infarction heart
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2022 ◽  
pp. 80-127
Author(s):  
Viswanathan Rajagopalan ◽  
Houwei Cao

Despite significant advancements in diagnosis and disease management, cardiovascular (CV) disorders remain the No. 1 killer both in the United States and across the world, and innovative and transformative technologies such as artificial intelligence (AI) are increasingly employed in CV medicine. In this chapter, the authors introduce different AI and machine learning (ML) tools including support vector machine (SVM), gradient boosting machine (GBM), and deep learning models (DL), and their applicability to advance CV diagnosis and disease classification, and risk prediction and patient management. The applications include, but are not limited to, electrocardiogram, imaging, genomics, and drug research in different CV pathologies such as myocardial infarction (heart attack), heart failure, congenital heart disease, arrhythmias, valvular abnormalities, etc.


Author(s):  
Claudio Humeres ◽  
Arti V. Shinde ◽  
Anis Hanna ◽  
Linda Alex ◽  
Silvia C. Hernandez ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Zhenzhen Chen ◽  
Youyou Yan ◽  
Chao Qi ◽  
Jia Liu ◽  
Longbo Li ◽  
...  

Cardiovascular diseases (CVDs) are the leading cause of deaths worldwide with regulated cell death playing an important role in cardiac pathophysiology. However, the classical mode of cell death cannot fully explain the occurrence and development of heart disease. In recent years, much research has been performed on ferroptosis, a new type of cell death that causes cell damage and contributes to the development of atherosclerosis, myocardial infarction, heart failure, and other diseases. In this review, we discuss the role of different organelles in ferroptosis and also focus on the relationship between autophagy and ferroptosis. Additionally, we describe the specific mechanism by which ferroptosis contributes to the development of CVD. Finally, we summarize the current research on ferroptosis-related pathway inhibitors and the applications of clinically beneficial cardiovascular drugs.


2021 ◽  
Vol 22 (19) ◽  
pp. 10885
Author(s):  
Katarzyna Fiedorowicz ◽  
Weronika Wargocka-Matuszewska ◽  
Karolina A. Ambrożkiewicz ◽  
Anna Rugowska ◽  
Łukasz Cheda ◽  
...  

Current treatment protocols for myocardial infarction improve the outcome of disease to some extent but do not provide the clue for full regeneration of the heart tissues. An increasing body of evidence has shown that transplantation of cells may lead to some organ recovery. However, the optimal stem cell population has not been yet identified. We would like to propose a novel pro-regenerative treatment for post-infarction heart based on the combination of human skeletal myoblasts (huSkM) and mesenchymal stem cells (MSCs). huSkM native or overexpressing gene coding for Cx43 (huSKMCx43) alone or combined with MSCs were delivered in four cellular therapeutic variants into the healthy and post-infarction heart of mice while using molecular reporter probes. Single-Photon Emission Computed Tomography/Computed Tomography (SPECT/CT) performed right after cell delivery and 24 h later revealed a trend towards an increase in the isotopic uptake in the post-infarction group of animals treated by a combination of huSkMCx43 with MSC. Bioluminescent imaging (BLI) showed the highest increase in firefly luciferase (fluc) signal intensity in post-infarction heart treated with combination of huSkM and MSCs vs. huSkM alone (p < 0.0001). In healthy myocardium, however, nanoluciferase signal (nanoluc) intensity varied markedly between animals treated with stem cell populations either alone or in combinations with the tendency to be simply decreased. Therefore, our observations seem to show that MSCs supported viability, engraftment, and even proliferation of huSkM in the post-infarction heart.


2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Alexander S Milliken ◽  
Sergiy M Nadtochiy ◽  
Paul S Brookes

Succinate is a metabolite that plays a central role in ischemia-reperfusion (IR) injury,which is relevant to myocardial infarction (heart attack) and stroke. Succinateaccumulates during ischemia and is rapidly consumed at reperfusion driving reactiveoxygen species (ROS) generation at complex-I (Cx-I) and III of the mitochondrial electrontransport chain. This ROS production triggers cell-death, leading to tissue necrosis.Although succinate oxidation has been extensively studied and exploited as a noveltherapeutic target, only 1/3 of the succinate accumulated in ischemia is oxidized atreperfusion, with the remaining 2/3 being released from the cell via monocarboxylatetransporter 1 (MCT1). Extracellular succinate is thought to be pro-inflammatory, and ithas been proposed that preventing succinate release may be therapeutically beneficial.To determine the impact of preventing succinate release on IR injury, we comparedfunctional recovery (i.e. rate x pressure product, RPP) and infarction (i.e. tissue necrosis)of Langendorff perfused mouse hearts treated with an MCT1 inhibitor, AR-C155858,versus vehicle control. This revealed that succinate retention worsens IR injury (i.e.increased infarction and decreased functional recovery) likely due to increased ROS. Totest this hypothesis, we utilized a Langendorff apparatus positioned within aspectrofluorimeter, which permits real-time fluorescence measurements in beatingmouse hearts. Using the mitochondria targeted superoxide probe, MitoSOX red tomeasure ROS production at reperfusion + AR-C155858, demonstrated that succinateretention leads to enhanced mitochondrial ROS generation at the onset of reperfusion.Overall, these results suggest that inhibiting succinate release in the context of IR injurymay not be a viable therapeutic approach, regardless of any downstream anti-inflammatory effects.


2021 ◽  
Vol 7 (3) ◽  
pp. 70-76
Author(s):  
Botond Matyas ◽  
Stefania Polexa ◽  
Imre Benedek ◽  
Andreea Buicu ◽  
Theodora Benedek

Abstract Background: The aim of this study was to investigate the correlation between serum biomarkers of left ventricular dysfunction and systemic inflammation in the first days after the acute episode, and to investigate their role for early identification of patients at high risk for post-infarction heart failure. Materials and methods: In total, 123 subjects admitted to the Intensive Cardiovascular Care Unit of the Cardiology Clinic of the Târgu Mureș County Clinical Emergency Hospital, Romania, with acute myocardial infarction were retrospectively analyzed in this study. Based on the level of NT-proBNP, the study population was divided into 2 groups: Group 1 (n = 92), with NT-proBNP <3,000 pg/mL, and Group 2 (n = 31), with NT-proBNP >3,000 pg/mL. Results: Biomarkers reflecting systemic inflammation presented significantly higher values in patients with elevated NT-proBNP (hs-CRP – 12.3 ± 8.9 mg/L vs. 3.6 ± 6.7 mg/L, p <0.0001, and interleukin 6 – 27.6 ± 30.7 pg/mL vs. 8.6 ± 6.2 pg/mL, p <0.0001). However, cell adhesion molecules VCAM and ICAM were not significantly different between the groups. Patients in Group 2 presented significantly higher rates of major cardiovascular events and rehospitalizations in the first year after the acute coronary event, with 13.33% event rate for patients in Group 2 compared to 8.7% in Group 1 (p <0.05). Conclusions: Serum biomarkers of ventricular dysfunction are strongly associated with systemic inflammation and ventricular impairment in the immediate phase after an acute myocardial infarction. Systemic inflammation has a higher impact on the clinical outcomes and progression to heart failure than the local coronary inflammation expressed by cell adhesion molecules.


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