Myocardial Infarction Research Articles

Hypoxia-inducible factor-2α enhances neutrophil survival to promote cardiac injury following myocardial infarction.

Heart failure is a major cause of mortality following myocardial infarction. Neutrophils are among the first immune cells to accumulate in the infarcted region. Although beneficial functions of neutrophils in heart injury are now appreciated, neutrophils are also well known for their ability to exacerbate inflammation and promote tissue damage. Myocardial infarction induces hypoxia, where hypoxia-inducible factors (HIFs) are activated and play critical roles in cellular functions. In this context, the role of Hif2α in neutrophils during myocardial infarction is unknown. Here, we demonstrate that neutrophil Hif2α deletion markedly attenuates myocardial infarct size, improves cardiac function, reduces neutrophil survival and tissue accumulation, and correlates with increased macrophage engulfment rates. Mechanistic studies revealed that Hif2α promotes neutrophil survival through binding to hypoxia response element (HRE) in the promoter region of Birc2 to regulate expression of the prosurvival factor, cellular inhibitor of apoptosis protein-1 (cIAP1). Inhibition of cIAP1 in neutrophils using the pharmacological agent, Birinapant resulted in increased cell death, establishing a critical role of cIAP1 downstream of Hif2α in neutrophil survival. Taken together, our data demonstrate a protective effect of Hif2α deletion in neutrophils on cardiac injury outcomes through modulation of neutrophil cell survival.NEW & NOTEWORTHY Hif2α in neutrophils increases infarct size, cardiac dysfunction, and ventricular scar after myocardial infarction. Hif2α in neutrophils supports neutrophil survival via cIAP-1 signaling and delays macrophage engulfment.

“I think we should wait and see”: A qualitative study of call-takers’ decision-making in consultations with patients suffering unrecognized myocardial infarction

ObjectivesCall-takers face a complex situation when assessing medical problems in emergency medical services calls. Patients with myocardial infarction experiencing atypical symptoms risk misinterpretation. We examined development in call-takers' decision-making process in telephone consultations with patients having imminent myocardial infarction. MethodsRecording of 38 calls among 19 patients (two per patient) who contacted Copenhagen Emergency Medical Services (Denmark) at least twice within one week before myocardial infarction diagnosis. The penultimate and last call were compared using qualitative content analysis. ResultsCall-takers’ assessment of the condition changed from symptom picture and dismissal of heart disease in penultimate call to severe condition, not heart-related, and possible heart disease in last call. Call-takers recommended watchful waiting in the penultimate call. Both calls involved response negotiation, while caution regarding misinterpretation was only seen in the penultimate call. ConclusionCall-takers used different decision-making approaches when the caller’s symptom descriptions appeared unclear and not corresponding with the medical understanding of severe conditions. Call-takers did not negotiate the condition's assessment but engaged in discussions about the response choice. Practice implicationsA protocol to negotiate response choice with callers having unclear clinical conditions should be developed. Clarifying watchful waiting as a recommendation may assist call-takers’ decision-making.

Invasive Treatment of Left Main Coronary Artery Disease: From Anatomical Features to Mechanistic Differences.

There is debate on the best treatment for significant stenoses of the left main (LM) coronary artery. The available evidence is based on four randomized trials, which were either performed specifically to assess patients with LM disease (EXCEL, NOBLE, PRECOMBAT) or had a significant fraction of patients with this disease pattern (SYNTAX). A meta-analysis revealed no difference in periprocedural and 5-year mortality but demonstrated a significant reduction of spontaneous myocardial infarction (MI) with CABG. Furthermore, the recently published SWEDEHEART registry data have shown survival advantage and fewer MACCE with CABG for LM disease after adjustment. In general, patients with more severe coronary artery disease (CAD) appear to have a survival advantage with CABG both over PCI and medical therapy (independent of the presence or absence of LM stenosis), which is always associated with a reduction of spontaneous MI in the CABG arm. Since the nomenclature of LM disease does not automatically reflect the complexity of CAD, we review the nature of LM disease in this article. We mechanistically assess the treatment effects of PCI and CABG for patients with LM disease, which is rarely isolated, often distal, and mostly associated with varying degrees of single and multi-vessel disease. We conclude that in patients with isolated LM shaft lesions and associated diseases of low complexity, the risk of spontaneous MI is lower, and PCI may achieve similar long-term outcomes compared to CABG. Thus, heart teams are essential for selecting the best treatment option and should focus on assessing infarction risk in chronic CAD.

Integration of network pharmacology and transcriptomics to explore the mechanism of isoliquiritigenin in treating heart failure induced by myocardial infarction

BackgroundThe inflammatory response and myocardial remodeling play critical roles in the progression of heart failure (HF) following myocardial infarction (MI). Isoliquiritigenin (ISL) possesses anti-inflammatory properties and has been investigated in cardiovascular diseases such as atherosclerosis. However, the effects and mechanism of ISL on MI-induced HF remain unclear. This research aimed to explore the effects and mechanism of ISL in the treatment of HF on the basis of network pharmacology, transcriptomics, and experimental verification. Methods and resultsWe established an MI-induced HF mouse model in which ISL was administered via gavage for 28 days. Ultrasonic cardiogram data were collected from the mice, and pathological staining was conducted. Then, network pharmacology and molecular docking were performed. Transcriptomic analysis was also conducted on mouse myocardial tissue. Ultimately, we integrated transcriptomic data and network pharmacology to reveal the underlying mechanism, with the results verified through in vivo experiments. Our experiments indicated that ISL improved cardiac function, preserved myocardial structure, inhibited collagen fiber accumulation, reduced inflammatory factor secretion, and mitigated myocardial cell apoptosis in mice with MI-induced HF. A combination of transcriptomics and network pharmacology analysis revealed that core targets of ISL related to HF were significantly enriched in the Tumor Necrosis Factor (TNF) signaling pathway. Molecular docking validation demonstrated that ISL shows strong binding to these core targets. Additionally, in vivo experiments verified that ISL protects against HF post-MI by inhibiting the TNF signaling pathway. ConclusionWe clarified the anti-inflammatory and antimyocardial remodeling mechanisms of ISL in the treatment of HF post-MI, which involves the TNF signaling pathway.

The impact of door to extracorporeal cardiopulmonary resuscitation time on mortality and neurological outcomes among out-of-hospital cardiac arrest acute myocardial infarction patients treated by primary percutaneous coronary intervention

BackgroundFew previous studies evaluated the impact of time from the hospital arrival to the implementation of extracorporeal cardiopulmonary resuscitation (ECPR) (door to ECPR time) on outcomes among out-of-hospital cardiac arrest (OHCA) acute myocardial infarction (MI) patients. Methods50 patients with OHCA who received both ECPR and percutaneous coronary intervention (PCI) at Cardiovascular Division, NHO Osaka National Hospital were analyzed. Patients were divided into 2 groups according to the median of door to ECPR time. The primary outcome was all-cause death. Survival analyses were conducted to compare all-cause mortality at 90 days between 2 groups. Neurological outcome at 30 days was also compared between 2 groups using the Cerebral Performance Category (CPC). ResultsThe multivariable Cox proportional-hazards model showed that all-cause mortality at 90 days was significantly higher among patients with door to ECPR time ≥ 25 min compared with those with door to ECPR time < 25 min (adjusted hazard ratio [HR]: 3.14; 95 % confidence interval [CI]: 1.21–8.18). The proportion of patients with CPC at 30 days ≤ 2 was significantly higher among patients with shorter door to ECPR time (P = 0.048). ConclusionAmong patients with OHCA due to acute MI who received ECPR and PCI, the shorter door to ECPR time was associated with the lower mortality and favorable neurological outcomes.

A cohort analysis of familial partial lipodystrophy from two Mediterranean countries.

To assess the disease burden of familial partial lipodystrophy (FPLD) caused by LMNA (FPLD2) and PPARG (FPLD3) variants to augment the knowledge of these rare disorders characterized by selective fat loss and metabolic complications. An observational longitudinal study, including 157 patients (FPLD2: 139 patients, mean age 46 ± 17 years, 70% women; FPLD3: 18 patients, mean age: 44 ± 17 years, 78% women) from 66 independent families in two countries (83 from Turkey and 74 from Spain), was conducted. Patients were diagnosed at a mean age of 39 ± 19 years, 20 ± 16 years after the first clinical signs appeared. Men reported symptoms later than women. Symptom onset was earlier in FPLD2. Fat loss was less prominent in FPLD3. In total, 92 subjects (59%) had diabetes (age at diagnosis: 34 ± 1 years). Retinopathy was more commonly detected in FPLD3 (P < .05). Severe hypertriglyceridaemia was more frequent among patients with FPLD3 (44% vs. 17%, P = .01). Hepatic steatosis was detected in 100 subjects (66%) (age at diagnosis: 36 ± 2 years). Coronary artery disease developed in 26 patients (17%) and 17 (11%) suffered from a myocardial infarction. Turkish patients had a lower body mass index, a higher prevalence of hepatic steatosis, greater triglyceride levels and a tendency towards a higher prevalence of coronary artery disease. A total of 17 patients died, with a mean time to death of 75 ± 3 years, which was shorter in the Turkish cohort (68 ± 2 vs. 83 ± 4 years, P = .01). Cardiovascular events were a major cause of death. Our analysis highlights severe organ complications in patients with FPLD, showing differences between genotypes and Mediterranean countries. FPLD3 presents a milder phenotype than FPLD2, but with comparable or even greater severity of metabolic disturbances.

Prognostic Effect of Obstructive Sleep Apnea in Acute Coronary Syndrome Patients with Heart Failure

Acute coronary syndrome (ACS), heart failure (HF) and obstructive sleep apnea (OSA) often overlap and interact, the impact of OSA on ACS patients with HF remains unclear. The study sought to comprehensively evaluate the effects of the interaction between OSA and HF on long-term cardiovascular outcomes in ACS patients. Between June 2015 and January 2020, patients hospitalized for ACS were prospectively enrolled and underwent portable sleep monitoring after clinically stabilization. OSA was defined as an apnea hypopnea index ≥15 events/h. HF was defined using medical records. The primary endpoint was major adverse cardiovascular and cerebrovascular event (MACCE), including death, myocardial infarction, stroke, ischemia-driven revascularization, and hospitalization for unstable angina. Among all 1927 included patients, 214 (11.1%) had HF, and 1014 (52.6%) had OSA. For 2.9 years (1.5, 3.6 years) follow-up, OSA was independently associated with the risk of MACCE in HF patients (adjusted hazard ratio [HR], 2.11; 95%CI, 1.16-3.84; P=0.014), but not in those without HF (adjusted HR, 1.15; 95%CI, 0.92-1.45; P=0.228). Further analysis showed OSA exerted more prognostic effect in HF patients with preserved eject fraction (adjusted HR, 2.45; 95% CI, 1.11-5.41; P=0.027) than those with reduced eject fraction (adjusted HR, 1.62; 95% CI, 0.63-4.20; P=0.319). In the settings of ACS, OSA was independently associated with poor prognosis in patients with concomitant HF especially those with persevered ejection fraction. Screening and treatment for OSA are highly recommended in ACS patients with HF. URL: www.clinicaltrails.gov; Unique Identifier: NCT03362385.

Nociceptive withdrawal reflex in Göttingen minipigs with myocardial infarction: a case series

Nociceptive withdrawal reflex in Göttingen minipigs with myocardial infarction: a case series

Effect of Intensive Blood Pressure Lowering on the Risk of Incident Silent Myocardial Infarction: A Post Hoc Analysis of a Randomized Controlled Trial.

Silent myocardial infarction (SMI) frequently goes undetected, yet it is associated with increased cardiovascular morbidity and mortality. The impact of intensive systolic blood pressure (SBP) lowering on the risk of SMI in those with hypertension remains uncertain. In this post hoc analysis of the Systolic Blood Pressure Intervention Trial (SPRINT), participants with serial electrocardiograms (ECGs) during the trial were included. SPRINT investigated the benefit of intensive SBP lowering, aiming for < 120 mmHg compared to the standard SBP goal of < 140 mmHg. Incident SMI was defined as evidence of new MI on an ECG without adjudicated recognized myocardial infarction (RMI). During a median follow-up of 3.9 years, a total of 234 MI events (55 SMI and 179 RMI) occurred. Intensive, compared to standard, SBP lowering resulted in a lower rate of SMI (incidence rate 1.1 vs. 2.3 cases per 1000 person-years, respectively; HR [95% CI]: 0.48 [0.27-0.84]). Similarly, intensive, compared to standard, BP lowering reduced the risk of RMI (incidence rate 4.6 vs. 6.5 cases per 1000 person-years, respectively; HR [95% CI]: 0.71 [0.52-0.95]). No significant differences were noted between the strength of the association of intensive BP control on lowering the risk of SMI and RMI (p-value for HR differences = 0.23). This study shows that in adults with hypertension, the benefits of intensive SBP lowering, compared with standard BP lowering, go beyond the prevention of RMI to include the prevention of SMI. ClinicalTrials.gov Identifier: NCT01206062.

Sevoflurane Affects Myocardial Autophagy Levels After Myocardial Ischemia Reperfusion Injury via the microRNA-542-3p/ADAM9 Axis.

This research focused on investigating the effects of sevoflurane (Sev) on myocardial autophagy levels after myocardial ischemia reperfusion (I/R) injury via the microRNA-542-3p (miR-542-3p)/ADAM9 axis. Mice underwent 30min occlusion of the left anterior descending coronary (LAD) followed by 2h reperfusion. Cardiac infarction was determined by 2,3,5-triphenyltetrazolium chloride triazole (TTC) staining. Cardiac function was examined by echocardiography. Cardiac markers and oxidative stress factors were evaluated by ELISA. Autophagy-associated factors were detected by western blot. Relationship between miR-542-3p and ADAM9 was tested by dual-luciferase reporter gene assay, RT-qPCR, and western blot. Sev treatment ameliorated cardiac dysfunction, myocardial oxidative stress, and histopathological damages, decreased myocardial infarction size and myocardial apoptotic cells after myocardial I/R injury. Sev treatment elevated miR-542-3p expression and decreased ADAM9 expression in myocardial tissues after myocardial I/R injury. miR-542-3p overexpression could enhance the ameliorative effects of Sev on myocardial injury and myocardial autophagy in I/R mice. miR-542-3p targeted and negatively regulated ADAM9 expression. ADAM9 overexpression reversed the ameliorative effects of miR-542-3p up-regulation on myocardial injury and myocardial autophagy in Sev-treated I/R mice. Sev treatment could ameliorate myocardial injury and myocardial autophagy in I/R mice, mediated by mechanisms that include miR-542-3p up-regulation and ADAM9 down-regulation.

Heat and cause-specific cardiopulmonary mortality in Germany: a case-crossover study using small-area assessment

High temperatures have been associated with increased mortality, with evidence reported predominately in large cities and for total cardiovascular or respiratory deaths. This case-crossover study examined heat-related cause-specific cardiopulmonary mortality and vulnerability factors using small-area data from Germany. We analyzed daily counts of cause-specific cardiopulmonary deaths from 380 German districts (2000-2016) and daily mean temperatures estimated by spatial-temporal models. We applied conditional quasi-Poisson regression using distributed lag nonlinear models to examine heat effects during May-September in each district and random-effects meta-analysis to pool the district-specific estimates. Potential individual- and district-level vulnerability factors were examined by subgroup analyses and meta-regressions, respectively. Heat was associated with increased mortality risks for all cardiopulmonary sub-causes. The relative risk (RR) of total cardiovascular and respiratory mortality for a temperature increment from the 75th to the 99th percentile was 1.24 (95% confidence interval: 1.23, 1.26) and 1.34 (1.30, 1.38), respectively. The RRs of cardiovascular sub-causes ranged from 1.16 (1.13, 1.19) for myocardial infarction to 1.32 (1.29, 1.36) for heart failure. For respiratory sub-causes, the RR was 1.27 (1.22, 1.31) for COPD and 1.49 (1.42, 1.57) for pneumonia. We observed greater susceptibility related to several individual- and district-level characteristics, e.g., among females or in highly urbanized districts. Heat vulnerability factors remained consistent between urban and rural areas. Our study highlights heat-related increases in cause-specific cardiopulmonary mortality across Germany and identifies key vulnerability factors, offering insights for improving public health practices to mitigate heat-related health impacts. European Union's Horizon 2020 research and innovation program; Helmholtz Associations Initiative and Networking Fund.

Le coroscanner peut-il être réalisé en dépistage à grande échelle en prévention des syndromes coronaires aigus et de l'insuffisance cardiaque ischémique ?

Coronary CT-Scan permits non-invasive visualization of all stages of coronary artery atherosclerosis allowing early therapeutic interventions, lifestyle changes and accurate follow-up all of which result in an improved prognosis. We discuss the possibility of a systematic coronary CT-scan in the global population at certain ages such as fifty or sixty years-old (or both). May this strategy decrease the onset of myocardial infarction or ischemic chronic heart failure thus improving quality (and quantity) of life? May it also reduce the medical costs for the individual and the society? Is it technically possible to deploy such a strategy? What would be the obstacles for its set up and what solutions might be proposed?

Cardioprotective effects of novel antioxidants post-myocardial infarction: An integrative review of preclinical and clinical data

Myocardial infarction (MI), is still a major public health problem, and oxidative stress contributes to the degree of myocardial damage after MI. Oxygen-derived free radicals (ODFR) worsen myocardial injury and result in chronic heart failure in many patients. These harms have led to interest in antioxidant treatment to reduce these adverse effects; new antioxidants with the potential for cardioprotection are the subject of significant interest. This review summarizes basic and clinical research comparing the effectiveness of newly synthesized antioxidants in attenuating oxidative stress and enhancing recovery after myocardial infarction. The review synthesizes evidence of a reduction in infarct size, enhancement of cardiac function, and repression of apoptosis in myocardial cells by the use of antioxidants from animal models. Melatonin, N-acetylcysteine, edaravone, and coenzyme Q10 demonstrated a wide range of preclinical positive effects by acting as ROS free radicals scavengers, modulating mitochondria dysfunction, and reducing inflammation. These findings are extrapolated from humans, although advances in antioxidant therapy are beginning to be viewed in initial clinical trials. From human data, although clinical trials are scarce, the evidence of new antioxidants can improve point and long-term outcomes in patients undergoing MI, help to increase the contractility of the injured myocardium, and decrease the mortality level. However, some issues are still there, such as high inter- and intra-individual variability in patient response and dosing schedule, as well as adverse effects such as pro-oxidant activity at high Oral administered doses of melatonin. The limitations of the current research discussed in this review include the general lack of large-scale, well-controlled clinical trials and the need for long-term follow-up studies. This review also proposed future research directions for improving antioxidant applications in post-MI management.

A study on QT dispersion and thrombolytic therapy in acute myocardial infarction

Background: Myocardial infarction is a major manifestation of ischemic heart disease, a leading cause of death in developed nations and the third globally. QTc dispersion is an important marker of ventricular repolarization variations and arrhythmogenic risk. This study examines the effects of thrombolytic therapy on QTc dispersion in acute myocardial infarction Materials and methods: 88 patients admitted to Al Ameen Medical College Hospital, Vijayapur, for acute MI were included in the study. Over a period of 8±2 days, all patients underwent monitoring, with standard 12-lead ECGs conducted upon admission and before discharge. QT interval, QTc interval, and QT and QTc dispersion parameters were calculated from these ECGs. Results: Analysis revealed significant variations in QT parameters between patients treated and not treated with thrombolytic therapy. Patients receiving thrombolytic therapy exhibited greater reductions in QT parameters by day 8±2 compared to those without treatment. Additionally, anterior wall infarctions demonstrated significantly higher QT and QTc dispersions compared to inferior wall infarctions, with these differences being statistically significant. Conclusion: In the early stages of acute myocardial infarction, patients, especially those diagnosed with anterior myocardial infarction, exhibited significantly elevated QT and QTc dispersions. Thrombolytic treatment resulted in substantial reductions in these dispersions compared to untreated individuals. Typically peaking within the initial hours of the condition, these dispersions subsequently decline following successful thrombolysis, underscoring their significance in risk assessment for malignant ventricular tachyarrhythmias and reinforcing the efficacy of thrombolytic therapy

Lung Ultrasound in the Acute Phase of ST-Segment-Elevation Acute Myocardial Infarction: 1-Year Prognosis and Improvement in Risk Prediction.

Lung ultrasound (LUS) has emerged as a useful tool in the acute phase of patients admitted for ST-segment-elevation myocardial infarction. However, its long-term significance remains uncertain, and risk scores do not include LUS findings as a predictor. This study aims to assess the 1-year prognostic value of LUS and its ability to enhance existing risk scores. This is a multicenter prospective cohort study involving 373 patients with ST-segment-elevation myocardial infarction. LUS was performed during the first 24 hours after angiography. LUS results were assessed both as a categorical (wet/dry lung) and continuous variable (LUS score). The primary end point comprised the following major adverse cardiovascular events: all-cause mortality or hospitalization for heart failure, acute coronary syndrome, or stroke within 1 year. We also evaluated whether LUS could enhance the predictive value of the GRACE (Global Registry of Acute Coronary Events) score. Major adverse cardiovascular events occurred in 51 (13.7%) patients over a median follow-up of 368 days. After multivariate analysis, the LUS score was an independent predictor (hazard ratio [HR], 1.06 [95% CI, 1.01-1.10]; P=0.009] for each additional B-line), whereas the categorical classification was an independent predictor in patients with ST-segment-elevation myocardial infarction Killip I (HR, 3.12 [95% CI, 1.34-7.31]; P=0.009). Incorporating LUS into GRACE resulted in a net reclassification index of 31.6% and a significant increase in the area under the curve; GRACE alone scored 0.705 compared with GRACE+LUS 0.791 (P=0.002). Detecting B-lines on LUS at the acute phase predicts major adverse cardiovascular events at 1 year in patients with ST-segment-elevation myocardial infarction and enhances the predictive value of the GRACE score. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04526535.

Immediate Versus Staged Complete Revascularization for Patients With ST-Segment-Elevation Myocardial Infarction and Multivessel Disease: A Network Meta-Analysis of Randomized Trials.

The comparative outcomes with immediate, staged in-hospital, and staged out-of-hospital complete revascularization for patients with ST-segment-elevation myocardial infarction and multivessel disease remain unclear. An electronic search of MEDLINE, SCOPUS, and Cochrane databases was performed through August 2023 for randomized trials evaluating immediate, staged in-hospital, and staged out-of-hospital complete revascularization for patients with ST-segment-elevation myocardial infarction and multivessel disease. The primary outcome was major adverse cardiac events (MACEs). The final analysis included 9 trials with 4270 patients. The weighted follow-up duration was 13.8 months. On pairwise meta-analysis, there were no statistically significant differences between immediate versus staged nonculprit percutaneous coronary intervention (PCI) in MACEs (odds ratio, 0.79 [95% CI, 0.54-1.16]). Network meta-analysis showed that there was no statistically significant difference in MACEs with staged in-hospital nonculprit PCI (odds ratio, 1.29-[95% CI, 0.91-1.82]) compared with immediate nonculprit PCI, while there were higher odds of MACEs with out-of-hospital nonculprit PCI (odds ratio, 1.67-[95% CI, 1.21-2.30]) compared with immediate nonculprit PCI. Compared with immediate nonculprit PCI, there were higher odds of ischemia-driven repeat revascularization with staged out-of-hospital nonculprit PCI (odds ratio, 2.26-[95% CI, 1.37-3.72]), but not with in-hospital staged nonculprit PCI. There were no significant differences for the other outcomes among the 3 strategies. Among patients with ST-segment-elevation myocardial infarction with multivessel disease, an immediate nonculprit PCI approach was associated with similar clinical outcomes to the staged nonculprit PCI approach. The staged out-of-hospital nonculprit PCI approach was associated with a higher incidence of MACEs compared with the other strategies, which was driven by higher risk for ischemia-driven repeat revascularization.

Association of Risk Factors of Acute Myocardial Infarction and Heart Blockage Among non-diabetic Patients in a Tertiary Care Hospital – An Observational Study

Introduction: Cardiovascular diseases (CVDs) are a leading cause of death in the world. In 2015, an estimated 442.7 million prevalent cases of CVD were present worldwide. Cardiovascular diseases account for more than 17 million deaths globally each year. Previous studies identified diabetes mellitus, hypertension, hypercholesterolemia, smoking, alcohol consumption, obesity and sedentary lifestyle as risk factors. Aim of the study: The aim of this study was to determine the risk factors for acute myocardial infarction associated with heart blockage among non-diabetic patients. Methods: This was an observational study conducted in the Department of Cardiology of Jashore Medical College Sadar Hospital, Jashore, Bangladesh during the period from April, 2021 to March, 2022. In this study, we included 120 non-diabetic patients who were diagnosed with myocardial infarction. Result: Mean age was 53.03±11.3 years &amp; most of our patients were male. Among all patients, majority (65%) patients had &gt;60% blockage, followed by 30(25%) patients had 40%-60% artery blockage, and &lt;40% blockage was found in 10% patients. Hypertension, dyslipidemia &amp; dyslipidemia with hypertension, age ≥60 years, family history of CHD, smoking, diabetes &amp; obesity were individual risk factors of CHD among non-diabetic patients. The most common risk factors for heart blockage were age &gt;45 years, high blood pressure, high LDL, unhealthy diet, and stressful life. Conclusion: In our study, we found hypertension, history of CHD, dyslipidemia, dyslipidemia with hypertension, stress, age ≥60 years, and obesity were individual risk factors for CHD. These elements work as crucial risk factors for myocardial infarction in non-diabetic patients. Risk factors like age &gt;45 years, high blood pressure, high LDL, unhealthy diet, and stressful life were responsible for the highest heart blockage in myocardial infarction patients. J Inv Clin Cardiol 2023; 5(2): 38-44

Lesion Characterization by 99mTc-MIBI Myocardial Perfusion Imaging (MPI) &amp; 18F-FDG Cardiac PET Following Myocardial Infarction Before Revascularization &amp; Outcome Prediction: Initial Experience in Bangladesh

99mTc-MIBI SPECT myocardial perfusion imaging (MPI) and 18F-FDG cardiac positron emission tomography (Cardiac PET) can assess the extent and severity of myocardial perfusion and metabolic defect following myocardial infarction (MI) and also able to predict the outcome before revascularization in known coronary artery disease patients. About 135 cases of known coronary artery disease patients were enrolled here for combined nuclear imaging tests, rest only ECG gated MPI and FDG cardiac PET to assess myocardial perfusion and viability status following MI prior to revascularization. In this study we want to figure out the utility of this combined protocol for myocardial lesion characterization and its role for clinical decision-making in-patient selection prior to revascularization and treatment planning. We are also intended to share the initial outcome in available follow up cases. J Inv Clin Cardiol 2023; 5(2): 45-52

Cardiomyocyte-Specific Overexpression of Activated Yes-Associated Protein Modified-RNA Promotes Cardiomyocyte Proliferation and Myocardial Regeneration.

The proliferative capacity of cardiomyocytes in adult mammalian hearts is far too low to replace the cells that are lost to myocardial infarction. Both cardiomyocyte proliferation and myocardial regeneration can be improved via the overexpression of a constitutively active variant of YAP5SA (Yes-associated protein, 5SA [active] mutant), but persistent overexpression of proliferation-inducing genes could lead to hypertrophy and arrhythmia, whereas off-target expression in fibroblasts and macrophages could increase fibrosis and inflammation. Transient overexpression of YAP5SA or GFP (green fluorescent protein; control) was targeted to cardiomyocytes via our cardiomyocyte-specific modified mRNA translation system (YAP5SACM-SMRTs or GFPCM-SMRTs, respectively). YAP5SA-cardiomyocyte specificity was confirmed via invitro experiments in cardiomyocytes and cardiac fibroblasts that had been differentiated from human induced- pluripotent stem cells and in human umbilical-vein endothelial cells, and the regenerative potency of YAP5SACM-SMRTs was evaluated in a mouse myocardial infarction model. In cultured human induced-pluripotent stem cells-cardiomyocytes, YAP was abundantly expressed for 3 days after YAP5SACM-SMRTs administration and was accompanied by increases in the expression of markers for proliferation, before declining to near-background levels after day 7, whereas GFP fluorescence remained high from days 1 to 3 after GFPCM-SMRTs treatment and then slowly declined. GFP fluorescence was also observed in human induced-pluripotent stem cells-cardiac fibroblasts and human umbilical-vein endothelial cells on day 1 after GFPCM-SMRTs administration but declined substantially by day 3. In the mouse myocardial infarction model, echocardiographic assessments of left-ventricular ejection fraction and fractional shortening were significantly greater, whereas infarct sizes were significantly smaller in YAP5SACM-SMRTs-treated mice than in vehicle-treated control animals, and YAP5SACM-SMRTs appeared to promote cardiomyocyte proliferation. The CM-SMRTs can be used to transiently and specifically overexpress YAP5SA in cardiomyocytes, and this treatment strategy significantly promoted cardiomyocyte proliferation and myocardial regeneration in a mouse myocardial infarction model.

Acute Myocardial Infarction in a Amphetamine Abuser with Low ASCVD Risk: A Case Report

Wide availability of recreational drugs, like amphetamine, cocaine, cannabis etc has spread out these drugs to all classes and age groups in the society of Bangladesh. Among them association cocaine and cannabis with acute myocardial infarction has been well established. But the popular drug, amphetamine, which is available in tablet form containing the active ingredient named 3,4 methylenedioxymethamphetamine (MDMA), has been reported to have significant cardiac and CNS toxicity. Repeated angina, even myocardial infarction due to active coronary vasospasm and accelerated atherothrombosis in amphetamine abusers has been reported in several case studies worldwide. But, only a few cases has been reported in Bangladesh. Here we present a case of acute myocardial infarction in a amphetamine abuser with low 10 years ASCVD risk. J Inv Clin Cardiol 2023; 5(2): 53-55