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Ventricular remodeling

April 13, 2024

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]

Pathophysiology edit

 
Myocardiocyte

The cardiac myocyte is the major cell involved in remodeling. Fibroblasts, collagen, the interstitium, and the coronary vessels to a lesser extent, also play a role. A common scenario for remodeling is after myocardial infarction. There is myocardial necrosis (cell death) and disproportionate thinning of the heart. This thin, weakened area is unable to withstand the pressure and volume load on the heart in the same manner as the other healthy tissue. As a result, there is dilatation of the chamber arising from the infarct region. The initial remodeling phase after a myocardial infarction results in repair of the necrotic area and myocardial scarring that may, to some extent, be considered beneficial since there is an improvement in or maintenance of LV function and cardiac output. Over time, however, as the heart undergoes ongoing remodeling, it becomes less elliptical and more spherical. Ventricular mass and volume increase, which together adversely affect cardiac function. Eventually, diastolic function, or the heart's ability to relax between contractions may become impaired, further causing decline.[7]

After a myocardial infarction (MI), cardiac myocyte death can be triggered by necrosis, apoptosis, or autophagy, leading to thinning of the cardiac wall.[8] The surviving cardiac myocytes either arrange in parallel or in series to each other, contributing to ventricular dilatation or ventricular hypertrophy, depending on the loading stress on the ventricular wall.[7] Besides, reduced expression of V1 myosin and L-type calcium channels on cardiac myocytes are also thought to cause cardiac remodeling. Under normal body conditions, fatty acid accounts for 60 to 90% of the energy supply of the heart. Post MI, as fatty acid oxidation decreases, it leads to reduced energy supply for the cardiac myocytes, accumulation of fatty acids to toxic levels, and dysfunction of mitochondria. These consequences also led to the increase in oxidative stress on the heart, causing the proliferation of fibroblasts, activation of metalloproteinases, and induction of apoptosis, which would be explained below. Besides, inflammatory immune response after MI also contributes to the above changes.[8]

Besides, the cardiac interstitium which consisted of largely Type I and Type III collagen fibres are also involved in cardiac remodeling. Cardiac collagen is synthesized by fibroblasts and degraded by metalloproteinases.[7] Fibroblasts are activated post MI, leading to increased collagen synthesis and fibrosis of the heart.[8] Increase expression of MMP1 and MMP9 led to degradation of collagen fibres, and subsequently dilatation of the heart.[7] Several signal pathways such as Angiotensin II, Transforming growth factor beta (TGF-beta), and Endothelin 1 are known to trigger synthesis and degradation of collagen fibres in the heart.[8]

Other factors such as high blood pressure, activation of sympathetic system which releases norepinephrine, activation of renin–angiotensin system which releases renin and anti-diuretic hormones are important contributors of cardiac remodelling. However, atrial natriuretic peptide is thought to be cardio-protective.[7]

Evaluation edit

Remodeling of the heart is evaluated by performing an echocardiogram. The size and function of the atria and ventricles can be characterized using this test.[citation needed]

Treatment edit

Many factors influence the time course and extent of remodeling, including the severity of the injury, secondary events (recurrent ischemia or infarction), neurohormonal activation, genetic factors and gene expression, and treatment. Medications may attenuate remodeling. Angiotensin-converting enzyme (ACE) inhibitors have been consistently shown to decrease remodeling in animal models or transmural infarction and chronic pressure overload. Clinical trials have shown that ACE inhibitor therapy after myocardial infarction leads to improved myocardial performance, improved ejection fraction, and decreased mortality compared to patients treated with placebo. Likewise, inhibition of aldosterone, either directly or indirectly, leads to improvement in remodeling.[9] Carvedilol, a 3rd generation beta blocker, may actually reverse the remodeling process by reducing left ventricular volumes and improving systolic function.[10][11] Cardiac resynchronization therapy (CRT) has shown the ability to reverse left ventricular remodeling in some patients.[12][13] Early correction of congenital heart defects, if appropriate, may prevent remodeling, as will treatment of chronic hypertension or valvular heart disease. Often, reverse remodeling, or improvement in left ventricular function, will also be seen.[citation needed]

See also edit

References edit

  1. ^ 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.
  2. ^ Ventricular+remodeling at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
  3. ^ 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.
  4. ^ 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.
  5. ^ 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.
  6. ^ 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.
  7. ^ a b c d e Cohn, Jay N; Colucci, Wilson S; Yeon, Susan B. "Cardiac remodeling: Basic aspects". UpToDate.com. Retrieved 8 November 2017.
  8. ^ a b c d Azevedo, Paula S; Polegato, Bertha F; Minicucci, Marcos F (January 2016). "Cardiac Remodeling: Concepts, Clinical Impact, Pathophysiological Mechanisms and Pharmacologic Treatment". Arquivos Brasileiros de Cardiologia. 106 (1): 62–69. doi:10.5935/abc.20160005. PMC 4728597. PMID 26647721.
  9. ^ Pitt, Bertram; Remme, Willem; Zannad, Faiez; Neaton, James; Martinez, Felipe; Roniker, Barbara; Bittman, Richard; Hurley, Steve; Kleiman, Jay; Gatlin, Marjorie (2003). "Eplerenone, a Selective Aldosterone Blocker, in Patients with Left Ventricular Dysfunction after Myocardial Infarction". New England Journal of Medicine. 348 (14): 1309–21. doi:10.1056/NEJMoa030207. PMID 12668699.
  10. ^ Khattar, R. S. (2003). "Effects of ACE-inhibitors and beta-blockers on left ventricular remodeling in chronic heart failure". Minerva Cardioangiologica. 51 (2): 143–54. PMID 12783070.
  11. ^ Reis Filho JR, Cardoso JN, Cardoso CM, Pereira-Barretto AC (2015). "Reverse Cardiac Remodeling: A Marker of Better Prognosis in Heart Failure". Arquivos Brasileiros de Cardiologia. 104 (6): 502–06. doi:10.5935/abc.20150025. PMC 4484683. PMID 26131706.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Leyva, Francisco; Nisam, Seah; Auricchio, Angelo (2014). "20 Years of Cardiac Resynchronization Therapy". Journal of the American College of Cardiology. 64 (10). Elsevier BV: 1047–1058. doi:10.1016/j.jacc.2014.06.1178. ISSN 0735-1097. PMID 25190241.
  13. ^ St John Sutton, Martin G.; Plappert, Ted; Hilpisch, Kathryn E.; Abraham, William T.; Hayes, David L.; Chinchoy, Edward (2006-01-17). "Sustained Reverse Left Ventricular Structural Remodeling With Cardiac Resynchronization at One Year Is a Function of Etiology". Circulation. 113 (2). Ovid Technologies (Wolters Kluwer Health): 266–272. doi:10.1161/circulationaha.104.520817. ISSN 0009-7322. PMID 16401777.

Further reading edit

  • "Left Ventricular Remodeling in Heart Failure: Current Concepts in Clinical Significance and Assessment". imaging.onlinejacc.org. Retrieved 2016-02-12.

April 13, 2024
ventricular, remodeling, cardiology, ventricular, remodeling, cardiac, remodeling, refers, changes, size, shape, structure, function, heart, this, happen, result, exercise, physiological, remodeling, after, injury, heart, muscle, pathological, remodeling, inju. 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 Contents 1 Pathophysiology 2 Evaluation 3 Treatment 4 See also 5 References 6 Further readingPathophysiology edit nbsp MyocardiocyteThe cardiac myocyte is the major cell involved in remodeling Fibroblasts collagen the interstitium and the coronary vessels to a lesser extent also play a role A common scenario for remodeling is after myocardial infarction There is myocardial necrosis cell death and disproportionate thinning of the heart This thin weakened area is unable to withstand the pressure and volume load on the heart in the same manner as the other healthy tissue As a result there is dilatation of the chamber arising from the infarct region The initial remodeling phase after a myocardial infarction results in repair of the necrotic area and myocardial scarring that may to some extent be considered beneficial since there is an improvement in or maintenance of LV function and cardiac output Over time however as the heart undergoes ongoing remodeling it becomes less elliptical and more spherical Ventricular mass and volume increase which together adversely affect cardiac function Eventually diastolic function or the heart s ability to relax between contractions may become impaired further causing decline 7 After a myocardial infarction MI cardiac myocyte death can be triggered by necrosis apoptosis or autophagy leading to thinning of the cardiac wall 8 The surviving cardiac myocytes either arrange in parallel or in series to each other contributing to ventricular dilatation or ventricular hypertrophy depending on the loading stress on the ventricular wall 7 Besides reduced expression of V1 myosin and L type calcium channels on cardiac myocytes are also thought to cause cardiac remodeling Under normal body conditions fatty acid accounts for 60 to 90 of the energy supply of the heart Post MI as fatty acid oxidation decreases it leads to reduced energy supply for the cardiac myocytes accumulation of fatty acids to toxic levels and dysfunction of mitochondria These consequences also led to the increase in oxidative stress on the heart causing the proliferation of fibroblasts activation of metalloproteinases and induction of apoptosis which would be explained below Besides inflammatory immune response after MI also contributes to the above changes 8 Besides the cardiac interstitium which consisted of largely Type I and Type III collagen fibres are also involved in cardiac remodeling Cardiac collagen is synthesized by fibroblasts and degraded by metalloproteinases 7 Fibroblasts are activated post MI leading to increased collagen synthesis and fibrosis of the heart 8 Increase expression of MMP1 and MMP9 led to degradation of collagen fibres and subsequently dilatation of the heart 7 Several signal pathways such as Angiotensin II Transforming growth factor beta TGF beta and Endothelin 1 are known to trigger synthesis and degradation of collagen fibres in the heart 8 Other factors such as high blood pressure activation of sympathetic system which releases norepinephrine activation of renin angiotensin system which releases renin and anti diuretic hormones are important contributors of cardiac remodelling However atrial natriuretic peptide is thought to be cardio protective 7 Evaluation editRemodeling of the heart is evaluated by performing an echocardiogram The size and function of the atria and ventricles can be characterized using this test citation needed Treatment editMany factors influence the time course and extent of remodeling including the severity of the injury secondary events recurrent ischemia or infarction neurohormonal activation genetic factors and gene expression and treatment Medications may attenuate remodeling Angiotensin converting enzyme ACE inhibitors have been consistently shown to decrease remodeling in animal models or transmural infarction and chronic pressure overload Clinical trials have shown that ACE inhibitor therapy after myocardial infarction leads to improved myocardial performance improved ejection fraction and decreased mortality compared to patients treated with placebo Likewise inhibition of aldosterone either directly or indirectly leads to improvement in remodeling 9 Carvedilol a 3rd generation beta blocker may actually reverse the remodeling process by reducing left ventricular volumes and improving systolic function 10 11 Cardiac resynchronization therapy CRT has shown the ability to reverse left ventricular remodeling in some patients 12 13 Early correction of congenital heart defects if appropriate may prevent remodeling as will treatment of chronic hypertension or valvular heart disease Often reverse remodeling or improvement in left ventricular function will also be seen citation needed See also edit nbsp Anatomy portalDor procedure Athlete s heartReferences edit 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 a b c d e Cohn Jay N Colucci Wilson S Yeon Susan B Cardiac remodeling Basic aspects UpToDate com Retrieved 8 November 2017 a b c d Azevedo Paula S Polegato Bertha F Minicucci Marcos F January 2016 Cardiac Remodeling Concepts Clinical Impact Pathophysiological Mechanisms and Pharmacologic Treatment Arquivos Brasileiros de Cardiologia 106 1 62 69 doi 10 5935 abc 20160005 PMC 4728597 PMID 26647721 Pitt Bertram Remme Willem Zannad Faiez Neaton James Martinez Felipe Roniker Barbara Bittman Richard Hurley Steve Kleiman Jay Gatlin Marjorie 2003 Eplerenone a Selective Aldosterone Blocker in Patients with Left Ventricular Dysfunction after Myocardial Infarction New England Journal of Medicine 348 14 1309 21 doi 10 1056 NEJMoa030207 PMID 12668699 Khattar R S 2003 Effects of ACE inhibitors and beta blockers on left ventricular remodeling in chronic heart failure Minerva Cardioangiologica 51 2 143 54 PMID 12783070 Reis Filho JR Cardoso JN Cardoso CM Pereira Barretto AC 2015 Reverse Cardiac Remodeling A Marker of Better Prognosis in Heart Failure Arquivos Brasileiros de Cardiologia 104 6 502 06 doi 10 5935 abc 20150025 PMC 4484683 PMID 26131706 a href Template Cite journal html title Template Cite journal cite journal a CS1 maint multiple names authors list link Leyva Francisco Nisam Seah Auricchio Angelo 2014 20 Years of Cardiac Resynchronization Therapy Journal of the American College of Cardiology 64 10 Elsevier BV 1047 1058 doi 10 1016 j jacc 2014 06 1178 ISSN 0735 1097 PMID 25190241 St John Sutton Martin G Plappert Ted Hilpisch Kathryn E Abraham William T Hayes David L Chinchoy Edward 2006 01 17 Sustained Reverse Left Ventricular Structural Remodeling With Cardiac Resynchronization at One Year Is a Function of Etiology Circulation 113 2 Ovid Technologies Wolters Kluwer Health 266 272 doi 10 1161 circulationaha 104 520817 ISSN 0009 7322 PMID 16401777 Further reading edit Left Ventricular Remodeling in Heart Failure Current Concepts in Clinical Significance and Assessment imaging onlinejacc org Retrieved 2016 02 12 Retrieved from https en wikipedia org w index php title Ventricular remodeling amp oldid 1170128340, wikipedia, wiki, book, books, library,

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