Irreversible morphological changes contributing to depressed cardiac function after surgery for chronic aortic regurgitation.

Donaldson, R M; Florio, R; Rickards, Anthony F.; Bennett, J. G.; Mh, Yacoub; Ross, D. N.; Olsen, E. G. J.

doi:10.1136/hrt.48.6.589

Cited by 38 publications

(14 citation statements)

References 17 publications

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“…Left ventricle (LV) VOL secondary to aortic valve insufficiency induces LV remodeling, in which cardiac fibroblasts are activated to modulate the extracellular matrix [ 4 ] and in which cardiomyocytes develop mitochondrial dysfunction-associated pathological hypertrophy [ 5 , 6 ]. This leads to dilation of the LV cavity and impairment of systolic and diastolic LV function.…”

Section: Introductionmentioning

confidence: 99%

“…This leads to dilation of the LV cavity and impairment of systolic and diastolic LV function. Volume-unloading surgery, such as aortic valve replacement, can pathologically and functionally reverse VOL-induced LV remodeling [ 4 ]. Mitochondrial dysfunction in cardiomyocytes is an early predictor of irreversible LV remodeling and may therefore be an indication for surgical intervention for VOL [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

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Functional and pathological characteristics of reversible remodeling in a canine right ventricle in response to volume overloading and volume unloading

et al. 2014

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PurposesPatients who undergo right ventricular (RV) outflow augmentation inevitably develop RV remodeling due to pulmonary insufficiency-related volume overload (VOL). However, the reversibility of this remodeling is not fully understood. The goal of this study was to establish an animal model of VOL and unloading to characterize the functional and pathological characteristics and reversibility of RV remodeling.MethodsVOL-RV was successfully induced by establishing direct RV-pulmonary artery (PA) bypass for 12 weeks in beagle canines. There were no procedure-related mortalities (n = 8).ResultsThe RV developed typical functional features of VOL-related remodeling, such as a significant increase in end-diastolic/systolic volume and end-systolic pressure and a significant reduction in ejection fraction at 12 weeks, as assessed by three-dimensional echocardiography and cardiac catheterization. The RV developed typical pathological signs of remodeling, microstructural disorganization of cardiomyocytes, and/or structural/functional deterioration of the mitochondria. Volume unloading by division of the RV-PA bypass reversed the increase in the end-systolic/diastolic volume over 4 weeks when compared with a sham operation (n = 4 each). In addition, the bypass division also reversed the pathological changes seen in VOL-RV.ConclusionsVOL-RV that yielded typical functional and pathological features of RV remodeling was reproducibly achieved by direct RV-PA bypass in canines. The RV remodeling due to VOL was functionally and pathologically reversed by volume unloading via the bypass division.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Functional and pathological characteristics of reversible remodeling in a canine right ventricle in response to volume overloading and volume unloading

et al. 2014

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“…As a result, the relationships between histopathology and cardiac function in AR have not been well defined. It is not suprising, then, that studies relating myocardial histology and surgical outcome have yielded varying results [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Fibrosis, Myocyte Degeneration and Heart Failure in Chronic Experimental Aortic Regurgitation

Liu¹,

Magid

Fox³

et al. 1998

Cardiology

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Myocardial fibrosis and myocyte degeneration have been reported in patients with chronic aortic regurgitation (AR), and may be related to the pathophysiology of congestive heart failure (CHF) in this disease. To define the relationship between myocardial histopathologic variations and CHF in chronic AR, we performed gross and microscopic evaluations of postmortem tissue from a rabbit model of chronic AR manifesting left ventricular (LV) responses to AR similar to those in humans. Moderate-to-severe chronic AR (echocardiographic regurgitant fraction = 52 ± 13%) was induced by closed-chest aortic valve perforation in 11 New Zealand White rabbits; 5 control rabbits were sham operated. Six of the 11 AR rabbits died 1.5 ± 0.8 years (range 0.6–2.8 years) after AR induction; all 6 had gross and histologic anatomic evidence of CHF at necropsy. The remaining 5 AR rabbits survived until sacrifice at 2.9 ± 0.1 years of AR; none had pathologic evidence of CHF. Cardiac hypertrophy and the extent of LV fibrosis and myocyte necrosis all were greatest among the 6 AR CHF rabbits. No inflammatory response was apparent in any animal. Moderate-to-severe chronic experimental AR frequently results in CHF which is strongly associated with myocardial fibrosis and necrosis, without evidence of inflammation. These histopathologic variations may be pathophysiologically related to CHF development.

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“…Many patients will develop symptoms (typically dyspnea, sometimes angina) while having normal LV systolic function; a significant number will develop symptoms at the onset of LV systolic dysfunction, whereas others may remain asymptomatic in the presence of varying degrees of LV systolic dysfunction. AVR should be undertaken to alleviate symptoms and before LV impairment becomes irreversible [12].…”

Section: Chronic Aortic Regurgitationmentioning

confidence: 99%

Indications for surgery for aortic regurgitation

Nkomo

2003

Curr Cardiol Rep

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Aortic valve replacement for isolated aortic regurgitation (AR) is usually not indicated unless the regurgitation is severe. However, not all patients with severe AR require aortic valve replacement. This review focuses on the causes of AR and the pathophysiology of acute versus chronic AR, and the attendant adaptive mechanisms of the left ventricle that ultimately determine their different natural histories. Aortic valve surgery must be performed in a timely manner to prevent cardiac death, ameliorate symptoms, and limit late postoperative excess mortality.

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Irreversible morphological changes contributing to depressed cardiac function after surgery for chronic aortic regurgitation.

Cited by 38 publications

References 17 publications

Functional and pathological characteristics of reversible remodeling in a canine right ventricle in response to volume overloading and volume unloading

Functional and pathological characteristics of reversible remodeling in a canine right ventricle in response to volume overloading and volume unloading

Fibrosis, Myocyte Degeneration and Heart Failure in Chronic Experimental Aortic Regurgitation

Indications for surgery for aortic regurgitation

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