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Cardiology & Current Research

Review Article Volume 5 Issue 5

Types of Myocardial Necrosis: The Possible Role of Cigarette Smoking

Aurelio Leone1,2,3

1Fellow of the American Society of Hypertension (FASH), USA
2Fellow of the Royal Society for Promotion of Health (FRSPH), UK
3Editor in Chief of the Journal of Cardiology & Current Research, USA

Correspondence: Aurelio Leone, Fellow of the American Society of Hypertension (FASH), Fellow of the Royal Society for Promotion of Health (FRSPH), Editor in Chief of the Journal of Cardiology & Current Research, Via Provinciale 27, 19033 Castelnuovo Magra, Italy

Received: December 20, 2015 | Published: May 9, 2016

Citation: Leone A (2016) Types of Myocardial Necrosis: The Possible Role of Cigarette Smoking. J Cardiol Curr Res 5(5): 00177. DOI: 10.15406/jccr.2016.05.00177

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Abstract

Three types of myocardial necrosis have been experimentally documented to be the result of cigarette smoking action: coagulation necrosis, colliquative myocytolysis and coagulative myocytolysis. They may be the response to a direct action of nicotine and carbon monoxide on heart muscle as well as consequence of a vascular mechanisms of coronary artery harm. While the vascular pathogenic mechanism is able to induce mainly coagulative necrosis, which is the specific necrosis of the acute myocardial infarction, the toxic action of the smoking compounds develops all types of necrosis with myocardial alterations variably combined among themselves.

Keywords: Cigarette smoking; Myocardial necrosis, Pathogenic mechanism

Introduction

A large number of both dated and very recent papers [1-10] undoubtedly show that cigarette smoking harms the cardiovascular system mainly causing mild, moderate and severe lesions variably combined among them, to heart muscle.

A wide spectrum of alterations up to myocardial necrosis, a dramatic outcome characterized by cell death, affects myocardial fibers and interstitium. Of over 4,000 toxics of tobacco smoke, only a few exert a harmful effect on the heart structure. These are nicotine and its metabolite cotinine, and carbon monoxide that act by different, but synergistic mechanisms.

It is worth noting that necrosis is the final results of all morphological changes, which contribute to cell death and following remodeling of the affected structure [11-13]. Therefore, all these factors able to cause such a lesion are also responsible of an abnormal re-building of the cells and tissues which are its constituents.

Usually, the dead cell shows both cytoplasmic and nuclear changes that determine loss of its function, although repairing phenomena mainly of fibrotic type accompany structural alterations. Cigarette smoking mainly affects the myocardium by various mechanisms that, however, cause ischemic alterations. In addition, various types of necrosis may be seen as a result of smoking by experimental studies. This brief review aims to describe the type of necrosis of myocardial cells, the underlying mechanisms, and the severe alterations occurred to heart muscle.

Types of Myocardial Necrosis

As aforesaid, the necrosis is the death of a cell, but the death cell does not meet early the complete loss of its structure, unless in some sudden events usually not smoking-related. This fact determines variable steps of intermediate damage, which, however, is the door of myocardial cell death. Three types of myocardial necrosis (Table 1) have been clinically and experimentally documented to be the result of tobacco smoke: coagulation necrosis, colliquative myocytolysis, and coagulation myocytolysis.

Necrosis

Underlying Mechanism

Coagulation necrosis

Reduced vascular supply

Colliquative myocytolysis

Lysis of cell structure

Coagulation myocytolysis

Sympathetic nervous system hyper stimulation

Table 1: Types of myocardial necrosis.

Coagulation necrosis (Figure 1) is the common pattern of necrosis characterized by cytoplasmic coagulation. Myocardial cells become acidophilic, but the features of myocardial fibers can be recognized for a long time from the onset of the pathologic process. However, the specific details of the structure change their properties. This type of necrosis commonly has to be recognized as a result of a vascular mechanism related to a reduced perfusion of specific areas of the myocardium, although other chemical, physical and biological factors may play their effects.

With regard to this type of necrosis, Katz [14] & Schwartz [15] hypothesized a loss of contractile properties of myocardial fibers as an effect of intracellular acidosis derived by the anaerobic glycolysis due to the hypoxia. Hypoxia should be responsible of a shift of Calcium ions and contractile myocardial protein coupling. There is evidence that cigarette smoking can biochemically determine these changes [16]. These coagulate cells may meet a liquefactive process or be removed by fragmentation and phagocytosis due to macrophages and leukocytes migrating in the altered area (Figure 1).

Colliquative myocytolysis (also named liquefaction necrosis) displays an evident liquefaction of the necrotic tissue due to the action of hydrolytic enzymes released from myocardial fibers undergone autolysis. They result from the migration of leukocytes in the ischemic area (Figure 2). Marked nuclear alterations with fragmentation, basophilia and degeneration characterize this type of necrosis, which determines myocardial lysis, vacuolization with loss of contractile proteins of the myocardium, and edema, all lesions that precede the development of heart failure [17] (Figure 2).

Figure 1: Coagulative necrosis of myocardium. The myocardial tissue under necrosis shows altered structure of muscular fibers, although with still evident composition. Leukocyte infiltration may be seen in the infarct area. Hematoxylin-Eosinstaining.

Figure 2: Colliquative myocytolysis. Evident vacuolization of the myocardium undergone lysis as a result of leukocyte infiltration. Hematoxylin-Eosin staining.

Coagulative myocytolysis (Figure 3) is undoubtedly the type of myocardial necrosis more closely related to the action of both smoking toxics, nicotine and carbon monoxide [18-20]. The histologic features and pathogenic mechanisms can be easily recognized because being similar to that due to catecholamine release and sympathetic nervous system stimulation [21,22].

Figure 3: Coagulative myocytolysis. Myocardial fibers are deeply altered and contractbands due to cell death in hypercontraction, similarly to what observed in the “stone heart”, may be seen. Hematoxylin-Eosin staining.

The main alterations that characterize coagulative necrosis consist of a variety of changes of myocardial fibers, which meet hypercontraction with the formation of transverse bands, fragmentation, and rupture. This picture evokes the pattern defined as “alveolar pattern” [23] responsible of a strong myocardial disarray considered as an architectural disorganization of the myocardium. It has beenclosely linked with the adrenergic stress [24]. It is worth noting that smoke cardiomyopathy takes a significant place in the context of the various types of myocardial necrosis.

This pattern is a result of a direct effect of carbon monoxide on myocardial cells and intracellular structures of the heart muscle [25-27]. The lesions observed are an association of some features of the necrosis described and consist of hyalinosis, interstitial edema, perivascular cellular infiltrates and hemorrhagic foci resulting from myocardial fiber fragmentation.

As can be seen a wide spectrum of alterations characterize myocardial necrosis making possible multiple patterns typical of the underlying disease. However, it can be also determined by cigarette smoking as experimentally documented. Therefore, even if it is hard to clearly attribute the different morphology of myocardial necrosis to tobacco toxics, nevertheless some of the alterations can lead to this way.

Pathogenic Mechanisms

It is worth noting that a large number of pathogenic mechanisms can be attributed to the cigarette smoking, but, with regard to myocardial necrosis, only two are worthy of mention (Table 2): a toxic, and a coronarogenic mechanism.

There is evidence that all infarcts of the heart muscle belong to the group of necrotic lesions, but not all cardiac necrosis are necessarily infarcts [28]. Starting from this assumption, the different types of necrosis described can be interpreted to have the same, but also different pathogenic mechanisms.

Vascular mechanism of necrosis primarily recognizes pathological alterations of the coronary arteries, which undergo narrowing and/or occlusion as a consequence of a thrombus formation. Morpho-pathological substrate is coagulation necrosis, which occurs because of reduced coronary blood flow and hypoxia due to the action of nicotine and carbon monoxide. The two pathogenic mechanisms are often associated. Thus, it has been well documented the effects of both nicotine, mainly by endothelial dysfunction [29,30], and carbon monoxide on the coronary tree. Increased concentrations of carboxyhemoglobin [31] contributeto activating the vascular mechanism.

Toxic mechanism, mainly exerted by nicotine in the first phases of damage through an increased catecholamine release and sympathetic nervous system stimulation [32,33], and later as a direct effect of the hypoxia chronically caused by carbon monoxide [34,35], may be responsible of the different types of necrosis described, and primarily smoke cardiomyopathy.

Toxic Mechanism

Vascular Mechanism

Carbon monoxide (carboxyhemoglobin)

Coronary atherosclerosis

Nicotine (adrenergic and sympathetic stimulation)

Coronary narrowing

Table 2: Pathogenic mechanisms of myocardial necrosis from cigarette smoking.

Conclusion

There is no doubt that some chemical compounds of cigarette smoke, primarily nicotine and carbon monoxide, play a severely adverse effect on heart muscle cells causing a wide spectrum of structural lesions mainly of ischemic type. These involve both myocardial fibers and intracellular structure, and are able to determine different types of myocardial necrosis, which have been certainly documented in the experimental pathology of the animals.

References

  1. Leone A, Landini L, Leone A (2010) What is tobacco smoke? Sociocultural dimensions of the association with cardiovascular risk. Curr Pharm Des 16(23): 2510-2517.
  2. Glantz SA, Parmley WW (1995) Passive smoking and heart disease: mechanisms and risk. JAMA 273(13): 1047-1053.
  3. Leone A (2003) Relationship between cigarette smoking and other coronary risk factors in atherosclerosis: risk of cardiovascular disease and preventive measures. Curr Pharm Des 9(29): 2417-2423.
  4. Ambrose JA, Barua RS (2004) The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol 43(10): 1731-1737.
  5. Leone A (2014) Relation between coronary lesions and cigarette smoking of subjects deceased from acute myocardial infarction. A histopathological study. J Cardiobiol 2(2): 5.
  6. Leone A (1993) Cardiovascular damage from smoking: a fact or belief? Int J Cardiol 38(2): 113-117.
  7. Davis J, Shelton L, Watanabe I, Arnold J (1989) Passive smoking affects endothelium and platelets. Arch Intern Med 149(2): 386-389.
  8. Auerbach O, Carter HW, Garfinkel L, Hammond EC (1976) Cigarette smoking and coronary heart disease, a macroscopic and microscopic study. Chest 70(6): 697-705.
  9. Leone A, Giannini D, Bellotto C, Balbarini A (2004) Passive smoking and coronary heart disease. Curr Vasc Pharmacol 2(2): 175-182.
  10. Meinert CL, Forman S, Jacobs DR, Stamler J (1979) Cigarette smoking as a risk factor in men with a prior history of myocardial infarction. J Chronic Dis 32(6): 415-425.
  11. Leone A (2015) Toxics of tobacco smoke and cardiovascular system: from functional to cellular damage. Curr Pharm Des 21(30): 4370-4379.
  12. McGill HC (1988) The cardiovascular pathology of smoking. Am Heart J 115 (1 Part 2): 250-257.
  13. Leone A (2014) What has taught almost half a century of research on the relationship between passive smoking and cardiovascular system? J CardiolCurr Res 1(1): 00004.
  14. Katz AM (1971) Effect of ischemia on the cardiac contractile proteins. Cardiology 56(1): 276-283.
  15. Schwartz A (1971) Calcium and the sarcoplasmic reticulum. In: Harris P, Opie LH (Eds.) Calcium and the Heart, Academic Press, London, New York, USA.
  16. Opie LH (2005) Mechanisms of cardiac contraction and relaxation. In: Zipes DP, Libby P, Bonow RO, Braunwald E, (Eds.), A Textbook of Cardiovascular Medicine; Braunwald’s Heart Disease. Elsevier-Saunders, Philadelphia, Penn, USA, pp. 457-489.
  17. Leone A, Bertanelli F, Mori L, Fabiano P, Battaglia A (1994) Features of ischaemic cardiac pathology from cigarette smoking. J Smoking-Related Dis 5: 109-114.
  18. Benowitz NL, Jacob P III, Jones RT, Rosemberg J (1982) Interindividual variability in the metabolism and cardiovascular effects of nicotine in man. J Pharmacol Exp Ther 221(2): 368-372.
  19. Samuels MA (1993) Neurally induced cardiac damage: definition of the problem. Neurol Clin 11(2): 273-292.
  20. Leone A (2005) Biochemical markers of cardiovascular damage from tobacco smoke. Curr Pharm Des 11(17): 2199-2208.
  21. Csapò Z, Dusek J, Rona G (1972) Early alterations of the cardiac muscle cells in isoproterenol-induced necrosis. Arch Pathol 93(4): 356-365.
  22. Ferrans VJ, Hibbs RG, Cipriano PR, Buja ML (1972) Histochemical and electron microscopic studies of norepinephrine-induced myocardial necrosis in rats. In: Bajusz E, Rona G (Eds.): Recent Advances in Studies on Cardiac Structure and Metabolism; Myocardiology, University Park Press, Baltimore, USA, 495-525.
  23. Baroldi G (1974) Letter: Myocardial necrosis: the need for definition. J Mol Cell Cardiol 6(4): 401-402.
  24. Fineschi V, Silver MD, Karch SB, Parolini M, Turillazzi E, et al. (2005) Myocardial disarray: an architectural disorganization linked with adrenergic stress ? Int J Cardiol 99(2): 277-282.
  25. Astrup P (1972) Some physiological and pathological effects of moderate carbon monoxide exposure. Br Med J 4(5838): 447-452.
  26. Lough J (1978) Cardiomyopathy produced by cigarette smoke. Ultra structural observations in guinea pigs. Arch Pathol Lab Med 102(7): 377-380.
  27. Gvozdjakova A, Bada V, Sani L, Kucharská J, Krutý F, et al (1984) Smoke cardiomyopathy: disturbance of oxidative processes in myocardial mitochondria. Cardiovasc Res 18(4): 229-232.
  28. Leone A, Landini L , Biadi O, Balbarini A (2008) Smoking and cardiovascular system: cellular features of the damage. Curr Pharm Des 14(18): 1771-1777.
  29. Ross R (1993) The pathogenesis of atherosclerosis. A perspective for the 1990s. Nature 362(6423): 801-809.
  30. Desideri G, Ferri C (2005) Endothelial activation. Sliding door to atherosclerosis. Curr Pharm Des 11(17): 2163-2175.
  31. Melley DD, Finney SJ, Elia A, Lagan AL, Quinlan GJ, et al. (2007) Arterial carboxyhemoglobin level and outcome in critically ill patients. Crit Car Med 35(8): 1882-1887.
  32. Baer L, Radichevich I (1985) Cigarette smoking in hypertensive patients: Blood pressure and endocrine responses. Am J Med 78(4): 564-568.
  33. Hill P, Winder EL (1974) Smoking and cardiovascular disease. Effects of nicotine on the serum epinephrine and corticoids. Am Heart J 87(4): 491-496.
  34. Wald N, Howard S, Smith PG, Kjeldsen K (1973) Association between atherosclerotic diseases and carboxyhemoglobin levels in tobacco smokers. Br Med J 1(5856): 761-765.
  35. Leone A (2015) Morphological alterations of the heart and blood vessels from tobacco smoke: the steps of the damage. Journal of Cardiol Ther 2(4): 355-359.
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