Left ventricular remodelling: common process in patients with different primary myocardial disorders

Florea, Viorel G.; Mareyev, V.Y.; Самко, А. Н.; Orlova, Ya. A.; Coats, Andrew J.S.; Belenkov, Y.

doi:10.1016/s0167-5273(98)00362-3

Cited by 47 publications

(24 citation statements)

References 19 publications

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“…Remodeling of the ventricle, clinically manifested as changes in size, shape, and function of the heart after cardiac injury, 26 is an important mechanism underlying the progression of heart failure. 27 It is a process that is common to multiple causes of heart failure 28,29 and that can be delayed or even reversed by appropriate treatment. 23 Eccentric remodeling in the control animals was suggested in the present study by a higher magnitude of ventricular and left atrial enlargement associated with thinning of the infarct-related posterior wall and the overall increase in heart weight.…”

Section: Discussionmentioning

confidence: 99%

Ventricular Preexcitation Modulates Strain and Attenuates Cardiac Remodeling in a Swine Model of Myocardial Infarction

et al. 2007

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Background-Myocardial infarction modifies the distribution of stress within the heart, increasing wall stress in ischemic and surrounding tissue, which often leads to adverse left ventricular remodeling. Electrical preexcitation pacing with appropriate timing of high-stress regions can reduce local strain and may attenuate global remodeling. Methods and Results-Myocardial infarction was induced in 24 swine to study the short-term (nϭ12) and long-term (nϭ12) effects of therapy. Sonomicrometry and hemodynamic measurements were used to show the mechanistic effects of preexcitation and to determine the optimal stimulation site and atrioventricular delay. Lagrangian strain was used to assess regional loading characteristics. Long-term study animals were randomized to 8 weeks of preexcitation (therapy) or no pacing (control). Echocardiograms were performed 2 days after myocardial infarction and repeated at 60 days, when tissue weights and apoptosis were assessed. Preexcitation reduced regional strain in the short term, with the best results achieved when the border region was paced at an atrioventricular delay of 50% of the intrinsic PR interval. In the long term, the changes in left ventricular internal diameter and left atrial size were decreased in therapy animals versus control animals (0.9Ϯ0.3 versus 1.5Ϯ0.5 cm, Pϭ0.03, and 1.06Ϯ0.78 versus 2.32Ϯ0.88 cm, PϽ0.04, respectively). Heart weight was significantly lower in the therapy animals than in the control animals (319.8Ϯ20.8 versus 359.6Ϯ29.3 g, Pϭ0.02). Although not significant, cardiomyocyte apoptosis trended lower in the therapy group. Conclusions-Preexcitation of the left ventricle after myocardial infarction reduced strain and stroke work in the infarct and border regions in the short term and attenuated adverse ventricular remodeling in the long term.

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Section: Discussionmentioning

confidence: 99%

Ventricular Preexcitation Modulates Strain and Attenuates Cardiac Remodeling in a Swine Model of Myocardial Infarction

et al. 2007

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“…Cardiac remodeling involves a series of structural, biochemical, molecular and geometric LV changes, such as reexpression of fetal genes that codify isoforms of myosin; enzymes that regulate the intracellular calcium cycle; imbalance between supply and demand of myocardial oxygen; induction of myocytes to necrosis and/or apotosis and to the abnormal collagen accumulation that occur as a consequence of the direct mechanical stimulation and/or of the activation of several neurohormonal factors, notably angiotensin II, endothelin, norepinephrine and aldosterone [1][2][3][4]6,7,30,31 . Together, these mechanisms progressively affect the global cardiac function, culminating in CHF or sudden death [1][2][3][4][5][6][30][31][32][33] .…”

Section: Discussionmentioning

confidence: 99%

“…In chronic pressure overloads the mechanisms triggering CHF include geometric alterations of the LV cavity 5,6,32 , morphological alterations of the myocardium [1][2][3][4]7,33 , impairment of the myocardial contractile function 1,2,8,10,11 , or a combination of these factors [2][3][4]11,33 .…”

Section: Discussionmentioning

confidence: 99%

Papel relativo da remodelação geométrica do ventrículo esquerdo, morfológica e funcional do miocárdio na transição da hipertrofia compensada para a falência cardíaca em ratos com estenose aórtica supravalvar

Bregagnollo

Mestrinel

Okoshi

et al. 2007

Arq. Bras. Cardiol.

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SummaryObjectives: To evaluate the relative contribution of left ventricular (LV) geometric remodeling and of morphological and functional myocardial changes in rats with induced supravalvar aortic stenosis (SAS), in the transition from compensated hypertrophy to congestive heart failure (CHF).Methods: Twenty one weeks after induction of SAS, the rats were classified as controls (CG, n=13), without congestive heart failure (SG, n=11), or with congestive heart failure (SG-HF, n=12). All groups were evaluated with echocardiographic, hemodynamic and morphological study of the myocardium.Results: Twenty one weeks after SAS: mass index (SG-HF>SG>CG, p<0.05); systolic pressure (SG-HF= SG>CG, p<0.05); diastolic pressure (SG-HF>SG>CG, p<0.05); systolic and diastolic meridional stress (SG-HF>SG>CG, p<0.05); LV myocyte cross-sectional area (SG-HF>SG>CG, p<0.05) and hydroxyproline content (SG-HF>SG>CG, p<0.05). In the SG-HF group, LV geometric remodeling was characterized by a significant increase in dimensions and relative thickness of the normal wall (excentric remodeling), whereas the SG group presented a concentric remodeling. Indexes of LV performance in the SG-HF group were significantly lower than those of the SG group.Conclusions: The SG-HF and SG groups differed primarily in the LV geometric remodeling and structural myocardial remodeling process, which established a chronically compensated state in the SG group and triggered CHF in the SG-HF group in the presence of equivalent degrees of impaired contractility.

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“…However, long-lasting or excessive exposure to mechanical stress results in chamber dilation and cardiac dysfunction. Independent of etiology, a similar remodeling process is seen in these myocardial disorders, suggesting common mechanisms for the development of LV remodeling (4).…”

mentioning

confidence: 92%

Targeted deletion of apoptosis signal-regulating kinase 1 attenuates left ventricular remodeling

Yamaguchi

Higuchi

Hirotani

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

215

191

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Left ventricular remodeling that occurs after myocardial infarction (MI) and pressure overload is generally accepted as a determinant of the clinical course of heart failure. The molecular mechanism of this process, however, remains to be elucidated. Apoptosis signalregulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase that plays an important role in stress-induced apoptosis. We used ASK1 knockout mice (ASK ؊/؊ ) to test the hypothesis that ASK1 is involved in development of left ventricular remodeling. ASK ؊/؊ hearts showed no morphological or histological defects. Echocardiography and cardiac catheterization revealed normal global structure and function. Left ventricular structural and functional remodeling were determined 4 weeks after coronary artery ligation or thoracic transverse aortic constriction (TAC). ASK ؊/؊ had significantly smaller increases in left ventricular end-diastolic and end-systolic ventricular dimensions and smaller decreases in fractional shortening in both experimental models compared with WT mice. The number of terminal deoxynucleotidyl transferase biotin-dUDP nick end-labeling-positive myocytes after MI or TAC was decreased in ASK ؊/؊ compared with that in WT mice. Overexpression of a constitutively active mutant of ASK1 induced apoptosis in isolated rat neonatal cardiomyocytes, whereas neonatal ASK ؊/؊ cardiomyocytes were resistant to H2O2-induced apoptosis. An in vitro kinase assay showed increased ASK1 activity in heart after MI or TAC in WT mice. Thus, ASK1 plays an important role in regulating left ventricular remodeling by promoting apoptosis.

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Left ventricular remodelling: common process in patients with different primary myocardial disorders

Cited by 47 publications

References 19 publications

Ventricular Preexcitation Modulates Strain and Attenuates Cardiac Remodeling in a Swine Model of Myocardial Infarction

Ventricular Preexcitation Modulates Strain and Attenuates Cardiac Remodeling in a Swine Model of Myocardial Infarction

Papel relativo da remodelação geométrica do ventrículo esquerdo, morfológica e funcional do miocárdio na transição da hipertrofia compensada para a falência cardíaca em ratos com estenose aórtica supravalvar

Targeted deletion of apoptosis signal-regulating kinase 1 attenuates left ventricular remodeling

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