 versus 0.14+/-0.03 versus 0.11+/-0.01 ml. g(-1). min(-1), respectively; P<0. 05, LVH- versus other groups) were increased in the LVH- group. Myocardial efficiency was reduced in the LVH+ group (18.1+/-4.1% versus 15.1+/-2.3% versus 13.5+/-1.9%, respectively; P<0.05, LVH+ versus CONT).
  
  
  CONCLUSIONS
  Myocardial oxygen consumption per unit weight is increased in hypertensive patients without LVH but is normal in those with LVH. The normalization of oxygen consumption via hypertrophy occurs at the expense of efficiency, which may predispose hypertensive patients with LVH to heart failure.
authors.affiliation: Department of Medicine, and Clinical Physiology, University of Turku, Finland. hannal@pet.tyks.fi
authors.forename: H
authors.initials: H
authors.lastname: Laine
authors.forename: C
authors.initials: C
authors.lastname: Katoh
authors.forename: M
authors.initials: M
authors.lastname: Luotolahti
authors.forename: H
authors.initials: H
authors.lastname: Yki-Järvinen
authors.forename: I
authors.initials: I
authors.lastname: Kantola
authors.forename: A
authors.initials: A
authors.lastname: Jula
authors.forename: T O
authors.initials: TO
authors.lastname: Takala
authors.forename: U
authors.initials: U
authors.lastname: Ruotsalainen
authors.forename: H
authors.initials: H
authors.lastname: Iida
authors.forename: M
authors.initials: M
authors.lastname: Haaparanta
authors.forename: P
authors.initials: P
authors.lastname: Nuutila
authors.forename: J
authors.initials: J
authors.lastname: Knuuti
mesh_terms: D000328:Adult; D001786:Blood Glucose; D001794:Blood Pressure; D003326:Coronary Circulation; D004452:Echocardiography; D004734:Energy Metabolism; D005947:Glucose / Q000493:pharmacokinetics; D006321:Heart / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D014055:Tomography, Emission-Computed
chemical_list: D001786:Blood Glucose; D007328:Insulin; D005947:Glucose; D010100:Oxygen