title: Myocardial fatty acid metabolism: independent predictor of left ventricular mass in hypertensive heart disease.
abstract: The expression of myocardial fatty acid beta-oxidation enzymes is downregulated at the gene transcriptional level in animal models of left ventricular hypertrophy and of heart failure. Humans with idiopathic dilated cardiomyopathy have decreased myocardial fatty acid oxidation. The extent to which molecular mechanisms, such as a reduction in myocardial fatty acid oxidation, regulate the cardiac hypertrophic response in humans in vivo is unknown. Positron emission tomography was used to measure myocardial blood flow, oxygen consumption, fatty acid utilization, and oxidation in two groups of patients: (1) hypertensive left ventricular hypertrophy (n=19; left ventricular mass, 211+/-39 g; left ventricular ejection fraction, 67+/-4%) and (2) left ventricular dysfunction (n=9; left ventricular mass, 210+/-36 g; left ventricular ejection fraction, 31+/-10%); these were compared with a normal control group (n=36; left ventricular mass, 139+/-25 g; left ventricular ejection fraction, 66+/-6%). Left ventricular mass showed significant correlation with gender, diastolic and systolic blood pressure, myocardial fatty acid uptake, utilization and oxidation, myocardial blood flow, body mass index, and left ventricular ejection fraction (all P<0.02). Independent predictors of increased left ventricular mass were male gender (r=0.38, P<0.001), myocardial fatty acid oxidation (r=-0.24, P<0.018), systolic blood pressure (r=0.41, P<0.001), and left ventricular ejection fraction (r=-0.29, P=0.005). Thus, myocardial fatty acid metabolism is an independent predictor of left ventricular mass in hypertension and in left ventricular dysfunction. The extent to which reduced myocardial fatty acid metabolism affects cardiovascular morbidity and mortality and whether pharmacologic modulation results in improved outcomes remains to be determined.
authors.affiliation: Cardiovascular Imaging and Clinical Research Core Laboratory, Washington University School of Medicine, St Louis, Mo 63110, USA.
authors.forename: Lisa
authors.initials: L
authors.lastname: de las Fuentes
authors.forename: Pilar
authors.initials: P
authors.lastname: Herrero
authors.forename: Linda R
authors.initials: LR
authors.lastname: Peterson
authors.forename: Daniel P
authors.initials: DP
authors.lastname: Kelly
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Gropler
authors.forename: Víctor G
authors.initials: VG
authors.lastname: Dávila-Román
mesh_terms: D000328:Adult; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000000981:diagnostic imaging; D005227:Fatty Acids / Q000378:metabolism*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D012307:Risk Factors; D012737:Sex Factors; D014055:Tomography, Emission-Computed; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism
chemical_list: D005227:Fatty Acids