Wall stress and patterns of hypertrophy in the human left ventricle.

Grossman, William; Jones, Davy; McLaurin, Lambert P.

doi:10.1172/jci108079

Cited by 2,190 publications

(1,090 citation statements)

References 28 publications

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“…Although the underlying mechanism by which E 2 prevented the increase of LVEDP remains undetermined, a role for nitric oxide may be postulated. In the myocardium, nitric oxide has been shown to increase diastolic distensibility (Prendergast et al, 1997;Paulus et al, 1994), and nitric oxide synthase activity in the heart can be enhanced by oestrogen treatment (Neudling et al, 1999) A sustained increase in systolic load, as observed in systemic hypertension leads to a concentric pattern of cardiac hypertrophy, characterized by the increased expression of the putative hypertrophic marker prepro-ANP mRNA and the progression of interstitial ®brosis (Boluyt & Bing, 1995;Calderone et al, 1995;Weber & Brilla, 1991;Grossman et al, 1975). Direct morphological examination was not performed to determine whether a concentric pattern of cardiac remodelling had occurred.…”

Section: Discussionmentioning

confidence: 99%

Elevated mean arterial pressure in the ovariectomized rat was normalized by ET_A receptor antagonist therapy: absence of cardiac hypertrophy and fibrosis

Mercier

Pham-Dang

Clement

et al. 2002

British J Pharmacology

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1 The in¯uence of menopause on ventricular function and remodelling remains unde®ned. The following study examined the e ect of ovariectomy on ventricular contractility, cardiac hypertrophy and extracellular matrix protein expression. 2 Elevated circulating levels of the vasoconstrictor endothelin-1 have been reported in postmenopausal women. Moreover, endothelin-1 has been shown to in¯uence blood pressure, ventricular function and cardiac remodelling. In this regard, the potential pathophysiological role of endothelin-1 in the ovariectomized rat was assessed via the administration of the selective endothelin A receptor (ET A ) antagonist BMS-182874.3 In 3 and 6 week ovariectomized female Sprague ± Dawley rats, uterus atrophy was associated with a signi®cant increase in mean arterial pressure, and left ventricular systolic pressure, as compared to sham. By contrast, right ventricular contractile indices were normal in the ovariectomized rat. Despite increased systolic load, left ventricular hypertrophy was not evident, prepro-atrial natriuretic peptide (prepro-ANP) mRNA levels and collagen protein content were similar to sham. 4 The treatment of ovariectomized rats with BMS-182874 (60 mg kg 71 per day) did not reverse uterus atrophy. However, BMS-182874 normalized mean arterial pressure, and left ventricular systolic pressure in the ovariectomized rat. 5 Thus, despite elevated blood pressure, ovariectomized rats were not associated with either cardiac hypertrophy or ®brosis. Lastly, endothelin-1, acting via the stimulation of the ET A receptor represents an integral mechanism implicated in the increase of mean arterial pressure following ovariectomy.

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Section: Discussionmentioning

confidence: 99%

Elevated mean arterial pressure in the ovariectomized rat was normalized by ET_A receptor antagonist therapy: absence of cardiac hypertrophy and fibrosis

Mercier

Pham-Dang

Clement

et al. 2002

British J Pharmacology

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“…A mathematical description of this physical relationship was developed by the eighteenth century French physicist, Pierre Laplace, and reveals that wall stress (in the heart, afterload) is directly proportional to the radius of the chamber (r) and its intracavitary pressure (p), and is inversely proportional to the chamber wall thickness (h); stress ¼ pr/2h. Thus, any primary injury to the heart that causes cardiomyocyte dropout and ventricular remodeling produces a secondary stress on the heart in the form of increased afterload that is chronic and unremitting (Grossman et al, 1975). Studies performed over the past decade have shown that this hemodynamic stress is a powerful stimulus for programmed cardiomyocyte death, initiating a vicious cycle of unfavorable geometrical remodeling that stimulates yet more cell death (Foo et al, 2005;Dorn II, 2009).…”

Section: Introductionmentioning

confidence: 99%

Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

Dorn

Kirshenbaum

2008

Oncogene

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Programmed cardiac myocyte death contributes to pathological ventricular remodeling and the progression of myocardial infarction or pressure overload hypertrophy to dilated cardiomyopathy. Recent work has identified importance of stress-mediated transcriptional induction of BNIP3 (BCL2 and 19-kDa interacting protein-3) and NIX/BNIP3L in cardiac remodeling. Here, the regulatory mechanisms for these two factors in the heart and their effects on programmed cardiomyocyte death are reviewed, with a focus on information derived from studies using mouse models of cardiac BNIP3 and NIX/BNIP3L overexpression and gene ablation.

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“…It is believed that this process is due to cardiomyocyte elongation and hypertrophy that compensate volume overload and normalize wall stress (Grossman et al, 1975). Despite cardiac output being often increased (such as in the case of chronic arteriovenous fistula-AVF), substantial part of stroke volume is shunted or recirculated and is not contributing to systemic perfusion.…”

mentioning

confidence: 99%

Myocardial Morphological Characteristics and Proarrhythmic Substrate in the Rat Model of Heart Failure Due to Chronic Volume Overload

Beneš

Melenovský

Škaroupková

et al. 2010

The Anatomical Record

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Chronic volume overload leads to cardiac hypertrophy and later to heart failure (HF), which are both associated with increased risk of cardiac arrhythmias. The goal of this study was to describe changes in myocardial morphology and to characterize arrhythmogenic substrate in rat model of developing HF due to volume overload. An arteriovenous fistula (AVF) was created in male Wistar rats between the inferior vena cava and abdominal aorta using needle technique. Myocardial morphology, tissue fibrosis, and connexin43 distribution, localization and phosphorylation were examined using confocal microscopy and Western blotting in the stage of compensated hypertrophy (11 weeks), and decompensated HF (21 weeks). Heart to body weight (BW) ratio was 89% and 133% higher in AVF rats at 11 and 21 weeks, respectively. At 21 weeks but not 11 weeks, AVF rats had pulmonary congestion (increased lung to BW ratio) indicating presence of decompensated HF. The myocytes in left ventricular midmyocardium were significantly thicker (þ8% and þ45%) and longer (þ88% and þ97%). Despite extensive hypertrophy, there was no excessive fibrosis in the AVF ventricles. Distribution and localization of connexin43 were similar between groups, but its phosphorylation was significantly lower in AVF hearts at 21st week, but not 11th week, suggesting that HF,

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Wall stress and patterns of hypertrophy in the human left ventricle.

Cited by 2,190 publications

References 28 publications

Elevated mean arterial pressure in the ovariectomized rat was normalized by ET_A receptor antagonist therapy: absence of cardiac hypertrophy and fibrosis

Elevated mean arterial pressure in the ovariectomized rat was normalized by ET_A receptor antagonist therapy: absence of cardiac hypertrophy and fibrosis

Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

Myocardial Morphological Characteristics and Proarrhythmic Substrate in the Rat Model of Heart Failure Due to Chronic Volume Overload

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Wall stress and patterns of hypertrophy in the human left ventricle.

Cited by 2,190 publications

References 28 publications

Elevated mean arterial pressure in the ovariectomized rat was normalized by ETA receptor antagonist therapy: absence of cardiac hypertrophy and fibrosis

Elevated mean arterial pressure in the ovariectomized rat was normalized by ETA receptor antagonist therapy: absence of cardiac hypertrophy and fibrosis

Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

Myocardial Morphological Characteristics and Proarrhythmic Substrate in the Rat Model of Heart Failure Due to Chronic Volume Overload

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Elevated mean arterial pressure in the ovariectomized rat was normalized by ET_A receptor antagonist therapy: absence of cardiac hypertrophy and fibrosis

Elevated mean arterial pressure in the ovariectomized rat was normalized by ET_A receptor antagonist therapy: absence of cardiac hypertrophy and fibrosis