全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Similarities and Differences between the Pathogenesis and Pathophysiology of Diastolic and Systolic Heart Failure

DOI: 10.1155/2013/824135

Full-Text   Cite this paper   Add to My Lib

Abstract:

Pathophysiology of heart failure has been considered to be a damaged state of systolic function of the heart followed by a state of low cardiac output that is, systolic heart failure. Even if systolic function is preserved, left ventricular filling in diastole can be impeded and resulted in elevation of filling pressure and symptoms of heart failure. This kind of heart failure is called diastolic heart failure. Nowadays, diastolic heart failure is referred to as heart failure with preserved ejection fraction (HFpEF), whereas systolic heart failure is referred to as heart failure with reduced ejection fraction (HFrEF). In this paper, the similarities and differences between the pathogenesis and pathophysiology of diastolic and systolic heart failure were reviewed. Although diastolic heart failure is a common condition of heart failure worldwide, its pathophysiology has not been sufficiently elucidated. This is thought to be the most significant reason for a lack of established treatment methods for diastolic heart failure. We hope to proceed with future studies on this topic. 1. Introduction Pathophysiology of heart failure has been considered to be a damaged state of systolic function of the heart followed by a state of low cardiac output (systolic heart failure). However, even if systolic function is preserved, left ventricular filling in diastole is impeded due to various factors. This condition leads to congestive heart failure due to the rise in left ventricular end-diastolic pressure and the decrease in cardiac output. This kind of pathophysiology is now known as diastolic heart failure [1, 2]. In recent years, diastolic heart failure caused by the affected left ventricle has become a clinical issue [3]. Nowadays, diastolic heart failure is referred to as heart failure with preserved ejection fraction (HFpEF), whereas systolic heart failure is referred to as heart failure with reduced ejection fraction (HFrEF). This is because evaluating accurate pathophysiology and diagnosis of diastolic heart failure is in fact difficult. 2. Diastolic Dysfunction Diastole of the left ventricle is composed of isovolumic relaxation and ventricular filling. Relaxation of the left ventricle is an active process that occurs as a result of energy-dependent uptake of intracellular calcium by the sarcoplasmic reticulum, whose concentration has risen during the systolic phase. Relaxation of the left ventricle is impaired in a disease state caused by energy metabolism disorders or calcium-handling abnormalities such as myocardial ischemia and myocardial hypertrophy. Left

References

[1]  M. Ouzounian, D. S. Lee, and P. P. Liu, “Diastolic heart failure: mechanisms and controversies,” Nature Clinical Practice Cardiovascular Medicine, vol. 5, pp. 375–386, 2008.
[2]  M. T. Maeder and D. M. Kaye, “Heart failure with normal left ventricular ejection fraction,” Journal of the American College of Cardiology, vol. 53, no. 11, pp. 905–918, 2009.
[3]  B. A. Borlaug and W. J. Paulus, “Heart failure with preserved ejection fraction: pathophysiology, diagnosis, and treatment,” European Heart Journal, vol. 32, no. 6, pp. 670–679, 2011.
[4]  E. H. García, E. R. Perna, E. F. Farías et al., “Reduced systolic performance by tissue Doppler in patients with preserved and abnormal ejection fraction: new insights in chronic heart failure,” International Journal of Cardiology, vol. 108, no. 2, pp. 181–188, 2006.
[5]  G. Yip, M. Wang, Y. Zhang, J. W. H. Fung, P. Y. Ho, and J. E. Sanderson, “Left ventricular long axis function in diastolic heart failure is reduced in both diastole and systole: time for a redefinition?” Heart, vol. 87, no. 2, pp. 121–125, 2002.
[6]  S. J. Skaluba and S. E. Litwin, “Mechanisms of exercise intolerance: insights from tissue Doppler imaging,” Circulation, vol. 109, no. 8, pp. 972–977, 2004.
[7]  K. Yamamoto, Y. Sakata, T. Ohtani, Y. Takeda, and T. Mano, “Heart failure with preserved ejection fraction: what is known and unknown,” Circulation Journal, vol. 73, no. 3, pp. 404–410, 2009.
[8]  S. A. Hunt, W. T. Abraham, M. H. Chin et al., “ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society,” Circulation, vol. 112, no. 12, pp. e154–e235, 2005.
[9]  R. S. Vasan and D. Levy, “Defining diastolic heart failure: a call for standardized diagnostic criteria,” Circulation, vol. 101, no. 17, pp. 2118–2121, 2000.
[10]  M. R. Zile, W. H. Gaasch, J. D. Carroll et al., “Heart failure with a normal ejection fraction: is measurement of diastolic function necessary to make the diagnosis of diastolic heart failure?” Circulation, vol. 104, no. 7, pp. 779–782, 2001.
[11]  M. R. Zile, C. F. Baicu, and W. H. Gaasch, “Diastolic heart failure—abnormalities in active relaxation and passive stiffness of the left ventricle,” The New England Journal of Medicine, vol. 350, no. 19, pp. 1953–1959, 2004.
[12]  T. E. Owan, D. O. Hodge, R. M. Herges, S. J. Jacobsen, V. L. Roger, and M. M. Redfield, “Trends in prevalence and outcome of heart failure with preserved ejection fraction,” The New England Journal of Medicine, vol. 355, no. 3, pp. 251–259, 2006.
[13]  R. S. Bhatia, J. V. Tu, D. S. Lee et al., “Outcome of heart failure with preserved ejection fraction in a population-based study,” The New England Journal of Medicine, vol. 355, no. 3, pp. 260–269, 2006.
[14]  S. F. Nagueh, C. P. Appleton, T. C. Gillebert et al., “Recommendations for the evaluation of left ventricular diastolic function by echocardiography,” European Journal of Echocardiography, vol. 10, no. 2, pp. 165–193, 2009.
[15]  D. J. van Veldhuisen, G. C. Linssen, T. Jaarsma, et al., “B-type natriuretic Peptide and prognosis in heart failure patients with preserved and reduced ejection fraction,” Journal of the American College of Cardiology, vol. 61, no. 14, pp. 1498–1506, 2013.
[16]  F. P. Brouwers, R. A. de Boer, P. van der Harst, et al., “Incidence and epidemiology of new onset heart failure with preserved vs. reduced ejection fraction in a community-based cohort: 11-year follow-up of PREVEND,” European Heart Journal, vol. 34, pp. 1424–1431, 2013.
[17]  R. Santhanakrishnan, J. P. Chong, T. P. Ng, et al., “Growth differentiation factor 15, ST2, high-sensitivity troponin T, and N-terminal pro brain natriuretic peptide in heart failure with preserved vs. reduced ejection fraction,” European Journal of Heart Failure, vol. 14, pp. 1338–1347, 2012.
[18]  R. R. J. van Kimmenade and J. L. Januzzi Jr., “Emerging biomarkers in heart failure,” Clinical Chemistry, vol. 58, no. 1, pp. 127–138, 2012.
[19]  H. K. Gaggin and J. L. Januzzi Jr., “Biomarkers and diagnostics in heart failure,” Biochimica et Biophysica Acta, 2013.
[20]  J. G. F. Cleland, M. Tendera, J. Adamus, N. Freemantle, L. Polonski, and J. Taylor, “The perindopril in elderly people with chronic heart failure (PEP-CHF) study,” European Heart Journal, vol. 27, no. 19, pp. 2338–2345, 2006.
[21]  S. Yusuf, M. A. Pfeffer, K. Swedberg et al., “Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-preserved trial,” The Lancet, vol. 362, no. 9386, pp. 777–781, 2003.
[22]  B. M. Massie, P. E. Carson, J. J. McMurray et al., “Irbesartan in patients with heart failure and preserved ejection fraction,” The New England Journal of Medicine, vol. 359, no. 23, pp. 2456–2467, 2008.
[23]  A. F. Hernandez, B. G. Hammill, C. M. O'Connor, K. A. Schulman, L. H. Curtis, and G. C. Fonarow, “Clinical effectiveness of beta-blockers in heart failure. Findings from the OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients With Heart Failure) Registry,” Journal of the American College of Cardiology, vol. 53, no. 2, pp. 184–192, 2009.
[24]  H. Fukuta, D. C. Sane, S. Brucks, and W. C. Little, “Statin therapy may be associated with lower mortality in patients with diastolic heart failure: a preliminary report,” Circulation, vol. 112, no. 3, pp. 357–363, 2005.
[25]  W. J. Paulus and J. J. M. van Ballegoij, “Treatment of heart failure with normal ejection fraction: an inconvenient truth!,” Journal of the American College of Cardiology, vol. 55, no. 6, pp. 526–537, 2010.
[26]  B. A. Borlaug, V. Melenovsky, T. Marhin, P. Fitzgerald, and D. A. Kass, “Sildenafil inhibits β-adrenergic-stimulated cardiac contractility in humans,” Circulation, vol. 112, no. 17, pp. 2642–2649, 2005.
[27]  C. Vlachopoulos, K. Hirata, and M. F. O'Rourke, “Effect of sildenafil on arterial stiffness and wave reflection,” Vascular Medicine, vol. 8, no. 4, pp. 243–248, 2003.
[28]  S. D. Katz, K. Balidemaj, S. Homma, H. Wu, J. Wang, and S. Maybaum, “Acute type 5 phosphodiesterase inhibition with sildenafil enhances flow-mediated vasodilation in patients with chronic heart failure,” Journal of the American College of Cardiology, vol. 36, no. 3, pp. 845–851, 2000.
[29]  G. D. Lewis, J. Lachmann, J. Camuso et al., “Sildenafil improves exercise hemodynamics and oxygen uptake in patients with systolic heart failure,” Circulation, vol. 115, no. 1, pp. 59–66, 2007.
[30]  H. H. Chen, “Heart failure: a state of brain natriuretic peptide deficiency or resistance or both!,” Journal of the American College of Cardiology, vol. 49, no. 10, pp. 1089–1091, 2007.
[31]  M. M. Redfield, K. L. Lee, and E. Braunwald, “Evaluating the effectiveness of Sildenafil at improving health outcomes and exercise ability in people with diastolic heart failure (The RELAX Study),” NCT00763867, 2008, http://clinicaltrials.gov/.
[32]  K. R. Daniel, G. Wells, K. Stewart, B. Moore, and D. W. Kitzman, “Effect of aldosterone antagonism on exercise tolerance, doppler diastolic function, and quality of life in older women with diastolic heart failure,” Congestive Heart Failure, vol. 15, no. 2, pp. 68–74, 2009.
[33]  P. V. Vaitkevicius, M. Lane, H. Spurgeon et al., “A cross-link breaker has sustained effects on arterial and ventricular properties in older rhesus monkeys,” Proceedings of the National Academy of Sciences of the United States of America, vol. 98, no. 3, pp. 1171–1175, 2001.
[34]  D. A. Kass, E. P. Shapiro, M. Kawaguchi et al., “Improved arterial compliance by a novel advanced glycation end-product crosslink breaker,” Circulation, vol. 104, no. 13, pp. 1464–1470, 2001.
[35]  W. C. Little, M. R. Zile, D. W. Kitzman, W. G. Hundley, T. X. O'Brien, and R. C. Degroof, “The effect of alagebrium chloride (ALT-711), a novel glucose cross-link breaker, in the treatment of elderly patients with diastolic heart failure,” Journal of Cardiac Failure, vol. 11, no. 3, pp. 191–195, 2005.
[36]  B. A. Borlaug, V. Melenovsky, S. D. Russell et al., “Impaired chronotropic and vasodilator reserves limit exercise capacity in patients with heart failure and a preserved ejection fraction,” Circulation, vol. 114, no. 20, pp. 2138–2147, 2006.
[37]  T. T. Phan, K. Abozguia, G. Nallur Shivu et al., “Heart failure with preserved ejection fraction is characterized by dynamic impairment of active relaxation and contraction of the left ventricle on exercise and associated with myocardial energy deficiency,” Journal of the American College of Cardiology, vol. 54, no. 5, pp. 402–409, 2009.
[38]  D. W. Kitzman, M. B. Higginbotham, F. R. Cobb, K. H. Sheikh, and M. J. Sullivan, “Exercise intolerance in patients with heart failure and preserved left ventricular systolic function: failure of the Frank-Starling mechanism,” Journal of the American College of Cardiology, vol. 17, no. 5, pp. 1065–1072, 1991.
[39]  C. S. Smith, P. A. Bottomley, S. P. Schulman, G. Gerstenblith, and R. G. Weiss, “Altered creatine kinase adenosine triphosphate kinetics in failing hypertrophied human myocardium,” Circulation, vol. 114, no. 11, pp. 1151–1158, 2006.
[40]  M. Frenneaux, “Perhexiline therapy in heart failure with preserved ejection fraction syndrome,” NCT00839228, 2009, http://clinicaltrials.gov/.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133