These abstracts have been selected for presentation in 4 sessions throughout the meeting. Please refer to the PROGRAM for more details.
Fischer K., Guensch DP., Shie N., Friedrich MG., Captur G., Zemrak F., Muthurangu V., Chunming L., Petersen SE., Kawel-Boehm N., Bassett P., Elliott PM., Lima JAC., Bluemke DA., Moon JC., Pontone G., Bertella E., Loguercio M., Baggiano A., Mushtaq S., Aquaro GD., Salerni S., Rossi C., Andreini D., Masci P., Moschetti K., Petersen SE., Pilz G., Wasserfallen JB., Lombardi M., Korosoglou G., Van Rossum AC., Bruder O., Mahrholdt H., Schwitter J., Florian A., Ludwig A., Rösch S., Sechtem U., Yilmaz A., Barison A., Pugliese NR., Masci PG., Del Franco A., Vergaro G., Del Torto A., Passino C., Perfetto F., Emdin M., Aquaro GD., Yoshihara HAI., Bastiaansen JAM., Berthonneche C., Comment A., Schwitter J.
Background: Altered metabolism is thought to play an important role in the pathogenesis of heart failure. Study of the metabolism may provide insights into the pathology of heart failure and may provide new diagnostic tools. Proton magnetic resonance spectroscopy (MRS) allows us to quantify total creatine, which plays an essential role in the transport of energy from the mitochondria to the myofibrils. Experimental autoimmune myocarditis (EAM) in rodents is an accepted model of myocarditis and dilated cardiomyopathy. As of yet, proton MRS has not been used to study the changes occurring in this model of heart failure. We aimed to study the metabolic changes occurring in an animal model of EAM, and compare these to the findings in healthy animals. Methods: Myocardial tissue of 10 male young Lewis rats with EAM (35 days after immunization with 0.25 mg porcine myocardial myosine) was analysed using 1H-MAS-MRS (Bruker 600 MHz). The metabolic profile was compared to fresh (n = 7) and frozen (n = 8) healthy controls and to the results from histology and immunohistochemistry (CD68). For fresh control samples the spectra were taken less than 10 min after death. Frozen control samples and myocarditis samples were shock-frozen in liquid nitrogen and stored for 4-6 months at –80°C before measurements. Myocardial tissue from a basal-cavity slice of the the left ventricle (30-40 mg) excluding epicardial tissue was placed in a 4 mm zirconium rotor, packed homogeneously using a spacer and spun at 4 kHz at 293 K. A water suppression pulse sequence was applied to obtain the proton spectrum (ns = 128, t = 7 min). Spectra were phased and baseline correction using polynomial fit to the region of interest was applied before integration of the peaks. Results: The metabolic ratio of taurine to creatine obtained by spectral analysis proved to be a significant biomarker for diagnosis of myocarditis compared to healthy controls (taurine/creatine ratio in myocarditis: 4.47(±0.83), fresh control: 2.59(±0.09), frozen control: 2.59(±0.28); P < 0.001). Myocarditis was confirmed histologically with an inflammatory cellular infiltrate and CD68 positive staining. Conclusions: Myocardial taurine/creatine ratio as detected by proton MRS is able to differentiate between healthy myocardium and myocardium from rats with EAM. This variation may occur due to creatine depletion as described in heart failure and/or an increase in taurine due to its antioxidant activity in inflammatory reactions. Objectives: The relationship between the severity of coronary stenosis and the severity of stress perfusion abnormalities was important in the validation of quantitative Positron Emission Tomography stress perfusion. We studied myocardial blood flow (MBF) derived from regadenoson stress Cardiac MRI (CMR) quantified to the pixel level in units of ml/min/g and compared results with quantitative coronary angiography (QCA) at the vessel level. Methods: Regadenoson perfusion CMR (steady state free precession and 0.05 mmol/kg gadolinium) was quantified at the pixel level with model-constrained Fermi deconvolution. QCA was available in 51 subjects after excluding patients with coronary artery bypass, congenital disease, hypertrophic cardiomyopathy, and catheterization technical issues. Five subjects were excluded for CMR technical issues. Regions of interest were drawn in the three layers of the myocardium. Endocardial/epicardial MBF ratio was defined as endocardial MBF/(average epicardial MBF in that coronary distribution). Results: The 46 patients in this study averaged 61.3 ± 10.8 years, 61% were male, and 35% had prior percutaneous coronary intervention. At a QCA threshold of 50%, the Left Anterior Descending was abnormal in 32, Right Coronary Artery in 24, Circumflex in 18, and leaving 63 coronary arteries with 0-49% stenosis. Stress endocardial MBF averaged 2.28 ml/min/g in normal segments which was higher than in segments with ≥50% QCA stenosis (1.24 ml/min/g; p < 0.0001). There was a graded severity in stress endocardial/epicardial MBF ratio vs severity of QCA stenosis (Figure). In receiver operating characteristics curve analysis, endocardial/epicardial MBF discriminated ≥50% QCA stenosis from normal (area under the curve (AUC) 0.949, p < 0.001); absolute endocardial MBF had an AUC of 0.903 (p < 0.001) and myocardial perfusion reserve had an AUC of 0.881 (p < 0.001). Conclusions: Myocardial perfusion quantified at the pixel level detects significant coronary artery disease at the coronary vessel level objectively and with high diagnostic discrimination from normal.