Transient Myocardial Ischemia Research Articles

Atrioventricular (AV) block and sinus arrest associated with dipyridamole infusion.

The use of dipyridamole for thallium-201 imaging has proved very successful in demonstrating coronary arterial disease, and a combination of dipyridamole and dynamic exercise is becoming widely used. Dipyridamole is safe when given intravenously, although transient noncardiac side effects are common; side effects such as chest pain, headache, and dizziness. These side effects are mostly mild, and can be treated with aminophylline. We describe a 45-year-old woman with normal baseline electrocardiography (ECG) and unremarkable physical examination, referred for myocardial thallium scan with dipyridamole. A few seconds after infusion of dipyridamole, her ECG developed first-degree atrioventricular (AV) block, then, 2:1 AV block, complete heart block (CHB), and sinus arrest. After aminophylline infusion, junctional escape rhythm was seen, and a few seconds later, rhythm changed to sinus rhythm. Thallium scan was negative for ischemia. High-grade AV block after dipyridamole has been described in few case reports, and mostly was associated with transient myocardial ischemia; it seems that the presence of conduction abnormalities at baseline is a risk factor. But in our case, the sinus arrest and AV block occurred without evidence of ischemia in myocardial perfusion imaging, and we think it can be an unwanted complication of dipyridamole; clinicians should be aware of bradyarrhythmia as a possible complication of dipyridamole. An alternative explanation is that this arrhythmia can be caused by vagal activity; and another possibility is that the imaging study was false negative.

Fragmented QRS complex as a marker of myocardial fibrosis in patients with coronary artery disease

Aim– to analyze the relationship between fQRS and myocardial fibrosis in CAD patients using SPECT.
 Material and methods.Retrospectively, we have analyzed the anamnesis and examinations of 116 patients with suspected coronary heart disease. The fQRS was assessed according to the criteria of Das M. et al., 2006, along with the presence of a pathological Q wave and a slow increase in the amplitude of the R wave. We analysed the transient myocardial ischemia and/or myocardial scarring using stress/rest SPECT with technetium-99m.
 Results.fQRS was significantly more frequently detected in patients with stable and partially reversible perfusion defects – 44.1% and 52.2%, respectively, versus 13.0% and 5.5% in patients without perfusion defects or with reversible perfusion defects, p 0.05. Among 28 patients with QRS fragmentation and myocardial fibrosis, 19 (67.8%) had classical signs of fibrosis on the ECG, 9 (32.1%) had no ECG-registered fibrosis but fQRS was detected. The sensitivity of fQRS marker in detecting myocardial fibrosis reached 84.4%, the specificity was 63.3%.
 Conclusion.fQRS complex is an informative marker for detecting myocardial scarring in patients with coronary artery disease. Analysis of fQRS in daily clinical practice may increase the diagnostic value of electrocardiography in the detection of fibrosis.

Ischemic Pre-Conditioning is Present in Patients with Non-ST Elevation Myocardial Infarction and ECG Derived Moderate Obstructive Sleep Apnea.

Obstructive Sleep Apnea (OSA) is associated with an increased risk of cardiovascular events, including Acute Coronary Syndrome (ACS). There is conflicting evidence that suggests OSA has a cardioprotective effect (i.e., lower troponin), via ischemic pre-conditioning, in patients with ACS. This study had two aims: (1) compare peak troponin between non-ST elevation (NSTE) ACS patients with and without moderate OSA identified using a Holter derived respiratory disturbance index (HDRDI); and (2) determine the frequency of transient myocardial ischemia (TMI) between NSTE-ACS patients with and without moderate HDRDI. This was a secondary analysis. OSA events were identified from 12-lead ECG Holter recordings using QRSs, R-R intervals, and the myogram. Moderate OSA was defined as an HDRDI ≥15 events per/hour. TMI was defined as ≥1 millimeter of ST-segment ↑ or ↓, in ≥ 1 ECG lead, ≥ 1 minute. In 110 NSTE-ACS patients, 39% (n=43) had moderate HDRDI. Peak troponin was higher in patients with moderate HDRDI (6.8 ng/ml yes vs. 10.2 ng/ml no; p=0.037). There was a trend for fewer TMI events, but there were no differences (16% yes vs. 30% no; p=0.081). NSTE-ACS patients with moderate HDRDI have less cardiac injury than those without moderate HDRDI measured using a novel ECG derived method. These findings corroborate prior studies suggesting a possible cardioprotective effect of OSA in ACS patients via ischemic pre-condition. There was a trend for fewer TMI events in moderate HDRDI patients, but there was no statistical difference. Future research should explore the underlying physiologic mechanisms of this finding.

АДАПТИВНАЯ РОЛЬ ОКСИДА АЗОТА У НЕДОНОШЕННЫХ НОВОРОЖДЕННЫХ ДЕТЕЙ С ИШЕМИЕЙ МИОКАРДА В РАННЕМ НЕОНАТАЛЬНОМ ПЕРИОДЕ

Objective of the study: to study the role of nitric oxide (NO) in adaptive reactions of the circulatory system in premature infants with transient myocardial ischemia (TMI). Materials and methods of research: a clinical, prospective, comparative study was carried out from 2016 to 2018. 82 infants with gestational age of 31–36 weeks who have had respiratory failure were included. Newborns were divided into groups: 1st – 14 newborns with TMI ECG criteria and troponin I (TrI) >0.139 ng/ml, 2nd – 39 newborns with TMI ECG criteria and TrI<0.139 ng/ml, 3rd – 29 children with normal ECG and TrI<0.139 ng/ml. In the early neonatal period, the clinical status, blood gas analysis, ECG, echocardiography and determination of TrI and NO were carried out. Quantitative data are presented as median, 25th and 75th percentiles; qualitative – in absolute values and %. The statistical significance was assessed by the Mann–Whitney test, the analysis of the relationship was assessed by the Spearman's rank correlation coefficient. Results: the level of NO by the 7th day of life in premature newborns of the 1st group increased 3.8 times, in the 2nd and 3rd groups – 1.7 and 2.5 times. A correlation relationship was revealed between TrI and NO on the 7th day of life (r=0.793, p=0.006), between NO and pH (r=–0.738, p=0.036), NO and pCO2 (r=0.857, p=0.006) on the 1st day. Also, on the 1st day there was a statistically significant increase in the end diastolic (EDS) and end systolic sizes (EDS) of the left ventricle (LV), the relationship of LV EDS with NO (r=0.722, p=0.042) and TrI (r=0.666, p=0.049), as well as NO with the LA size (r=0.731, p=0.038) in the 1st group. Conclusions: in premature infants with TMI and destructive changes in the myocardium, an increase in NO is probably necessary to optimize LV contractility and compensate for damage to cardiomyocytes. In children with TMI in the absence of myocardial injury, a compensatory increase in NO contributes to limiting the effects of hypoxia by functional disorders of LV, which persist by the end of the early neonatal period.

Left ventricular regional longitudinal strain assessed during speckle-tracking stress echocardiography with physical exercise may identify severe coronary artery disease

Abstract Funding Acknowledgements Type of funding sources: None. Background. Assessment of global longitudinal strain of the left ventricular (LV) myocardium during stress echocardiography showed promising results in diagnosing transient myocardial ischemia. Regional longitudinal strain (RLS) allows to evaluate LV systolic function more precisely. However, due to the heterogeneity of LV segments contraction, an isolated assessment of LV RLS values can be challenging. We suggest that evaluation of the mean LV RLS values for the basal, middle and apical regions of the LV during stress echocardiography may be more useful in clinical setting. Aim of the study. The aim of the study was to determine the diagnostic capabilities of the LV RLS assessed during stress echocardiography with exercise on the treadmill in defining the presence and significance of coronary artery disease (CAD). Methods. The study included 132 patients (65.0 ± 9.3 years, 85 men) with known or suspected CAD. All patients underwent speckle-tracking stress echocardiography with exercise on the treadmill. At rest and after treadmill test all patients were measured for the values of LV RLS using the AFI (Automated functional imaging) algorithm. The LV RLS values for basal, middle and apical regions were calculated as the ratio of the sum of LV RLS values of the segments of each region to the number of segments. Segments of the LV were represented with the standard 17-segment model of the LV, 1-6 segments were assigned as basal segments; 7-12 segments as middle segments and 13-17 as apical segments (Picture 1). All patients underwent coronary angiography; the severity of CAD was assessed using the Gensini score. According to the results of coronary angiography, patients were divided into 3 groups: group 1 – 42 patients without CAD, group 2 – 63 patients with moderate CAD (<34 points on the Gensini score) and group 3 – 27 patients with severe CAD (≥ 35 points on the Gensini score). Results. At rest LV RLS values in basal, middle and apical regions did not significantly differ between the groups. Picture 2 shows that after the load, LV RLS values in basal, middle and apical regions in patients with severe CAD were significantly lower than in groups of patients without CAD and with moderate CAD. The values of LV RLS in patients with severe CAD decreased in all regions after the load, while in patients without CAD and with moderate CAD, LV RLS values increased in middle and apical regions and decreased in basal region. Conclusion. In patients with severe CAD (≥ 35 points on the Gensini score) after the load on the treadmill LV RLS values in all regions were significantly lower than in patients without CAD and with moderate CAD. Thus, LV RLS assessed during speckle-tracking stress echocardiography on the treadmill may be useful in identifying patients with severe CAD. Abstract Figure. Picture 1. 17-segment model of the LV Abstract Figure. Picture 2. Results of stress test

Transient Myocardial Ischemia in a Case Post Intra-Muscular Adrenaline

Background: Anaphylaxis is a medical emergency and requires immediate medical attention. Kounis syndrome is myocardial infarction or injury occurring in the setting of anaphylaxis and can also be due to the effects of epinephrine. Adrenaline is a common drug in the management of anaphylaxis but the electrocardiographic consequences of its administration post an attack are seldomly seen. Vasospasm is generally the cause for myocardial injury in an acute setting following the administration of epinephrine.
 Case Presentation: A 21-year- old female developed sudden onset breathlessness and giddiness post vaccination with the oxford –AstraZeneca COVID -19 vaccine. She was administered 0.5 ml adrenaline (1:1000) intramuscularly on the lateral aspect of the left thigh, following which she complained of chest tightness and palpitations. This was accompanied by hypotension and global ST segment depression on her Electrocardiogram. The second electrocardiogram, done after 30 minutes showed a relative resolution in ST segment depressions with sinus rhythm in the one done at 16:00 hours. Creatine Kinase- MB and Troponin I were within normal limits and the patient experienced symptomatic improvement with normalization of blood pressure post fluid challenge.
 Conclusion: This case report highlights the case of a young female with no comorbidities who developed transient myocardial ischemia after administration of intramuscular adrenalin in therapeutic dose in view of an anaphylactic reaction. The probable action is alpha mediated coronary vasospasm. The potential adverse effects in an acute setting are hence outlined in this case report without discouraging its use given the potential benefits outweigh the risks.

Efficacy of add-on Danhong injection in patients with unstable angina pectoris: A double-blind, randomized, placebo-controlled, multicenter clinical trial

Ethnopharmacological relevanceDanhong injection (DHI)，which is extracted from Salviae miltiorrhizae and Flos carthami，has been widely prescribed to patients with unstable angina pectoris (UAP) in China. However, a high quality clinical trial is needed. Aim of the studyTo determine whether DHI can relieve symptoms of transient myocardial ischemia in patients with unstable angina pectoris. Materials and methodsA double-blind, placebo-controlled, randomized clinical trial was conducted in nine hospitals in China. Inpatients with UAP with blood stasis syndrome (BSS) were randomized 1:1 to receive DHI or placebo. The primary outcome was improvement rate in the quantification score of angina pectoris. Secondary outcomes included blood stasis syndrome scale, nitrates use, electrocardiogram recordings, PCI procedures, Seattle Angina Questionnaire (SAQ) and biochemical indexes. Results160 participants were enrolled and 159 were analyzed. There was no significant difference in primary outcome as compared with control group at the end of 7-day treatment, but significant difference at 28-day follow up (70.53% [95% CI, 59.97–81.09%] and 54.34% [95% CI, 42.68–65.99%]; P = 0.0423). The BSS score was significantly lower in the DHI group than that in the control group at day 28 (6.49 [6.96] vs 10.53 [9.07], P = 0.0034). In addition, DHI was significantly superior to placebo in the angina stability score of SAQ (91.10 [17.37] versus 78.21 [22.08], P < 0.001). There were no significant differences in other secondary outcome measures. ConclusionsA small decrease in the total effective rate and an increase in the angina stability score were observed 28 days after implementation of DHI in UAP with a total blood stasis syndrome score decrease, but the efficacy was not observed at day 7. The findings support that DHI may potentially relieve clinical symptoms and can benefit angina stability. Clinical trial registrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT02007187.

Transient myocardial ischemia due to corticosteroid use in a patient with multiple sclerosis diagnosed with myocardial perfusion imaging

Transient myocardial ischemia due to corticosteroid use in a patient with multiple sclerosis diagnosed with myocardial perfusion imaging

Comparative evaluation of empagliflozin, canagliflozin and sitagliptin cardioprotective properties in rats with experimental type 2 diabetes mellitus

Background: Myocardial infarction (MI) is one of the leading causes of mortality in patients with type 2 diabetes mellitus (DM), therefore it is essential to give preference to a glucose-lowering drug having optimal cardioprotective properties. A comparative study of the various sodium-glucose co-transporter inhibitors representatives’ protective effects in experimental MI was not carried out within the framework of one study.Aim: To evaluate the influence of empagliflozin (EMPA) and canagliflozin (CANA), in comparison with sitagliptin (SITA), on hemodynamic parameters and myocardial damage area in rats with diabetes type 2 model in experimental MI.Materials and methods: Type 2 DM was modelled in Wistar rats by means of 4-week high-fat diet followed by nicotinamide 230 mg/kg and streptozotocin 60 mg/kg administration. 4 weeks after DM induction the following groups were made: «DM+SITA» — treatment with SITA 50 mg/kg, «DM+EMPA» — treatment with EMPA 2 mg/kg, «DM+CANA» — treatment with CANA 25 mg/kg per os once daily for 8 weeks. Animals in «DM» group remained untreated for the following 8 weeks. Rats in control group were fed with standard chow. 16 weeks after the experiment beginning transient global myocardial ischemia was modelled in all rats. Hemodynamic parameters and myocardium necrosis area were evaluated.Results: The necrosis area was larger in «DM» group, than in control one (p=0.018). Infarction size in «DM+SITA» did not differ from that in «DM» group (62.92(41.29;75.84) and 57.26(45.51;70.08)%, р=0.554). Necrosis area in «DM+EMPA» and «DM+CANA» groups was smaller than in «DM» group (37.90(20.76;54.66)%, 46.15(29.77;50.55) vs 57.26(45.51;70.08)%, р=0.008 and р=0.009, respectively). Necrosis size did not differ between «DM+EMPA» and «DM+CANA» groups (p=0.630). Ischemic contracture in «DM+CANA» group was less prominent than under the use of all other glucose-lowering drugs. We observed increase of coronary blood flow in «DM+EMPA» group, in comparison with «DM», «DM+CANA» and «DM+SITA» groups.Conclusions: SITA does not have cardioprotective effect in ischemia-reperfusion injury in diabetic rats. EMPA and CANA have similarly prominent infarct-limiting properties. EMPA is able to increase coronary blood flow, whereas cardioprotective action of CANA is associated with ischemic contracture diminishing.

Nesfatin-1 inhibits myocardial ischaemia/reperfusion injury through activating Akt/ERK pathway-dependent attenuation of endoplasmic reticulum stress.

Nesfatin‐1 (encoded by NUCB2) is a cardiac peptide possessing protective activities against myocardial ischaemia/reperfusion (MI/R) injury. However, the regulation of NUCB2/nesfatin‐1 and the molecular mechanisms underlying its roles in MI/R injury are not clear. Here, by investigating a mouse MI/R injury model developed with transient myocardial ischaemia followed by reperfusion, we found that the levels of NUCB2 transcript and nesfatin‐1 amount in the heart were both decreased, suggesting a transcriptional repression of NUCB2/nesfatin‐1 in response to MI/R injury. Moreover, cardiac nesfatin‐1 restoration reduced infarct size, troponin T (cTnT) level and myocardial apoptosis, supporting its cardioprotection against MI/R injury in vivo. Mechanistically, the Akt/ERK pathway was activated, and in contrast, endoplasmic reticulum (ER) stress was attenuated by nesfatin‐1 following MI/R injury. In an in vitro system, similar results were obtained in nesfatin‐1‐treated H9c2 cardiomyocytes with hypoxia/reoxygenation (H/R) injury. More importantly, the treatment of wortmannin, an inhibitor of Akt/ERK pathway, abrogated nesfatin‐1 effects on attenuating ER stress and H/R injury in H9c2 cells. Furthermore, nesfatin‐1‐mediated protection against H/R injury also vanished in the presence of tunicamycin (TM), an ER stress inducer. Lastly, Akt/ERK inhibition reversed nesfatin‐1 effects on mouse ER stress and MI/R injury in vivo. Taken together, these findings demonstrate that NUCB2/nesfatin‐1 inhibits MI/R injury through attenuating ER stress, which relies on Akt/ERK pathway activation. Hence, our study provides a molecular basis for understanding how NUCB2/nesfatin‐1 reduces MI/R injury.

Protective role of Gremlin-1 in myocardial function.

Gremlin-1 is a cystine knot protein and is expressed in organs developing fibrosis. Transient ischaemia leads to myocardial fibrosis, a major determinant of impaired myocardial function. Expression of Gremlin-1 was investigated in infarcted myocardium by real-time PCR, Western blot analysis, histological and immunohistochemistry staining. We further elaborated the colocalization of Gremlin-1 and TGF-β proteins by confocal microscopy and co-immunoprecipitation experiments. The interaction between Gremlin-1 and TGF-β was analysed by photon correlation spectroscopy. Gremlin-1 modulation of the TGF-β-dependent collagen I synthesis in fibroblasts was investigated using ELISA and immunohistochemistry experiments. The effect of prolonged administration of recombinant Gremlin-1 on myocardial function following ischaemia/reperfusion was accessed by echocardiography and immunohistochemistry. Gremlin-1 is expressed in myocardial tissue and infiltrating cells after transient myocardial ischaemia (P<.05). Gremlin-1 colocalizes with the pro-fibrotic cytokine transforming growth factor-β (TGF-β) expressed in fibroblasts and inflammatory cell infiltrates (P<.05). Gremlin-1 reduces TGF-β-induced collagen production of myocardial fibroblasts by approximately 20% (P<.05). We found that Gremlin-1 binds with high affinity to TGF-β (KD =54nmol/L) as evidenced by photon correlation spectroscopy and co-immunoprecipitation. intravenous administration of m Gremlin-1-Fc, but not of equivalent amount of Fc control, significantly reduced infarct size by approximately 20%. In the m Gremlin-1-Fc group, infarct area was reduced by up to 30% in comparison with mice treated with Fc control (I/LV: 4.8±1.2% vs 6.0±1.2% P<.05; I/AaR: 15.2±1.5% vs 21.1±5%, P<.05). The present data disclose Gremlin-1 as an antagonist of TGF-β and presume a role for Gremlin-1/TGF-β interaction in myocardial remodelling following myocardial ischaemia.

Effects of Tranilast on Inflammasome and Macrophage Phenotype in a Mouse Model of Myocardial Infarction.

Acute myocardial infarction (AMI) has been a devastating actuality and accounts for half of cardiovascular emergency department visits. Nucleotide oligomerization domain, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome participates in the mediation of myocardial inflammation during AMI. Therefore, this study aimed to reveal the therapeutic function of tranilast, an agent targeting NLRP3, for AMI. AMI mouse model was first established by transient myocardial ischemia. Western blot and quantitative reverse transcription polymerase chain reaction assay were performed to estimate the expression levels of related genes. Flow cytometry was used to analyze the macrophage types, and the therapeutic effects of tranilast were estimated by echocardiographic analysis and Masson's trichrome stain. We demonstrated that AMI induced the activation of NLRP3 inflammasome in the heart tissues of mice with AMI. Tranilast decreased the expression of interleukin-1β and cleaved caspase-1 in bone marrow-derived macrophages and thus re-educated M1-macrophages toward the M2-phenotype both in vitro and in vivo. Tranilast inhibited the activation in the heart tissues of AMI mice and thus improved cardiac functional recovery in the AMI mouse model. In conclusion, we revealed that tranilast ameliorated myocardial infarction by inhibiting NLRP3 inflammasome and re-educating macrophage phenotype in this study.

Evaluation of strain parameters during stress-echocardiography with physical exercise may be significant in detecting severe coronary artery disease

Abstract Funding Acknowledgements Type of funding sources: None. Background. Assessment of the left ventricular strain during speckle-tracking stress echocardiography may be significant in diagnosing transient myocardial ischemia. So it is challenging to evaluate left ventricular global longitudinal strain (GLS) and post-systolic shortening indicators during stress-echocardiography and compare their diagnostic value with the data obtained with invasive methods of diagnosing coronary artery disease (CAD). Aim of the study. The aim of this study was to determine the diagnostic capabilities of the left ventricular GLS, delta GLS, left ventricular post-systolic index (PSI) and post-systolic time (PST) obtained during stress echocardiography with exercise on the treadmill in defining the presence and significance of CAD. Methods. The study included 113 patients (mean age 64.8 ± 9.4 years; 43 females) with known or suspected CAD. All patients underwent stress echocardiography with exercise on the treadmill. At rest and after treadmill-test, all patients were measured for the values of left ventricular GLS, left ventricular PSI and PST using the AFI (Automated functional imaging) algorithm. The delta of the left ventricular GLS values was also counted. The delta of the left ventricular GLS values was counted as the difference of the left ventricular GLS values after the load and at rest. All patients underwent coronary angiography, assessment of the severity of CAD was counted according to the Gensini score. According to the results of coronary angiography, the patients were divided into 3 groups: 41 patients without CAD, 53 patients with moderate CAD (≤34 points on the Gensini score) and 19 patients with severe CAD (&amp;gt;35 points on the Gensini score). Results. In the group of patients with severe CAD, values of left ventricular GLS after the load significantly differed from the group of patients without CAD (16,1 compared with 20,3; p = 0,003) and from the group of patients with moderate CAD (16,1 compared with 19,4; p = 0,003). At rest GLS values didn’t differ significantly between all groups. Left ventricular GLS delta in the group of patients with severe CAD differed significantly with the group of patients without CAD (-1,8 compared with 1,3; p = 0,003) and with the group of patients with moderate CAD (-1,8 compared with 0,6; p = 0,03). Left ventricular PSI differed significantly between the group of patients with severe CAD and the group of patients without CAD after the load (8,4 compared with 5,1; p = 0,03) and at rest didn’t differ significantly. Left ventricular PST values didn’t differ significantly at rest and after the load in all groups. Conclusions. Strain parameters such as left ventricular GLS, left ventricular GLS delta and left ventricular PSI assessed during stress-echocardiography on the treadmill may be useful in identifying patients with severe CAD. Left ventricular PST didn’t show significance in identifying CAD.

Speckle Tracking Echocardiography: Early Predictor of Diagnosis and Prognosis in Coronary Artery Disease.

Echocardiography represents a first level technique for the evaluation of coronary artery disease (CAD) which supports clinicians in the diagnostic and prognostic workup of these syndromes. However, visual estimation of wall motion abnormalities sometimes fails in detecting less clear or transient myocardial ischemia and in providing accurate differential diagnosis. Speckle tracking echocardiography (STE) is a widely available noninvasive tool that could easily and quickly provide additive information over basic echocardiography, since it is able to identify subtle myocardial damage and to localize ischemic territories in accordance to the coronary lesions, obtaining a clear visualization with a “polar map” useful for differential diagnosis and management. Therefore, it has increasingly been applied in acute and chronic coronary syndromes using rest and stress echocardiography, showing good results in terms of prediction of CAD, clinical outcome, left ventricular remodeling, presence, and quantification of new/residual ischemia. The aim of this review is to illustrate the current available evidence on STE usefulness for the assessment and follow-up of CAD, discussing the main findings on bidimensional and tridimensional strain parameters and their potential application in clinical practice.

Prediction of the fact and degree of coronary artery disease using the processing of clinical and instrumental data by artificial intelligence

Aim of the study was to analyze the possibility of using neural network analysis to predict the severity of coronary bed lesion. The study was also designated to determine the performance and accuracy of the trained neural network model receiving input as the structured data and EGG images with the parameters and leads positioning differ from the training sample, and also to compare the efficiency of detecting transient myocardial ischemia with traditional diagnostic methods, such as 24-hour Holter monitoring, treadmill test. Neural network analysis of the available clinical, laboratory and instrumentation data allow to configure the network parameters for further prediction of coronary artery disease. The results obtained in the form of an AUC score allow to consider this method to be effective in the coronary artery disease diagnosis using recorded ECG tape with parameters and lead positioning differ from initial training sample. The efficiency of transient myocardial ischemia detection on the training sample of the trained neural network is higher in comparison with traditional diagnostic methods, such as 24-hour Holter monitoring, treadmill test.

Percutaneous Coronary Intervention in Anomalous Single Coronary Artery From the Anterior Right Sinus of Valsalva

An anomalous single coronary artery (SCA) is extremely rare with registry studies suggesting a prevalence of 0.014%-0.066%. SCA may be associated with symptomatic transient myocardial ischaemia, arrhythmias, and sudden cardiac death regardless of the presence of coronary atherosclerosis.

Safety and Effectiveness of Volumetric Computed Tomography of the Heart in Combination with a PharmacologicaTest with Adenosine Triphosphate in the Diagnosis of Coronary Heart Disease

Aim To evaluate safety and efficacy of sodium adenosine triphosphate (ATP) as a vasodilator in assessment of left ventricular (LV) myocardial perfusion and in verification of ischemia by cardiac volumetric computed tomography (CT).Material and methods The study included 58 patients with suspected ischemic heart disease (IHD). For all included patients, cardiac volumetric CT with a pharmacological ATP test was performed. The rate of adverse effects was analyzed during the ATP infusion. Results of the study were compared with data from using other noninvasive methods for IHD diagnosis by calculating Cohen's kappa, the measure of agreement between two variables.Results The test performed during CT showed good tolerability of the ATP infusion, a low rate of moderate adverse reactions (8.6 %), and the absence of severe side effects. Results of diagnosing IHD with cardiac volumetric CT with the ATP pharmacological test were comparable with data from using other methods for noninvasive verification of LV myocardial ischemia (bicycle ergometry, treadmill test, stress echocardiography) in combination with coronarography or CT coronarography.Conclusion ATP appears a safe pharmacological agent for diagnosing transient LV myocardial ischemia. ATP can be recommended as a vasodilator for evaluation of perfusion using cardiac volumetric CT.

Coronary vasospasm-induced syncope with dynamic changes of regional wall motion abnormalities confirmed real-time: a case report.

BackgroundCoronary vasospasm is primarily characterized by transient and reversible vasoconstriction causing myocardial ischaemia and can manifest with various clinical features, including syncope.Case summaryA 50-year-old man presented with recurrent episodes of syncope for 3 days. The last syncope history occurred during an early morning walk, accompanied by dizziness and loss of consciousness. There was no clear history of chest pain at the time. He smoked one pack of cigarettes daily and frequently consume alcohol. Approximately 3 h after admission, echocardiography initially revealed normal systolic function; however, during the examination, the patient suddenly complained of dizziness and regional wall motion abnormalities (RWMA) of the left anterior descending artery (LAD) territory were observed. Both RWMA and dizziness spontaneously improved within a few minutes. Emergency coronary angiography (CAG) was performed to confirm vasospasm. Coronary angiography revealed mild atherosclerosis of proximal LAD. After 3 min, he complained of dizziness and vague chest discomfort, and electrocardiogram revealed ST-segment elevation. We immediately performed angiography of the left coronary artery, and CAG revealed total occlusion of the proximal LAD without any provocation. After administration of intracoronary nitroglycerine, coronary flow was restored completely and ST-segment deviation normalized along with relief in chest discomfort. The patient’s symptoms have not recurred for 3 months while being on calcium channel blocker and long-acting nitrates.DiscussionCoronary vasospasm can present as transient and dynamic myocardial ischaemia along with angina. Coronary vasospasm should always be considered in the differential diagnosis for syncope.

Old unsolved problems: when and how to treat silent ischaemia.

Silent myocardial ischaemia (SMI) is defined as objective evidence of ischaemia without angina (or equivalent symptoms) in the presence of coronary artery disease, differing from silent coronary artery disease. Silent myocardial ischaemia represents the majority of episodes of myocardial ischaemia at Holter monitoring. During transient myocardial ischaemia, the symptoms appear after the contraction anomalies of the left ventricle and after the ECG changes. The cause of silent myocardial ischaemia is still not well established. The severity and duration of ischaemia have been theorized as important elements in the SMI mechanism. Another possible mechanism responsible for SMI is represented by changes in the perception of painful stimuli with an increased pain threshold. Finally, a neuronal dysfunction of the diabetic, in post-infarction or a cardiac neuronal ‘stunning’ could play a role in SMI. In the pre-stent era, the SMI was associated with a worse prognosis. In patients with diabetes mellitus, SMI seems to be more represented because autonomic dysfunction is present in this category of patients. In conclusion, SMI is more frequent than symptomatic ischaemia. However, despite the presence of countless studies on the subject, it is not clear today whether medical therapy has equalized the risk and what the real prognosis of SMI is.

Extracellular miR-146a-5p Induces Cardiac Innate Immune Response and Cardiomyocyte Dysfunction.

Previous studies have demonstrated that transient myocardial ischemia leads to release of cellular nucleic acids such as RNA. Extracellular RNA reportedly plays a pivotal role in myocardial inflammation and ischemic injury in animals. RNA profiling has identified that numerous microRNA (miRNAs), such as ss-miR-146a-5p, are upregulated in plasma following myocardial ischemia, and certain uridine-rich miRNAs exhibit strong proinflammatory effects in immune cells via ssRNA-sensing mechanism. However, the effect of extracellular miRNAs on myocardial inflammation and cardiac cell function remains unknown. In this study, we treated adult mouse cardiomyocytes with miR-146a-5p loaded in extracellular vesicles and observed a dose- and TLR7-dependent production of CXCL-2, IL-6, and TNF-α. In vivo, a single dose of myocardial injection of miR-146a-5p induced both cytokine expression (CXCL2, IL-6, and TNF-α) and innate immune cell activation (CD45+ leukocytes, Ly6Cmid+ monocytes, Ly6G+ neutrophils), which was significantly attenuated in the hearts of TLR7 KO mice. We discovered that conditioned media from miR-146a-treated macrophages stimulated proinflammatory cytokine production in adult cardiomyocytes and significantly inhibited their sarcomere shortening. Finally, using an electric cell impedance-sensing assay, we found that the conditioned media from miR-146a-treated cardiac fibroblasts or cardiomyocytes impaired the barrier function of coronary artery endothelial cells. Taken together, these data demonstrate that extracellular miR-146a-5p activates multiple cardiac cells and induces myocardial inflammation and cardiomyocyte dysfunction via intercellular interaction and innate immune TLR7 nucleic acid sensing.