Nonischemic heart failure: epidemiology, pathophysiology, and progression of disease
- PMID: 10442682
- DOI: 10.1097/00005344-199906003-00004
Nonischemic heart failure: epidemiology, pathophysiology, and progression of disease
Abstract
The prevalence of nonischemic heart failure including idiopathic dilative cardiomyopathy is not well known. It may vary considerably in different population sub-groups and geographic areas. In ambulatory and hospitalized patients with clinically manifest heart failure primary cardiomyopathy is diagnosed in 2-15%, while in recent large scale therapeutic trials the proportion of patients with nonischemic heart failure ranged from 18% to 53%. There is a relation between sex, age and etiology of chronic heart failure, nonischemic cardiomyopathy being more frequent in women and in younger individuals. In contrast to ischemic heart failure, where the severity usually correlates with the extent of coronary artery lesions, the pathophysiology of cardiomyopathy is less clear. Genetic factors, myocarditis from infectious agents, auto-immune mechanisms, cytokine activation, hormonal and metabolic influences can play a role. The functional consequences of myocardial damage in nonischemic heart failure is a global instead of localized abnormality of ventricular contractility. There is epidemiological evidence that in general the prognosis of nonischemic heart failure is better than in ischemic heart failure. The mortality of patients with ischemic heart failure was usually higher in the placebo groups of recent heart failure trials than in patients with nonischemic etiology. Furthermore, therapeutic responses to angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, amlodipine and amiodarone were also different in some studies. The outcome of nonischemic heart failure is better even in transplant candidates with the most advanced stages of heart failure, they survive longer and respond better to intensified drug regimens than patients with similar clinical severity of ischemic heart failure. Thus, an early and precise diagnosis of the etiology of heart failure should be encouraged not only in clinical trials but also in every day patient management. As more therapeutic options are developed, individualized drug selection for patients with various etiologies of heart failure may become possible.
Similar articles
-
Ischemic and nonischemic heart failure do not require different treatment strategies.J Cardiovasc Pharmacol. 1999 Jun;33 Suppl 3:S1-7. doi: 10.1097/00005344-199906003-00001. J Cardiovasc Pharmacol. 1999. PMID: 10442679 Review.
-
Etiology and response to drug treatment in heart failure.J Am Coll Cardiol. 1998 Nov;32(5):1167-72. doi: 10.1016/s0735-1097(98)00400-8. J Am Coll Cardiol. 1998. PMID: 9809921 Review.
-
Heart failure etiology affects peripheral vascular endothelial function after cardiac transplantation.J Am Coll Cardiol. 2001 Jan;37(1):195-200. doi: 10.1016/s0735-1097(00)01057-3. J Am Coll Cardiol. 2001. PMID: 11153738
-
Ischemic versus non-ischemic heart failure: should the etiology be determined?Heart Fail Monit. 2001;1(4):122-5. Heart Fail Monit. 2001. PMID: 12634896 Review.
-
Contemporary Characteristics and Outcomes in Chagasic Heart Failure Compared With Other Nonischemic and Ischemic Cardiomyopathy.Circ Heart Fail. 2017 Nov;10(11):e004361. doi: 10.1161/CIRCHEARTFAILURE.117.004361. Circ Heart Fail. 2017. PMID: 29141857
Cited by
-
Young at Heart: Pioneering Approaches to Model Nonischaemic Cardiomyopathy with Induced Pluripotent Stem Cells.Stem Cells Int. 2016;2016:4287158. doi: 10.1155/2016/4287158. Epub 2016 Mar 24. Stem Cells Int. 2016. PMID: 27110250 Free PMC article. Review.
-
Dilated cardiomyopathy in mice deficient for the lysosomal cysteine peptidase cathepsin L.Proc Natl Acad Sci U S A. 2002 Apr 30;99(9):6234-9. doi: 10.1073/pnas.092637699. Epub 2002 Apr 23. Proc Natl Acad Sci U S A. 2002. PMID: 11972068 Free PMC article.
-
Melatonin in Heart Failure: A Promising Therapeutic Strategy?Molecules. 2018 Jul 22;23(7):1819. doi: 10.3390/molecules23071819. Molecules. 2018. PMID: 30037127 Free PMC article. Review.
-
Protective role of ErbB3 signaling in myeloid cells during adaptation to cardiac pressure overload.J Mol Cell Cardiol. 2021 Mar;152:1-16. doi: 10.1016/j.yjmcc.2020.11.009. Epub 2020 Nov 28. J Mol Cell Cardiol. 2021. PMID: 33259856 Free PMC article.
-
Implementation of guidelines for implantable cardioverter-defibrillator therapy in clinical practice: Which patients do benefit?Neth Heart J. 2013 Jun;21(6):274-83. doi: 10.1007/s12471-013-0407-x. Neth Heart J. 2013. PMID: 23572330 Free PMC article.
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Medical
Research Materials
Miscellaneous