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Diagnosis and Treatment of Asymptomatic Left Ventricular Systolic Dysfunction after Myocardial Infarction

DOI: 10.1155/2013/731285

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Abstract:

The increased survival after acute myocardial infarction induced an increase in heart failure with left ventricular systolic dysfunction. Early detection and treatment of asymptomatic left ventricular systolic dysfunction give the chance to improve outcomes and to reduce costs due to the management of patients with overt heart failure. 1. Introduction Despite substantial progresses in the diagnosis and treatment of acute myocardial infarction (AMI), about 22% of men and 46% of women will be disabled with heart failure (HF) within six years [1]. About 40% of patients with an AMI develop left ventricular systolic dysfunction (LVSD) with or without signs of HF, which adversely influences quality of life, hospitalization rates, and mortality [2]. Considering the high survival rate after an AMI and the higher incidence of LVSD, early detection of people at risk of developing HF after an AMI should constitute a priority. Patients who have had an AMI, but who do not show signs of HF, could be burdened with an asymptomatic LVSD or stage B HF (Figure 1), according to ACC/AHA Guidelines of 2009 [3]. This condition is often not diagnosed and, for this reason, not treated, even if morbidity and mortality are similar to those of symptomatic HF [3]. Besides this, these patients run a higher risk because they are not aware of their pathology. Our aim is to underline the importance of an early detection of patients with asymptomatic LVSD in order to take all the measures that are necessary to reduce morbidity and mortality connected to this condition. Figure 1: Stages of heart failure (Adapted from [ 3]). 2. Epidemiology In occidental countries, coronary heart disease (CHD) is the most important cause of LVSD and HF [4]. Ischemic cardiomyopathy is the underlying cause in about 61% of patients with signs and symptoms of HF [5]. In the SAVE trial, asymptomatic LVSD was present in 58% of patients after an AMI [6]. Robust epidemiological data about the prevalence of asymptomatic LVSD after an AMI are hard to find. Surveys indicate that only about 60% of patients with an AMI have their ventricular function assessed [7]. Hellermann et al. conducted a review of the literature between 1978 and 2000, finding that the incidence of HF was reported only in few studies and in none of these studies diagnostic criteria for assessing HF were given [8]. If the Killip classification is used, patients with asymptomatic LVSD should be classified as Killip class 1 (no evidence of pulmonary congestion or shock). Possibly the most relevant data on the incidence, prevalence, and persistence

References

[1]  W. Rosamond, K. Flegal, K. Furie et al., “Heart disease and stroke statistics-2008 Update: a report from the American heart association statistics committee and stroke statistics subcommittee,” Circulation, vol. 117, no. 4, pp. e25–e46, 2008.
[2]  L. K?ber, C. Torp-Pedersen, S. J?rgensen, P. Eliasen, and A. J. Camm, “Changes in absolute and relative importance in the prognostic value of left ventricular systolic function and congestive heart failure after acute myocardial infarction,” American Journal of Cardiology, vol. 81, no. 11, pp. 1292–1297, 1998.
[3]  ACC/AHA, “Guidelines update for the diagnosis and managenment of chronic heart failure in the adult,” Journal of the American College of Cardiology, vol. 53, pp. 1343–1382, 2009.
[4]  M. Gheorghiade and R. O. Bonow, “Chronic heart failure in the United States: a manifestation of coronary artery disease,” Circulation, vol. 97, no. 3, pp. 282–289, 1998.
[5]  C. G. Frazier, K. P. Alexander, L. K. Newby et al., “Association of gender and etiology with outcomes in heart failure with systolic dysfunction,” Journal of the American College of Cardiology, vol. 49, no. 13, pp. 1450–1458, 2007.
[6]  L. M. Mielniczuk, G. A. Lamas, G. C. Flaker et al., “Left ventricular end-diastolic pressure and risk of subsequent heart failure in patients following an acute myocardial infarction,” Congestive Heart Failure, vol. 13, no. 4, pp. 209–214, 2007.
[7]  J. G. F. Cleland, A. Torabi, and N. K. Khan, “Epidemiology and management of heart failure and left ventricular systolic dysfunction in the aftermath of a myocardial infarction,” Heart, vol. 91, supplement 2, pp. ii7–ii13, 2005.
[8]  J. P. Hellermann, S. J. Jacobsen, B. J. Gersh, R. J. Rodeheffer, G. S. Reeder, and V. L. Roger, “Heart failure after myocardial infarction: a review,” American Journal of Medicine, vol. 113, no. 4, pp. 324–330, 2002.
[9]  L. K?ber, C. Torp-Pedersen, J. E. Carlsen et al., “A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction,” The New England Journal of Medicine, vol. 333, no. 25, pp. 1670–1676, 1995.
[10]  P. Giannuzzi, P. L. Temporelli, E. Bosimini et al., “Heterogeneity of left ventricular remodeling after acute myocardial infarction: results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-3 Echo Substudy,” American Heart Journal, vol. 141, no. 1, pp. 131–138, 2001.
[11]  E. Bosimini, P. Giannuzzi, P. L. Temporelli et al., “Electrocardiographic evolutionary changes and left ventricular remodeling after acute myocardial infarction: results of the GISSI-3 Echo substudy,” Journal of the American College of Cardiology, vol. 35, no. 1, pp. 127–135, 2000.
[12]  D. Hasdai, E. J. Topoi, R. Kilaru et al., “Frequency, patient characteristics, and outcomes of mild-to-moderate heart failure complicating ST-segment elevation acute myocardial infarction: lessons from 4 international fibrinolytic therapy trials,” American Heart Journal, vol. 145, no. 1, pp. 73–79, 2003.
[13]  P. G. Steg, O. H. Dabbous, L. J. Feldman et al., “Determinants and prognostic impact of heart failure complicating acute coronary syndromes: observation from GRACE,” Circulation, vol. 109, no. 4, pp. 494–499, 2004.
[14]  M. A. Pfeffer, E. Braunwald, L. A. Moye et al., “Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction—results of the survival and ventricular enlargement trial,” The New England Journal of Medicine, vol. 327, no. 10, pp. 669–677, 1992.
[15]  S. D. Solomon, S. Zelenkofske, J. J. V. McMurray et al., “Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both,” The New England Journal of Medicine, vol. 352, no. 25, pp. 2581–2588, 2005.
[16]  D. L. Mann and M. R. Bristow, “Mechanisms and models in heart failure: the biomechanical model and beyond,” Circulation, vol. 111, no. 21, pp. 2837–2849, 2005.
[17]  B. Pitt, W. Remme, F. Zannad et al., “Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction,” The New England Journal of Medicine, vol. 348, no. 14, pp. 1309–1321, 2003.
[18]  H. J. Dargie, “Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: The CAPRICORN randomised trial,” The Lancet, vol. 357, no. 9266, pp. 1385–1390, 2001.
[19]  T. J. Wang, J. C. Evans, E. J. Benjamin, D. Levy, E. C. LeRoy, and R. S. Vasan, “Natural history of asymptomatic left ventricular systolic dysfunction in the community,” Circulation, vol. 108, no. 8, pp. 977–982, 2003.
[20]  ACC/AHA, “ACC/AHA 2008 performance measures for adults With ST-elevation and non–ST-elevation myocardial infarction,” Circulation, vol. 118, pp. 2596–2648, 2008.
[21]  The SOLVD Investigators, “Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions,” The New England Journal of Medicine, vol. 327, no. 10, pp. 685–691, 1992.
[22]  P. Jong, S. Yusuf, M. F. Rousseau, S. A. Ahn, and S. I. Bangdiwala, “Effect of enalapril on 12-year survival and life expectancy in patients with left ventricular systolic dysfunction: a follow-up study,” The Lancet, vol. 361, no. 9372, pp. 1843–1848, 2003.
[23]  The SOLVD Investigators, “Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure,” The New England Journal of Medicine, vol. 325, no. 5, pp. 293–302, 1991.
[24]  J. G. Crilley and M. Farrer, “Left ventricular remodelling and brain natriuretic peptide after first myocardial infarction,” Heart, vol. 86, no. 6, pp. 638–642, 2001.
[25]  P. Bettencourt, A. Ferreira, N. Pardal-Oliveira et al., “Clinical significance of brain natriuretic peptide in patients with postmyocardial infarction,” Clinical Cardiology, vol. 23, no. 12, pp. 921–927, 2000.
[26]  G. F. Mitchell, G. A. Lamas, D. E. Vaughan, and M. A. Pfeffer, “Left ventricular remodeling in the year after first anterior myocardial infarction: a quantitative analysis of contractile segment lengths and ventricular shape,” Journal of the American College of Cardiology, vol. 19, no. 6, pp. 1136–1144, 1992.
[27]  G. A. lamas, D. E. Vaughan, A. F. Parisi, and M. A. Pfeffer, “Effects of left ventricular shape and captopril therapy on exercise capacity after anterior wall acute myocardial infarction,” American Journal of Cardiology, vol. 63, no. 17, pp. 1167–1173, 1989.
[28]  N. Sharpe, H. Smith, J. Murphy, S. Greaves, H. Hart, and G. Gamble, “Early prevention of left ventricular dysfunction after myocardial infarction with angiotensin-converting-enzyme inhibition,” The Lancet, vol. 337, no. 8746, pp. 872–876, 1991.
[29]  R. N. Doughty, G. A. Whalley, G. Gamble, S. MacMahon, and N. Sharpe, “Left ventricular remodeling with carvedilol in patients with congestive heart failure due to ischemic heart disease,” Journal of the American College of Cardiology, vol. 29, no. 5, pp. 1060–1066, 1997.
[30]  P. Vantrimpont, J. L. Rouleau, C. C. Wun et al., “Additive beneficial effects of beta-blockers to angiotensin-converting enzyme inhibitors in the Survival and Ventricular Enlargement (SAVE) study,” Journal of the American College of Cardiology, vol. 29, no. 2, pp. 229–236, 1997.
[31]  D. V. Exner, D. L. Dries, M. A. Waclawiw, B. Shelton, and M. Domanski, “Beta-adrenergic blocking agent use and mortality in patients with asymptomatic and symptomatic left ventricular systolic dysfunction: a post hoc analysis of the Studies of Left Ventricular Dysfunction,” Journal of the American College of Cardiology, vol. 33, no. 4, pp. 916–923, 1999.
[32]  E. Ambrosioni, C. Borhi, and B. Magnani, “The effect of the ACE inhibitor zofenopril on mortality and morbility after anteriormyocardial infarction. The SMILE Study Investigators,” The New England Journal of Medicine, vol. 332, pp. 1715–1716, 1995.
[33]  P. J. de Kam, A. A. Voors, M. P. Van Den Berg et al., “Effect of very early angiotensin-converting enzyme inhibition on left ventricular dilation after myocardial infarction in patients receiving thrombolysis: results of a meta-analysis of 845 patients,” Journal of the American College of Cardiology, vol. 36, no. 7, pp. 2047–2053, 2000.
[34]  Heart Failure Society of America, “Executive summary: HFSA 2010 comprehensive heart failure practice guideline,” Journal of Cardiac Failure, vol. 16, no. 6, pp. 475–539, 2010.
[35]  W. S. Colucci, T. J. Kolias, K. F. Adams et al., “Metoprolol reverses left ventricular remodeling in patients with asymptomatic systolic dysfunction: The REversal of VEntricular Remodeling with Toprol-XL (REVERT) Trial,” Circulation, vol. 116, no. 1, pp. 49–56, 2007.
[36]  M. G. Shlipak, W. S. Browner, H. Noguchi, B. Massie, C. D. Frances, and M. McClellan, “Comparison of the effects of angiotensin converting-enzyme inhibitors and beta blockers on survival in elderly patients with reduced left ventricular function after myocardial infarction,” American Journal of Medicine, vol. 110, no. 6, pp. 425–433, 2001.
[37]  R. Garg, R. Gorlin, T. Smith, and S. Yusuf, “The effect of digoxin on mortality and morbidity in patients with heart failure,” The New England Journal of Medicine, vol. 336, no. 8, pp. 525–533, 1997.
[38]  S. S. Rathore, Y. Wang, and H. M. Krumholz, “Sex-based differences in the effect of digoxin for the treatment of heart failure,” The New England Journal of Medicine, vol. 347, no. 18, pp. 1403–1411, 2002.
[39]  K. Fox, I. Ford, P. G. Steg, M. Tendera, and R. Ferrari, “Ivabradine for patients with stable coronary artery disease and left-ventricular systolic dysfunction (BEAUTIFUL): a randomised, double-blind, placebo-controlled trial,” The Lancet, vol. 372, no. 9641, pp. 807–816, 2008.
[40]  A. E. Buxton, K. L. Lee, J. D. Fisher, M. E. Josephson, E. N. Prystowsky, and G. Hafley, “A randomized study of the prevention of sudden death in patients with coronary artery disease,” The New England Journal of Medicine, vol. 341, no. 25, pp. 1882–1890, 1999.
[41]  A. J. Moss, W. Zareba, W. Jackson Hall et al., “Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction,” The New England Journal of Medicine, vol. 346, no. 12, pp. 877–883, 2002.
[42]  S. H. Hohnloser, K. H. Kuck, P. Dorian et al., “Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction,” The New England Journal of Medicine, vol. 351, no. 24, pp. 2481–2488, 2004.
[43]  F. Van de Werf, J. Bax, A. Betriu, et al., “Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation,” European Heart Journal, vol. 29, pp. 2909–2945, 2008.
[44]  A. J. Moss, W. J. Hall, D. S. Cannom et al., “Cardiac-resynchronization therapy for the prevention of heart-failure events,” The New England Journal of Medicine, vol. 361, no. 14, pp. 1329–1338, 2009.
[45]  ESC Guidelines 201, “Focused update on device therapy in heart failure,” European Heart Journal, vol. 31, pp. 2677–2687, 2010.
[46]  F. A. Spencer, T. E. Meyer, J. M. Gore, and R. J. Goldberg, “Heterogeneity in the management and outcomes of patients with acute myocardial infarction complicated by heart failure: the national registry of myocardial infarction,” Circulation, vol. 105, no. 22, pp. 2605–2610, 2002.
[47]  W. B. Kannel, “Lessons from curbing the coronary artery disease epidemic for confronting the impending epidemic of heart failure,” Medical Clinics of North America, vol. 88, no. 5, pp. 1129–1133, 2004.

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