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Introduction: Acute coronary syndromes (ACS) encompass a spectrum of clinical conditions that result from a sudden occlusion or severe narrowing of the coronary arteries, leading to myocardial ischemia. Early and accurate diagnosis of ACS is critical to improv e patient outcomes. The frontal QRS-T angle, a parameter measured on the electrocardiogram (ECG), has been proposed as a potential marker for cardiovascular events. This study aims to evaluate the effectiveness of the frontal QRS -T angle in differentiating between various subtypes of ACS (STEMI, non-STEMI, USAP) and stable angina pectoris (SAP). Materials and Methods: A prospective observational study was conducted on patients admitted to the emergency department between January 9, 2023, and January 3, 2024. The study population included patients diagnosed with ACS or SAP and a control group without cardiac pathology. The frontal QRS-T angle was calculated from 12-lead ECGs. Statistical analyses, including Kruskal -Wallis and ROC curve analysis, were performed to assess the diagnostic utility of the QRS-T angle. Results: The study included 169 patients, with a mean age of 61.96±13.90 yea rs. The frontal QRS-T angle was significantly higher in the STEMI group compared to other groups. ROC analysis demonstrated that the QRS-T angle could significantly differentiate between noncardiac patients and those with STEMI, non-STEMI, and USAP. The cutoff value for differentiating non-cardiac patients from those with STEMI was >30, with an AUC of 0.784, sensit ivity of 81.25%, and specificity of 66.67%. The frontal QRS-T angle was also significant in predicting mortality, with a cutoff value of 58.00, AUC of 0.825, sensitivity of 84.20%, and specificity of 72.00%. Conclusion: The frontal QRS-T angle is a significant marker for distinguishing between different ACS subtypes and non-cardiac patients. Its role in identifying STEMI and predicting mortality highlights its potential utility in clinical practice. Further studies are needed to validate these findings and explore the broader implications of the QRS-T angle in cardiovascular diagnosis and management. [ABSTRACT FROM AUTHOR]

Ventricular fibrillation (VF) in dogs is characterized by a rapid increase in its dominant frequency during the 1st minute of reperfusion followed by its decrease during the 2nd minute of reperfusion. The longer is ischemia in VF, the greater is the increase in dominant VF frequency during reperfusion. The 1st minute of reperfusion is characterized by a 1.2-fold increase in dominant VF frequency after 1-min ischemia in VF, by 1.4-fold increase after 2-min ischemia, by 2-fold increase after 3 min, and by 2.6-fold increase after 4-min ischemia. During the 2nd minute of reperfusion, the dominant VF frequency decreased by 1.1-1.3 times, and during 3rd-10th minutes of reperfusion, the dominant VF frequency is stabilized. [ABSTRACT FROM AUTHOR]

Ischemic events can culminate in acute myocardial infarction, which is generated by irreversible cardiac lesions that cannot be restored due to the limited regenerative capacity of the heart. Cardiac cell therapy aims to replace injured or necrotic cells with healthy and functional cells. Tissue engineering and cardiovascular regenerative medicine propose therapeutic alternatives using biomaterials that mimic the native extracellular environment and improve cellular and tissue functionality. This investigation evaluates the effect of thermosensitive hydrogels, and murine fetal ventricular cardiomyocytes encapsulated in thermosensitive hydrogels, on the contractile function of cardiomyocyte regeneration during an ischemic event. Chitosan and hydrolyzed collagen thermosensitive hydrogels were developed, and they were physically and chemically characterized. Likewise, their biocompatibility was evaluated through cytotoxicity assays by MTT, LDH, and their hemolytic capacity. The hydrogels, and cells inside the hydrogels, were used as an intervention for primary cardiomyocytes under hypoxic conditions to determine the restoration of the contractile capacity by measuring intracellular calcium levels and the expressions of binding proteins, such as a-actinin and connexin 43. These results evidence the potential of natural thermosensitive hydrogels to restore the bioelectrical functionality of ischemic cardiomyocytes. [ABSTRACT FROM AUTHOR]

Abstract Background Amiodarone-induced thyroid dysfunction (AIT) is a side-effect associated with the use of Amiodarone for the treatment of refractory arrythmias. Resulting hyperthyroidism can precipitate cardiac complications, including cardiac ischemia and myocardial infarction, although this has only been described in a few case reports. Case presentation We present here a clinical scenario involving a 66-year-old male Caucasian patient under Amiodarone for atrial fibrillation, who developed AIT. In the presence of dyspnea, multiple cardiovascular risk factors and ECG abnormalities, a transthoracic echocardiogram was performed, showing inferobasal hypokinesia. This led to further investigations through a cardiac PET-CT, where cardiac ischemia was suspected. Ultimately, the coronary angiography revealed no abnormalities. Nonetheless, these extensive cardiologic investigations led to a delay in initiating an emergency endovascular revascularization for acute-on-chronic left limb ischemia. Although initial treatment using Carbimazole was not successful after three weeks, the patient reached euthyroidism after completion of the treatment with Prednisone so that eventually thyroidectomy was not performed. Endovascular revascularization was finally performed after more than one month. Conclusions We discuss here cardiac abnormalities in patients with AIT, which may be due to relative ischemia secondary to increased metabolic demand during hyperthyroidism. Improvement of cardiac complications is expected through an optimal AIT therapy including medical therapy as the primary approach and, when necessary, thyroidectomy. Cardiac investigations in the context of AIT should be carefully considered and may not justify delaying other crucial interventions. If considered mandatory, diagnostic procedures such as coronary angiography should be preferred to functional testing.

Background and Aims: Curcumin has potential anti-inflammatory effects. The aim of this study was to investigate the protective effect of curcumin against cardiac ischemia -reperfusion injury in rats fed a high-fat diet. Materials and Methods: In this experimental study, male Wistar rats were divided into four groups: control (C), high-fat diet (H), curcumin 100 (HyperC100, 100 mg/kg) and curcumin 200 (HyperC200), with the last two groups receiving oral curcumin daily for 3 weeks. The rats were fed a high-fat diet for 7 weeks to induce obesity. After anesthesia, hearts were removed and placed on the Langendorff perfusion system andbegan beating. After 20 minutes of stabilization, 35 minutes of ischemia and 60 minutes of nutrient fluid reflux were performed. During this interval, ventricular (LV) functional indices including LVSP, LVDP, LVEDP and +dp/dt were recorded. The relative size of the infarction was measured by using 2,3,5-triphenyltetrazolium chloride staining. Results: Hyperlipidemia caused dysfunction with changes in ventricular parameters, but curcumin could to improve some LV contractile parameters such as systolic pressure and increase diastolic pressure (P≤0.05). Curcumin could not significantly reduce the infarct size. Conclusion: Curcumin may have an cardio protection effects against ischemia/reperfusion injury in normal and hyperlipidemic rats.

Background: Diagnosing ischemia in emergency department (ED) patients with suspected acute coronary syndrome (sACS) is challenging with equivocal disposition of intermediate risk patients. Objective: Compare sensitivity and specificity of magnetocardiography (MCG) versus standard of care (SOC) stress testing in diagnosing myocardial ischemia. Methods: Multicenter, prospective, observational cohort study. ED patients with sACS and HEART score ≥ 3 underwent 90 s noninvasive MCG to detect myocardial ischemia. Results were blinded to the patient's clinicians. MCGs were read independently by 3 physicians blinded to clinical data. Myocardial ischemia was ≥70 % epicardial coronary artery stenosis, revascularization within 30 days, or 30-day major adverse cardiac events (MACE). Time to first test (TTT) and patient satisfaction for MCG and SOC were compared. Results: Of enrolled patients (N = 390) (mean age 59 ± 12 years, 45 % female), 99 (25 %) underwent a non-invasive stress test: 42 (14 %) diagnosed with ischemia. MCG sensitivity was 66.7 % (50.5–80.4 %, 95 % CI) and specificity 57.1 % (50.0–63.3 %, 95 % CI) for detecting coronary ischemia. Noninvasive stress testing (stress echo, nuclear stress, and exercise stress) had the same sensitivity 66.7 % (95 % CI 29.9 % to 92.5 %) and a specificity of 89.9 % (95 % CI 81.7–95.3 %). Mean TTT was shorter for MCG, 3.18 h (SD 1.91) vs. SOC stress testing 22.71 (SD 15.23), p

Abstract Background Cardiovascular diseases (CVDs) are one of the main causes of death worldwide. Data on the effect of eggs consumption on the risk of CVDs are still unreliable. Therefore, this study aimed to investigate the association between CVDs and the consumption of eggs. Methods In this case-control study, the required data were extracted from the Prospective Epidemiologic Research Studies in Iran (PERSIAN) cohort in Sabzevar, Iran. A total of 4241 adults participated including 1535 patients with CVDs as the case group and 2706 healthy people as controls. Egg consumption was assessed using a valid food frequency questionnaire (FFQ). Results A significant association was observed between eggs consumption and stroke after adjustment for physical activity, body mass index (BMI), smoking, systolic blood pressure (SBP), diastolic blood pressure (DBP), using alcohol, lipid profile, diabetes, and the intake of energy, lipid, protein, carbohydrate, and cholestrol (OR:1.007, 95% CI:1.001–1.013, P = 0.03). No association was found between egg consumption with hypertension, cardiac ischemia, and myocardial infarction. Conclusions There was a significant association between the consumption of eggs and stroke. However, more studies are needed to examine the effect of eggs on CVDs.

Aim: to study the effect of reperfusion on the organized frequency-amplitude structure of ventricular fibrillation (VF) in the dog heart.Materials and methods. We conducted 4 experiments on 8 dogs. In each experiment, the isolated heart of one dog was perfused with the blood of the second (supporting) dog. In 4 experiments on an isolated artificially perfused heart, 6 episodes of 3 min ischemia and 10 min reperfusion of the heart were performed in VF (1–2 episodes of ischemia-reperfusion in one experiment). Each episode of 3 min ischemia in VF was preceded by a 10 min perfusion of the heart in VF. Ventricular electrogram was recorded during VF episodes. A frequencyamplitude (spectral) analysis of 1 sec segments of the electrogram was performed, and the proportion (in %) of 0.5–15 Hz frequency oscillations in 10 sec segments of the electrogram was determined in 6 episodes of perfusion, ischemia and reperfusion in VF (M±m, N=60). The VF frequency-amplitude structures during ischemia and reperfusion were compared with the stable VF frequency-amplitude structure during perfusion taken as the control. The nonparametric Welch criterion in the «The R Project for Statistical Computing» software environment was used to compare the VF parameters during perfusion, ischemia and reperfusion. Results. 9–10 Hz frequency oscillations dominated in the VF frequency-amplitude structure during heart perfusion, taken as the control. In the first 30 sec of ischemia, the frequency and amplitude of the dominant oscillations did not significantly change vs VF control obtained during cardiac perfusion. A decrease of dominant oscillations frequency up to 6.5–7.5 Hz, and of the proportion of oscillations — up to 26% was documented at the 3rd min of ischemia. At the 1st min of reperfusion, the frequency of dominant oscillations increased to 13.5–14.5 Hz, but the proportion of oscillations remained reduced to 26%, as at the 3rd min of ischemia. At the 2nd min of reperfusion, the frequency of dominant oscillations decreased to 9.5–10.5 Hz, and the proportion of dominant oscillations increased to 33%. The frequency and amplitude of the dominant oscillations stabilized at 3–10 min of reperfusion: oscillations at 9–10 Hz frequency accounted for 32–33% of the spectral power.Conclusion. Reperfusion in VF is characterized by transient destabilization of VF organized structure at the 1st min of the procedure. VF organized structure regains stabilization within 2–10 min of reperfusion. Cardiac perfusion in intentionally induced VF can be used instead of cardioplegia during major cardiac surgery to boost cardiac resistance to ischemia and prevent or reduce reperfusion complications.

Introduction. In recent years, the clinical and practical interest in malignant neoplasms and diseases of the cardiovascular system has been extremely high. These nosologies are the leading causes of hospitalisations and deaths worldwide.Objective. To assess the prevalence of coronary heart disease and risk factors among patients with newly diagnosed prostate cancer, as well as to identify their relationship with the severity of prostate cancer.Materials & methods. The study included 140 newly diagnosed prostate cancer (PCa) patients with a median age of 65 [62; 70] years. All patients had the level of prostate-specific antigen, pelvic MRI, prostate biopsy with determination of Gleason score, all patients filled out the questionnaire of the International Index of Erectile Function (IIEF-5). Depending on the presence of coronary heart disease (CHD), all patients were divided into two groups: Group 1 — 94 (67%) PCa patients without CHD; Group 2 — 46 (33%) PCa patients with CHDResults. In a comparative analysis, the groups did not differ in indicators such as age, BMI, prostate volume, incidence of diabetes mellitus type 2, and lipid status level. However, in PCa patients with CHD, erectile dysfunction was statistically significantly more pronounced than in patients without CHD (10 vs 18 IIEF5 points, p = 0.03), respectively. In terms of PSA levels, it turned out that in Group 2, this indicator was significantly higher than in Group 1 (15.8 ng/ml vs 10.1 ng/ml, p = 0.03), respectively, which indicates possibly more high malignancy of the process. Furthermore, in Group 2, patients with a high grade PCa according to the classification of The International Society of Urological Pathology (ISUP) 4 / 5 were statistically significantly more common compared to patients of Group 1 (12 (26%) vs. 10 (11%), p = 0.01), respectively. In a comparative analysis of patients depending on the risk of a possible PCa recurrence of , which was taken into account by such parameters as PSA level, Gleason index + ISUP grade, it turned out that in Group 2 there were statistically significantly more patients with a higher risk of PCa progression compared to Group 1 (20 (44%) vs 26 (28%), p = 0.02), respectively.Conclusion. PCa patients with concomitant CHD are characterized by a higher waist circumference, they had lower indicators of erectile function, a more pronounced comorbid background, and more often had a history of stroke. In addition, PCa patients with CHD had a high grade PCa and a higher risk of PCa progression.

Ischemic events can culminate in acute myocardial infarction, which is generated by irreversible cardiac lesions that cannot be restored due to the limited regenerative capacity of the heart. Cardiac cell therapy aims to replace injured or necrotic cells with healthy and functional cells. Tissue engineering and cardiovascular regenerative medicine propose therapeutic alternatives using biomaterials that mimic the native extracellular environment and improve cellular and tissue functionality. This investigation evaluates the effect of thermosensitive hydrogels, and murine fetal ventricular cardiomyocytes encapsulated in thermosensitive hydrogels, on the contractile function of cardiomyocyte regeneration during an ischemic event. Chitosan and hydrolyzed collagen thermosensitive hydrogels were developed, and they were physically and chemically characterized. Likewise, their biocompatibility was evaluated through cytotoxicity assays by MTT, LDH, and their hemolytic capacity. The hydrogels, and cells inside the hydrogels, were used as an intervention for primary cardiomyocytes under hypoxic conditions to determine the restoration of the contractile capacity by measuring intracellular calcium levels and the expressions of binding proteins, such as a-actinin and connexin 43. These results evidence the potential of natural thermosensitive hydrogels to restore the bioelectrical functionality of ischemic cardiomyocytes.

MicroRNAs are small non-coding post-translational biomolecules which, when expressed, modify their target genes. It is estimated that microRNAs regulate production of approximately 60% of all human proteins and enzymes that are responsible for major physiological processes. In cardiovascular disease pathophysiology, there are several cells that produce microRNAs, including endothelial cells, vascular smooth muscle cells, macrophages, platelets, and cardiomyocytes. There is a constant crosstalk between microRNAs derived from various cell sources. Atherosclerosis initiation and progression are driven by many pro-inflammatory and pro-thrombotic microRNAs. Atherosclerotic plaque rupture is the leading cause of cardiovascular death resulting from acute coronary syndrome (ACS) and leads to cardiac remodeling and fibrosis following ACS. MicroRNAs are powerful modulators of plaque progression and transformation into a vulnerable state, which can eventually lead to plaque rupture. There is a growing body of evidence which demonstrates that following ACS, microRNAs might inhibit fibroblast proliferation and scarring, as well as harmful apoptosis of cardiomyocytes, and stimulate fibroblast reprogramming into induced cardiac progenitor cells. In this review, we focus on the role of cardiomyocyte-derived and cardiac fibroblast-derived microRNAs that are involved in the regulation of genes associated with cardiomyocyte and fibroblast function and in atherosclerosis-related cardiac ischemia. Understanding their mechanisms may lead to the development of microRNA cocktails that can potentially be used in regenerative cardiology.

Aim. In an open-label clinical trial, to evaluate the effectiveness and impact on metabolic parameters of triple antihypertensive combination therapy with amlodipine, indapamide and perindopril arginine (perindopril A) in patients with hypertension (HTN) and stable coronary artery disease (CAD) in combination with abdominal obesity (AO), who have not had an adequate response to dual antihypertensive therapy for at least 4 weeks.Material and methods. The study included 68 adult patients aged 42 to 64 years (51 (47; 60) years) with AO, stable CAD and uncontrolled HTN, despite treatment with two drugs: an angiotensin-converting enzyme (ACE) inhibitor and a thiazide and thiazide-like diuretic. In the study, patients, in accordance with the general characteristics of the drug, after prescribing a free triple-dose combination of amlodipine, indapamide, perindopril in appropriate dosages, received one of the following combination of amlodipine/indapamide/perindopril for 24 weeks: group 1 (n=34) — 10/2,5/10 mg and group 2 (n=34) — 5/1,25/5 mg, one tablet daily. The analysis of the primary endpoint was to assess the change in mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) in the sitting position from baseline to 24 weeks. Secondary efficacy endpoints included the proportion of patients achieving target mean SBP and DBP values for this category in the sitting position of 120-130 mm Hg and 70-79 mm Hg, respectively, at 12, 16, 20 and 24 weeks. Safety was assessed throughout the study. The effect on metabolic parameters was assessed at 24 weeks of the study.Results. Sixty-seven (98,5%) patients completed the study. The mean decrease in blood pressure from the initial level (group 1159/96 mm Hg; group 2161/95 mm Hg) to 24 weeks (group 1 126/76 mm Hg; group 2 132/84 mm Hg) was significant (p

Background Cardiovascular diseases (CVDs) are one of the main causes of death worldwide. Data on the effect of eggs consumption on the risk of CVDs are still unreliable. Therefore, this study aimed to investigate the association between CVDs and the consumption of eggs. Methods In this case-control study, the required data were extracted from the Prospective Epidemiologic Research Studies in Iran (PERSIAN) cohort in Sabzevar, Iran. A total of 4241 adults participated including 1535 patients with CVDs as the case group and 2706 healthy people as controls. Egg consumption was assessed using a valid food frequency questionnaire (FFQ). Results A significant association was observed between eggs consumption and stroke after adjustment for physical activity, body mass index (BMI), smoking, systolic blood pressure (SBP), diastolic blood pressure (DBP), using alcohol, lipid profile, diabetes, and the intake of energy, lipid, protein, carbohydrate, and cholestrol (OR:1.007, 95% CI:1.001-1.013, P=0.03). No association was found between egg consumption with hypertension, cardiac ischemia, and myocardial infarction. Conclusions There was a significant association between the consumption of eggs and stroke. However, more studies are needed to examine the effect of eggs on CVDs. [ABSTRACT FROM AUTHOR]

Numerous physiological and pathological roles have been attributed to the formation of mitochondrial reactive oxygen species (ROS). However, the individual contribution of different mitochondrial processes independently of bioenergetics remains elusive and clinical treatments unavailable. A notable exception to this complexity is found in the case of monoamine oxidases (MAOs). Unlike other ROS-producing enzymes, especially within mitochondria, MAOs possess a distinct combination of defined molecular structure, substrate specificity, and clinically accessible inhibitors. Another significant aspect of MAO activity is the simultaneous generation of hydrogen peroxide alongside highly reactive aldehydes and ammonia. These three products synergistically impair mitochondrial function at various levels, ultimately jeopardizing cellular metabolic integrity and viability. This pathological condition arises from exacerbated MAO activity, observed in many cardiovascular diseases, thus justifying the exploration of MAO inhibitors as effective cardioprotective strategy. In this context, we not only summarize the deleterious roles of MAOs in cardiac pathologies and the positive effects resulting from genetic or pharmacological MAO inhibition, but also discuss recent findings that expand our understanding on the role of MAO in gene expression and cardiac development. [ABSTRACT FROM AUTHOR]

MicroRNAs are small non-coding post-translational biomolecules which, when expressed, modify their target genes. It is estimated that microRNAs regulate production of approximately 60% of all human proteins and enzymes that are responsible for major physiological processes. In cardiovascular disease pathophysiology, there are several cells that produce microRNAs, including endothelial cells, vascular smooth muscle cells, macrophages, platelets, and cardiomyocytes. There is a constant crosstalk between microRNAs derived from various cell sources. Atherosclerosis initiation and progression are driven by many pro-inflammatory and pro-thrombotic microRNAs. Atherosclerotic plaque rupture is the leading cause of cardiovascular death resulting from acute coronary syndrome (ACS) and leads to cardiac remodeling and fibrosis following ACS. MicroRNAs are powerful modulators of plaque progression and transformation into a vulnerable state, which can eventually lead to plaque rupture. There is a growing body of evidence which demonstrates that following ACS, microRNAs might inhibit fibroblast proliferation and scarring, as well as harmful apoptosis of cardiomyocytes, and stimulate fibroblast reprogramming into induced cardiac progenitor cells. In this review, we focus on the role of cardiomyocyte-derived and cardiac fibroblast-derived microRNAs that are involved in the regulation of genes associated with cardiomyocyte and fibroblast function and in atherosclerosis-related cardiac ischemia. Understanding their mechanisms may lead to the development of microRNA cocktails that can potentially be used in regenerative cardiology. [ABSTRACT FROM AUTHOR]

Stem cell therapy provides a hope to no option heart disease patient group. Stem cells work via different mechanisms of which paracrine mechanism is reported to justify most of the effects. Therefore, identifying the control arms for paracrine cocktail production is necessary to tailor stem cell functions in disease contextual manner. In this study, we describe a novel paracrine cocktail regulatory axis, in stem cells, to enhance their cardioprotective abilities. We identified that HSF1 knockout resulted in reduced cardiac regenerative abilities of mesenchymal stem cells (MSCs) while its overexpression had opposite effects. Altered exosome biognesis and their miRNA cargo enrichment were found to be underlying these altered regenerative abilities. Decreased production of exosomes by MSCs accompanied their loss of HSF1 and vice versa. Moreover, the exosomes derived from HSF1 depleted MSCs showed significantly reduced candidate miRNA expression (miR-145, miR-146, 199-3p, 199b and miR-590) compared to those obtained from HSF1 overexpressing MSCs. We further discovered that HSF1 mediates miRNAs' enrichment into exosomes via Y binding protein 1 (YBX1) and showed, by loss and gain of function strategies, that miRNAs' enrichment in mesenchymal stem cell derived exosomes is deregulated with altered YBX1 expression. It was finally demonstrated that absence of YBX1 in MSCs, with normal HSF1 expression, resulted in significant accumulation of candidate miRNAs into the cells. Together, our data shows that HSF1 plays a critical role in determining the regenerative potential of stem cells. HSF1 does that by affecting exosome biogenesis and miRNA cargo sorting via regulation of YBX1 gene expression. [ABSTRACT FROM AUTHOR]

Background and Aims: Curcumin has potential anti-inflammatory effects. The aim of this study was to investigate the protective effect of curcumin against cardiac ischemia -reperfusion injury in rats fed a high-fat diet. Materials and Methods: In this experimental study, male Wistar rats were divided into four groups: control (C), high-fat diet (H), curcumin 100 (HyperC100, 100 mg/kg) and curcumin 200 (HyperC200), with the last two groups receiving oral curcumin daily for 3 weeks. The rats were fed a high-fat diet for 7 weeks to induce obesity. After anesthesia, hearts were removed and placed on the Langendorff perfusion system andbegan beating. After 20 minutes of stabilization, 35 minutes of ischemia and 60 minutes of nutrient fluid reflux were performed. During this interval, ventricular (LV) functional indices including LVSP, LVDP, LVEDP and +dp/dt were recorded. The relative size of the infarction was measured by using 2,3,5-triphenyltetrazolium chloride staining. Results: Hyperlipidemia caused dysfunction with changes in ventricular parameters, but curcumin could to improve some LV contractile parameters such as systolic pressure and increase diastolic pressure (P≤0.05). Curcumin could not significantly reduce the infarct size. Conclusion: Curcumin may have an cardio protection effects against ischemia/reperfusion injury in normal and hyperlipidemic rats. [ABSTRACT FROM AUTHOR]

A blockage of the blood vessels feeding the area causes ischemia, which is defined as a localized absence of blood flow. If an organ is not getting enough oxygen and blood flow, such as the heart, or brain it is said to be ischemic. To describe the progress made in the detection, characterization, and prediction of cardiac ischemia using Machine Learning (ML)-based Artificial Intelligence (AI) processes including together Single Photon Emission Computed Tomography (SPECT) and Positron Emission Tomography (PET). In the relatively recent past, the use of machine learning algorithms in the area of cardiology has increasingly centered on image processing for the goals of diagnosis, prognosis, and type identification analysis. The main objective of this study was to Improve Nuclear Cardiology (NC) Images for cardiac ischemia Patients using Image Processing Techniques. Clinical research is being significantly changed by the application of AI. By the examination of very big datasets and the recent convergence of potent ML algorithms and rising computer capacity, it has been shown that experimental categorization as well as prediction may be improved through examining extremely highdimensional non-linear features. Machine learning is improving the identification of perfusion abnormalities in myocardial ischemia and predicting adverse cardiovascular events at the patient level. [ABSTRACT FROM AUTHOR]

Objective: To investigate the therapeutic effects of supplemental oxygen on patients with myocardial infarction. Methods: This study was a randomized, double-blind clinical trial. The study population included all patients who were admitted to the emergency room of Ali-ibn-Abitaleb and Khatam-al-Anbia hospitals in Zahedan within six hours of the onset of classic symptoms of myocardial infarction. The patients (n=47) were divided into two groups: the case group (with oxygen therapy) and the control group (without oxygen therapy). The initial follow-up was evaluated after one month and the second follow-up was evaluated after three months in the target population in terms of mortality caused by acute myocardial infarction, mortality caused by any other cause, and re-hospitalization caused by acute myocardial infarction. Results: Out of the 47 patients, 27 were male (57.4%). The average age of the patients was (60.9±8.1) years. One month after admission, 2 patients (8.7%) in the case group and 2 patients (8.3%) in the control group died due to acute myocardial infarction. A total of 7 patients (14.9%) died three months after admission. There was no significant difference between the control and case groups in terms of mortality caused by acute ischemia within one and three months. After one month, 2 patients (8.7%) in the case group and 1 patient (4.2%) in the control group died of other causes. After three months, 4 patients (8.5%) in total died for other causes. There was no significant difference between the control and case groups in terms of mortality due to other causes within one and three months. One month after admission, 5 patients (21.7%) of the case group and 4 patients (16.7%) of the control group were re-hospitalized due to acute myocardial ischemia. During the next three months, 3 patients (13.0%) of the case group and 5 patients (20.8%) of the control group were re-hospitalized. There was no significant difference between the control and case groups regarding the rate of re-hospitalization caused by acute myocardial infarction within one and three months after admission. Conclusions: There is no significant relationship between oxygen therapy and death by acute myocardial ischemia, or any other causes. The relationship between oxygen therapy and the rate of re-hospitalization caused by acute myocardial ischemia is not found within one and three months after admission. The results show that oxygen therapy does not affect patients with acute myocardial ischemia within three months after admission.

Abstract Paclitaxel-induced cardiac ischemia is a rare but life-threatening complication. Although it may be difficult to distinguish from hypersensitivity or infusion reactions, it should not be overlooked. We herein report a rare case of ST-segment elevation following the administration of paclitaxel for uterine cervical cancer and review the literature regarding paclitaxel-induced cardiac ischemia. A 48-year-old woman with uterine cervical cancer with no cardiovascular risk factors was admitted to our hospital for concurrent chemoradiotherapy (CCRT) and planned to receive weekly paclitaxel and carboplatin for a total of 5 weeks. Just after the completion of the first cycle of paclitaxel infusion, she presented with diaphoresis and her consciousness level decreased. Electrocardiography showed ST elevation, suggesting acute myocardial infarction. Laboratory testing revealed troponin I positivity. Emergency coronary angiography (CAG) revealed a normal coronary artery, suggesting paclitaxel-induced vasospasm. After CAG, the patient was hemodynamically stable and was returned to the gynecologic unit two days after CAG. CCRT without paclitaxel was continued and the patient was uneventfully discharged from hospital.

The present study hypothesizes that the ischemic insults activate epicardial adipose tissue-derived stem cells (EATDS) to secrete extracellular vesicles (EVs) packed with regenerative mediators to alter the gene expression in cardiac fibroblasts (CF). EATDS and CF were isolated from hyperlipidemic microswine and EVs were harvested from control, simulated ischemia (ISC) and ischemia-reperfusion (ISC/R) groups. The in vitro interaction between ISC-EVs and CF resulted in the upregulation of cardiomyocyte-specific transcription factors including GATA4, Nkx2.5, IRX4, and TBX5 in CF and the healing marker αSMA and the downregulation of fibroblast biomarkers such as vimentin, FSP1, and podoplanin and the cardiac biomarkers such as troponin-I and connexin-43. These results suggest a cardiomyocyte-like phenotype as confirmed by immunostaining and Western blot. The LC-MS/MS analysis of ISC-EVs LGALS1, PRDX2, and CCL2 to be the potent protein mediators which are intimately involved in versatile regenerative processes and connected with a diverse array of regenerative genes. Moreover, the LGALS1+, PRDX2+, and CCL2+ EATDS phenotypes were deciphered at single cell resolution revealing corresponding sub-populations with superior healing potential. Overall, the findings unveiled the healing potential of EATDS-derived EVs and sub-populations of regenerative EATDS promising novel translational opportunities in improved cardiac healing following ischemic injury. [ABSTRACT FROM AUTHOR]

Objective: To investigate the therapeutic effects of supplemental oxygen on patients with myocardial infarction. Methods: This study was a randomized, double-blind clinical trial. The study population included all patients who were admitted to the emergency room of Ali-ibn-Abitaleb and Khatam-al-Anbia hospitals in Zahedan within six hours of the onset of classic symptoms of myocardial infarction. The patients (n=47) were divided into two groups: the case group (with oxygen therapy) and the control group (without oxygen therapy). The initial follow-up was evaluated after one month and the second follow-up was evaluated after three months in the target population in terms of mortality caused by acute myocardial infarction, mortality caused by any other cause, and rehospitalization caused by acute myocardial infarction. Results: Out of the 47 patients, 27 were male (57.4%). The average age of the patients was (60.9±8.1) years. One month after admission, 2 patients (8.7%) in the case group and 2 patients (8.3%) in the control group died due to acute myocardial infarction. A total of 7 patients (14.9%) died three months after admission. There was no significant difference between the control and case groups in terms of mortality caused by acute ischemia within one and three months. After one month, 2 patients (8.7%) in the case group and 1 patient (4.2%) in the control group died of other causes. After three months, 4 patients (8.5%) in total died for other causes. There was no significant difference between the control and case groups in terms of mortality due to other causes within one and three months. One month after admission, 5 patients (21.7%) of the case group and 4 patients (16.7%) of the control group were re-hospitalized due to acute myocardial ischemia. During the next three months, 3 patients (13.0%) of the case group and 5 patients (20.8%) of the control group were re-hospitalized. There was no significant difference between the control and case groups regarding the rate of re-hospitalization caused by acute myocardial infarction within one and three months after admission. Conclusions: There is no significant relationship between oxygen therapy and death by acute myocardial ischemia, or any other causes. The relationship between oxygen therapy and the rate of rehospitalization caused by acute myocardial ischemia is not found within one and three months after admission. The results show that oxygen therapy does not affect patients with acute myocardial ischemia within three months after admission. [ABSTRACT FROM AUTHOR]

IntroductionIn this study, a new probe was designed to enable electrocardiography of a rotated heart during cardiac surgery when skin electrodes became non-functional. This probe adhered non-invasively to the epicardium and collected the ECG signal independently from the position of the heart. The study compared the accuracy of cardiac ischemia detection between classic skin and epicardial electrodes in an animal model.MethodsUsing six pigs, an open chest model was devised with cardiac ischemia induction by coronary artery ligation in two non-physiologic heart positions. Both the accuracy and the time of detection of electrocardiographic symptoms of acute cardiac ischemia were compared between skin and epicardial methods of signal collection.ResultsHeart rotation to expose either the anterior or the posterior wall resulted in a distortion or loss of the ECG signal collected by skin electrodes after coronary artery ligation, standard skin ECG monitoring did not reveal any ischemia symptoms. Attachment of an epicardial probe on the anterior and posterior walls helped in the recovery of the normal ECG wave. After ligation of the coronary artery, the epicardial probes recorded cardiac ischemia within 40 s.DiscussionThis study highlighted the effectiveness of ECG monitoring with epicardial probes in a rotated heart. It can be concluded that epicardial probes can detect the presence of acute ischemia of a rotated heart when skin ECG monitoring becomes ineffective.

Coronary artery disease (CAD) is the number one cause of death in the United States, and it is estimated that every 40 seconds one person experiences a heart attack. Among patients with chronic CAD, many will experience a potentially fatal complication known as acute coronary syndrome (ACS). Wellens syndrome is a rare form of ACS that indicates critical left anterior descending coronary artery occlusion and can be identified by its characteristic T-wave patterns on ECG. This syndrome also may go unrecognized by clinicians because of a lack of familiarity with the ECG findings. This article describes the Wellens ECG pattern and its significance in patients with chest pain. [ABSTRACT FROM AUTHOR]

Myocardial regenerative strategies are promising where the choice of ideal cell population is crucial for successful translational applications. Herein, we explored the regenerative/repair responses of infarct zone cardiac fibroblast(s) (CF) by unveiling their phenotype heterogeneity at single-cell resolution. CF were isolated from the infarct zone of Yucatan miniswine that suffered myocardial infarction, cultured under simulated ischemic and reperfusion, and grouped into control, ischemia, and ischemia/reperfusion. The single-cell RNA sequencing analysis revealed 19 unique cell clusters suggesting distinct subpopulations. The status of gene expression (log2 fold change (log2 FC) > 2 and log2 FC < −2) was used to define the characteristics of each cluster unveiling with diverse features, including the pro-survival/cardioprotective (Clusters 1, 3, 5, 9, and 18), vasculoprotective (Clusters 2 and 5), anti-inflammatory (Clusters 4 and 17), proliferative (Clusters 4 and 5), nonproliferative (Clusters 6, 8, 11, 16, 17, and 18), proinflammatory (Cluster 6), profibrotic/pathologic (Clusters 8 and 19), antihypertrophic (Clusters 8 and 10), extracellular matrix restorative (Clusters 9 and 12), angiogenic (Cluster 16), and normal (Clusters 7 and 15) phenotypes. Further understanding of these unique phenotypes of CF will provide significant translational opportunities for myocardial regeneration and cardiac management. [ABSTRACT FROM AUTHOR]

Human P2Y4 is a UTP receptor, while in mice it is activated by both ATP and UTP. P2Y4 knockout (KO) in mice protects against myocardial infarction and is characterized by increased adiponectin secretion by adipocytes, and decreased cardiac inflammation and permeability under ischemic conditions. The relevance of these data has, however, not been explored to date in humans. In a population study comprising 50 patients with coronary artery disease (CAD) and 50 age-matched control individuals, we analyzed P2RY4 mutations and their potential association with CAD severity and fasting plasma parameters. Among the mutations identified, we focused our attention on a coding region polymorphism (rs3745601) that results in replacement of the asparagine at residue 178 with threonine (N178T) located in the second extracellular loop of the P2Y4 receptor. The N178T variant is a loss-of-function mutation of the human P2Y4 receptor and is encountered less frequently in coronary patients than in control individuals. In coronary patients, carriers of the N178T variant had significantly reduced jeopardy and Gensini cardiac severity scores, as well as lower resting heart rates and plasma levels of N-terminal pro-brain natriuretic peptide (NT-proBNP). Regarding fasting plasma parameters, the N178T variant was associated with a lower concentration of glucose. Accordingly, P2Y4 KO mice had significantly improved glucose tolerance and insulin sensitivity compared with their WT littermate controls. The improvement of insulin sensitivity resulting from lack of the P2Y4 receptor was no longer observed in the absence of adiponectin. The present study identifies a frequent loss-offunction P2Y4 variant associated with less severe coronary artery atherosclerosis and lower fasting plasma glucose in coronary patients. The role of the P2Y4 receptor in glucose homeostasis was confirmed in mouse. P2Y4 antagonists could thus have therapeutic applications in the treatment of myocardial infarction and type 2 diabetes. [ABSTRACT FROM AUTHOR]

Disclaimer. The EAC Guidelines represent the views of the EAC, and were produced after careful consideration of the scientific and medical knowledge, and the evidence available at the time of their publication. The EAC is not responsible in the event of any contradiction, discrepancy, and/or ambiguity between the EAC Guidelines and any other official recommendations or guidelines issued by the relevant public health authorities, in particular in relation to good use of healthcare or therapeutic strategies. Health professionals are encouraged to take the EAC Guidelines fully into account when exercising their clinical judgment, as well as in the determination and the implementation of preventive, diagnostic, or therapeutic medical strategies; however, the EAC Guidelines do not override, in any way whatsoever, the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of each patient’s health condition and in consultation with that patient and, where appropriate and/or necessary, the patient’s caregiver. Nor do the EAC Guidelines exempt health professionals from taking into full and careful consideration the relevant official updated recommendations or guidelines issued by the competent public health authorities, in order to manage each patient’s case in light of the scientifically accepted data pursuant to their respective ethical and professional obligations. It is also the health professional’s responsibility to verify the applicable rules and regulations relating to drugs and medical devices at the time of prescription.

The purpose of the research was exploration of the impact of the conventional treatment in combination with simvastatin and iodine-containing pumpkin oil “Fortuna vita” on the values of lipid metabolism in cardiac ischemia patients residing in the setting of iodine deficit. The patients were divided into 2 groups: group 1– patients underwent conventional treatment with application of simvastatin of 20mg/day during the whole course of observation; group 2 – same treatment in combination with iodine-containing pumpkin oil “Fortuna vita” of 10ml/day, which contains 200μg of organically combined iodine form. The level of total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL cholesterol) and lowdensity lipoprotein cholesterol (LDL cholesterol) in serum, and aspartate aminotransferase and alanine aminotrasferase in patients before treatment, after 10 days, and after 1 month of treatment was measured. It was determined, that simvastatin is an effective and safe cholesterol-reducing preparation for cardiac ischemia patients which results in reduction of cholesterol level by 18% and LDL by 23% in one month. A combination of simvastatin and iodine-containing pumpkin oil appears more effective, probably because of potentiation of their effects, which also facilitate growth of antiatherogenic HDL and consequently decrease the atherogenicity coefficient. The general clinical state of both groups improved as a result of the treatment, though more so for the patients treated in combination with iodine-containing pumpkin oil. We are inclined to explain this fact by normalization of iodine-thyroid status, and consequently, of the general metabolism of the patients in the setting of ecologic iodine deficit because of iodine-containing fatty acids.

Objective: Inflammatory markers are among the possible contributing factors with a proposed role in hepatic and ischemic heart disease. The present study aimed to determine the association between high-sensitivity-C-reactive protein (hs-CRP), liver elastography, and cardiac ischemic diseases in patients with fatty liver. Methods: In this cross-sectional comparative study, 103 consecutive patients with fatty liver were enrolled to undergo angiography. They were divided into groups with and without cardiac ischemia. Results: The results demonstrated that the mean hs-CRP was 2.3 and 10.9 mg/L in normal and ischemic angiography groups, respectively (P = 0.001). According to the receiver operating characteristic (ROC) analysis, the predictive role for hs-CRP was 94.5% that had sensitivity and specificity of 95.2% and 90%, respectively, with a cut-off point of 3.1. Conclusion: This study showed that there is an association between the fatty liver, cardiac ischemia, and hs-CRP level.

Human P2Y4 is a UTP receptor, while in mice it is activated by both ATP and UTP. P2Y4 knockout (KO) in mice protects against myocardial infarction and is characterized by increased adiponectin secretion by adipocytes, and decreased cardiac inflammation and permeability under ischemic conditions. The relevance of these data has, however, not been explored to date in humans. In a population study comprising 50 patients with coronary artery disease (CAD) and 50 age-matched control individuals, we analyzed P2RY4 mutations and their potential association with CAD severity and fasting plasma parameters. Among the mutations identified, we focused our attention on a coding region polymorphism (rs3745601) that results in replacement of the asparagine at residue 178 with threonine (N178T) located in the second extracellular loop of the P2Y4 receptor. The N178T variant is a loss-of-function mutation of the human P2Y4 receptor and is encountered less frequently in coronary patients than in control individuals. In coronary patients, carriers of the N178T variant had significantly reduced jeopardy and Gensini cardiac severity scores, as well as lower resting heart rates and plasma levels of N-terminal pro-brain natriuretic peptide (NT-proBNP). Regarding fasting plasma parameters, the N178T variant was associated with a lower concentration of glucose. Accordingly, P2Y4 KO mice had significantly improved glucose tolerance and insulin sensitivity compared with their WT littermate controls. The improvement of insulin sensitivity resulting from lack of the P2Y4 receptor was no longer observed in the absence of adiponectin. The present study identifies a frequent loss-of-function P2Y4 variant associated with less severe coronary artery atherosclerosis and lower fasting plasma glucose in coronary patients. The role of the P2Y4 receptor in glucose homeostasis was confirmed in mouse. P2Y4 antagonists could thus have therapeutic applications in the treatment of myocardial infarction and type 2 diabetes.

Background and Objectives: Myocardial ischemia is one of the leading causes deaths among cardiac pathological conditions. Doxorubicin belongs to anthracycline class of drug which is effective against a wide variety of neoplasms. However, doxorubicininduced cardiotoxicity limits the clinical utility of the drug. One of the major causes of myocardial ischemia is oxidative stress. Adhatoda vasica have been shown to possess strong anti-inflammatory during ischemia reperfusion injury induced by doxorubicin in zebrafish model. Materials and Methods: Cardiac ischemia was induced in Zebrafish using doxorubicin. Adhatoda vasica was further supplemented and the antioxidants enzymes were analysed. Zebrafish was also infected with MRSA and the anti-microbial activity of A. vasica was analysed. Results: Supplementation with Adhatoda vasica extract to doxorubicin reduces the oxidative stress induced by doxorubicin through improvement of catalase, superoxide dismutase and GSH activities and subsequently reduces lipid peroxidation. Doxorubicin mediated inflammatory response in cardiac tissue is neutralized by supplementation with Adhatoda vasica plant extract and improves the cardiac tissue architecture. A. vasica plant extract is effective against inhibiting the growth of MRSA which has been shown to cause serious complications during cardiac surgery and cardiac prosthetic implantation. A. vasica plant extract causes a dose-dependent suppression of virulence gens such as spA and m ecA. Conclusion: Therefore, A. vasica extract may be useful in controlling microbial infections during cardiac complications. In conclusion, the present study indicates that A. vasica can be useful during cardiac complications. [ABSTRACT FROM AUTHOR]

Objective: Inflammatory markers are among the possible contributing factors with a proposed role in hepatic and ischemic heart disease. The present study aimed to determine the association between high-sensitivity-C-reactive protein (hs-CRP), liver elastography, and cardiac ischemic diseases in patients with fatty liver. Methods: In this cross-sectional comparative study, 103 consecutive patients with fatty liver were enrolled to undergo angiography. They were divided into groups with and without cardiac ischemia. Results: The results demonstrated that the mean hs-CRP was 2.3 and 10.9 mg/L in normal and ischemic angiography groups, respectively (P = 0.001). According to the receiver operating characteristic (ROC) analysis, the predictive role for hs-CRP was 94.5% that had sensitivity and specificity of 95.2% and 90%, respectively, with a cut-off point of 3.1. Conclusion: This study showed that there is an association between the fatty liver, cardiac ischemia, and hs-CRP level. [ABSTRACT FROM AUTHOR]

Bergapten (BeG) is explored for its anti‐inflammatory and antioxidant properties. Myocardial infarction (MI) is reported to be one of the leading cardiovascular diseases characterized by mitochondrial dysfunction and apoptosis. The main purpose of this study is to assess the cardiopreventive effects of BeG (50 mg/kg) in isoproterenol (ISO)‐induced MI in Wistar rats. The increased infarct size after ISO induction was reduced simultaneously on treatment with BeG. Similarly, augmented levels of cardiac biomarkers, namely cardiac troponin T, creatine kinase (CK), cardiac troponin I, and CK‐MB were also suppressed by BeG. The increased rate of lipid hydroperoxides and thiobarbituric acid reactive substances owing to the oxidative stress caused by free radical generation in ISO‐induced rats were also inhibited by BeG. Antioxidants reduce oxidative stress by scavenging free radicals. ISO induction reduces these antioxidant enzymes glutathione peroxidase, catalase, superoxide dismutase, and glutathione, and levels causing oxidative cardiac damage to the heart tissue. BeG supplementation improved these enzymes synthesis preventing potential damage to the myocardium. Inflammation caused by ISO pretreatment increased the secretion of proinflammatory cytokines in ISO‐induced rats. Pretreatment with BeG suppressed these inflammatory cytokines to a normal level in ISO + BeG‐treated rats. The histopathological examination of the morphological characteristics showed that the intensity of cardiac damage caused by ISO induction was less in BeG pretreated rats with less inflammatory cells and no necrosis. BeG also showed promising results in the molecular alteration of AMP‐activated protein kinase/endothelial nitric oxide synthase/protein kinase B signaling molecules. These observations emphasize the cardioprotective effects of BeG and its potential use as a drug in the near future. [ABSTRACT FROM AUTHOR]

We present the case of a 45-year-old physically active female who presented to the cardiology clinic with subacute chest pain. Despite an extensive diagnostic cardiac workup revealing no significant findings, her chest pain persisted. The patient was finally referred to thoracic surgery for the management of severe pectus excavatum deformity, and her symptoms improved following surgical correction of the condition. Our case report details a symptomatic case of pectus excavatum, emphasizing the importance of recognizing that this condition can be associated with clinical symptoms., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Khunger et al.)

Cardiac ischemia, such as angina pectoris or myocardial infarction, is associated with pain in the oral cavity, lower jaw, head, or neck, or spanning from the left upper arm to the shoulder. When presenting to a dentist, however, appropriate treatment for such patients is often delayed, as dental problems are usually the first to be suspected when the chief complaint is orofacial pain. This report describes a case of a 70-year-old woman who was aware of pain and a burning sensation in the oral cavity upon exertion for a year prior to presenting at our clinic. She had been examined by her family physician, an otolaryngologist, and another dentist, none of whom found any abnormalities other than suspected periodontal disease and caries, for which she was treated. An examination at our clinic revealed no abnormal dental findings that would have been consistent with the mandibular pain, however. Although no chest symptoms were reported, pain was elicited on exertion, suggesting cardiogenic toothache. An immediate referral to a cardiologist was therefore made on the same day. The patient visited the cardiology department of the University Hospital of Tokyo Dental College 6 days later. The increased frequency of symptoms on exertion suggested unstable angina, and the patient was admitted to the emergency department on the same day. Emergency coronary angiography showed that right coronary artery #1 was 99% stenosed proximally (highly calcified plaque). The diagnosis was unstable angina pectoris, with the right coronary artery #1 as the responsible lesion, and percutaneous coronary angioplasty was performed on the same day. Subsequently, all the orofacial pain disappeared, confirming unstable angina as the cause. The pain characteristics in this case were consistent with pain associated with cardiac ischemia, which led to the immediate referral to the cardiology department. In cases of toothache associated with cardia ischemia, it is essential to seek cardiological care as soon as possible.

Adipose tissue is a source of stem cells with a high potential of differentiation for cell-based regenerative therapies. We previously identified mouse P2Y2, an ATP and UTP nucleotide receptor, as a regulator of adipogenic and endothelial differentiation of cardiac adipose-derived stem cells (cADSC). We investigated here the potential involvement of P2Y2 receptor in the cardioprotective action of undifferentiated cADSC transplantation in mouse ischemic heart. Transplantation of cADSC was realized in the periphery of the infarcted zone of ischemic heart, 3 days after left anterior descending artery ligation. A strong reduction of collagen stained area was observed 14 days after cADSC injection, compared to PBS injection. Interestingly, loss of P2Y2 expression totally inhibits the ability of transplanted cADSC to reduce cardiac fibrosis. A detailed gene ontology enrichment analysis was realized by comparing RNA-sequencing data obtained for UTP-treated wild type cASDC and UTP-treated P2Y2-null cASDC. We identified UTP target genes linked to extracellular matrix organization such as matrix metalloproteinases and various collagen types, UTP target genes related to macrophage chemotaxis and differentiation into pro-fibrotic foam cells, and a significant number of UTP target genes linked to angiogenesis regulation. More particularly, we showed that UTP regulated the secretion of CCL5, CXCL5, and CCL12 chemokines and serum amyloid apolipoprotein 3, in the supernatants of UTP-treated cADSC. Interestingly, CCL5 is reported as a key factor in post-infarction heart failure and in the reparative and angiogenic action of transplanted ADSC on ischemic tissue. We investigated then if a UTP-pretreatment of cADSC amplifies their effect on cardiac revascularization in mouse ischemic heart. Transplantation of cADSC was able to increase peri-infarct capillary density, 14 days after their injection. This beneficial effect on cardiac revascularization was enhanced by a UTP-pretreatment of cADSC before their transplantation, and not observed using P2Y2-null cADSC. Our data support that the efficacy of transplanted cADSC can be regulated by the release of inflammatory mediators such as extracellular nucleotides in the ischemic site. The present study highlights the P2Y2 receptor as a regulator of cADSC cardioprotective action, and as a potential target for the therapeutic use of undifferentiated cADSC in post-ischemic cardiac ischemia. [ABSTRACT FROM AUTHOR]

Adipose tissue is a source of stem cells with a high potential of differentiation for cell-based regenerative therapies. We previously identified mouse P2Y2, an ATP and UTP nucleotide receptor, as a regulator of adipogenic and endothelial differentiation of cardiac adipose-derived stem cells (cADSC). We investigated here the potential involvement of P2Y2 receptor in the cardioprotective action of undifferentiated cADSC transplantation in mouse ischemic heart. Transplantation of cADSC was realized in the periphery of the infarcted zone of ischemic heart, 3 days after left anterior descending artery ligation. A strong reduction of collagen stained area was observed 14 days after cADSC injection, compared to PBS injection. Interestingly, loss of P2Y2 expression totally inhibits the ability of transplanted cADSC to reduce cardiac fibrosis. A detailed gene ontology enrichment analysis was realized by comparing RNA-sequencing data obtained for UTP-treated wild type cASDC and UTP-treated P2Y2-null cASDC. We identified UTP target genes linked to extracellular matrix organization such as matrix metalloproteinases and various collagen types, UTP target genes related to macrophage chemotaxis and differentiation into pro-fibrotic foam cells, and a significant number of UTP target genes linked to angiogenesis regulation. More particularly, we showed that UTP regulated the secretion of CCL5, CXCL5, and CCL12 chemokines and serum amyloid apolipoprotein 3, in the supernatants of UTP-treated cADSC. Interestingly, CCL5 is reported as a key factor in post-infarction heart failure and in the reparative and angiogenic action of transplanted ADSC on ischemic tissue. We investigated then if a UTP-pretreatment of cADSC amplifies their effect on cardiac revascularization in mouse ischemic heart. Transplantation of cADSC was able to increase peri-infarct capillary density, 14 days after their injection. This beneficial effect on cardiac revascularization was enhanced by a UTP-pretreatment of cADSC before their transplantation, and not observed using P2Y2-null cADSC. Our data support that the efficacy of transplanted cADSC can be regulated by the release of inflammatory mediators such as extracellular nucleotides in the ischemic site. The present study highlights the P2Y2 receptor as a regulator of cADSC cardioprotective action, and as a potential target for the therapeutic use of undifferentiated cADSC in post-ischemic cardiac ischemia.

High-frequency QRS (HFQRS) analysis of surface ECG is a reliable marker of cardiac ischemia (CI). This study aimed to assess the response of HFQRS signals from standard intracardiac electrodes (iHFQRS) to CI in swine and compare them with conventional ST-segment deviations. Devices with three intracardiac leads were implanted in three swine in a controlled environment. CI was induced by inflating a balloon in epicardial coronary arteries. A designated signal-processing algorithm was applied to quantify the iHFQRS content before, during, and after each occlusion. iHFQRS time responses were compared to conventional ST-segment deviations. Thirty-three over thirty-nine (85%) of the occlusions presented significant reduction in the iHFQRS signal, preceding ST-segment change, being the only indicator of CI in brief occlusions. iHFQRS was found to be an early indicator for the onset of CI and demonstrated superior sensitivity to conventional ST-segment deviations during brief ischemic episodes. [ABSTRACT FROM AUTHOR]

The conventional management strategies of myocardial infarction (MI) are effective to sustain life; however, myocardial regeneration has not been achieved owing to the inherently poor regenerative capacity of the native myocardium. Stem cell-based therapies are promising; however, lineage specificity and undesired differentiation profile are challenging. Herein, we focused on the epicardial fat (EF) as an ideal source for mesenchymal stem cells (MSCs) owing to the proximity and same microvasculature with cardiac muscle. Unfortunately, the epicardial adipose tissue derived stem cells (EATDS) remain understudied regarding their phenotype heterogeneity and cardiac regeneration potential. As EF closely reflects the cardiac pathology during ischemia, the present study aims to determine the EATDS subpopulations under simulated ischemic and reperfused conditions employing single cell RNA sequencing (scRNAseq). EATDS were isolated from three hyperlipidemic Yucatan microswine and were divided into Control, Ischemia (ISC), and Ischemia/reperfusion (ISC/R). The scRNAseq analysis was performed using 10 genomics platform which revealed 18 unique cell clusters suggesting the existence of heterogeneous phenotypes. The upregulated genes were taken into consideration and subsequent functional assessment revealed the cardioprotective phenotypes with diverse mechanisms including epigenetic regulation (Cluster 1), myocardial homeostasis (Cluster 1), cell integrity and cell cycle (Clusters 2 and 3), prevention of fibroblast differentiation (Cluster 4), differentiation to myocardial lineage (Cluster 6), anti-inflammatory responses (Clusters 5, 8, and 11), prevention of ER-stress (Cluster 9), and increasing the energy metabolism (Cluster 10). These unique phenotypes of heterogeneous EATDS population open significant translational opportunities for myocardial regeneration and cardiac management. [ABSTRACT FROM AUTHOR]

Background: Obesity is associated with an augmented risk of myocardial ischemia/reperfusion (I/R) injury. Reduction of I/R injury by effective cardioprotective strategies needs to be investigated in obese subjects. This study aimed to evaluate the combined effects of sitagliptin and melatonin on inflammatory response and TLR4/IκBα/NF-κB signaling following cardiac I/R damage in obese rats. Methods: Sixty-six male Wistar rats (180–200 g) were fed a low fat diet (10% Kcal from lipids) or high fat (45% Kcal from lipids) diets for 12 weeks. High fat-fed (obese) rats experienced 30 min left anterior descending occlusion followed by 24 h reperfusion. Obese rats received sitagliptin (20 mg/kg/day) for 1 month before I/R surgery. Melatonin (10 mg/kg) was injected at early reperfusion. Myocardial infarct size (IS), cTn-I release, pro-inflammatory cytokines, myeloperoxidase (MPO), COX-2 and iNOS, and the protein expressions of TLR4, p-NF-κB/p65, and p-IκBα were evaluated. Results: Monotherapies with sitagliptin-preconditioning or melatonin-postconditioning had no cardioprotective effects in obese rats. However, combined therapy with sitagliptin and melatonin significantly reduced IS, and the release of cTn-I, in comparison to untreated obese rats (p <.01) Moreover, this combination decreased the production of pro-inflammatory cytokines, MPO, COX-2 and iNOS, and the expression of TLR4 and p-NF-κB/p65, while reduced the expression of p-IκBα, in comparison with untreated or monotherapies-received obese rats (p <.01 for all). Conclusion: Combination therapy with sitagliptin and melatonin was a good cardioprotective strategy to modulate the inflammatory responses and TLR4/NF-κB signaling pathway in obese patients with cardiac I/R injury. [ABSTRACT FROM AUTHOR]

Marfan syndrome (MFS) is a life-threatening connective tissue disorder that affects multiple organs and systems. We report a case of MFS with recurrent lower left posterior toothache as the first symptom. A 23-year-old Asian man walked into the dental emergency room with a chief complaint of recurrent spontaneous and intermittent toothache in his lower left posterior tooth region, mimicking acute symptomatic pulpitis. He self-reported a relatively healthy medical status without any hereditary disease. However, his disproportionately elongated body structure, high myopia, and positive wrist sign were immediately recognizable. Although there were no remarkable findings on the dental examination, pectus carinatum deformity and abnormal blood pressure were later detected. He was immediately referred to a cardiologist in a medical hospital. The timely diagnosis of MFS and early surgical intervention helped to avoid severe lethal consequences. The symptoms of toothache completely resolved after surgery. [ABSTRACT FROM AUTHOR]

BackgroundPain symptoms related to cardiac ischemia can vary greatly from patient to patient. However, should emergency physicians consider the possibility of myocardial infarction in patients who present solely with dental pain?ObjectiveThis is a systematic review of the literature investigating the incidence of jaw, tooth, or facial pain as the sole symptom of cardiac ischemia.MethodsStudies investigating jaw, tooth, or facial pain of cardiac origin were identified using the PubMed database. All English studies in which cardiac pain originated in the face, teeth, or jaw were screened for inclusion. Data were abstracted from each study utilizing a structured review process, and rated for methodological quality.ResultsEighteen studies met study criteria: 16 were case reports, and the remaining 2 were prospective cohort studies. After quality assessment and categorization, nine reports were categorized as weak, eight moderate, and one strong methodological quality.ConclusionCardiac ischemia may present in no anatomic location other than face or jaw. However, despite frequent claims in the literature to the contrary, the lack of methodological quality of the studies investigated impedes a firm conclusion of face, jaw, or tooth pain as the only symptom of cardiac insufficiency.

Abstract Background Weaning-induced cardiac pulmonary edema (WiPO) is one of the main mechanisms of weaning failure during mechanical ventilation. We hypothesized that weaning-induced cardiac ischemia (WiCI) may contribute to weaning failure from cardiac origin. Methods A prospective cohort study of patients mechanically ventilated for at least 24 h who failed a first spontaneous breathing trial (SBT) was conducted in four intensive care units. Patients were explored during a second SBT using multiple tools (echocardiography, continuous 12-lead ST monitoring, biomarkers) to scrutinize the mechanisms of weaning failure. WiPO definition was based on three criteria (echocardiographic signs of increased left atrial pressure, increase in B-type natriuretic peptides, or increase in protein concentration during SBT) according to a conservative definition (at least two criteria) and a liberal definition (at least one criterion). WiCI was diagnosed according to the third universal definition of myocardial infarction proposed by the European Society of Cardiology (ESC) and the American Heart Association (AHA) statement for exercise testing. Results Among patients who failed a first SBT, WiPO occurred in 124/208 (59.6%) and 44/208 (21.2%) patients, according to the liberal and conservative definition, respectively. Among patients with ST monitoring, WiCI was diagnosed in 36/177 (20.3%) and 12/177 (6.8%) of them, according to the ESC and AHA definitions, respectively. WiCI was not associated with WiPO and was not associated with weaning outcomes. Only two patients of the cohort were treated for an acute coronary syndrome after the second SBT, and seven other patients required coronary angiography during the weaning period. Conclusions This observational study showed the common occurrence of pulmonary edema in mechanically ventilated patients who failed a first SBT, but the association with cardiac ischemia and weaning outcomes was weak.

This paper presents the results of studying the psychological aspects of attitudes to personal security of patients with coronary artery disease (CAD) and heart defects. The research involved 40 patients aged 45 to 81 years (47.5 % male, 52.5 % female): 20 patients with ischemic heart disease with stable angina and 20 patients with acquired heart defects. In the course of the research conducted with the help of the techniques based on subjective scaling, the attitudes to personal security, including the sources of threats, the consequences of the realization of threats and the assessment of efforts on the counteraction to these threats, posing in the author’s theoretical model as the components of the system of the attitudes to personal security, have been studied. The results show that in the patients with heart diseases, the assessments for a variety of threats, the consequences of their realization and the efforts on the counteraction to them are significantly higher, than in the patients with CAD. In general, the estimates for all the parameters in the group of the patients with CAD were closer to the estimates of healthy people, obtained in the previous studies. In the patients with heart defects, characterized by a greater duration and disease severity, the results of the indicators of the attitudes to personal security, in general, are higher and less differentiated. The conclusion is made that the attitudes to personal security as a part of the system of the psychological attitudes in general, can act as a diagnostic criterion and the indicator of the efficiency of the adaptation in cardiovascular diseases and also can be an independent target of the correctional work in a psychological consultation and psychotherapy of the patients with cardiovascular diseases. In the conclusion the recommendations for the experts who are engaged in the psychological help to the patients with cardiovascular diseases in diagnostic and correctional work with the attitudes to personal security are formulated.

Exosomes transport biologically active cargo (e.g., proteins and microRNA) between cells, including many of the paracrine factors that mediate the beneficial effects associated with stem-cell therapy. Stem cell derived exosomes, in particular mesenchymal stem cells (MSCs), have been shown previously to largely replicate the therapeutic activity associated with the cells themselves, which suggests that exosomes may be a useful cell-free alternative for the treatment of cardiovascular disorders. However, the mechanisms that govern how exosomes home to damaged cells and tissues or the uptake and distribution of exosomal cargo are poorly characterized, because techniques for distinguishing between exosomal proteins and proteins in the targeted tissues are lacking. Here, we report the development of an in vivo model that enabled the visualization, tracking, and quantification of proteins from systemically administered MSC exosomes. The model uses bioorthogonal chemistry and cell-selective metabolic labeling to incorporate the non-canonical amino acid azidonorleucine (ANL) into the MSC proteome. ANL incorporation is facilitated via expression of a mutant (L274G) methionyl-tRNA-synthetase (MetRS∗) and subsequent incubation with ANL-supplemented media; after which ANL can be covalently linked to alkyne-conjugated reagents (e.g., dyes and resins) via click chemistry. Our results demonstrate that when the exosomes produced by ANL-treated, MetRS∗-expressing MSCs were systemically administered to mice, the ANL-labeled exosomal proteins could be accurately and reliably identified, isolated, and quantified from a variety of mouse organs, and that myocardial infarction (MI) both increased the abundance of exosomal proteins and redistributed a number of them from the membrane fraction of intact hearts to the cytosol of cells in infarcted hearts. Additionally, we found that Desmoglein-1c is enriched in MSC exosomes and taken up by ischemic myocardium. Collectively, our results indicate that this newly developed bioorthogonal system can provide crucial insights into exosome homing, as well as the uptake and biodistribution of exosomal proteins.