ReviewCureus2026
Myocardial Metabolism and Postoperative Risk Stratification in Cardiac Surgery: A Narrative Review and Conceptual Framework.
Review in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Retracted
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Postoperative complications following cardiac surgery remain a significant source of morbidity and mortality despite substantial advances in operative technique and perioperative care, underscoring the need for more precise and individualized risk stratification strategies. Existing prediction models rely primarily on demographic variables, comorbid conditions, and structural measures of cardiac function. However, they do not account for myocardial energetic resilience or the heart's capacity to tolerate ischemia-reperfusion injury and hemodynamic stress. Myocardial metabolism, encompassing substrate utilization, mitochondrial oxidative phosphorylation, bioenergetic reserve, redox homeostasis, calcium handling, and inflammatory signaling, represents a biologically plausible and mechanistically relevant contributor to perioperative risk, though the strength and consistency of this relationship across study types remain heterogeneous. Impairments in metabolic flexibility, reduced mitochondrial respiratory capacity, inefficient adenosine triphosphate (ATP) generation, and heightened oxidative stress have been associated with, though not consistently shown to predict directly, adverse postoperative outcomes, including low cardiac output syndrome, arrhythmias, prolonged inotropic support, and significant morbidity or mortality, even among patients with similar structural and demographic risk profiles. Emerging approaches to metabolic phenotyping, including noninvasive metabolic imaging, circulating metabolite and redox biomarker panels, and ex vivo mitochondrial functional assays, offer complementary pathways for quantifying myocardial energetic state; however, much of this evidence remains early-stage, indirect, or translational in nature, derived largely from preclinical models, small cohorts, or non-cardiac surgical populations, with limited standardization and prospective clinical validation to date. Collectively, the available mechanistic and early clinical evidence support further investigation into myocardial metabolic profiling as a potential adjunct to established clinical risk scores, rather than immediate clinical integration, with the longer-term potential to refine perioperative risk assessment, identify metabolically vulnerable patients with greater precision, and advance a physiology-driven, personalized framework for cardiac surgical care.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.