PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 14717385

Ventricular remodeling.

Sara Paul
View original source ↗Export metadata ↓

Abstract

Ventricular remodeling is an extremely complicated process that is not well understood. There seem to be multiple feedback loops that respond to mechanical events as well as to neurohormonal stimulation, cytokine release, and other, yet unidentified, agents. The progression of ventricular remodeling after the index event includes: Myocyte slippage and thinning of infarct area, chamber dilatation. Fibrosis and scar formation. Collagen strut dissolution and excessive accumulation of interstitial matrix. Increased wall stress. Myocyte hypertrophy. Neurohormonal activation. Cytokine release. Ongoing myocyte hypertrophy. Cell apoptosis and necrosis. Continued deterioration of cardiac function. It is impossible to place the sequence of events in order, because the multiple feedback systems create a complex interactive process. A basic awareness of the pathophysiology of ventricular remodeling can aid in understanding current and future treatments for heart failure. It is clear that therapeutic interventions solely aimed at improving cardiac pump function do not slow the progression of heart failure or reduce mortality. Drugs that block the neuroendocrine contribution to the remodeling process have been shown to have a greater impact. Current therapies with angiotensin-converting enzyme inhibition, beta blockade, and aldosterone antagonism are associated with significant reductions in morbidity and mortality in heart failure. Other therapeutic strategies suggested by knowledge of remodeling mechanisms, such as drugs to block cytokines, endothelins, and MMPs, may offer further benefit to patients with heart failure in the future.

Explore related subjects

CytokinesDiabetes ComplicationsDisease ProgressionHeart FailureHumansHypertensionHypertrophy, Left VentricularMyocardial InfarctionNeurotransmitter AgentsPrognosisRenin-Angiotensin SystemRisk FactorsSystoleTime FactorsVentricular RemodelingJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Sara Paul. 2003. Ventricular remodeling.. https://doi.org/10.1016/s0899-5885(02)00089-8

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Placental cytokines and preeclampsia.

Preeclampsia is a serious and life-threatening pregnancy complication. Reduced uteroplacental perfusion and oxygen tension, impaired trophoblast differentiation and invasion, and altered placental production of immunomodulators and growth factors are all considered to be important aspects in the aetiology of the condition. The placenta expresses a variety of pro and anti-inflammatory cytokines, adipokines and cytokine-like angiogenic growth factors, production of which is altered in preeclampsia, driven (at least in part) by hypoxia. Altered levels of cytokines have been measured in the circulation of women with preeclampsia, although for reasons that are not always apparent much of the data are disturbingly inconsistent. While the placenta undoubtedly makes an important contribution to plasma cytokine levels, production by maternal peripheral blood mononuclear cells (PBMCs) and other tissues is also likely to be significant, although to what extent remains undetermined. Increased placental expression of soluble receptors occurs with preeclampsia, resulting in elevated circulating concentrations which confer impaired angiogenesis, deficient placental vascularisation, increased placental apoptosis and endothelial dysfunction. The extent to which these changes reflect a response to the disorder, as opposed to being a causative factor in the development of maternal disease, is a matter of some debate. Nevertheless, convincing evidence is now accruing that autocrine/paracrine interactions between placental cytokines/growth factors and the maternal endothelium play a central role in the pathogenesis of preeclampsia.

Cytokines↗
PubMed2006

Radiation pneumonitis and fibrosis: mechanisms underlying its pathogenesis and implications for future research.

Radiation pneumonitis and subsequent radiation pulmonary fibrosis are the two main dose-limiting factors when irradiating the thorax that can have severe implications for patients' quality of life. In this article, the current concepts about the pathogenetic mechanisms underlying radiation pneumonitis and fibrosis are presented. The clinical course of fibrosis, a postulated acute inflammatory stage, and a late fibrotic and irreversible stage are discussed. The interplay of cells and the wide variety of molecules orchestrating the immunologic response to radiation, their interactions with specific receptors, and the cascade of events they trigger are elucidated. Finally, the implications of this knowledge with respect to the therapeutic interventions are critically presented.

Cytokines↗
PubMed2006

Nutritional modulation of exercise-induced immunodepression in athletes: a systematic review and meta-analysis.

BACKGROUND: Heavy exercise induces marked immunodepression that is multifactorial in origin. Nutrition can modulate normal immune function. OBJECTIVE: To assess the efficacy of nutritional supplements in exercise-induced immunodepression in athletes. DESIGN: Systematic review. REVIEW METHODS: Randomised and/or controlled trials of athletes undertaking nutritional supplements to minimise the immunodepression after exercise were retrieved. The primary outcome measure was incidence of upper respiratory tract (URT) illness symptoms after exercise, and secondary outcomes included cortisol, cell counts, plasma cytokine concentration, cell proliferative response, oxidative burst, natural killer cell activity and immunoglobulins. When data were available for a pooled estimate of the effect of intervention, meta-analyses were conducted for direct comparisons. RESULTS: Forty-five studies were included (1603 subjects). The studies were heterogeneous in terms of exercise interventions, selection of athletes, settings and outcomes. The overall methodological quality of most of the trials was poor. Twenty studies addressed carbohydrate supplementation, eight glutamine, 13 vitamin C and four others interventions. Three trials assessed the effect of intervention on prevention of URT infections. The pooled rate ratio for URT infections after vitamin C supplementation against placebo was 0.49 (0.34-0.71). Carbohydrate supplementation attenuated the increase in cortisol and neutrophils after exercise; vitamin C attenuated the decrease in lymphocytes after exercise. No other interventions had significant or consistent effect on any of the studied outcomes. CONCLUSIONS: Although the prevention of URT infections by vitamin C was supported by two trials, further studies are needed. The available evidence failed to support a role for other nutritional supplements in preventing exercise-induced immune suppression. Larger trials with clinically relevant and uniform end points are necessary to clarify the role of these nutritional interventions.

Cytokines↗