Lviv clinical bulletin 2013, 2(2): 18-22

https://doi.org/10.25040/lkv2013.02.018

Myocardial Hibernation in Patients with Arterial Hypertension and Ischemic Heart Disease as a Cause of Heart Failure

Posted onAuthorAdminЗалишити коментар / Leave a comment

O. Barnett, Y. Kyyak, H. Kyyak, V. Kovalyshyn, D. Besh

Danylo Halytsky Lviv National Medical University

Introduction. Myocardial hibernation refers to “new ischemic syndromes,” which in recent years have increasingly attracted the attention of cardiologists and cardiac surgeons. Hibernation includes a number of adaptive responses: inhibition of metabolic processes to more complex and lengthy pathophysiological changes that lead to myocardial contractile weakness, and their degeneration of cardiomyocytes and their apoptosis.

Aim. To find out the pathophysiological mechanisms of occurrence and ultrastructural signs of cardiomyocyte hibernation in patients with arterial hypertension (AH) and myocardial infarction (MI), as well as the role of hibernation in the occurrence of heart failure (HF). To determine the dependence of segmental disorders of the left ventricular myocardial contractility (hypokinesia, akinesia, dyskinesia) on the presence of hybridized cardiomyocytes and to reveal the duration of their life.

Materials and methods. For 36 patients with hypertension and coronary artery disease were examined, were examined the ultrastructure of myocardial biopsy material (n = 10) obtained during coronary artery bypass graft (CABG) and aneurysmectomy, as well as express neoplastic lesions (n​​= 26) in those who died of heart attack. Myocardial biopsies were obtained during the execution of the CABG for angina pectoris (n = 10) or ventriculoplasty in combination with CABG (n = 6).

Ultra-structured study of 10 myocardial biopsies during CABG and ventriculoplasty, as well as 26 express-necropsies of the myocardium of those died due to the MI who were ill with hypertension were made.

Results. It has been determined that hypertrophy and cardiomyocyte hybridization correlate with the severity of hypertension, MI, besides necrosis, causes stunning, hypertension, apoptosis, and necrosis of cardiomyocytes, mainly in the parainfarction and intact regions of the left venticle. The hepatized cardiomyocytes (irreversibly altered, hybridized cardiomyocytes containing α-glucogens) were first detected. The correlation between the percentage of remodulated cells (from 50.0 to > 75.0%) and the emergence of segmental lesions of the contractility of left ventricle (hypo-, aki-, dyskinesia), which leads to acute and chronic HF was found.

Conclusions. Myocardial hibernation is a clinically important syndrome, which is often accompanied, under certain circumstances, by the transient left ventricle dysfunction. It is important to consider it in clinical practice, since hibernation is present in patients with almost all forms of coronary heart disease and requires both medical and surgical treatment.

Reference

  1. Zakharov VN. About the Acute Focal Dystrophy of the Myocardium with a Hibernating (“Sleeping”) or “Stunned” Myocardium. Clinical Medicine. 2002;6:67-70. (Russian)
  2. Kovalenko VM. The Current State of Cardiology in Ukraine and the Prospects for the Implementation of New Diagnostic and Treatment Technologies. Journal of the Academy of Medical Sciences of Ukraine. 2004;10(2):268-273. (Ukrainian)
  3. Lutai M. Systolic Dysfunction of the Left Ventricle in Patients with Ischemic Heart Disease. Clinical Significance of the Hibernated Myocardium. Doctor. 2001;4:30-34. (Russian)
  4. Sokolov RI, Zhdanov VS. Hibernation and Stunning as a Manifestation of Ischemic Myocardial Dysfunction. Archive of Pathology. 2002;64(1):50-54. (Russian)
  5. Rahimtoola SH. Hibernating myocardium: introduction, validation and clinical significance of a concept in cardiac pathophysiology. Medicographia. 1999;21(2):158-161.
  6. Rahimtoola SH. The hibernating myocardium. Am Heart J. 1989;117:211-221. https://doi.org/10.1016/0002-8703(89)90685-6
  7. Chen C, Chen L, Fallon JT, Ma L, Li L, Bow L et al. Functional and structural alterations with 24-hour myocardial hibernation and recovery after reperfusion: a pig model of myocardial hibernation. Circulation. 1996;94(3):507-516. https://doi.org/10.1161/01.CIR.94.3.507
  8. Heusch G, Schultz R. Characterization on hibernating and stunned myocardium. Eur Heart J. 1997;18(D):D102-110.
  9. Heusch G, Schultz R. Features of short-term myocardial hibernation. Mol Cell Bio. 1998;186(1-2):185-193.
  10. Heusch G, Sipido KR. Myocardial Hibernation. Circ Res. 2004;94(8):1005-1007. https://doi.org/10.1161/01.RES.0000128071.90075.e3
  11. Heusch G, Schultz R. Myocardial hibernation: adaptation to ischaemia. Eur Heart J. 1996;17:824-828. https://doi.org/10.1093/oxfordjournals.eurheartj.a014962
  12. Ferrari R, Visioli O, Ferrari F et al. Hibernating myocardium: its pathophysiology and clinical role. Mol Cell Bio. 1998;l86(1-2):190.
  13. Hughes G. Cellular models of hibernating myocardium : implications for future research. Cardiovasc Res. 2001;51(2):191-193. https://doi.org/10.1016/S0008-6363(01)00352-2
  14. Swarz ER, Schaper J, vom Dahl J et al. Myocyte degeneration and cell death in hibernating human myocardium. J Am Coll Cardiol. 1998;186:147-158.
  15. Opie LH. The new ischemic syndromes and endogenous cardiac cytoprotection: what is the present and future meaning for the clinician? Medicografhia. 1999;21(2):149-155.
  16. Schulz R, Heusch G. Myocardium Hibernating. Heart. 2000;84(6):587-594. https://doi.org/10.1136/heart.84.6.587
  17. Vanoverschelde JJ, Melin JA. The Pathophisiology of Myocardial Hibernation: Current Controversies and Future Directions. Progr Cardiovasc Dis. 2001;43(5):387-398. https://doi.org/10.1053/pcad.2001.20655