In cardiology, ventricular remodeling (or cardiac remodeling)[1] refers to changes in the size, shape, structure, and function of the heart. This can happen as a result of exercise (physiological remodeling) or after injury to the heart muscle (pathological remodeling).[2] The injury is typically due to acute myocardial infarction (usually transmural or ST segment elevation infarction), but may be from a number of causes that result in increased pressure or volume, causing pressure overload or volume overload (forms of strain) on the heart. Chronic hypertension, congenital heart disease with intracardiac shunting, and valvular heart disease may also lead to remodeling. After the insult occurs, a series of histopathological and structural changes occur in the left ventricular myocardium that lead to progressive decline in left ventricular performance. Ultimately, ventricular remodeling may result in diminished contractile (systolic) function and reduced stroke volume.
Physiological remodeling is reversible while pathological remodeling is mostly irreversible. Remodeling of the ventricles under left/right pressure demand make mismatches inevitable. Pathologic pressure mismatches between the pulmonary and systemic circulation guide compensatory remodeling of the left and right ventricles. The term "reverse remodeling" in cardiology implies an improvement in ventricular mechanics and function following a remote injury or pathological process.[3][4][5]
Ventricular remodeling may include ventricular hypertrophy, ventricular dilation, cardiomegaly, and other changes. It is an aspect of cardiomyopathy, of which there are many types. Concentric hypertrophy is due to pressure overload, while eccentric hypertrophy is due to volume overload.[6]
- ^ Mihl, C.; Dassen, W. R. M.; Kuipers, H. (2008). "Cardiac remodelling: Concentric versus eccentric hypertrophy in strength and endurance athletes". Netherlands Heart Journal. 16 (4): 129–33. doi:10.1007/BF03086131. PMC 2300466. PMID 18427637.
- ^ Ventricular+remodeling at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
- ^ Yu, Cheuk-Man; Bleeker, Gabe B.; Fung, Jeffrey Wing-Hong; Schalij, Martin J.; Zhang, Qing; Wall, Ernst E. van der; Chan, Yat-Sun; Kong, Shun-Ling; Bax, Jeroen J. (2005-09-13). "Left Ventricular Reverse Remodeling but Not Clinical Improvement Predicts Long-Term Survival After Cardiac Resynchronization Therapy". Circulation. 112 (11): 1580–86. doi:10.1161/circulationaha.105.538272. ISSN 0009-7322. PMID 16144994.
- ^ Ypenburg, Claudia; Bommel, Rutger J. van; Borleffs, C. Jan Willem; Bleeker, Gabe B.; Boersma, Eric; Schalij, Martin J.; Bax, Jeroen J. (2009). "Long-Term Prognosis After Cardiac Resynchronization Therapy Is Related to the Extent of Left Ventricular Reverse Remodeling at Midterm Follow-Up". Journal of the American College of Cardiology. 53 (6): 483–90. doi:10.1016/j.jacc.2008.10.032. PMID 19195605.
- ^ Saavedra, W.Federico; Tunin, Richard S; Paolocci, Nazareno; Mishima, Takayuki; Suzuki, George; Emala, Charles W; Chaudhry, Pervaiz A; Anagnostopoulos, Petros; Gupta, Ramesh C (2002). "Reverse remodeling and enhancedadrenergic reserve from passive externalsupport in experimental dilated heart failure". Journal of the American College of Cardiology. 39 (12): 2069–76. doi:10.1016/s0735-1097(02)01890-9. PMID 12084610.
- ^ Katz, Daniel H.; Beussink, Lauren; Sauer, Andrew J.; Freed, Benjamin H.; Burke, Michael A.; Shah, Sanjiv J. (2013). "Prevalence, Clinical Characteristics, and Outcomes Associated with Eccentric Versus Concentric Left Ventricular Hypertrophy in Heart Failure with Preserved Ejection Fraction". The American Journal of Cardiology. 112 (8): 1158–64. doi:10.1016/j.amjcard.2013.05.061. PMC 3788852. PMID 23810323.