A new insight into oxidative stress is based on oxidative deoxyribonucleic acid (DNA) damage. DNA is the pivotal biopolymer for life and health. Arterial hypertension (HT) is a globally common disease and a major risk factor for numerous cardiovascular (CV) conditions and non-cardiac complications, making it a significant health and socio-economic problem. The aetiology of HT is multifactorial. Oxidative stress is the main driver. Oxidative DNA damage (oxidised guanosine (8OHdG), strand breaks (SSBs, DSBs)) seems to be the crucial and initiating causal molecular mechanism leading to HT, acting through oxidative stress and the resulting consequences (inflammation, fibrosis, vascular remodelling, stiffness, thickness, and endothelial dysfunction). In light of the current European Society of Cardiology (ESC) guidelines with defined gaps in the evidence, this manuscript, for the first time, (1) summarizes evidence for oxidative DNA damage in HT and other CV risk factors, (2) incorporates them into the context of known mechanisms in HT genesis, (3) proposes the existing concept of HT genesis innovatively supplemented with oxidative DNA damage, and (4) mentions consequences such as promising new targets for the treatment of HT (DNA damage response (DDR) pathways).

• MeSH
• hypertenze * MeSH
• lidé MeSH
• oxidační stres * MeSH
• poškození DNA * MeSH
• směrnice pro lékařskou praxi jako téma MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Oxidative DNA damage markers (8OHdG, comet assay, gammaH2AX) are becoming widely used in clinical cardiology research. To conduct this review of DNA damage in relation to hypertension in humans, we used databases (e.g. PubMed, Web of Science) to search for English-language publications up to June 30, 2022 and the terms: DNA damage, comet assay, gammaH2AX, 8OHdG, strand breaks, and arterial hypertension. Exclusion criteria were: children, absence of relevant controls, extra-arterial hypertensive issues, animal, cell lines. From a total of 79526, 15 human studies were selected. A total of 902 hypertensive patients (pts): (comet: N=418 pts; 8OHdG: N=484 pts) and 587 controls (comet: N=203; 8OHdG: N=384) were included. DNA damage was significantly higher in hypertensive pts than healthy controls (comet 26.6±11.0 vs 11.7±4.07 arbitrary units /A.U./; P<0.05 and="" 8ohdg="" 13="" 1="" 4="" 12="" vs="" 6="" 97="" 2="" 67="" ng="" mg="" creatinine="" i=""> P<0.05) confirmed with meta-analysis for both. Greater DNA damage was observed in more adverse cases (concentric cardiac hypertrophy 43.4±15.4 vs 15.6±5.5; sustained/untreated hypertension 31.4±12.1 vs 14.2±5/35.0±5.0 vs 25.0 ±5.0; non-dippers 39.2±15.5 vs 29.4±11.1 A.U.; elderly 14.9±4.5 vs 9.3±4.1 ng/mg creatinine; without carvedilol 9.1±4.2 vs 5.7±3.9; with coronary heart disease 0.5±0.1 vs 0.2±0.1 ng/mL) (P<0.05) confirmed with meta-analysis. DNA damage correlated strongly positively with serum glycosylated haemoglobin (r=0.670; P<0.05) and negatively with total antioxidant status (r=-0.670 to -0.933; P<0.05). This is the first systematic review with meta-analysis showing that oxidative DNA damage was increased in humans with arterial hypertension compared to controls.

• MeSH
• 8-hydroxy-2'-deoxyguanosin MeSH
• dítě MeSH
• hypertenze * MeSH
• kometový test MeSH
• kreatinin MeSH
• lidé MeSH
• poškození DNA * MeSH
• senioři MeSH
• zvířata MeSH
• Check Tag
• dítě MeSH
• lidé MeSH
• senioři MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• metaanalýza MeSH
• přehledy MeSH
• systematický přehled MeSH

• MeSH
• antiarytmika farmakologie   terapeutické užití   MeSH
• antikoagulancia terapeutické užití   MeSH
• bradykardie diagnóza   etiologie   terapie   MeSH
• defibrilátory implantabilní MeSH
• fibrilace síní diagnóza   etiologie   komplikace   terapie   MeSH
• komorová tachykardie diagnóza   patofyziologie   terapie   MeSH
• lidé MeSH
• srdeční arytmie * diagnóza   patologie   terapie   MeSH
• synkopa diagnóza   etiologie   terapie   MeSH
• tachykardie diagnóza   patologie   terapie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy MeSH

• MeSH
• lidé MeSH
• náhlá srdeční smrt * etiologie   prevence a kontrola   MeSH
• rizikové faktory MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy MeSH

OBJECTIVE: This study aimed to investigate whether out-of-hospital cardiac arrest (OHCA) may induce severe DNA damage measured using comet assay in successfully resuscitated humans and to evaluate a short-term prognostic role. METHODS: In this prospective, controlled, blinded study (1/2013-1/2014), 41 patients (age, 63±14 years) successfully resuscitated from non traumatic OHCA and 10 healthy controls (age, 53±17 years) were enrolled. DNA damage [double-strand breaks (DSBs) and single-strand breaks (SSBs)] was measured using comet assay in peripheral lymphocytes sampled at admission. Clinical data were recorded (according to Utstein style). A good short-term prognosis was defined as survival for 30 days. RESULTS: Among the patients, there were 71% (29/41) short-term survivors. After OHCA, DNA damage (DSBs and SSBs) was higher (11.0±7.6% and 0.79±2.41% in tail) among patients than among controls (1.96±1.63% and 0.02±0.03% in tail), and it was more apparent for DSBs (p<0.001 and p=0.085). There was no difference in the DNA damage between patients with cardiac and non-cardiac etiology, or between survivors and nonsurvivors. Among Utstein style parameters, ventricular fibrillation, asystole, and early electrical defibrillation influenced DSBs; none of the factors influenced SSBs. Factors influencing survival were SSBs, ventricular fibrillation, length of cardiopulmonary resuscitation by professionals ≤15 min, cardiogenic shock, and postanoxic encephalopathy. In contrast to DSBs [area under the curve (AUC)=0.520], SSBs seem to have a potential in prognostication (AUC=0.639). CONCLUSION: This study for the first time demonstrates revelation of DNA damage using comet assay in patients successfully resuscitated from OHCA. Whether DNA damage measured using comet assay may be a prognostic marker remains unknown, although our data may encourage some suggestions.

• MeSH
• analýza přežití MeSH
• dospělí MeSH
• dvojitá slepá metoda MeSH
• elektrická defibrilace MeSH
• kardiopulmonální resuscitace MeSH
• kometový test MeSH
• lidé středního věku MeSH
• lidé MeSH
• lymfocyty metabolismus   MeSH
• poškození DNA * MeSH
• prognóza MeSH
• prospektivní studie MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• senzitivita a specificita MeSH
• studie případů a kontrol MeSH
• zástava srdce mimo nemocnici mortalita   terapie   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• hodnotící studie MeSH
• Geografické názvy
• Turecko MeSH

• MeSH
• dospělí MeSH
• kardiopulmonální resuscitace škodlivé účinky   MeSH
• lidé středního věku MeSH
• lidé MeSH
• poškození DNA * MeSH
• prospektivní studie MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• urgentní zdravotnické služby MeSH
• zástava srdce mimo nemocnici genetika   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• dopisy MeSH
• práce podpořená grantem MeSH

• MeSH
• dospělí MeSH
• koarktace aorty diagnóza   epidemiologie   terapie   MeSH
• lidé MeSH
• nemocnice univerzitní MeSH
• retrospektivní studie MeSH
• terapie náhlých příhod statistika a číselné údaje   MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• dopisy MeSH
• Geografické názvy
• Turecko epidemiologie   MeSH

• MeSH
• akční potenciály účinky léků   MeSH
• antiarytmika * farmakokinetika   klasifikace   terapeutické užití   MeSH
• lidé MeSH
• Check Tag
• lidé MeSH

• MeSH
• náhlá srdeční smrt epidemiologie   etiologie   patologie   prevence a kontrola   MeSH
• prognóza MeSH
• rizikové faktory MeSH

• Konspekt
• Patologie. Klinická medicína
• NLK Obory
• kardiologie
• NLK Publikační typ
• studie

Pharmacorefractory chronic heart failure is a serious world-wide problem of systolic dysfunction not improving despite evidence based chronic heart failure pharmacotherapy. With the aim to reverse the poor pharmacorefractory chronic heart failure prognosis, severe sophisticated technical therapeutic approaches (from cardiac resynchronization usually with implantable cardioverter-defibrillator to heart transplantation) have been clinically adopted and detached at least for the most eligible pharmacorefractory chronic heart failure patients. However, both significant limitations of these highly specialised therapeutic techniques (cost, uncertain individual effect, complication, adverse effect, waiting list) and the pharmacorefractory chronic heart failure hopelessness for unfit patients make the effort to stop the pharmacorefractory chronic heart failure genesis never ending longing. Regarding growing knowledge on differences in pharmacokinetics, authors assume that the relative undertreatment despite fixed doses may explain the pharmacorefractory chronic heart failure genesis. If this hypothesis proves to be correct, the evidence based chronic heart failure pharmacotherapy innovatively personalized according to steady state drug serum level may reduce the pharmacorefractory chronic heart failure epidemiology with the lower need for cost-consuming techniques and be the promising strategy for patients left on individually ineffective evidence based chronic heart failure pharmacotherapy.

• MeSH
• chronická nemoc MeSH
• kardiovaskulární látky aplikace a dávkování   terapeutické užití   MeSH
• lidé MeSH
• srdeční selhání farmakoterapie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH