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A comparison of visual and quantitative assessment of left ventricular ejection fraction by cardiac magnetic resonance.
To determine the accuracy of visual analysis of left ventricular (LV) function in comparison with the accepted quantitative gold standard method, cardiac magnetic resonance (CMR). Cine CMR imaging was performed at 1.5 T on 44 patients with a range of ejection fractions (EF, 5-80%). Clinicians (n = 18) were asked to visually assess EF after sequentially being shown cine images of a four chamber (horizontal long axis; HLA), two chamber (vertical long axis; VLA) and a short axis stack (SAS) and results were compared to a commercially available analysis package. There were strong correlations between visual and quantitative assessment. However, the EF was underestimated in all categories (by 8.4% for HLA, 8.4% for HLA + VLA and 7.9% for HLA + VLA + SAS, P all < 0.01) and particularly underestimated in mild LV impairment (17.4%, P < 0.01), less so for moderate (4.9%) and not for severe impairment (1%). Assessing more than one view of the heart improved visual assessment of LV, EF, however, clinicians underestimated EF by 8.4% on average, with particular inaccuracy in those with mild dysfunction. Given the important clinical information provided by LV assessment, quantitative analysis is recommended for accurate assessment.
Mice over-expressing the myocardial creatine transporter develop progressive heart failure and show decreased glycolytic capacity.
The metabolic phenotype of the failing heart includes a decrease in phosphocreatine and total creatine concentration [Cr], potentially contributing to contractile dysfunction. Surprisingly, in 32- week-old mice over-expressing the myocardial creatine transporter (CrT-OE), we previously demonstrated that elevated [Cr] correlates with left ventricular (LV) hypertrophy and failure. The aim of this study was to determine the temporal relationship between elevated [Cr] and the onset of cardiac dysfunction and to screen for potential molecular mechanisms. CrT-OE mice were compared with wild-type (WT) littermate controls longitudinally using cine-MRI to measure cardiac function and single-voxel (1)H-MRS to measure [Cr] in vivo at 6, 16, 32, and 52 weeks of age. CrT-OE mice had elevated [Cr] at 6 weeks (mean 1.9-fold), which remained constant throughout life. Despite this increased [Cr], LV dysfunction was not apparent until 16 weeks and became more pronounced with age. Additionally, LV tissue from 12 to 14 week old CrT-OE mice was compared to WT using 2D difference in-gel electrophoresis (DIGE). These analyses detected a majority of the heart's metabolic enzymes and identified seven proteins that were differentially expressed between groups. The most pronounced protein changes were related to energy metabolism: alpha- and beta-enolase were selectively decreased (p<0.05), while the remaining enzymes of glycolysis were unchanged. Consistent with a decrease in enolase content, its activity was significantly lower in CrT-OE hearts (in WT, 0.59+/-0.02 micromol ATP produced/microg protein/min; CrT-OE, 0.31+/-0.06; p<0.01). Additionally, anaerobic lactate production was decreased in CrT-OE mice (in WT, 102+/-3 micromol/g wet myocardium; CrT-OE, 78+/-13; p=0.02), consistent with decreased glycolytic capacity. Finally, we found that enolase may be regulated by increased expression of the beta-enolase repressor transcription factor, which was significantly increased in CrT-OE hearts. This study demonstrates that chronically increased myocardial [Cr] in the CrT-OE model leads to the development of progressive hypertrophy and heart failure, which may be mediated by a compromise in glycolytic capacity at the level of enolase.
Increased mitochondrial uncoupling proteins, respiratory uncoupling and decreased efficiency in the chronically infarcted rat heart.
Heart failure patients have abnormal cardiac high energy phosphate metabolism, the explanation for which is unknown. Patients with heart failure also have elevated plasma free fatty acid (FFA) concentrations. Elevated FFA levels are associated with increased cardiac mitochondrial uncoupling proteins (UCPs), which, in turn, are associated with decreased mitochondrial respiratory coupling and low cardiac efficiency. Here, we determined whether increased mitochondrial UCP levels contribute to decreased energetics in the failing heart by measuring UCPs and respiration in mitochondria isolated from the viable myocardium of chronically infarcted rat hearts and measuring efficiency (hydraulic work/O(2) consumption) in the isolated, working rat heart. Ten weeks after infarction, cardiac levels of UCP3 were increased by 53% in infarcted, failing hearts that had ejection fractions less than 45%. Cardiac UCP3 levels correlated positively with non-fasting plasma FFAs (r=0.81; p<0.01). Mitochondria from failing hearts were less coupled than those from control hearts, as demonstrated by the lower ADP/O ratio of 1.9+/-0.1 compared with 2.5+/-0.2 in controls (p<0.05). The decreased ADP/O ratio was reflected in an efficiency of 14+/-2% in the failing hearts when perfused with 1 mM palmitate, compared with 20+/-1% in controls (p<0.05). We conclude that failing hearts have increased UCP3 levels that are associated with high circulating FFA concentrations, mitochondrial uncoupling, and decreased cardiac efficiency. Thus, respiratory uncoupling may underlie the abnormal energetics and low efficiency in the failing heart, although whether this is maladaptive or adaptive would require direct investigation.
Is MR spectroscopy of the heart ready for humans?
Cardiac magnetic resonance spectroscopy (MRS) is a non-invasive in vivo technique that can be used to measure high-energy phosphate metabolism in heart without harmful radiation or radio-isotopes. Using the property of atomic nuclear spin, this technique provides real-time information on cardiac metabolite composition, including creatine content. Cardiac (31)P MR spectroscopy has shown most promise for the prognosis and treatment of heart failure, but has also been used as a powerful research tool for uncovering energy deficits in cardiomyopathies, ischaemic heart disease and valvular heart disease. Information provided by cardiac (1)H MRS includes myocardial creatine levels, which are decreased in heart failure, and myocardial fat content. Hyperpolarisation is an emerging MRS technique, which allows the (13)C MR signal to be increased many orders of magnitude in studies of substrate metabolism and enzyme kinetics. Cardiac MRS has predominantly been used in research and is not currently ready for routine clinical practice. However, higher MR field strengths, which provide greater signal and spectral resolution, may allow spectroscopy to become more widespread. This article reviews the applications of cardiac MRS, concentrating on the (31)P nucleus, and the current limitations that prevent routine use in research and clinical practice.
Ventricular hypertrophy and cavity dilatation in relation to body mass index in women with uncomplicated obesity.
OBJECTIVE: The traditionally accepted mechanism for ventricular adaptation to obesity suggests that cavity dilatation in response to increased blood volume and elevated filling pressure results in ventricular hypertrophy as a compensatory mechanism. Our hypothesis was that, instead, initiation of ventricular hypertrophy in obesity may be explained by changes in hormonal milieu and not by cavity dilatation. RESEARCH DESIGN AND METHODS: 88 female subjects without identifiable cardiovascular risk factors, covering a wide range of body mass indices (BMI), from normal (21.2 ± 1.6 kg/m(2)) to severely obese (45.0 ± 4.6 kg/m(2)), underwent cardiovascular MRI to determine left ventricular (LV) and right ventricular (RV) mass and volumes. RESULTS: BMI correlated positively with LV and RV mass and end-diastolic volumes (EDV). However overweight is associated with a significant LV and RV hypertrophy (LV: 78 ± 11 g vs 103 ± 16 g, p<0.01; RV: 26 ± 7 g vs 40 ± 11 g, p<0.01) was observed in the absence of differences in LV and RV volumes (LV: EDV 119 ± 15 vs 121 ± 21 ml, p>0.99, RV: 131 ± 17 vs 130 ± 24 ml; p>0.99). Furthermore, significant increases of serum leptin occurred at this pre-obese stage (15.6 ± 19 vs 36.5 ± 22 ng/ml; p=0.013). CONCLUSION: In a cohort of healthy female subjects with a wide range of BMIs, ventricular hypertrophy occurs without associated cavity dilatation in overweight individuals, while in manifest obesity, both cavity dilatation and ventricular hypertrophy occur. Elevated leptin levels may have a role in this effect on ventricular mass.