In human heart failure due to DCM, both PCr and ATP are significantly reduced. Ratios of PCr to ATP underestimate changes of high-energy phosphate levels.
We examined possible age- and gender-specific differences in the function and mass of left (LV) and right (RV) ventricles in 36 healthy volunteers using cine gradient-recalled echo magnetic resonance imaging. Subjects were divided into four groups (nine men and nine women in each): men aged under 45 years (32 +/- 7), women aged under 45 (27 +/- 6), men aged over 45 (59 +/- 8), and women aged over 45 (57 +/- 9). Functional analysis of cardiac volume and mass and of LV wall motion was performed by manual segmentation of the endocardial and epicardial borders of the end-diastolic and end-systolic frame; both absolute and normalized (per square meter body surface area) values were evaluated. With age there was a significant decrease in both absolute and normalized LV and RV chamber volumes (EDV, ESV), while LV and RV masses remained unchanged. Gender-specific differences were found in cardiac mass and volume (for men and women, respectively: LV mass, 155 +/- 18 and 110 +/- 16 g; LV EDV, 118 +/- 27 and 96 +/- 21 ml; LV ESV, 40 +/- 13 and 29 +/- 9 ml; RV mass, 52 +/- 10 and 39 +/- 5 g; RV EDV, 131 +/- 28 and 100 +/- 23 ml; RV ESV, 53 +/- 17 and 33 +/- 15 ml). Normalization to body surface area eliminated differences in LV volumes but not those in LV mass, RV mass, or RV function. Functional parameters such as cardiac output and LV ejection fraction showed nonsignificant or only slight differences and were thus largely independent of age and gender. Intra- and interobserver variability ranged between 1.4% and 5.9% for all parameters. Cine magnetic resonance imaging thus shows age- and gender-specific differences in cardiac function, and therefore the evaluation of cardiac function in patients should consider age- and gender-matched normative values.
Objective: To compare the extent and distribution of focal fibrosis by gadolinium contrast-enhanced magnetic resonance imaging (MRI; delayed hyperenhancement) in severe left ventricular (LV) hypertrophy in patients with pressure overload caused by aortic stenosis (AS) and with genetically determined hypertrophic cardiomyopathy (HCM). Methods: 44 patients with symptomatic valvular AS (n = 22) and HCM (n = 22) were studied. Cine images were acquired with fast imaging with steady-state precession (trueFISP) on a 1.5 T scanner (Sonata, Siemens Medical Solutions). Gadolinium contrast-enhanced MRI was performed with a segmented inversion-recovery sequence. The location, extent and enhancement pattern of hyperenhanced myocardium was analysed in a 12-segment model. Results: Mean LV mass was 238.6 (SD 75.3) g in AS and 205.4 (SD 80.5) g in HCM (p = 0.17). Hyperenhancement was observed in 27% of patients with AS and in 73% of patients with HCM (p , 0.01). In AS, hyperenhancement was observed in 60% of patients with a maximum diastolic wall thickness > 18 mm, whereas no patient with a maximum diastolic wall thickness , 18 mm had hyperenhancement (p , 0.05). Patients with hyperenhancement had more severe AS than patients without hyperenhancement (aortic valve area 0.80 (0.09) cm 2 v 0.99 (0.3) cm 2 , p , 0.05; maximum gradient 98 (22) mm Hg v 74 (24) mm Hg, p , 0.05). In HCM, hyperenhancement was predominant in the anteroseptal regions and patients with hyperenhancement had higher end diastolic (125.4 (36.9) ml v 98.8 (16.9) ml, p , 0.05) and end systolic volumes (38.9 (18.2) ml v 25.2 (1.7) ml, p , 0.05). The volume of hyperenhancement (percentage of total LV myocardium), where present, was lower in AS than in HCM (4.3 (1.9)% v 8.6 (7.4)%, p, 0.05). Hyperenhancement was observed in 4.5 (3.1) and 4.6 (2.7) segments in AS and HCM, respectively (p = 0.93), and the enhancement pattern was mostly patchy with multiple foci. Conclusions: Focal scarring can be observed in severe LV hypertrophy caused by AS and HCM, and correlates with the severity of LV remodelling. However, focal scarring is significantly less prevalent in adaptive LV hypertrophy caused by AS than in genetically determined HCM. R emodelling in left ventricular (LV) hypertrophy is accompanied by several structural changes. Interstitial and replacement fibrosis are among the morphological alterations that have been observed in LV hypertrophy caused by pressure overload and in genetically determined hypertrophic cardiomyopathy (HCM).
Evidence of delayed hyperenhancement of dysfunctional myocardium may be used to predict lack of mechanical improvement or nonviability, whereas the lack of hyperenhancement can be correlated with improvement of regional contractility or viability after revascularization.
ce-CMR is comparable with a PET/SPECT imaging protocol for the prediction of regional and global functional improvement after revascularization. However, ce-CMR may be superior to nuclear imaging for the identification of segments that are unlikely to recover function at follow-up.
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