Background-Hypertension is an important clinical problem and is often accompanied by left ventricular (LV) hypertrophy and dysfunction. Whether the myocardial high-energy phosphate (HEP) metabolism is altered in human hypertensive heart disease and whether this is associated with LV dysfunction is not known. Methods and Results-Eleven patients with hypertension and 13 age-matched healthy subjects were studied with magnetic resonance imaging at rest and with phosphorus-31 magnetic resonance spectroscopy at rest and during high-dose atropine-dobutamine stress. Hypertensive patients showed higher LV mass (98Ϯ28 g/m 2 ) than healthy control subjects (73Ϯ13 g/m 2 , PϽ0.01). LV filling was impaired in patients, reflected by a decreased peak rate of wall thinning (PRWThn), E/A ratio, early peak filling rate, and early deceleration peak (all PϽ0.05), whereas systolic function was still normal. The myocardial phosphocreatine (PCr)/ATP ratio determined in patients at rest (1.20Ϯ0.18) and during stress (0.95Ϯ0.25) was lower than corresponding values obtained from healthy control subjects at rest (1.39Ϯ0.17, PϽ0.05) and during stress (1.16Ϯ0.18, PϽ0.05). The PCr/ATP ratio correlated significantly with PRWThn (rϭϪ0.55, PϽ0.01), early deceleration peak (rϭϪ0.56, PϽ0.01), and with the rate-pressure product (rϭϪ0.53, PϽ0.001). Conclusions-Myocardial HEP metabolism is altered in patients with hypertensive heart disease. In addition, there is an association between impaired LV diastolic function and altered myocardial HEP metabolism in humans.

Background-The question of whether training-induced left ventricular hypertrophy in athletes is a physiological rather than a pathophysiological phenomenon remains unresolved. The purpose of the present study was to detect any abnormalities in cardiac function in hypertrophic hearts of elite cyclists and to examine the response of myocardial high-energy phosphate metabolism to high workloads induced by atropine-dobutamine stress. Methods and Results-We studied 21 elite cyclists and 12 healthy control subjects. Left ventricular mass, volume, and function were determined by cine MRI. Myocardial high-energy phosphates were examined by 31 P magnetic resonance spectroscopy. There were no significant differences between cyclists and control subjects for left ventricular ejection fraction (59Ϯ5% versus 61Ϯ4%), left ventricular cardiac index (3.4Ϯ0.4 versus 3.4Ϯ0.4 L ⅐ min Ϫ1 ⅐ m Ϫ2 ), peak early filling rate (562Ϯ93 versus 535Ϯ81 mL/s), peak atrial filling rate (315Ϯ93 versus 333Ϯ65 mL/s), ratio of early and atrial filling volumes (3.0Ϯ1.0 versus 2.6Ϯ0.6), mean acceleration gradient of early filling (5.2Ϯ1.4 versus 5.8Ϯ1.9 L/s 2 ), mean deceleration gradient of early filling(Ϫ3.1Ϯ0.9 versus Ϫ3.2Ϯ0.7 L/s

Early after AVR, patients with aortic valve stenosis show a decrease in both LVMI and LVMI/LVEDVI and an improvement in diastolic filling, whereas in patients with aortic regurgitation, LVMI decreases less rapidly than LVEDVI, causing concentric remodeling of the LV, most likely explaining the observed deterioration of diastolic filling in these patients.

The phantom experiment shows that the in vivo decrease of myocardial PCr/ATP due to high-dose A-D stress we observed is not a motion artifact. Consequently, this indicates that myocardial high-energy phosphate metabolism of the normal human heart is altered at high workloads.