POTENTIALITIES OF HEART MRI IN DETECTION OF INFLAMMATION IN PATIENTS WITH IDIOPATHIC ABNORMALITIES OF CARDIAC CONDUCTION AND CLINICAL SYNDROME OF DILATED CARDIOMYOPATHY

To assess sensitivity and specificity of the inflammation criteria revealed using magnetic resonance imaging (MRI) as compared to the data of endomyocardial biopsy (EMB), 25 patients aged 39.5±11.3 years (12 men and 13 women) with the clinical syndrome of dilated cardiomyopathy (CMP Group) were examined. All study subjects had clinical signs of heart failure, which corresponded to Functional Class II-IV (NYHA classification). At the study entry, the patients of CMP group received therapy with inhibitors of angiotensin-converting enzyme, β blockers, and diuretics. To reveal MRI signs of inflammation in patients with “idiopathic” conduction abnormalities, 27 patients (11 men and 16 women) aged 40.7±11.4 years were examined (Block Group). MRI synchronized with ECG was carried out using the superconducting 1.5 T magnetic resonance tomograph Magnetom Avanto (Siemens, Germany) with superficial chest radiofrequency coil. To perform contrasting, immediately after cine-MR consequences, the contrast agent gadolinium-DTPA (Magnevist, Schering, Germany) was administered intravenously in a dose of 0.15 mmol/kg. The myocardial edema, as well as presence of the early (EC) and late contrasting (LC), was assessed in all 17 segments of the left ventricular (LV) myocardium on 3 cuts of the LV short axis according to the technique by M.D. Cerquera. According to the EMB data, signs of active myocarditis were found in GMP Group in 16 patients (64%) of 25. In 4 cases (16%), no active inflammatory infiltration was revealed; however, the considerable focal and interstitial fibrosis was observed in the biopsy samples which corresponded to post-myocarditic cardiosclerosis transforming into dilated cardiomyopathy. In 5 patients (20%), no inflammatory infiltration in the myocardium was observed, as well, morphological alterations were typical for idiopathic dilated cardiomyopathy. MRI showed edema in 3 11 segments in 10 patients (40%) of the CMP Group. EC was found in 3 17 segments in 7 patients (28%) of the above group, the LC foci were observed in 12 patients (48%). In the patients of the Block Group, signs of edema were found in 2-7 segments in 5 patients (18.5%), signs of myocardial hyperemia were observed in 3-10 segments in 9 patients (33.3%). Zones of accumulation of gadolinium were found in the LC phase only in 2 subjects (7.4%) of the Block Group. To clarify sensitivity and specificity of the MR criteria, presence of inflammation according to the MRI data was compared with the EMB data for the CMP Group. The Lake Louise criteria showed 33.3% of sensitivity and 77.8% of specificity. The sensitivity of the EC phenomenon was 31.3%, with 88.9% of specificity; the sensitivity of myocardial edema was 43.8%, and specificity, 66.7%. The maximal sensitivity (50%) with regard to the myocardial inflammation was shown for the LC phenomenon; however the specificity of the above phenomenon was 55.6%. Comparison of the heart MRI and EMB data in the CMP Group permitted one to determine sensitivity and specificity for both Lake Louise criteria and each particular MRI phenomenon. The most prevalent pathological MRI phenomenon in the CMP Group was LC foci revealed in 48% of cases. Thus, the data obtained indicate that heart MRI conducted according to three standard techniques permits one to reveal pathological signs in one third of the Block Group subjects. Prevalence of patients with signs of myocardial hyperemia, i.e. with the LC phenomenon, in the Block Group is the same as in the CMP Group (p=0.94). The percentage of patients with Lake Louise criteria in the Block Group was two times lower than in the CMP Group. At the same time, it should be noted that the difference in the number of patients with MRI signs of active myocarditis between the study groups was not statistically significant (p=0.29). The only peculiar feature of the CMP Group was LC foci observed more frequently than in the Block Group patients (p=0.01) and affecting a significant area of the myocardium.

magnetic resonance therapy, endomyocardial biopsy, dilated cardiomyopathy, atrio-ventricular block, inflammation, myocarditis

1. Грохотова В.В. и соавт. Диагностика некоронарогенных заболеваний у пациентов с желудочковыми тахикардиями. Всетник аритмологии, 2014, 75 41-48

2. Lecomte, D., et al., Isolated myocardial fibrosis as a cause of sudden cardiac death and its possible relation to myocarditis. J Forensic Sci, 1993. 38(3): p. 617-21.

3. Strain, J.E., et al., Results of endomyocardial biopsy in patients with spontaneous ventricular tachycardia but without apparent structural heart disease. Circulation, 1983. 68(6): p. 1171-81.

4. Sugrue, D.D., et al., Cardiac histologic findings in patients with life-threatening ventricular arrhythmias of unknown origin. J Am Coll Cardiol, 1984. 4(5): p. 952-7.

5. Cooper, L.T., et al., The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. Circulation, 2007. 116(19): p. 2216-33.

6. Friedrich, M.G., et al., Cardiovascular magnetic resonance in myocarditis: A JACC White Paper. J Am Coll Cardiol, 2009. 53(17): p. 1475-87.

7. Lurz, P., et al., Diagnostic performance of CMR imaging compared with EMB in patients with suspected myocarditis. JACC Cardiovasc Imaging, 2012. 5(5): p. 513-24.

8. Yilmaz, A., et al., Role of cardiovascular magnetic resonance imaging (CMR) in the diagnosis of acute and chronic myocarditis. Heart Fail Rev, 2013. 18(6): p. 747-60.

9. Abdel-Aty H., et al. Delayed enhancement cardiac magnetic resonance imaging reveals typical patterns of myocardial injury in patients with various forms of non-ischemic heart disease. Int J Cardiovasc Imaging 2008.

10. De Cobelli F., Pieroni M., Esposito A et al. Delayed gadoliniumenhanced cardiac magnetic resonance in patients with chronic myocarditis presenting with heart failure or recurrent arrhythmias. J Am Coll Cardiol 2006; 47: 1649 -1654

11. Mahmod, M., et al., Prevalence of cardiomyopathy in asymptomatic patients with left bundle branch block referred for cardiovascular magnetic resonance imaging. Int J Cardiovasc Imaging, 2012. 28(5): p. 1133-40.

12. Prochnau, D., et al., Cardiac magnetic resonance imaging as a tool to link cardiac conduction disease to myocarditis with minimal left ventricular impairment. J Electrocardiol, 2012. 45(2): p. 161-3.

13. Maisch, B. and S. Pankuweit, Standard and etiologydirected evidence-based therapies in myocarditis: state of the art and future perspectives. Heart failure reviews, 2013.18(6): p. 761-95.

14. Cerqueira MD., W.N., Dilsizian V., et al, Standardized myocardial segmentation andnomenclature for tomographic imaging of the heart: a statement for healthcare professionalsfrom the Cardiac Imaging Committee of the Council on Clinical Cardiology of the AmericanHeart Association // Circulation. - 2002. Vol. 105, № 4. - P. 539-542.

15. Francone, M., et al., CMR Sensitivity Varies With Clinical Presentation and Extent of Cell Necrosis in Biopsy-Proven Acute Myocarditis. JACC Cardiovasc Imaging, 2014. 7(3): p. 254-63.

16. Mahrholdt H., Wagner A., Deluigi CC et al. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis. Circulation 2006; 114: 1581-90.

17. Lev, M., The Pathology of Complete Atrioventricular Block. Progress in cardiovascular diseases, 1964. 6: p. 317-26.

18. Lenegre, J., Etiology and Pathology of Bilateral Bundle Branch Block in Relation to Complete Heart Block. Progress in cardiovascular diseases, 1964. 6: p. 409-44.