The sFlt-1/PlGF ratio and PlGF are superior to sFlt-1, UAPI and UARI for preeclampsia diagnosis. For early-onset preeclampsia diagnostics either sFlt-1 or PlGF is sufficient.
LV strain analysis in conjunction with NT-proBNP evaluation is a useful tool in assessing LV function in AR patients.
Background. Left ventricular remodeling is a complex pathologic process of progressive left ventricular dilatation, leading to dysfunction and heart failure in patients after myocardial infarction. Objective. To evaluate biochemical markers, reflecting cardiac remodeling process after first myocardial infarction and compare those markers with clinical characteristics of left ventricular remodeling. Material and methods. Brain natriuretic peptide, troponin I, creatine kinase, creatine kinase MB mass, lactate dehydrogenase levels were measured in 30 patients with acute myocardial infarction on days 1, 2, 3–7 . Brain natriuretic peptide was measured at 3 months, 6 months, and 2 years after myocardial infarction. Echocardiographic parameters of left ventricular remodeling were determined in acute phase (day 1–3), at 3 months, 6 months, and 2 years after MI. Results. In acute phase, brain natriuretic peptide level progressively increased according to worsening of left ventricular geometry: in normal left ventricle geometry group, brain natriuretic peptide level was 84.1 (58.7–121) pg/mL, in concentric remodeling group – 125 (69.2–165) pg/mL, in concentric hypertrophy group – 128 (74–368) pg/mL, and in eccentric hypertrophy group – 470 (459–494) pg/mL, P=0.02. Patients who had increased left ventricular end diastolic diameter index during 2-year period had higher brain natriuretic peptide level in the acute phase (584 (249–865) pg/mL vs. 120 (67–202) pg/mL, P=0.04) and also higher peak lactate dehydrogenase and troponin I levels. Conclusions. Brain natriuretic peptide level in acute phase of myocardial infarction is strongly associated with the markers of myocardial injury and related to left ventricular geometry changes and remodeling. Brain natriuretic peptide together with troponin I levels in acute phase of myocardial infarction might be useful in predicting subsequent cardiac function.
BACKGROUND AND PURPOSECytochrome c when released from mitochondria into cytosol triggers assembly of the apoptosome resulting in caspase activation. Recent evidence suggests that reduced cytochrome c is unable to activate the caspase cascade. In this study, we investigated whether a chemical reductant of cytochrome c, N,N,N′,N′-tetramethylphenylene-1,4-diamine (TMPD), which we have previously shown to block cytochrome c-induced caspase activation, could prevent ischaemia-induced apoptosis in the rat perfused heart. EXPERIMENTAL APPROACHThe Langendorff-perfused rat hearts were pretreated with TMPD and subjected to stop-flow ischaemia or ischaemia/reperfusion. The activation of caspases (measured as DEVD-p-nitroanilide-cleaving activity), nuclear apoptosis of cardiomyocytes (measured by dUTP nick end labelling assay), mitochondrial and cytosolic levels of cytochrome c (measured spectrophotometrically and by ELISA), and reperfusion-induced necrosis (measured as the activity of creatine kinase released into perfusate) were assessed. KEY RESULTSWe found that perfusion of the hearts with TMPD strongly inhibited ischaemia-or ischaemia/reperfusion-induced activation of caspases and partially prevented nuclear apoptosis in cardiomyocytes. TMPD did not prevent ischaemia-or ischaemia/ reperfusion-induced release of cytochrome c from mitochondria into cytosol. TMPD also inhibited ischaemia/reperfusioninduced necrosis. CONCLUSIONS AND IMPLICATIONSThese results suggest that TMPD or related molecules might be used to protect the heart against damage induced by ischaemia/reperfusion. The mechanism of this protective effect of TMPD probably involves electron reduction of cytochrome c (without decreasing its release) which then inhibits the activation of caspases. AbbreviationsAPAF-1, apoptosis activating factor 1; TMPD, N,N,N′,N′-tetramethylphenylene-1,4-diamine; TUNEL, dUTP nick end labelling IntroductionHeart ischaemia causes myocardial infarction and heart failure, which, according to the World Health Organization, are among the most common causes of human death in the world. Heart ischaemia or heart ischaemia plus reperfusion can induce necrosis and/or apoptosis of cardiomyocytes (Ganote et al., 1975;Freude et al., 1998;Lemasters et al., 1999). In general, it is found that relatively short periods of ischaemia induce apoptosis, longer periods of ischaemia induce necrosis, while reperfusion induces necrosis with additional apoptosis (Schumer et al., 1992;Fliss and Gattinger, 1996;Kametsu et al., 2003), but the relation between these events remains unclear. We and others have shown that ischaemia induces rapid cytochrome c release from mitochondria in rat perfused hearts, followed by caspase activation and nuclear apoptosis (De Moissac et al., 2000;Borutaite et al., 2001), and these events are prevented by inhibiting the mitochondrial permeability transition pore (Borutaite et al., 2003). Cytochrome c release activates apoptosis by binding to a cytosolic adaptor protein, APAF-1, which then recruits and activates procaspase-9 w...
Raktažodžiai: lėtinis širdies nepakankamumas, lėtinis nuovargis, kairiojo skilvelio išstūmimo frakcija, deguonies sunaudojimas. Santrauka. Tyrimo tikslas. Ištirti sergančiųjų lėtiniu III-IV Niujorko ĮvadasSergančiųjų lėtiniu širdies nepakankamumu (ŠN) simptomai ir funkcinis pajėgumas yra glaudžiai susiję su hemodinamikos rodikliais. Kai nuolatos yra sutrikusi širdies funkcija, aktyvuojasi renino-angiotenzinoaldosterono ir simpatinė nervų sistema. Tai sąlygoja širdies išstumiamo kraujo tūrio mažėjimą ir tolesnį širdies nepakankamumo simptomų: nuovargio ir dusulio progresavimą. Lėtinis nuovargis blogina tokių ligonių gyvenimo kokybę ir gali būti invalidumo priežastimi (1). Svarbūs simpatinio aktyvumo hormonaikatecholaminai išskiriami šerdinėje antinksčių dalyje. Kortikosteroidai yra išskiriami žievinėje antinksčių dalyje. Ten pat išskiriamas ir aldosteronas, kuris svarbus renino-angiotenzino-aldosterono grandinėje ir są-lygoja hemodinamikos rodiklius. Tyrimai rodo, kad ŠN simptomų ir prognozės pagerėjimas ypač gerai koreliuoja su neurohormoniniu gydymu beta adrenoblokatoriais, AKF inhibitoriais, angiotenzino 1 receptorių I blokatoriais, aldosterono antagonistais (2-4). Manoma, kad medikamentai negali užblokuoti visų simpatinio aktyvumo padidėjimą lemiančių grandžių ir dėl to, kad biologiškai aktyvių medžiagų yra daugiau nei veikia vaistai, ir dėl to, kad negalima skirti didesnių vaistų dozių dėl jų šalutinio veikimo.Sergančiųjų lėtiniu nuovargiu (LN) ir lėtiniu nuovargio sindromu (LNS) etiologijos veiksniai yra polimorfiniai. Galima teigti, kad LN ir sunkesnę ligos
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