Background: Beating-heart valve surgery appears to be a promising technique for protection of hypertrophied hearts. Normothermic normokalemic simultaneous antegrade/retrograde perfusion (NNSP) may improve myocardial perfusion. However, its effects on myocardial oxygenation and energy metabolism remain unclear. The present study was to determine whether NNSP improved myocardial oxygenation and energy metabolism of hypertrophied hearts relative to normothermic normokalemic antegrade perfusion (NNAP).
Methods: Twelve hypertrophied pig hearts underwent a protocol consisting of three 20-minute perfusion episodes (10 minutes NNAP and 10 minutes NNSP in a random order) with each conducted at a different blood flow in the left anterior descending coronary artery (LAD [100%, 50%, and 20% of its initial control]). Myocardial oxygenation was assessed using near-infrared spectroscopic imaging. Myocardial energy metabolism was monitored using localized phosphorus-31 magnetic resonance spectroscopy.
Results: With 100% LAD flow, both NNAP and NNSP maintained myocardial oxygenation, adenosine triphosphate, phosphocreatine, and inorganic phosphate at normal levels. When LAD flow was reduced to 50% of its control level, NNSP resulted in a small but significant decrease in myocardial oxygenation and phosphocreatine, whereas those measurements did not change significantly during NNAP. With LAD flow further reduced to 20% of its control level, both NNAP and NNSP caused a substantial decrease in myocardial oxygenation, adenosine triphosphate, and phosphocreatine with an increase in inorganic phosphate. However, the changes were significantly greater during NNSP than during NNAP.
Conclusions: Normothermic normokalemic simultaneous antegrade/retrograde perfusion did not improve, but slightly impaired myocardial oxygenation and energy metabolism of beating hypertrophied hearts relative to NNAP. Therefore, NNSP for protection of beating hypertrophied hearts during valve surgery should be used with extra caution.
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http://dx.doi.org/10.1016/j.athoracsur.2007.01.026 | DOI Listing |
J Physiol
January 2025
Center for Developmental Health, Oregon Health & Science University, Portland, OR, USA.
Robust preclinical models of asymmetric ventricular loading in late gestation reflecting conditions such as hypoplastic left heart syndrome are lacking. We characterized the morphometry and microvascular function of the hypoplastic left ventricle (LV) and remaining right ventricle (RV) in a sham-controlled late gestation fetal lamb model of impaired left ventricular inflow (ILVI). Singleton fetuses were instrumented at ∼120 days gestational age (dGA; term is ∼147 days) with vascular catheters, an aortic flow probe and a deflated left atrial balloon.
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Cardiology Department, Hospital de Santa Marta, Unidade Local de Saúde São José, Centro Clínico Académico de Lisboa, Rua de Santa Marta N.º 50, Lisbon, 1169-024, Portugal.
Background: Right ventricular myocardial work (RVMW) assessed by transthoracic echocardiography allows to study the right ventricular (RV) function using RV pressure-strain loops. The assessment of these novel indexes of RVMW has not yet been exten sively studied, namely in pre-capillary pulmonary hypertension (PH) population.
Objectives: to evaluate the relationship between RVMW and invasive indices of right heart catheterization (RHC) in a cohort of patients with group I and group IV PH and to compare with a control group without PH.
Nat Commun
January 2025
Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Energy deprivation and metabolic rewiring of cardiomyocytes are widely recognized hallmarks of heart failure. Here, we report that HEY2 (a Hairy/Enhancer-of-split-related transcriptional repressor) is upregulated in hearts of patients with dilated cardiomyopathy. Induced Hey2 expression in zebrafish hearts or mammalian cardiomyocytes impairs mitochondrial respiration, accompanied by elevated ROS, resulting in cardiomyocyte apoptosis and heart failure.
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January 2025
Department of Anesthesiology, Hainan Hosiptal of Chinese PLA General Hospital, No.80 Jianglin Street, Haitang District, Sanya City, Hainan Province, China.
Purpose: Myocardial ischemia/reperfusion injury (MIRI) is closely associated with ferroptosis. Dexmedetomidine (Dex) has good therapeutic effects on MIRI. This study investigates whether dexmedetomidine (Dex) regulates ferroptosis during MIRI by affecting ferroportin1 (FPN) levels and elucidates the underlying mechanisms.
View Article and Find Full Text PDFNat Cardiovasc Res
January 2025
Department of Pathology, Northwestern University, Chicago, IL, USA.
Myocardial infarction (MI) mobilizes macrophages, the central protagonists of tissue repair in the infarcted heart. Although necessary for repair, macrophages also contribute to adverse remodeling and progression to heart failure. In this context, specific targeting of inflammatory macrophage activation may attenuate maladaptive responses and enhance cardiac repair.
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