Heart remodelling Dotaz Zobrazit nápovědu
European heart journal ; Supplement Vol. 16. I
VI, 114 s. : obr., tab., grafy ; 26 cm
- MeSH
- hypertrofická kardiomyopatie MeSH
- kardiovaskulární nemoci komplikace MeSH
- myokard patologie MeSH
- srdeční komory patofyziologie patologie MeSH
- Publikační typ
- kongresy MeSH
- Konspekt
- Patologie. Klinická medicína
- NLK Obory
- kardiologie
- angiologie
Remodelace myokardu patří mezi základní adaptační schopnosti srdce. Umožňuje specificky reagovat na nejrůznější podněty a přizpůsobit se změněným podmínkám. Základními procesy remodelace jsou hypertrofie a fi bróza. Remodelace zahrnuje změny na mnoha úrovních, jejichž výsledkem je strukturální a následně i funkční změna myokardu. Pokud je nový stav kompenzován, označuje se za fyziologický. Příkladem je normální hypertrofický růst při opakované, dostatečně intenzivní fyzické zátěži (tzv. fyziologická hypertrofie). U patologické hypertrofie nejsou změny způsobené remodelací dostatečně kompenzovány. Po adaptaci na hemodynamické změny nebo pod vlivem hormonů propagujících patologický fenotyp dochází k přestavbě myokardu, která může vést až k srdečnímu selhání. Další formou remodelace myokardu je fibróza. Dochází k ní typicky po infarktu myokardu s cílem zachovat strukturní celistvost srdce. Proces fibrózy se aktivuje také při hemodynamickém přetížení, je pozorován u toxického poškození srdce a obecně u stavů vedoucích k zániku kardiomyocytů. Tyto stimuly aktivují v myokardu přítomné fibroblasty, které vytvoří nové komponenty mezibuněčné hmoty formující se ve vazivovou strukturu. Tento přehledový článek si klade za cíl shrnout aktuální poznatky týkající se mechanismů remodelace srdce. Článek poskytuje komplexní pohled na současný stav výzkumu a jeho potenciální přínos pro klinickou medicínu.
Remodelling is one of the fundamental processes in the heart adaptation. It allows the heart to respond specifically to various stimuli and adapt to changed conditions. The basic remodelling processes involve hypertrophy and fibrosis. Remodelling is present at various levels and results in structural and subsequently functional changes in the myocardium. If the new state is compensated, it is referred to as physiological. Such remodelling includes so-called physiological hypertrophy induced by repeated sufficiently in- tense physical exertion. In pathological hypertrophy, the changes caused by remodelling are not sufficiently compensated. After adaptation to hemodynamic changes or under the influence of hormones promot- ing a pathological phenotype, the myocardium undergoes remodelling, which may lead to heart failure. Another form of myocardial remodelling is fibrosis. It typically occurs after a myocardial infarction in order to preserve the structural integrity of the heart. The process of fibrosis is also activated during hemodynamic overload, can be observed in toxic myocardial damage and in general in situations leading to the myocardial loss. These stimuli activate the fibroblasts present in the myocardium, which create new components of the intercellular mass forming a fibrotic structure. This review article aims to summarize the current knowledge of the mechanisms of cardiac remodelling. The article provides a comprehensive view of the current state of research and its potential contribution to clinical medicine.
- MeSH
- fibróza etiologie klasifikace MeSH
- fyziologická adaptace fyziologie MeSH
- hypertrofická kardiomyopatie etiologie klasifikace patologie MeSH
- kardiomegalie indukovaná tělesnou námahou fyziologie MeSH
- lidé MeSH
- remodelace komor * MeSH
- remodelace síní * MeSH
- srdeční selhání diagnóza etiologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- práce podpořená grantem MeSH
- přehledy MeSH
- MeSH
- dysfunkce levé srdeční komory patologie MeSH
- kontraktilní proteiny MeSH
- lidé MeSH
- remodelace komor MeSH
- srdeční selhání patologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- přehledy MeSH
Myocardial remodelling involves structural and functional changes in the heart, potentially leading to heart failure. The deoxycorticosterone acetate (DOCA)/salt model is a widely used experimental approach to study hypertension-induced cardiac remodelling. It allows to investigate the mechanisms underlying myocardial fibrosis and hypertrophy, which are key contributors to impaired cardiac function. In this study, myocardial remodelling in rat deoxycorticosterone acetate/salt model was examined over a three-week period. The experiment involved 11 male Sprague-Dawley rats, divided into two groups: fibrosis (n=6) and control (n=5). Myocardial remodelling was induced in the fibrosis group through unilateral nephrectomy, deoxyco-rticosterone acetate administration, and increased salt intake. The results revealed significant structural changes, including increased left ventricular wall thickness, myocardial fractional volume, and development of myocardial fibrosis. Despite these changes, left ventricular ejection fraction was preserved and even increased. ECG analysis showed significant prolongation of the PR interval and widening of the QRS complex in the fibrosis group, indicating disrupted atrioventricular and ventricular conduction, likely due to fibrosis and hypertrophy. Correlation analysis suggested a potential relationship between QRS duration and myocardial hypertrophy, although no significant correlations were found among other ECG parameters and structural changes detected by MRI. The study highlights the advantage of the DOCA/salt model in exploring the impact of myocardial remodelling on electrophysiological properties. Notably, this study is among the first to show that early myocardial remodelling in this model is accompanied by distinct electrophysiological changes, suggesting that advanced methods combined with established animal models can open new opportunities for research in this field. Key words Myocardial fibrosis, Remodelling, Animal model, DOCA-salt, Magnetic resonance imaging.
- MeSH
- deoxykortikosteron-21-acetát * MeSH
- elektrokardiografie * MeSH
- fibróza MeSH
- krysa rodu rattus MeSH
- kuchyňská sůl škodlivé účinky MeSH
- modely nemocí na zvířatech MeSH
- myokard patologie MeSH
- potkani Sprague-Dawley * MeSH
- remodelace komor * MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
There is a great urgency of detecting and monitoring myocardial fibrosis in clinical practice with the aim to improve and personalize therapy against cardiac remodelling. Hence, the aim of this study was to describe alterations in and show potential correlations between the structural characteristics and the molecular and biochemical markers of cardiac remodelling on a model of isoproterenol-induced heart failure. Two groups of 3-month-old male Wistar rats (n = 8 per group) were sacrificed after four weeks of treatment: control (placebo), ISO (5 mg/kg/day intraperitoneally). Chronic ISO treatment led to heart failure (HF) characterized by significant reduction of systolic blood pressure (SBP) accompanied by an increase in left ventricular weight (LVW) along with increased collagen content in the LV. The collagen content correlated negatively with SBP (R = -0.776, P < 0.001) and positively with LVW (R = 0.796, P < 0.001), with Col1a1 (0.83; P < 0.001) and Acta2 (0.73; P < 0.01). Moreover, the mRNA expression of fibrotic remodelling indicator, i.e. TGF-β1 tended to increase, while the level of fibrinolysis markers (MCP-1, TIMP-2, MMP) were unchanged. The plasma markers of collagen, procollagen I C-terminal propeptide (PICP) was 37.34 ± 7.10 pg/mL in control and was reduced by 42% (P < 0.05) in the ISO group and procollagen III N-terminal propeptide (PIIINP) was 1216.7 ± 191.0 pg/mL in control and was decreased by 66% (P < 0.05) in the ISO group. Surprisingly, there was no positive correlation between plasma markers of collagen, i.e. PICP and PIIINP and collagen content or molecular markers of collagen. However, both PICP and PIIINP correlated with BW (R = 0.712, resp. 0.803, P < 0.001), which was significantly reduced (by 25%, P < 0.05) in the ISO group. In conclusion, we assume that the collagen content of the left ventricle does not need unavoidably correlate with plasma markers of collagen, which might be affected by confounding factors in heart failure, such as loss of body weight, presumably associated with a catabolic condition.
- MeSH
- isoprenalin MeSH
- kolagen metabolismus MeSH
- krevní tlak MeSH
- peptidové fragmenty krev MeSH
- potkani Wistar MeSH
- prokolagen krev MeSH
- remodelace komor * MeSH
- srdeční komory metabolismus MeSH
- srdeční selhání chemicky indukované metabolismus patofyziologie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
AIMS: Analysis of microvascular parameters in the retinal circulation-known to reflect those in the systemic circulation-allows us to differentiate between eutrophic and hypertrophic remodelling of small arteries. This study aimed to examine microvascular changes in patients with congestive heart failure (CHF) and reduced as well as mid-range ejection fraction. METHODS AND RESULTS: Forty subjects with CHF underwent measurement of retinal capillary flow (RCF), wall-to-lumen ratio (WLR), vessel and lumen diameter, wall thickness, and wall cross-sectional area (WCSA) of retinal arterioles of the right eye by scanning laser Doppler flowmetry (SLDF). Applying a matched pair approach, we compared this group with reference values of age-matched controls from a random sample in the population of Pilsen, Czech Republic. There was no significant difference in RCF and WLR between the groups (RCF: P = 0.513; WLR: P = 0.106). In contrast, wall thickness and WCSA, indicators of hypertrophic remodelling, were higher in CHF subjects (WT: 15.0 ± 4.2 vs. 12.7 ± 4.2 μm, P = 0.021; WCSA: 4437.6 ± 1314.5 vs. 3615.9 ± 1567.8 μm2 , P = 0.014). Similarly, vessel (109.4 ± 11.1 vs. 100.5 ± 14.4 μm, P = 0.002) and lumen diameter (79.0 ± 7.9 vs. 75.2 ± 8.5 μm, P = 0.009) were increased in CHF. CONCLUSIONS: In CHF subjects, we observed hypertrophic remodelling of retinal arterioles indicative of similar changes of small resistance arteries in the systemic circulation. Microvascular structure and function assessed by SLDF may thereby represent a useful, non-invasive method for monitoring of microvascular damage in patients with CHF and may offer innovative treatment targets for new CHF therapies.
- MeSH
- arterioly MeSH
- kapiláry MeSH
- laser doppler flowmetrie MeSH
- lidé MeSH
- retinální cévy * MeSH
- srdeční selhání * diagnóza MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Adverse remodelling following an initial insult is the hallmark of heart failure (HF) development and progression. It is manifested as changes in size, shape, and function of the myocardium. While cardiac remodelling may be compensatory in the short term, further neurohumoral activation and haemodynamic overload drive this deleterious process that is associated with impaired prognosis. However, in some patients, the changes may be reversed. Left ventricular reverse remodelling (LVRR) is characterized as a decrease in chamber volume and normalization of shape associated with improvement in both systolic and diastolic function. LVRR might occur spontaneously or more often in response to therapeutic interventions that either remove the initial stressor or alleviate some of the mechanisms that contribute to further deterioration of the failing heart. Although the process of LVRR in patients with new-onset HF may take up to 2 years after initiating treatment, there is a significant portion of patients who do not improve despite optimal therapy, which has serious clinical implications when considering treatment escalation towards more aggressive options. On the contrary, in patients that achieve delayed improvement in cardiac function and architecture, waiting might avoid untimely implantable cardioverter-defibrillator implantation. Therefore, prognostication of successful LVRR based on clinical, imaging, and biomarker predictors is of utmost importance. LVRR has a positive impact on prognosis. However, reverse remodelled hearts continue to have abnormal features. In fact, most of the molecular, cellular, interstitial, and genome expression abnormalities remain and a susceptibility to dysfunction redevelopment under biomechanical stress persists in most patients. Hence, a distinction should be made between reverse remodelling and true myocardial recovery. In this comprehensive review, current evidence on LVRR, its predictors, and implications on prognostication, with a specific focus on HF patients with non-ischaemic cardiomyopathy, as well as on novel drugs, is presented.
- MeSH
- echokardiografie MeSH
- funkce levé komory srdeční fyziologie MeSH
- kardiomyopatie * MeSH
- lidé MeSH
- remodelace komor fyziologie MeSH
- srdeční selhání * komplikace etiologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
AIMS: Reverse ventricular remodelling, defined as a decrease in left ventricular end-systolic volume indexed to body surface area (LVESVI) or an increase in left ventricular ejection fraction (LVEF), is associated with improved clinical outcomes in patients with heart failure with reduced ejection fraction (HFrEF). However, the underlying pathophysiological mechanisms remain unclear. METHODS AND RESULTS: We evaluated paired core-lab assessed echocardiograms and measurements of 92 biomarkers at baseline and 8 months thereafter in 419 participants with HFrEF. Reverse ventricular remodelling was defined as a >5% LVEF increase or >15% LVESVI relative decrease between baseline and 8 months. We evaluated the association between baseline biomarkers and their changes with reverse ventricular remodelling in the prospectively randomized controlled VICTORIA (Vericiguat Global Study in Subjects With Heart Failure With Reduced Ejection Fraction) trial. Of 419 patients (median age 66 [interquartile range 57-74] years, 27.4% women), 206 (49.2%) had reverse ventricular remodelling (either a 5% LVEF increase or a 15% LVESVI decrease). There were no differences in baseline biomarker concentrations between patients with versus those without reverse ventricular remodelling on follow-up. However, in patients with reverse ventricular remodelling there were significant decreases in biomarkers relating to inflammation and cardiac metabolism; particularly the tumour necrosis factor superfamily member 13B (ratio 0.82, 95% confidence interval [CI] 0.77-0.88), growth differentiation factor-15 (ratio 0.74, 95% CI 0.66-0.84), and insulin-like growth factor binding protein 7 (ratio 0.80, 95% CI 0.73-0.88). CONCLUSIONS: Reverse ventricular remodelling in patients with HFrEF is associated with a decrease of biomarkers related to inflammation and cardiac metabolism.
- MeSH
- biologické markery * MeSH
- echokardiografie * metody MeSH
- funkce levé komory srdeční fyziologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- prospektivní studie MeSH
- remodelace komor * fyziologie MeSH
- senioři MeSH
- srdeční selhání * patofyziologie MeSH
- tepový objem * fyziologie MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- randomizované kontrolované studie MeSH
