The effect of preventive administration of melatonin on the arrhythmogenic substrate in the myocardium was studied in the rabbit model of acute ischemia/reperfusion in vivo. The animals treated with melatonin 60 min before ischemia induction had shorter median activation time compared to the control group (p=0.039), less pronounced shortening of repolarization durations in the ischemic zone during coronary occlusion (p=0.008), and more complete recovery of repolarization during reperfusion (p=0.027). In the melatonin group, the dispersion of repolarization was less than in the control group during both ischemic period (p=0.043) and reperfusion (p=0.038). Thus, preventive administration of melatonin mitigated the arrhythmogenic substrate in the heart under conditions of ischemia/reperfusion.

• Klíčová slova
• dispersion of repolarization, ischemia/reperfusion, melatonin,
• MeSH
• ischemická choroba srdeční farmakoterapie   patofyziologie   MeSH
• králíci MeSH
• melatonin terapeutické užití   MeSH
• reperfuzní poškození myokardu farmakoterapie   patofyziologie   MeSH
• srdce fyziologie   MeSH
• srdeční elektrofyziologie MeSH
• zvířata MeSH
• Check Tag
• králíci MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• melatonin MeSH

Ambulatory monitoring represents an effective tool for the assessment of silent and transient myocardial ischemia during routine daily activities. Incidence of silent ischemia can provide important prognostic information about patients with coronary artery disease or acute coronary syndrome, as well as about post-myocardial infarction patients. The current technological progress enables development of powerful and miniaturized wearable devices for Holter monitoring. Higher sampling rates, dynamic range, and extended computational and storage capacity allow for considering of more complex methodological solutions such as high-frequency QRS analysis for diagnosing myocardial ischemia. Implementation of suitable methodologies for advanced detection of myocardial ischemia into modern ambulatory monitoring devices creates the potential of making the ambulatory myocardial ischemia monitoring a valuable diagnostic tool in clinical practice.

• Klíčová slova
• Ambulatory monitoring, HF-QRS, Holter monitoring, Myocardial Ischemia, Silent Ischemia,
• MeSH
• algoritmy * MeSH
• diagnóza počítačová metody   MeSH
• elektrokardiografie ambulantní metody   MeSH
• ischemická choroba srdeční diagnóza   MeSH
• lidé MeSH
• počítačové zpracování signálu MeSH
• reprodukovatelnost výsledků MeSH
• senzitivita a specificita MeSH
• určení tepové frekvence metody   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

Ischemia-modified albumin (IMA) is a laboratory biomarker of cardiac ischemia. Our study aims to determine whether IMA can estimate or represent to any degree the extent of myocardial ischemia. We expect that the higher the marker of cardiac necrosis (maximum value after serial measurements) the greater the preceding cardiac ischemia, indicated by IMA in patients diagnosed with STEMI prior to direct percutaneous coronary intervention (PCI). We studied 216 patients indicated for direct PCI with a diagnosis of ST elevation myocardial infarction. Biochemical analysis of IMA was carried out using the albumin cobalt binding (ACB®) test. We also obtained relevant values for markers of myocardial necrosis (CK, CK-MB, cTnT). In all patients, there was an increased level of IMA prior to the procedure (116 ± 16.9 kU/l); also raised were levels of CK (17.32 μkat/l), CK-MB (4.85 μkat/l) and cTnT (2.97 μg/l) taken as the maximum values obtained after serial measurements at 12, 18, and 24 h after the procedure. We observed that there was no significant association between increase in IMA and cTnT (R2 = 0.0068, p = 0.483). This was also the case for CK-MB (R2 = 0.0011, p = 0.637). IMA does not estimate the extent of ischemia in patients with ST elevation myocardial infarction. However, its absence can be used qualitatively to rule out cardiac ischemia.

• MeSH
• analýza rozptylu MeSH
• balónková koronární angioplastika MeSH
• biologické markery krev   MeSH
• časové faktory MeSH
• infarkt myokardu krev   diagnóza   etiologie   patologie   terapie   MeSH
• ischemická choroba srdeční krev   komplikace   diagnóza   patologie   terapie   MeSH
• kreatinkinasa, forma MB krev   MeSH
• lidé středního věku MeSH
• lidé MeSH
• lidský sérový albumin MeSH
• lineární modely MeSH
• myokard patologie   MeSH
• nekróza MeSH
• prediktivní hodnota testů MeSH
• prognóza MeSH
• senioři MeSH
• sérový albumin MeSH
• stupeň závažnosti nemoci MeSH
• troponin T krev   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Geografické názvy
• Česká republika MeSH
• Názvy látek
• biologické markery MeSH
• ischemia-modified albumin MeSH Prohlížeč
• kreatinkinasa, forma MB MeSH
• lidský sérový albumin MeSH
• sérový albumin MeSH
• troponin T MeSH

The effects of therapeutic or preventive-therapeutic administration of water-soluble echinochrome analog U-441 on arrhythmia severity assessed by a set of myocardial spatio-temporal depolarization and repolarization parameters were examined on the model of acute myocardial ischemia in cats. Coronary occlusion increased activation time and decreased repolarization time in the ischemic zone; in addition, it increased both global and borderline (local) dispersions of repolarization. The linear regression model showed that only activation time values measured at the initial state and at termination of occlusion were associated with total arrhythmia score during ischemia (regression coefficient β=0.338, 95%CI=0.074-0.602, p=0.015 and β=0.720, 95%CI=0.323-1.117, p=0.001, respectively). The study revealed no association between administration of echinochrome analog U-441 and arrhythmia severity.

• Klíčová slova
• cats, echinochrome analog U-441, ischemia, predictors, ventricular arrhythmias,
• MeSH
• antiarytmika izolace a purifikace   farmakologie   MeSH
• elektrokardiografie MeSH
• ischemická choroba srdeční farmakoterapie   patofyziologie   MeSH
• ježovky chemie   MeSH
• kočky MeSH
• koronární okluze chirurgie   MeSH
• modely nemocí na zvířatech MeSH
• myokard patologie   MeSH
• naftochinony izolace a purifikace   farmakologie   MeSH
• převodní systém srdeční účinky léků   patofyziologie   MeSH
• rozpustnost MeSH
• srdeční arytmie farmakoterapie   patofyziologie   MeSH
• stupeň závažnosti nemoci MeSH
• terapie neúspěšná MeSH
• voda chemie   MeSH
• zvířata MeSH
• Check Tag
• kočky MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antiarytmika MeSH
• echinochrome A MeSH Prohlížeč
• naftochinony MeSH
• voda MeSH

Apelin is a peptide known to have a vital role in cardiovascular diseases. It has been proven to induce proliferation and tube formation in endothelial cells, stabilise contacts between endothelial cells, and mediate pericyte recruitment. Since apelin level is reduced early after myocardial infarction, a supportive therapy with apelin is being investigated for its beneficial effect on blood vessel formation. It is becoming apparent, however, that the final effect of apelin often depends on stimuli the cell receives and the cross-talk with other molecules inside the cell. Hence, understanding the apelin pathway potentially can help us to improve angiogenic therapy. This review summarises recent knowledge regarding molecules involved in apelin signalling while focusing on their roles in angiogenesis within the ischemic environment after myocardial infarction.

• Klíčová slova
• Angiogenesis, Apelin, Apelin-12 (PubChem CID: 479167), Apelin-13 (PubChem CID: 71433878), Apelin-36 (PubChem CID: 16130451), Endothelial cells, Myocardial infarction, Signalling pathways, [Pyr1]-apelin-13 (PubChem CID: 25078060),
• MeSH
• endoteliální buňky metabolismus   MeSH
• fyziologická neovaskularizace fyziologie   MeSH
• infarkt myokardu metabolismus   MeSH
• intracelulární signální peptidy a proteiny metabolismus   MeSH
• ischemická choroba srdeční metabolismus   MeSH
• lidé MeSH
• patologická angiogeneze metabolismus   MeSH
• signální transdukce fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• intracelulární signální peptidy a proteiny MeSH

To investigate the possible role of endothelin in coronary vasoconstriction contributing to the development of myocardial ischemia, plasma endothelin concentrations at rest and during atrial pacing-induced myocardial ischemia have been measured in blood samples drawn from the aorta and coronary sinus in 12 patients with significant narrowing of the left anterior descending coronary artery. The plasma endothelin concentrations at rest were similar in the aorta (AO/R) and coronary sinus (CS/R) (4.8 +/- 2.4 and 4.5 +/- 1.7 pg/ml, respectively), the difference between coronary sinus and aorta plasma endothelin concentration (CS/R-AO/R) being -0.3 +/- 1.7 pg/ml. During atrial pacing-induced myocardial ischemia aortic plasma endothelin concentration (AO/P) did not change (4.6 +/- 2.6 pg/ml) and only an insignificant increase in the plasma endothelin concentration in the coronary sinus (CS/P) was observed (5.3 +/- 2.8 pg/ml). The difference between coronary sinus and aortic endothelin plasma concentration (CS/P-AO/P) was 0.6 +/- 2.5 pg/ml. Finally, the difference in endothelin concentrations between coronary sinus and aorta rose only insignificantly during pacing as compared to the resting values ([CS/P-AO/P]-[CS/R-AP/R] being 0.9 +/- 3.2 pg/ml). Thus, atrial pacing-induced myocardial ischemia in patients with significant left anterior descending coronary artery stenosis was not accompanied by significant changes in coronary sinus plasma endothelin concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

• MeSH
• aorta MeSH
• dospělí MeSH
• endoteliny krev   fyziologie   MeSH
• ischemická choroba srdeční krev   etiologie   patofyziologie   MeSH
• kardiostimulace umělá * MeSH
• koronární cévy * MeSH
• lidé středního věku MeSH
• lidé MeSH
• senioři MeSH
• vazokonstrikce fyziologie   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• endoteliny MeSH

The goal of the study was to determine whether postconditioning protects against different ischemia durations in the rabbit. Rabbits were assigned to a 20-, 25-, 45- or 60-min coronary occlusion followed by 24-h of reperfusion. Rabbits received no further intervention (control) or were postconditioned with four cycles of 30-s occlusion and 30-s reperfusion after myocardial infarction. Plasma levels of troponin I were quantified throughout reperfusion. In control conditions, infarct sizes (% area at risk using triphenyltetrazolium chloride) after 20, 25, 45 and 60 min of coronary occlusions were 23+/-3, 51+/-4, 70+/-3 and 81+/-3 %, respectively. With 20 and 25 min occlusion, postconditioning reduced infarct size by 43+/-10 and 73+/-21 %, respectively. On the other hand, with 45 or 60 min occlusion, postconditioning had no significant effects on infarct size (61+/-3 and 80+/-2 % of area at risk). Preconditioning protocol was performed with 25- and 60-min coronary occlusion. As expected, preconditioning significantly reduced infarct size. In conclusion, in the rabbit, the cardioprotection afforded by postconditioning is limited to less than 45 min coronary occlusion.

• MeSH
• hemodynamika MeSH
• ischemická choroba srdeční krev   patologie   prevence a kontrola   MeSH
• ischemické přivykání * MeSH
• králíci MeSH
• myokard patologie   MeSH
• troponin I krev   MeSH
• zvířata MeSH
• Check Tag
• králíci MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• troponin I MeSH

Aims of the study were to compare the development of electrocardiographic responses of the ischemia-induced heterogeneities of activation and repolarization in the ventricular myocardium of normal and diabetic animals. Body surface ECGs and unipolar electrograms in 64 epicardial leads were recorded before and during 20 min after the ligation of the left anterior descending artery in diabetic (alloxan model, 4 weeks, n=8) and control (n=8) rabbits. Activation times (ATs), end of repolarization times (RTs) and repolarization durations (activation-recovery intervals, ARIs) were determined in ischemic and periischemic zones. In contrast to the controls, the diabetic rabbits demonstrated the significant prolongation of ATs and shortening of ARIs (P<0.05) during ischemia in the affected region resulting in the development and progressive increase of the ARI and RT gradients across the ischemic zone boundary. The alterations of global and local dispersions of the RTs in diabetics correlated with the T(peak)-T(end) interval changes in the limb leads ECGs. In the ischemic conditions, the diabetic animals differed from the controls by the activation delay, significant repolarization duration shortening, and the increase of local repolarization dispersion; the latter could be assessed by the T(peak)-T(end) interval measurements in the body surface ECGs.

• MeSH
• elektrokardiografie MeSH
• epikardiální mapování MeSH
• experimentální diabetes mellitus patofyziologie   MeSH
• ischemická choroba srdeční patofyziologie   MeSH
• králíci MeSH
• převodní systém srdeční patofyziologie   MeSH
• srdeční komory patofyziologie   MeSH
• zvířata MeSH
• Check Tag
• králíci MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• srovnávací studie MeSH

RATIONALE: There is mounting evidence of a higher incidence of coronary heart disease in cytomegalovirus-seropositive individuals. OBJECTIVE: The aim of this study was to investigate whether acute myocardial infarction triggers an inflammatory T-cell response that might lead to accelerated immunosenescence in cytomegalovirus-seropositive patients. METHODS AND RESULTS: Thirty-four patients with acute myocardial infarction undergoing primary percutaneous coronary intervention were longitudinally studied within 3 months after reperfusion (Cohort A). In addition, 54 patients with acute myocardial infarction and chronic myocardial infarction were analyzed in a cross-sectional study (Cohort B). Cytomegalovirus-seropositive patients demonstrated a greater fall in the concentration of terminally differentiated CD8 effector memory T cells (TEMRA) in peripheral blood during the first 30 minutes of reperfusion compared with cytomegalovirus-seronegative patients (-192 versus -63 cells/μL; P=0.008), correlating with the expression of programmed cell death-1 before primary percutaneous coronary intervention (r=0.8; P=0.0002). A significant proportion of TEMRA cells remained depleted for ≥3 months in cytomegalovirus-seropositive patients. Using high-throughput 13-parameter flow cytometry and human leukocyte antigen class I cytomegalovirus-specific dextramers, we confirmed an acute and persistent depletion of terminally differentiated TEMRA and cytomegalovirus-specific CD8(+) cells in cytomegalovirus-seropositive patients. Long-term reconstitution of the TEMRA pool in chronic cytomegalovirus-seropositive postmyocardial infarction patients was associated with signs of terminal differentiation including an increase in killer cell lectin-like receptor subfamily G member 1 and shorter telomere length in CD8(+) T cells (2225 versus 3397 bp; P<0.001). CONCLUSIONS: Myocardial ischemia and reperfusion in cytomegalovirus-seropositive patients undergoing primary percutaneous coronary intervention leads to acute loss of antigen-specific, terminally differentiated CD8 T cells, possibly through programmed cell death-1-dependent programmed cell death. Our results suggest that acute myocardial infarction and reperfusion accelerate immunosenescence in cytomegalovirus-seropositive patients.

• Klíčová slova
• aging, cytotoxic T-lymphocytes, human cytomegalovirus, myocardial infarction, programmed cell death 1, reperfusion, telomere,
• MeSH
• antigeny CD8 krev   MeSH
• CD8-pozitivní T-lymfocyty imunologie   metabolismus   MeSH
• Cytomegalovirus imunologie   metabolismus   MeSH
• ischemická choroba srdeční krev   epidemiologie   virologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• longitudinální studie MeSH
• průřezové studie MeSH
• reperfuze myokardu metody   MeSH
• senioři MeSH
• stárnutí buněk fyziologie   MeSH
• syndromy imunologické nedostatečnosti krev   epidemiologie   virologie   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antigeny CD8 MeSH

Obesity is increasing at an alarming rate globally. Several studies have shown that premenopausal women have a reduced risk of CV disease and a reduced myocardial susceptibility to ischemia/reperfusion injury. The effect of obesity on myocardial tolerance to ischemia in women has not been established. To determine how obesity affects myocardial susceptibility to ischemia/reperfusion injury in both males and females, we fed male and female Wistar rats a high caloric diet (HCD) or a control rat chow diet (CD) for 18 weeks. Rats were subsequently fasted overnight, anesthetized and blood was collected. In separate experiments, 18-week-fed (HCD and CD) rats underwent 45 min in vivo coronary artery ligation (CAL) followed by 2 hours reperfusion. Hearts were stained with TTC and infarct size determined. Both male and female HCD fed rats had increased body and visceral fat weights. Homeostasis model assessment (HOMA) index values were 13.95+/-3.04 for CD and 33.58+/-9.39 for HCD male rats (p<0.01) and 2.98+/-0.64 for CD and 2.99+/-0.72 for HCD fed female rats. Male HCD fed rats had larger infarct sizes than CD fed littermates (43.2+/-9.3 % vs. 24.4+/-7.6 %, p<0.05). Female HCD and CD diet fed rats had comparable infarct sizes (31.8+/-4.3 % vs. 23.9+/-3.3 %). We conclude that male rats on the HCD became viscerally obese, dyslipidemic and insulin-resistant, while female HCD fed rats became viscerally obese without developing dyslipidemia or insulin resistance. Obesity increased myocardial infarct size in males but not the females.

• MeSH
• energetický příjem fyziologie   MeSH
• infarkt myokardu patofyziologie   MeSH
• inzulinová rezistence fyziologie   MeSH
• krysa rodu Rattus MeSH
• nitrobřišní tuk patofyziologie   MeSH
• obezita patofyziologie   MeSH
• potkani Wistar MeSH
• reperfuzní poškození myokardu patofyziologie   MeSH
• sexuální faktory MeSH
• tělesná hmotnost MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH