Regression of Left Ventricular Dilation and Hypertrophy after Removal of Volume Overload

Papadimitriou, John; Hopkins, Barry E.; Taylor, Roger R.

doi:10.1161/01.res.35.1.127

Cited by 67 publications

(24 citation statements)

References 12 publications

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“…30 Ultrastructural changes such as the appearance of small mitochondria and loss of alignment of sarcomeres reverses after several months. 31 In case of an atrophic response, after contractile arrest, the recovery of myofilament structure occurs within 2 weeks. 32 In the canine model of AF, Everett et al 10 did not observe reversion of structural atrial remodeling by 2 weeks of SR after 2 mo AF despite full recovery from electrical remodeling, possibly because of the remaining mitral valve insufficiency after cardioversion.…”

Section: Why Is Recovery From Structural Remodeling Slow?mentioning

confidence: 99%

Reverse Structural and Gap-Junctional Remodeling After Prolonged Atrial Fibrillation in the Goat

et al. 2003

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Background— Prolonged atrial fibrillation (AF) results in electrical, structural, and gap-junctional remodeling. We examined the reversibility of the changes in (ultra)structure and gap junctions. Methods and Results— Four groups of goats were used: (1) sinus rhythm (SR), (2) 4 months’ AF (4 mo AF), (3) 2 months’ SR after 4 mo AF (2 mo post-AF), and (4) 4 months’ SR after 4 mo AF (4 mo post-AF). Atria were characterized electrophysiologically, (ultra)structure was studied by light and electron microscopy, and structural and gap-junctional protein expression was studied by immunohistochemistry or Western blotting. The atrial effective refractory period had completely returned to normal values 2 mo post-AF. Induced AF episodes still lasted for minutes at 2 and 4 mo post-AF, compared with seconds in the SR group. Structural abnormalities were still present at 2 and 4 mo post-AF, although to a lesser extent. The increased atrial myocyte diameter was back to normal at 4 mo post-AF. The number of myocytes with severe myolysis had almost normalized 4 mo post-AF, whereas myocytes with mild myolysis remained significantly increased. Extracellular matrix area fraction after 4 mo AF was similar to SR. However, the extracellular matrix fraction per myocyte had increased after 4 mo AF and remained higher post-AF. Changes in expression of structural proteins were partially restored post-AF. The reduction of connexin 40 that was observed during AF was completely reversed at 4 mo post-AF. Conclusions— Recovery from structural remodeling after 4 mo AF is a slow process and is still incomplete 4 mo post-AF. Several months post-AF, the duration of AF episodes is still prolonged (minutes).

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Section: Why Is Recovery From Structural Remodeling Slow?mentioning

confidence: 99%

Reverse Structural and Gap-Junctional Remodeling After Prolonged Atrial Fibrillation in the Goat

et al. 2003

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“…If these late postop LV mass estimates are made assuming late postop ratios ranging from 1.7:1-2.0: 1, the decrease in muscle mass ranges from 43-37%. Assuming a constant geometry (either the unmodified 2:1 method of Troy or the cube method), calculated LV mass falls by 17% at the time of the early postop study and 46% by [12][13][14][15][16][17][18] months.…”

Section: V Mass and The R/ Th Ratiomentioning

confidence: 99%

Chronic aortic regurgitation: the effect of aortic valve replacement on left ventricular volume, mass and function.

Gaasch¹,

Andrias²,

Levine³

1978

Circulation

189

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CHRONIC AORTIC REGURGITATION/Gaasch et al. with the technical assistance ofL. M. Woodbury SUMMARY Serial echocardiographic left ventricular (LV) studies were performed in 19 patients before (preop) and after (postop) aortic valve replacement (AVR) for chronic aortic regurgitation (AR); the effect of AVR on LV volume, mass and function was determined from the echocardiographic data. In the 12 patients who were considered to have successful surgical results, the average LV end-diastolic dimension fell from a preop value of 6.9 ± 0.2 cm to 5.5 0.2 cm (P < 0.01) at the time of the early postop study (seven to 10 days). Muscle cross-sectional area (CSA) derived from dimension and wall thickness data was used as an index of LV muscle mass (preop CSA = 26 ± 1.3 cm2); CSA was unchanged at the early postop study, but subsequently fell to near normal within six months after AVR (20 1 cm2, P < 0.01). There was a trend toward improvement in systolic performance by the late postop studies (12+ months). In two out of three patients with postop paravalvular AR, LV dimension increased after an initial fall. Four patients without paravalvular AR failed to show a significant reduction in LV dimension in the postop studies. In this group the preop studies showed a tendency toward a large end-diastolic dimension and decreased fractional shortening, but the single preop parameter which differentiated these four from the successfully treated group was an end-diastolic radius-towall thickness (R/Th) ratio _ 4.Thus, successful AVR for chronic AR results in the normalization of LV volume and a decrease in LV muscle mass to near normal. The R/Th ratio has important prognostic value which appears to be independent of fractional shortening in some patients with chronic AR.OPTIMUM TIMING of valve replacement in patients with chronic left ventricular (LV) volume overload is a difficult and challenging problem. While aortic valve replacement often results in striking

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“…This phenomenon has not yet been studied quantitatively in postoperative patients with LV hypertrophy, and its relation to persistently depressed contractility 28 remains to be investigated. Studies in dogs with chronic volume overload 29 indicate that regression of hypertrophy is only partial after many weeks of observation.…”

Section: Function Of Hypertrophied Heart /Sasayama Etalmentioning

confidence: 99%

Adaptations of the left ventricle to chronic pressure overload.

Sasayama¹,

Ross²,

Franklin³

et al. 1976

Circulation Research

260

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SUMMARY Left ventricular (LV) function during the adaptationto chronic pressure overload produced by an ascending aortic constriction was analyzed in conscious dogs, instrumented with intraventricular micromanometers and pairs of ultrasonic crystals for measurement of LV wall thickness (WTh) and internal LV chamber diameter. During inflation of the cuff to produce LV pressures averaging 220 mm Hg, calculated peak wall stress (WSt) increased by 55% above control while percent shortening decreased by 24% and mean circumferential shortening velocity (V CF ) decreased by 39% from control. By 9 days (mean) after aortic constriction, the cross-sectional area (CSA) of the LV wall increased by 10% and peak WSt fell to 37% above control. End-diastolic diameter (EDD) increased to 4% above control, while percent shortening and mean V CT remained reduced at -12% and -20% of control, respectively.During the phase of concentric hypertrophy (mean 2V-i weeks), CSA increased further to 15% above control and WSt fell to 22% above control, while EDD and percent shortening returned to control and mean V CF increased to -7 % of control (not significant). At 24 hours after release of the cuff WSt, percent shortening, mean V CP , and peak velocity of LV pressure rise (peak dP/dt) were not significantly different from control. Rapid, partial regression of hypertrophy was observed in some dogs. Thus, the left ventricle responds to chronically elevated pressure by initial dilation with increased WSt followed by gradual wall thickening and consequent reduction of WSt to near normal. After successful adaptation to the pressure overload, hypertrophy per se did not produce intrinsic depression of the myocardial inotropic state.THE PERFORMANCE of the heart and of cardiac muscle in chronic hypertrophy has been investigated intensively, but whether the myocardium of the intact hypertrophied left ventricle exhibits depression of the inotropic state has remained unresolved.1 In addition, little information is available concerning the time course of the functional adaptations that follow the application of a chronic pressure overload.The canine left ventricle is a useful model for the study of experimental circulatory lesions, but investigations of chronic pressure overloading produced by aortic constriction have been complicated by the frequent occurrence of aortic rupture. 2 We have overcome this problem in part by placing a Dacron graft beneath an inflatable aortic cuff; in addition, the ultrasonic technique for measurement of left ventricular (LV) regional dimensions 3 has been adapted to allow serial measurements of LV wall thickness (WTh) and internal diameter. This model for chronic pressure overload in the conscious dog has been applied to assess LV function before and during sustained inflation of the ascending aortic cuff over several weeks, and following its release. MethodsTwelve mongrel dogs weighing 19-36 kg (average, 26.7 kg) underwent right thoracotomy in the 4th intercostal space under sodium pentobarbital anesthesia (25 mg/kg, iv...

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Regression of Left Ventricular Dilation and Hypertrophy after Removal of Volume Overload

Cited by 67 publications

References 12 publications

Reverse Structural and Gap-Junctional Remodeling After Prolonged Atrial Fibrillation in the Goat

Reverse Structural and Gap-Junctional Remodeling After Prolonged Atrial Fibrillation in the Goat

Chronic aortic regurgitation: the effect of aortic valve replacement on left ventricular volume, mass and function.

Adaptations of the left ventricle to chronic pressure overload.

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