BACKGROUND: Coronary microvascular dysfunction (CMD) is linked to adverse cardiovascular events. Definitive diagnosis of CMD requires invasive provocative testing during angiography. We developed and tested a novel computerized T wave analysis tool to identify electrocardiographic signatures of CMD. METHODS: 1552 patients underwent an invasive assessment of coronary microvascular function. Patients with interpretable pre-procedural ECGs were divided into 2 age and sex matched groups (n=261 in each group, 75% female): normal microvascular function, CFR>2.5 (CFR+), and abnormal microvascular function, CFR ≤ 2.5 (CFR-). ECGs were evaluated using a novel T wave program that quantified subtle changes in T wave morphology. RESULTS: T wave repolarization parameters were significantly different between patients with normal and abnormal microvascular function. The top 3 features in males comprised of T wave area in V6 (CFR+: 10091.4 mV(2) vs. CFR-: 8152.3 mV(2), p<0.05); T1 Y-center of gravity in lead II (CFR+: 17.8 mV vs. CFR-: 22.4, p<0.005) and T Peak-T End in lead II (CFR+: 97.6 msec vs. CFR-: 91.1 msec, p<0.05). These could identify the presence of an abnormal CFR with 74 ± 0.2% accuracy. In females, the top 3 features were T wave right slope lead V6 (CFR+: -2489.1 mV/msec vs. CFR-: -2352.3 mV/msec, p<0.005); Amplitude in V6 (CFR+: 190.4 mV vs. 172.7 mV, p=0.05) and Y-center of gravity in lead V1 (CFR+: 33.3 vs. CFR-: 40.0, p=0.001). These features could identify the presence of an abnormal CFR with 67 ± 0.3% accuracy. CONCLUSION: Our data demonstrates that a computer-based repolarization measurement tool may identify electrocardiographic signatures of CMD.

• MeSH
• automatizované zpracování dat metody   MeSH
• elektrokardiografie metody   MeSH
• intervenční ultrasonografie MeSH
• koronární angiografie MeSH
• koronární cévy patofyziologie   MeSH
• koronární cirkulace fyziologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mikrocirkulace fyziologie   MeSH
• následné studie MeSH
• nemoci koronárních tepen diagnóza   patofyziologie   MeSH
• reprodukovatelnost výsledků MeSH
• retrospektivní studie MeSH
• rychlost toku krve MeSH
• software * MeSH
• stupeň závažnosti nemoci MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH

• Publikační typ
• abstrakt z konference MeSH

Background: Takotsubo cardiomyopathy (TC) aetiology has not been completely understood yet. One proposed pathogenic mechanism was coronary microvascular dysfunction (MVD). This study compared coronary flow and myocardial perfusion in patients with TC, microvascular angina (MVA), and a control group (CG). Methods: Out of 42 consecutive patients presented to our centre with TC from 2013 to 2017; we retrospectively selected 27 patients. We compared them with a sex- and age-matched group of 27 MVA cases and 27 patients with normal coronary arteries (CG). The flow was evaluated in the three coronary arteries as TIMI flow and TIMI frame count (TFC). Myocardial perfusion was studied with Blush-Score and Quantitative Blush Evaluator (QuBE). Results: TFC, in TC, revealed flow impairment in the three arteries compared to the CG (left anterior descending artery (LAD): 22 ± 8, 15 ± 4; p = 0.001) (right coronary artery: 12 ± 4, 10 ± 3; p = 0,025) (left circumflex: 14 ± 4, CG 11 ± 3; p = 0,006). QuBE showed myocardial perfusion impairment in the LAD territory in TC comparing with both the CG (8,9 (7,2-11,5) versus 11,4 (10-15,7); p = 0,008) and the MVA group (8,9 (7,2-11,5) versus 13,5 (10-16); p = 0,006). Conclusions: Our study confirmed that coronary flow is impaired in TC, reflecting a MVD. Myocardial perfusion defect was detected only in the LAD area.

• MeSH
• echokardiografie metody   MeSH
• infarkt myokardu patofyziologie   MeSH
• koronární angiografie metody   MeSH
• koronární cévy patofyziologie   MeSH
• koronární cirkulace fyziologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mikrocévy patofyziologie   MeSH
• retrospektivní studie MeSH
• rychlost toku krve fyziologie   MeSH
• senioři MeSH
• takotsubo kardiomyopatie patofyziologie   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

• Publikační typ
• abstrakty MeSH

Angina pectoris bez obstrukce koronárních tepen je častý nález u pacientů s bolestmi na hrudi, v jehož patofyziologii se uplatňují zejména dva mechanismy – strukturální nebo funkční poškození mikrocirkulace či funkční poškození epikardiálních tepen, případně jejich kombinace. Souhrnný článek se zabývá dia- gnostikou koronární mikrovaskulární dysfunkce se zaměřením na kontinuální termodiluci jako bezpečnou, jednoduchou, rychlou a na operatérovi nezávislou metodu. Popisuje teoretický základ i praktické aspekty s grafickými ukázkami měření.

Angina with non-obstructive coronary artery disease is a frequent finding in patients with chest pain. Its pathophysiology involves two main mechanisms: structural and functional dysfunction of microcircula- tion, functional dysfunction of epicardial arteries, and their combination. The review article focuses on the diagnostics of microvascular dysfunction, particularly continuous thermodilution, as a safe, easy, fast, and operator-independent method. It describes both theoretical background and practical aspects with graphical examples of measurements.

• Klíčová slova
• koronární průtok,
• MeSH
• angina pectoris * diagnóza   klasifikace   patofyziologie   MeSH
• hemodynamické monitorování metody   MeSH
• koronární cévy patologie   MeSH
• lidé MeSH
• mikrocévy patologie   MeSH
• mikrocirkulace MeSH
• perikard fyziologie   MeSH
• termodiluce * metody   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• práce podpořená grantem MeSH
• přehledy MeSH

Background: We tested whether the level of endothelial dysfunction assessed by digital tonometry, and expressed as reactive hyperemia index (RHI), is related to occurrences of a discrepancy between fractional flow reserve (FFR) and the instantaneous wave free ratio (iFR) (ClinicalTrials.gov identifier: NCT03033810).Methods: We examined patients with coronary stenosis in the range of 40-70%, assessed by both FFR and iFR (system Philips-Volcano) for stable angina. We included consecutive patients with FFR and iFR in one native coronary artery, and who had had no previous intervention.Results: We included 138 patients. Out of those, 24 patients (17.4%) had a negative FFR (with an FFR value >0.8) and positive iFR (with a iFR value ≤0.89) - designated the FFRn/iFRp discrepancy group, and 22 patients (15.9%) had a positive FFR (≤0.8) and negative iFR (>0.89) - designated the FFRp/iFRn discrepancy. RHI was higher in the discrepancy groups compared the group without discrepancy (1.73 ± 0.79 vs. 1.48 ± 0.50, p = 0.025). However, this finding was not confirmed in multivariant logistic regression analyses. Patients with any type of discrepancy differed from the agreement group by having a higher occurrence of diabetes mellitus [9 patients (21.4%) vs. 36 patients (39.6%), p = 0.029], active smoking (23 patients or 54.8% vs. 26 patients or 28.6%, p = 0.003) and lower use of calcium channel blockers (9 patients, 21.4%, vs. 43 patients, 46.7%, p = 0.004).Conclusion: The presence of endothelial dysfunction can be associated with a discrepancy in FFR/iFR. However, RHI correlated with risk factors of atherosclerosis, not with FFR or iFR.

• MeSH
• cévní endotel patofyziologie   MeSH
• cévní rezistence MeSH
• frakční průtoková rezerva myokardu * MeSH
• koronární stenóza * diagnóza   patofyziologie   MeSH
• laser doppler flowmetrie * přístrojové vybavení   metody   MeSH
• lidé MeSH
• manometrie přístrojové vybavení   metody   MeSH
• mikrocirkulace fyziologie   MeSH
• navrhování softwaru * MeSH
• počítačové zpracování obrazu MeSH
• senioři MeSH
• software MeSH
• zobrazování myokardiální perfuze metody   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• pozorovací studie MeSH

We previously identified genomic instability as a causative factor for vascular aging. In the present study, we determined which vascular aging outcomes are due to local endothelial DNA damage, which was accomplished by genetic removal of ERCC1 (excision repair cross-complementation group 1) DNA repair in mice (EC-knockout (EC-KO) mice). EC-KO showed a progressive decrease in microvascular dilation of the skin, increased microvascular leakage in the kidney, decreased lung perfusion, and increased aortic stiffness compared with wild-type (WT). EC-KO showed expression of DNA damage and potential senescence marker p21 exclusively in the endothelium, as demonstrated in aorta. Also the kidney showed p21-positive cells. Vasodilator responses measured in organ baths were decreased in aorta, iliac and coronary artery EC-KO compared with WT, of which coronary artery was the earliest to be affected. Nitric oxide-mediated endothelium-dependent vasodilation was abolished in aorta and coronary artery, whereas endothelium-derived hyperpolarization and responses to exogenous nitric oxide (NO) were intact. EC-KO showed increased superoxide production compared with WT, as measured in lung tissue, rich in endothelial cells (ECs). Arterial systolic blood pressure (BP) was increased at 3 months, but normal at 5 months, at which age cardiac output (CO) was decreased. Since no further signs of cardiac dysfunction were detected, this decrease might be an adaptation to prevent an increase in BP. In summary, a selective DNA repair defect in the endothelium produces features of age-related endothelial dysfunction, largely attributed to loss of endothelium-derived NO. Increased superoxide generation might contribute to the observed changes affecting end organ perfusion, as demonstrated in kidney and lung.

• MeSH
• cévní endotel metabolismus   patologie   patofyziologie   MeSH
• DNA vazebné proteiny nedostatek   genetika   MeSH
• endonukleasy nedostatek   genetika   MeSH
• endoteliální buňky metabolismus   patologie   MeSH
• inhibitor p21 cyklin-dependentní kinasy genetika   metabolismus   MeSH
• kapilární permeabilita MeSH
• myši inbrední C57BL MeSH
• myši knockoutované MeSH
• oprava DNA * MeSH
• oxid dusnatý metabolismus   MeSH
• poškození DNA * MeSH
• stárnutí buněk genetika   MeSH
• stárnutí genetika   metabolismus   patologie   MeSH
• superoxidy metabolismus   MeSH
• synthasa oxidu dusnatého, typ III metabolismus   MeSH
• tuhost cévní stěny MeSH
• vazodilatace MeSH
• věkové faktory MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH

Syndróm inzulínovej rezistencie (metabolický syndróm, syndróm X, 5 H) predstavuje súhrn hlavných rizikových faktorov akcelerujúcich aterotrombogenézu. Mikrovaskulárna angina pectoris je tiež nepochybnou súčasťou syndrómu inzulínovej rezistencie, pretože hyperinzulinizmus, kompenzujúci inzulínovú rezistenciu sa našiel u 61,9 % pacientov s mikrovaskulárnou anginou pectoris a u 75 % pacientov s prekonaným srdcovým infarktom, podobne ako aj u 75 % ICHS so signifikantnými koronárnymi stenózami, kde hladiny inzulínu dokonca pozitívne korelovali s kvantitatívnym koronárnym skóre. Hyperinzulinizmus je teda významným jednotiacim patogenetickým článkom alebo aspoň spoločným markerom inzulínovej rezistencie u všetkých fenoménov syndrómu inzulínovej rezistencie. V súbore 500 na koronarografiu indikovaných pacientov sa našlo 70 prípadov (14 %), ktoré sa záverečne hodnotili ako mikrovaskulárna angina pectoris. Mikrovaskulárna a makrovaskulárna angina pectoris (ICHS) so signifikantnými koronárnymi stenózami, ak sa porovnávajú ich páry analogického veku, pohlavia a BMI, sa nelíšia v žiadnom z parametrov definujúcich inzulínovú rezistenciu, hyperinzulinizmus, obezitu a dyslipoproteinémiu! U mikrovaskulárnej anginy pectoris prevládali však 4,1 - krát androidne obézne, periklimakterické ženy. Mikrovaskulárna angina pectoris nie je bezvýznamné ochorenie, pretože u časti prípadov sa môžu neskôr za prítomnosti analogických rizikových faktorov vyvinúť aj signifikantné koronárne stenózy, blok ľavého Tawarovho ramienka, dilatačná kardiomyopatia, hoci väčšie, transmurálne infarkty myokardu tu obyčajne nevznikajú.

Insulin resistance syndrome (metabolic syndrome, syndrome X, 5HD) involves main risk factors accelerating atherothrombogenesis. Microvascular angina pectoris is also a part of syndrome (IRS), because hyperinsulinism compensating insulin resistance was found in 61.9 % of patients with microvascular angina pectoris and in 75 % of patients who have overcome myocardial infarction, and similarly in 75 % of patients with ischemic heart disease with significant coronary stenoses where insulin levels positively correlated with the quantitative coronary score. Therefore, hyperinsulinism is a significant integrating pathogenetic part or a common marker of insulin resistance in all phenomena of IRS. In the group of 500 patients indicated to coronarography 70 cases were found (14 %) that were at the end evaluated as patients with microvascular angina pectoris. Microvascular and macrovascular angina pectoris with significant coronary stenoses, if their pairs of analogical age, sex and BMI are compared, do not differ in any parameters defining insulin resistance, hyperinsulinism, obesity and dyslipoproteinaemia . However, in microvascular angina pectoris androidally obese, periclimacteric women prevailed 4.1 times. Microvascular angina pectoris is not a trivial disease, because some patients might later develop, if analogical risk factors are present, significant coronary stenoses, left Tawar`s branch blockage, dilated cardiomyopathy, though larger transmural myocardial infarctions here usually do not occur.

• MeSH
• ischemie MeSH
• koronární angiografie MeSH
• koronární cévy patofyziologie   MeSH
• koronární cirkulace MeSH
• lidé MeSH
• mikrocirkulace MeSH
• nemoci koronárních tepen * MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy MeSH

We review the current understanding of formation and development of the coronary microvasculature which supplies oxygen and nutrients to the heart myocardium and removes waste. We emphasize the close relationship, mutual development, and communication between microvasculature endothelial cells and surrounding cardiomyocytes. The first part of the review is focused on formation of microvasculature during embryonic development. We summarize knowledge about establishing the heart microvasculature density based on diffusion distance. Then signaling mechanisms which are involved in forming the microvasculature are discussed. This includes details of cardiomyocyte-endothelial cell interactions involving hypoxia, VEGF, NOTCH, angiopoietin, PDGF, and other signaling factors. The microvasculature is understudied due to difficulties in its visualization. Therefore, currently available imaging methods to delineate the coronary microvasculature in development and in adults are discussed. The second part of the review is dedicated to the importance of the coronary vasculature in disease. Coronary microvasculature pathologies are present in many congenital heart diseases (CHD), especially in pulmonary atresia, and worsen outcomes. In CHDs, where the development of the myocardium is impaired, microvasculature is also affected. In adult patients coronary microvascular disease is one of the main causes of sudden cardiac death, especially in women. Coronary microvasculature pathologies affect myocardial ischemia and vice versa; myocardial pathologies such as cardiomyopathies are closely connected with coronary microvasculature dysfunction. Microvasculature inflammation also worsens the outcomes of COVID-19 disease. Our review stresses the importance of coronary microvasculature and provides an overview of its formation and signaling mechanisms and the importance of coronary vasculature pathologies in CHDs and adult diseases. This article is categorized under: Cardiovascular Diseases > Stem Cells and Development Congenital Diseases > Molecular and Cellular Physiology Cardiovascular Diseases > Molecular and Cellular Physiology.

• MeSH
• COVID-19 MeSH
• dospělí MeSH
• endoteliální buňky MeSH
• kardiomyocyty * metabolismus   MeSH
• kardiovaskulární nemoci * metabolismus   MeSH
• lidé MeSH
• mikrocévy diagnostické zobrazování   MeSH
• myokard * metabolismus   MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH