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Background/Aims: Myocardial reperfusion has the potential to salvage the ischemic myocardium after a period of coronary occlusion. Reperfusion, however, can cause a wide spectrum of deleterious effects. Galectin-3 (GAL-3), a beta galactoside binding lectin, is closely associated with myocardial infarction (MI), myocardial fibrosis and heart failure. In our study, we investigated its role in ischemia-reperfusion injuries (IR) as this phenomenon is extremely relevant to the early intervention after acute MI. Methods: C57B6/J wild type (WT) mice and GAL-3 knockout (KO) mice were used for murine model of IR injury in the heart where a period of 30 minutes ischemia was followed by 24 hours of reperfusion. Heart samples were processed for immunohistochemical and immunofluorescent labeling, morphometric analysis, western blot and enzyme-linked immunosorbent assay to identify the apoptotic, inflammatory and oxidative stress role of GAL-3. Results: Our results show that there was a significant increase in GAL-3 levels in the heart which shows GAL-3 is playing a role in the ischemia reperfusion injury. Troponin I was also significantly higher in GAL-3-KO group than wild type. Our study shows that GAL-3 is associated with an increase in the antioxidant activity in the IR injured myocardium. Antioxidant enzymes superoxide dismutase, glutathione and catalase were found to be significantly raised in the GAL-3 wild type IR as compared to the GAL-3 KO IR group. A significant increase in apoptotic activity is seen in GAL-3 KO IR group as compared with GAL-3 wild IR group. Conclusion: Our study shows that GAL-3 can affect the redox pathways, controlling cell survival and death, and plays a protective role on the myocardium following IR injury.

Myocardial infarction (MI) is a leading cause of morbidity and mortality in the world and is characterized by ischemic necrosis of an area of the myocardium permanently devoid of blood supply. During reperfusion, reactive oxygen species are released and this causes further insult to the myocardium, resulting in ischemia-reperfusion (IR) injury. Since Nrf2 is a key regulator of redox balance, it is essential to determine its contribution to these two disease processes. Conventionally Nrf2 levels have been shown to rise immediately after ischemia and reperfusion but its contribution to disease process a week after the injury remains uncertain. Mice were divided into MI, IR injury, and sham surgery groups and were sacrificed 1 week after surgery. Infarct was visualized using H&E and trichrome staining and expression of Nrf2 was assessed using immunohistochemistry, Western blot, and ELISA. MI displayed a higher infarct size than the IR group (MI: 31.02 ± 1.45%, IR: 13.03 ± 2.57%; p < 0.01). We observed a significantly higher expression of Nrf2 in the MI group compared to the IR model using immunohistochemistry, spot densitometry of Western blot (MI: 2.22 ± 0.16, IR: 1.81 ± 0.10, Sham: 1.52 ± 0.13; p = 0.001) and ELISA (MI: 80.78 ± 27.08, IR: 31.97 ± 4.35; p < 0.01). There is a significantly higher expression of Nrf2 in MI compared to the IR injury group. Modulation of Nrf2 could be a potential target for therapeutics in the future, and its role in cardioprotection can be further investigated.

Myocardial infarction (MI) is the most serious manifestation of coronary artery disease and the cause of significant mortality and morbidity worldwide. Galectin-1(GAL-1), a divalent 14.5-kDa protein, is present both inside and outside cells, and has both intracellular and extracellular functions. Hypoxia inducible factor-1 alpha (HIF-1α) is a transcription factor mediating early and late responses to myocardial ischemia. Identification of the pattern of expression of GAL-1 and HIF-1α in the heart during the first 24 hours following acute MI will help in understanding early molecular changes in this event and may provide methods to overcome serious complications. Mouse model of MI was used and heart samples were processed for immunohistochemical and immunofluorescent labeling and Enzyme linked immunosorbent assay to identify GAL-1 and HIF 1α levels in the heart during the first 24 hours following MI. There was significant increase in left ventricular GAL-1 at 20 (p = 0.001) and 30 minutes (p = 0.004) following MI. There was also a significant increase in plasma GAL-1 at 4 hours (p = 0.012) and 24 hours (p = 0.001) following MI. A significant increase in left ventricular HIF-1 α was seen at 20 minutes (p = 0.047) following MI. In conclusion, we show for the first time that GAL-1 level in the left ventricle is increased in early ischemic period. We also report for the first time that HIF-1 α is significantly increased at 20 minutes following MI. In addition we report for the first time that mouse plasma GAL-1 level is significantly raised as early as 4 hours following MI.

Background It is generally agreed that basic and clinical sciences should be integrated throughout the undergraduate medical education, however, there is still need for continued formal integration of basic sciences into clinical clerkship in many medical schools across the globe. Methods Utilizing Kern’s Six-Step Model of Instructional Design, we aimed to develop an intervention that would facilitate cognitive integration of basic and clinical sciences. After problem identification and targeted needs assessment through focused group discussion with the students and faculty, objectives were devised with an implementation plan of using flipped class approach to develop a content-focused and learner-centered teaching strategy. This intervention was piloted in the 2-week cardiology clerkship in Year 5. Evaluation of the content, integration, student and faculty experiences were recorded through in-depth interviews, FGDs and a formative MCQ test. Results Flipped classroom based integrated sessions were successfully developed. The implementation phase was met with challenges that primarily stemmed from the diverse teaching styles among faculty members, hesitance to deviate from conventional practices, variations in clinic timings, and demanding schedules. Noteworthy observations were in terms of ownership of the project, the need for faculty development in modern student-centered teaching pedagogies, opportunities for content improvement, scheduling of sessions, and suggestion of revisiting fundamental concepts in basic sciences through a brief boot camp-style session at the onset of the clerkship. The role of flipped case model and clinical cases in integrating basic sciences into clinical sciences were appreciated by the students. Standardization in teaching practices was identified as the major challenge by the faculty. Conclusions A functional, learner-centered framework of cognitive integration of basic sciences in clinical sciences curriculum of cardiology rotation was developed with a potential to be implemented in other clerkship rotations.

Vectorcardiography (VCG) enables measurement of voltages and directions of resultant spatial vectors in the heart that are altered by myocardial ischemia. To validate the ability of VCG to detect electrophysiological effects of regional myocardial ischemia and identify blood vessels that obstruct blood flow significantly, VCG records of 37 patients who presented with unstable symptoms of ischemia requiring coronary angiography (CA) were processed and analyzed. The difference in magnitude and direction of electrical vectors were measured before and after percutaneous coronary intervention (PCI) to study the significance of changes after revascularization. Bio amplifiers recorded 3 simultaneous orthogonal lead ECG signals with low-pass frequency of 150 Hz without electronic filtration. The analogue signals were digitized and recorded for analysis. The numerical output was processed by algorithms to calculate and display the state of vectors. 36 of 37 patients showed congruence between VCG and CA results: 34 of the 36 showed changes in electrical vectors and insufficient blood supply. 2 showed no changes in electrical vectors and non-obstructive arteries on CA. 1 patient had ischemia detected by VCG, but CA was negative. Blood vessels that were opened with PCI corresponded with regions of myocardial ischemia and expected coronary blood supply on VCG interpretation.

Coronary artery calcification (CAC) is mainly associated with coronary atherosclerosis, which is an indicator of coronary artery disease (CAD). CAC refers to the accumulation of calcium phosphate deposits, classified as micro- or macrocalcifications, that lead to the hardening and narrowing of the coronary arteries. CAC is a strong predictor of future cardiovascular events, such as myocardial infarction and sudden death. Our narrative review focuses on the pathophysiology of CAC, exploring its link to plaque vulnerability, genetic factors, and how race and sex can affect the condition. We also examined the connection between the gut microbiome and CAC, and the impact of genetic variants on the cellular processes involved in vascular calcification and atherogenesis. We aimed to thoroughly analyze the existing literature to improve our understanding of CAC and its potential clinical and therapeutic implications.

IntroductionLeft ventricular diastolic dysfunction (LVDD) is common in patients with coronary artery disease (CAD) with prevalence estimates of 34% and constitutes a predictor of all-cause mortality. Although diastolic dysfunction is induced by myocardial ischemia and has been shown to alter the clinical course, the role of coronary artery disease in the diastolic dysfunction and its progression into heart failure has not been completely elucidated.ObjectiveThe present study was conducted to identify possible metabolites in coronary artery disease patients that are differentially regulated in patients with diastolic dysfunction.MethodsThe serum of CAD (n = 75) patients and young healthy volunteers (n = 43) were analysed by using gas chromatography mass spectrometry (GC–MS) technique. Pre-processing of data results in 1547 features; among them 1064 features were annotated using NIST library.Results and ConclusionFifteen metabolites were found to be statistically different between cases and control. Variation in metabolites were identified and correlated with several clinically important echocardiography parameters i.e. LVDD grades, ejection fraction (EF) and E/e’ values. The results suggested that metabolic products of fatty acid oxidation and glucose oxidation pathways such as oleic acid, stearic acid, palmitic acid, linoleic acid, galactose, pyruvic and lactic acids are predominantly up regulated in patients with coronary artery disease and severity of diastolic dysfunction appears to be linked to increase in fatty acid oxidation and inflammation. The metabolic fingerprints of these patients give us an insight into the pathophysiological mechanism of diastolic dysfunction in coronary artery disease patients although it did not identify validated novel markers.

Background: Cardiovascular diseases are the leading cause of death worldwide, including the United Arab Emirates. Ischemia–reperfusion (IR) injury results in the death of cardiac myocytes that were viable immediately before myocardial reperfusion. We aim to investigate the role of galectin-3 (Gal-3) in autophagy during ischemia–reperfusion injuries. Methods: Male C57B6/J and Gal-3 knockout (KO) mice were used for the murine model of IR injury. Heart samples and serum were collected 24 h post-IR and were processed for immunohistochemical and immunofluorescent labeling and an enzyme-linked immunosorbent assay. Results: There was a significant increase in left ventricle (LV) concentrations of Gal-3 in Gal-3 wild-type mice compared to sham mice. There were significantly higher concentrations of LV autophagy proteins and phospho-AMPK in IR Gal-3 KO mice than in IR Gal-3 wild-type mice, compared to lower concentrations of LV phospho-mTOR and p62 in IR Gal-3 KO than in IR wild-type mice. Antioxidant activities were higher in the LVs of IR Gal-3 wild-type mice, while oxidative stress was higher in the LVs of IR Gal-3 KO mice. Conclusions: Our study supports the interaction of Gal-3 with autophagy proteins, oxidative stress, and antioxidant proteins and demonstrates that the absence of Gal-3 can enhance autophagy in the heart after IR injury.

Ischemic heart disease (IHD) is the leading cause of death and chronic disability in the world. IHD affects both the systolic and diastolic function of the heart which progressively leads to heart failure; a structural and functional impairment of filling or ejection of blood from the heart. In this study, the progression of systolic and diastolic dysfunction characterized according to their echocardiographic parameters including left ventricular ejection fraction (EF), grades of diastolic dysfunction and ratio between early mitral inflow velocity and mitral annular early diastolic velocity (E/eʹ), were correlated with differential regulation of various metals in patients sera samples (n = 62) using inductive coupled plasma-mass spectrometry (ICP-MS). Chromium, nickel and selenium were found significant (p < 0.05) in patients having EF < 45% compared with EF > 45%. In patients with systolic dysfunction (EF < 45%), the level of selenium was decreased while the level of chromium and nickel was increased compared to patients with EF > 45%. Selenium level was also decreased significantly (p < 0.05) in grade 1A and 2 patients that are considered as higher grades of diastole dysfunction in comparison to grade 0–1. Overall, selenium deficiency was identified in both systolic and diastolic dysfunctions of IHD patients corresponding to the progression of disease that could be related to many metabolic and translational pathways specifically which involve selenoproteins.

Flipped classroom (FCR) is an active learning pedagogical method in which the students prepare prior to class using different modalities, for example, reading materials and videos, and afterward spend the time in class discussing the content and reinforcing the concepts. We chose to replace one problem-based case on “Shock” with flipped-style teaching in the respiration circulation module of a private medical university. Our objective was to use the clinical presentation of “Shock” to open a window to interrelate basic science concepts of cardiovascular physiology and pathology. It aimed to merge the case-based discussion with small-group discussions in the form of FCR activity. The qualitative study gives an overview of comments of facilitators, observers, and leadership of the Department and University obtained during focus group discussions and in-depth interviews. Thematic analysis of responses emphasized the importance of FCR as an effective teaching learning modality, which can be made more effective by careful selection of topic and provision of facilities to support technology-enhanced learning. The discussions with facilitators, observers, and leadership revealed its usefulness through student’s engagement and increased participation to build learning of the key concepts. Student satisfaction in these activities can be enhanced by construction of knowledge acquired in non–face-to-face component with substantial pre-reading materials, videos, peer discussions, quizzes, and prompt feedback.