Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
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ISSN 1899–5276 (print), ISSN 2451-2680 (online)
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Advances in Clinical and Experimental Medicine

2006, vol. 15, nr 1, January-February, p. 135–140

Publication type: review article

Language: Polish

Przerost mięśnia sercowego – patofizjologia, znaczenie prognostyczne, leczenie

Left Ventricular Hypertrophy – Pathophysiology, Prognostic Significance, Treatment

Wojciech Kosmala1,, Adam Spring1,, Monika Przewłocka−Kosmala1,

1 Katedra i Klinika Kardiologii AM we Wrocławiu

Streszczenie

Przerost mięśnia sercowego może być patologicznym następstwem różnych stanów klinicznych, takich jak: nadciśnienie tętnicze, zwężenie zastawki aortalnej, cukrzyca, otyłość, zawał mięśnia sercowego. Wystąpienie przerostu mięśnia sercowego wiąże się z niekorzystnym rokowaniem w postaci kilkakrotnego wzrostu ryzyka zgonu oraz powikłań sercowo−naczyniowych. Ze względu na to, iż przerost mięśnia lewej komory serca jest jednym z najsilniejszych czynników ryzyka wystąpienia poważnych powikłań pochodzących z układu krążenia, w tym również nagłego zgonu z przyczyn arytmicznych, poznanie jego mechanizmów patogenetycznych oraz sposobów profilaktyki i terapii może być bardzo ważne dla poprawy rokowania u chorych dotkniętych tą patologią. W rozpoznawaniu przerostu największe znaczenie ma echokardiografia, choć istotne miejsce w dalszym ciągu zajmuje badanie elektrokardiograficzne. Z leków zmniejszających przerost mięśnia sercowego w nadciśnieniu tętniczym najlepsze wyniki uzyskano po zastosowaniu antagonistów receptora AT1 dla angiotensyny II, inhibitorów enzymu konwertującego, trochę gorsze po antagonistach wapnia, diuretykach i lekach blokujcych receptory β. Zmniejszenie przerostu mięśnia sercowego, wiążące się z poprawą rokowania chorych, powinno być traktowane jako jeden z głównych celów terapeutycznych.

Abstract

Left ventricular hypertrophy is a pathological consequence of various clinical states such as: hypertension, aortic stenosis, diabetes, obesity, myocardial infarction. Finding of left ventricular hypertrophy indicates poor prognosis as several−fold increase in risk of death and serious cardiovascular complications. In diagnosis of LVH echocardiography has priority, although ECG is still very helpful. Among drugs diminishing LVH angiotensin receptor blockers, angiotensin converting enzyme inhibitors are the most efficacious, calcium antagonists, diuretics and β−blockers are less potent. Reduction of LVH should be one of main therapeutic purposes in terms of improvement of prognosis.

Słowa kluczowe

przerost mięśnia sercowego

Key words

left ventricular hypertrophy

References (40)

  1. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, Reichek N: Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 1986, 57, 450–456.
  2. Izzo JL Jr, Gradman AH: Mechanisms and management of hypertensive heart disease: from left ventricular hypertrophy to heart failure. Med Clin North Am 2004, 88, 1257–1271.
  3. Pokharel S, Sharma UC, Pinto YM: Left ventricular hypertrophy: virtuous intentions, malign consequences. Int J Biochem Cell Biol 2003, 35, 802–806.
  4. Sadoshima J, Izumo S: The cellular and molecular response of cardiac myocytes to mechanical stress. Ann Rev Physiol 1997, 59, 551–571.
  5. Swynghedauw B: Molecular mechanisms of cardiac remodeling. Physiol Rev 1999, 79, 215–262.
  6. Hannan RD, Jenkins A, Jenkins AK, Brandenburger Y: Cardiac hypertrophy: a matter of translation. Clin Exp Pharmacol Physiol 2003, 30, 517–527.
  7. Lips DJ, deWindt LJ, van Kraaij DJ, Doevendans PA: Molecular determinants of myocardial hypertrophy and failure: alternative pathways for beneficial and maladaptive hypertrophy. Eur Heart J 2003, 24, 883–896.
  8. Lewartowski B: Zmiany fenotypu komórkowego w przeroście i niewydolności serca. Kardiol Pol 2000, 53, 33–45.
  9. Collins JF, Pawloski−Dahm C, Davis MG, Ball N, Dorn GW 2nd, Walsh RA: The role of cytoskeleton in left ventricular pressure overload hypertrophy and failure. J Mol Cell Cardiol 1996, 628, 1435–1443.
  10. Boluyt MO, O’Neill L, Meredith AL, Bing OHL: Alteration in cardiac gene expression during the transition from table hypertrophy to heart failure. Marked upregulation of genes encoding extracellular matrix components. Circ Res 1994, 75, 23–32.
  11. Danser A, Vankesteren C, Bax W: Prorenin, renin, angiotensinogen, and angiotensin−converting enzyme in normal and failing human hearts: evidence for renin binding. Circulation 1997, 96, 220–226.
  12. Leri A, Claudio PP, Li Q, Wang X, Reiss K, Wang S, Malhotra A, Kajstura J, Anversa P: Stretch−mediated release of angiotensin II induces myocyte apoptosis by activating p53 that enhances the local renin–angiotensin system and decreases the Bcl−2−to−Bax protein ratio in the cell. J Clin Invest 1998, 101, 1326–1342.
  13. Cottone S, Vadala A, Vella MC, Nardi E, Mule G, Contorno A, Riccobene R, Cerasola G: Changes of plasma endothelin and growth factor levels, and of left ventricular mass after chronic AT1 receptor blockade in human hypertension. Am J Hypertens 1998, 11, 548–553.
  14. Karasek E, Witkowska M: Czynniki neurohumoralne u chorych na nadciśnienie tętnicze pierwotne z przerostem mięśnia lewej komory i bez przerostu. Pol Arch Med Wew 2000, CIII, 23–33.
  15. Krzesinski JM, Rorive G, Van Cauwenberge H: Hypertension and left ventricular hypertrophy. Acta Cardiol 1996, 2, 143–154.
  16. Frey N, Katus HA, Olson EN, Hill JA: Hypertrophy of the heart: a new therapeutic target? Circulation 2004, 109, 1580–1589.
  17. Molkentin JD, Lu J−R, Antos CL, Markham B, Richardson J, Robbins J, Grant SR, Olson EN: A calcineurin−dependent transcriptional pathway for cardiac hypertrophy. Cell 1998, 93, 215–228.
  18. Jennings G, Dart A, Meredith I, Korner P, Laufer E, Dewar E: Effects of exercise and other non−pharmacological measures on blood pressure and cardiac hypertrophy: J Cardiovasc Pharmacol 1991, 17 (Suppl. 2), 70–74.
  19. Kannel WB: Left ventricular hypertrophy as a risk factor: the Framingham experience. J Hypertens 1991, 9 (Suppl. 2), 3–9.
  20. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP: Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990, 332, 1561–1566.
  21. Sundstrom J, Lind L, Arnlov J, Zethelius B, Andren B, Lithell HO: Echocardiographic and electrocardiographic diagnoses of left ventricular hypertrophy predict mortality independently of each other in a population of elderly men. Circulation 2001, 103, 2346–2351.
  22. Ganau A, Devereux RB, Roman MJ, de Simone G, Pickering TG, Saba PS, Vargiu P, Simongini I, Laragh JH: Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol 1992, 19, 1550–1558.
  23. Aronow WS, Ahn C, Kronzon I, Koenigsberg M: Congestive heart failure, coronary events and atherothrombotic brain infarction in elderly blacks and whites with systemic hypertension and with and without echocardiographic and electrocardiographic evidence of left ventricular hypertrophy. Am J Cardiol 1991, 67, 295–299.
  24. Cooper RS, Simmons BE, Castaner A, Santhanam V, Ghali J, Mar M: Left ventricular hypertrophy is associated with worse survival independent of ventricular function and number of coronary arteries severely narrowed. Am J Cardiol 1990, 65, 441–445.
  25. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH: Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 1991, 114, 345–352.
  26. De Simone G, Palmieri V: Left ventricular hypertrophy in hypertension as a predictor of coronary events: relation to geometry. Curr Opin Nephrol Hypertens 2002, 11, 215–220.
  27. Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Gattobigio R, Zampi I, Santucci A, Santucci C, Reboldi G, Porcellati C: Prognostic value of left ventricular mass and geometry in systemic hypertension with left ventricular hypertrophy. Am J Cardiol 1996, 78, 197–202.
  28. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH: Changes in left ventricular mass predict risk essential hypertension. Circulation 1990, 82 (Suppl. III), 20.
  29. Muiesan ML, Salvetti M, Rizzoni D, Castellano M, Donato F, Agabiti−Rosei E: Association of change in left ventricular mass with prognosis during long−term antihypertensive treatment. J Hypertens 1996, 13, 1091–1095.
  30. Diez J, Gonzalez A, Lopez B, Ravassa S, Fortuno MA: Effects of antihypertensive agents on the left ventricle: clinical implications. Am J Cardiovasc Drugs 2001, 1, 263–279.
  31. Zhang R, Crump J, Reisin E: Regression of left ventricular hypertrophy is a key goal of hypertension management. Curr Hypertens Rep 2003, 5, 301–308.
  32. Liebson PR, Grandits GA, Dianzumba S, Prineas RJ, Grimm RH Jr, Neaton JD, Stamler J: Comparison of five antihypertensive monotherapies and placebo for change in left ventricular mass in patients receiving nutritional hygienic therapy in the Treatment of Mild Hypertension Study (TOMHS). Circulation 1995, 91, 698–706.
  33. Schmieder RE, Martus P, Klingbeil A: Reversal of left ventricular hypertrophy in essential hypertension: a meta−analysis of randomized double−blind trials. JAMA 1996, 275, 1507–1513.
  34. Cruickshank J, Lewes J, Moore EV, Dodd C: Reversibility of left ventricular hypertrophy by different types of antihypertensive therapy. J Hum Hypertens 1992, 6, 85–90.
  35. Dahlof B, Pennert K, Hansson L: Reversal of ventricular hypertrophy in hypertensive patients: a meta−analysis of 109 treatment studies. Am J Hypertens 1992, 5, 95–110.
  36. Schlaich MP, Schmieder RE: Left ventricular hypertrophy and its regression: pathophysiology and therapeutic approach; focus on treatment by antihypertensive agents. Am J Hypertens 1999, 12, 1048–1052.
  37. Klingbeil AU, Schneider M, Martus P, Messerli FH, Schmieder RE: A meta−analysis of the effects of treatment on left ventricular mass in essential hypertension. Am J Med 2003, 115, 41–46.
  38. Diamond JA, Phillips RA: Regression of left ventricular hypertrophy: are there preferred drugs? Curr Hypertens Rep 2003, 5, 368–371.
  39. Devereux R: Therapeutic options in minimizing left ventricular hypertrophy. Am Heart J 2000, 139, 9–14.
  40. Carey PA, Sheridan DJ, de Cordoue A, Guez D: Effect of indapamide on left ventricular hypertrophy in hypertension: a meta−analysis. Am J Cardiol 1996, 22, 17b–19b.
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