Despite considerable improvement in diagnostic modalities and therapeutic options over the last few decades, the global burden of ischemic heart disease is steadily rising, remaining a major cause of death worldwide. Thus, new strategies are needed to lessen cardiovascular events. Researchers in different areas such as biotechnology and tissue engineering have developed novel therapeutic strategies such as stem cells, nanotechnology, and robotic surgery, among others (3D printing and drugs). In addition, advances in bioengineering have led to the emergence of new diagnostic and prognostic techniques, such as quantitative flow ratio (QFR), and biomarkers for atherosclerosis. In this review, we explore novel diagnostic invasive and noninvasive modalities that allow a more detailed characterization of coronary disease. We delve into new technological revascularization procedures and pharmacological agents that target several residual cardiovascular risks, including inflammatory, thrombotic, and metabolic pathways.
A meu orientador Prof. Dr. Whady Hueb por toda paciência, pelo acolhimento, por dividir seu imenso conhecimento e experiência em Cardiologia e Pesquisa.Ter sido seu orientando representa uma grande honra e responsabilidade, visto sua mundialmente reconhecida referência na história e desenvolvimento da Cardiologia.Ao Dr. Paulo Cury Rezende, amigo e co-orientador, pelo exemplo inigualável de solicitude, apoio, dedicação, por não deixar de acreditar em minha tese, mesmo em momentos de grande desafio. Seu conhecimento e paixão pela pesquisa refletem-se em minha trajetória e estarão referenciados, como inspiração por toda minha carreira. Ao Dr. Eduardo Gomes Lima, espelho de cardiologista e pesquisador, por muito ter me ensinado sobre Cardiologia, pela amizade, por ter acreditado em meu potencial e apresentado-me ao Grupo MASS, como pós-graduando.A toda equipe do GRUPO MASS, Myrthes Takiuti, Eliana Lima, Laura Caringe e Marcela Silva pelo acolhimento, humanismo, competência técnica com trabalho primoroso, tornando o MASS mais que um grupo de pesquisa, mas também uma família acolhedora e alegre, deixando os dias de trabalho mais suaves.Aos amigos-irmãos, Guilherme Fernandes e Mauricio Mocha, exemplos de inteligência, criatividade, pela amizade desde a residência de Cardiologia, por muito me ensinarem, pelo apoio, por dividirem momentos divertidos e de descontração, mas também por estarem presentes nos momentos mais difíceis.
Background The correlation between the release of cardiac biomarkers after revascularization, in the absence of late gadolinium enhancement (LGE) or myocardial edema, and the development of myocardial tissue damage remains unclear. This study sought to identify whether the release of biomarkers is associated with cardiac damage by assessing myocardial microstructure on T1 mapping after on-pump (ONCAB) and off-pump coronary artery bypass grafting (OPCAB). Methods Seventy-six patients with stable multivessel coronary artery disease (CAD) and preserved systolic ventricular function were included. T1 mapping, high-sensitive cardiac troponin I (cTnI), creatine kinase myocardial band (CK-MB) mass, and ventricular dimensions and function were measured before and after procedures. Results Of the 76 patients, 44 underwent OPCAB, and 32 ONCAB; 52 were men (68.4%), and the mean age was 63±8.5 years. In both OPCAB and ONCAB the native T1 values were similar before and after surgeries. An increase in extracellular volume (ECV) values after the procedures was observed, due to the decrease in hematocrit levels during the second cardiac resonance. However, the lambda partition coefficient showed no significant difference after the surgeries. The median peak release of cTnI and CK-MB were higher after ONCAB than after OPCAB [3.55 (2.12–4.9) vs . 2.19 (0.69–3.4) ng/mL, P=0.009 and 28.7 (18.2–55.4) vs . 14.3 (9.3–29.2) ng/mL, P=0.009, respectively]. Left ventricular ejection fraction (LVEF) was similar in both groups before and after surgery. Conclusions In the absence of documented myocardial infarction, T1 mapping did not identify structural tissue damage after surgical revascularization with or without cardiopulmonary bypass (CPB), despite the excessive release of cardiac biomarkers.
Aims To analyze the association of myocardial edema (ME), observed as high T2-signal intensity (HT2) in cardiac magnetic resonance imaging (CMR), with the release of cardiac biomarkers, ventricular ejection, and clinical outcomes after revascularization. Methods and Results Patients with stable coronary artery disease with indication for revascularization were included. Biomarker levels (Troponin I [c-TnI] and creatine-kinase MB [CK-MB]) and T2-weighted and late gadolinium enhancement (LGE) images were obtained before and after the percutaneous or surgical revascularization procedures. The association of HT2 with the levels of biomarkers, with and without LGE, evolution of ejection fraction (LVEF), and 5-year clinical outcomes were assessed. A total of 196 patients were divided into two groups: Group 1 (HT2, 40) and Group 2 (no HT2, 156). Both peak c-TnI (8.9 and 1.6 ng/mL) and peak CK-MB values (44.7 and 12.1 ng/mL) were significantly higher in Group 1. Based on the presence of new LGE, patients were stratified into Groups A (no HT2/LGE, 149), B (HT2, 9), C (LGE, 7), and D (both HT2/LGE, 31). The peak c-TnI and CK-MB values were 1.5 and 12.0, 5.4 and 44.7, 5.0 and 18.3, and 9.8 and 42.8 ng/mL in Groups A, B, C, and D, respectively, and were significantly different. Average LVEF decreased 4.4% in Group 1 and increased 2.2% in Group 2 (p=0.057). Conclusion ME after revascularization procedures was associated with increased release of cardiac necrosis biomarkers, and a trend towards a difference in LVEF, indicating a role of ME in cardiac injury after interventions.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.