Targeting antioxidant mechanisms in myocardial ischemia-reperfusion injury: A review of therapeutic strategies and clinical progress.

Stress echocardiography (SE) detects myocardial ischemia while coronary computed tomography angiography (CCTA) detects structural abnormalities associated with coronary artery disease (CAD). A pilot retrospective study of 270 consecutive patients who underwent both SE and CCTA to explore which test is more accurate in patients with CAD. Health records and risk factors, SE, and CCTA outcomes were reviewed. SE outcomes were positive (n = 36) and negative (n = 234); CCTA outcomes were based on CAD severity (absent, mild, moderate, and severe). 219 (81.1%) patients had a positive CCTA, indicating the presence of CAD with mild, moderate, or severe stenosis. Despite a positive CCTA (n = 191), 70.7% had a negative SE. This discrepancy was most prevalent in the moderate CCTA category, where 110 patients had a negative SE but positive CCTA. Additionally, 9 patients demonstrated a positive SE despite no significant CCTA findings, indicating that functional abnormalities could have remained undetected by anatomical imaging. It is suggested that significant CAD detected by CCTA does not necessarily suggest myocardial ischemia, while the presence of myocardial ischemia is not necessarily associated with significant CAD, suggesting other causes (e.g., microvascular angina). A positive CCTA but negative SE findings may suggest the presence of coronary collaterals.

Effect of State-of-the-Art Treatment on Symptoms, Absolute Coronary Artery Flow, and Resistance Among Patients With Ischemia and Non-Obstructive Coronary Arteries (STAR-INOCA Study): Study Design and Rationale.

Isolated T-Wave Inversion in Lead aVL: A Diagnostic Blind Spot in Emergency Department Chest Pain Evaluation.

A comprehensive set of per-protocol analyses of the myocardial ischemia and transfusion (MINT) trial.

An integrative strategy combining network pharmacology, metabolomics, and gut microbiota analyses to elucidate the bioactive ingredients and underlying mechanisms of Xin-Shu-Ning tablets against myocardial ischemia.

Linagliptin enhances coronary microvascular function and collateralization in a large animal model of cardiometabolic syndrome.

Expanding Myocardial Ischemia in Heart Transplantation: The Impact of SherpaPak During Prolonged Ischemic Times in a Spanish Center

Withdrawal notice to "Relationship between coronary microvascular dysfunction (CMD) and left ventricular diastolic function in patients with symptoms of myocardial ischemia with non-obstructive coronary artery disease (INOCA) by cardiovascular magnetic resonance feature-tracking"[ClinRad 79(7) (July 2024) 536-543.

The role of lipoprotein(a) in coronary microvascular dysfunction: Mechanistic pathways, clinical evidence, and therapeutic perspectives.

Objective.Coronary microvascular dysfunction (CMD) causes myocardial ischemia and is associated with adverse cardiovascular events. This study explored the value of multidimensional electrocardiogram (ECG) features in capturing pathological changes linked to CMD.Approach.Global electrical heterogeneity (GEH) parameters were extracted from vectorcardiogram (VCG) signals synthesized from ECGs of 82 CMD patients and 252 controls. Temporal- and spatial-heterogeneity indices were extracted from VCG signals and cardiodynamicsgrams (CDGs), which were derived from VCGs' ST-T loops via deterministic learning algorithms. Entropy metrics were calculated across VCG waveforms, ECG signals, their ST-T segments, and CDGs. Feature selection was performed using sequential backward selection (SBS) and random forest (RF). The optimized feature sets were separately input into multilayer perceptron, support vector machine (SVM), XGBoost, and K-nearest neighbor algorithms to select the optimal model for CMD identification.Main results.Finally, the SVM models outperformed other models using both SBS- and RF-selected feature sets. The SVM model with SBS-selected features, comprising 5 GEH parameters, 3 VCG-based features, 1 CDG-based metrics, and 9 ECG-derived features, demonstrated superior discriminative performance compared to that with RF-selected features. It achieved high accuracy (0.923), specificity (0.925), sensitivity (0.917), and an area under the curve (0.970) in CMD classification. Generalization validation was performed on the 122 healthy ECGs from the Physikalisch-Technische Bundesanstalt diagnostic ECG database and 134 healthy ECGs from China Physiological Signal Challenge 2018 database further supported the superiority SVM model. It achieved high specificity values (>0.85) across both datasets.Significance.In conclusion, the integration of multidimensional ECG, VCG, CDG, and GEH features enhances the diagnostic performance of SVM model in detecting CMD. The developed methodology provides a non-invasive diagnostic tool with high sensitivity and specificity, showing promising prospects for potential clinical application.

Sleep is an active period of profound autonomic fluctuation, cycling between the parasympathetic dominance of nonrapid eye movement sleep and the sympathetic/parasympathetic volatility of rapid eye movement sleep. Sleep-disordered breathing, a spectrum of disorders marked by recurrent ventilatory instability and intermittent hypoxia during sleep, particularly obstructive sleep apnea, pathologically amplifies this volatility, transforming sleep into a nightly cascade of severe autonomic and hemodynamic stress. The cardinal features of sleep-disordered breathing, intermittent hypoxia, recurrent arousals, and marked intrathoracic pressure swings, act synergistically to drive chronic, 24-hour sympathetic overactivity, chemoreflex sensitization, and maladaptive neuroplasticity. These effects are mediated at a cellular level by oxidative stress, systemic inflammation, endothelial dysfunction, and neuroendocrine dysregulation. This persistent autonomic reset provides a direct mechanistic link to cardiovascular consequences. It is likely a primary driver of hypertension, blunting the nocturnal blood pressure dip and promoting sustained 24-hour sympathoexcitation. It fosters a proarrhythmic substrate for atrial fibrillation through mechanical stress, which drives atrial remodeling and autonomic conflict. Furthermore, sleep-disordered breathing contributes to myocardial ischemia by increasing myocardial oxygen demand and promoting a prothrombotic state. Beyond chronic disease, sleep-related autonomic shifts can act as acute triggers for malignant arrhythmias in individuals with vulnerable substrates, such as inherited channelopathies, a risk that may be significantly amplified by comorbid sleep-disordered breathing. This review delineates the critical neural and cellular pathways connecting sleep, autonomic dysregulation, and cardiovascular risk.

Safety, pharmacokinetics, and exploratory efficacy of the oral ghrelin receptor agonist AC01 in heart failure with reduced ejection fraction (GOAL-HF1): a randomised, double-blind, placebo-controlled, phase 1b/2a study.

This study aimed to conduct a comprehensive bibliometric analysis to map the global research landscape, identify evolving hotspots, and forecast future trends in the application of coronary computed tomography-derived fractional flow reserve (CT-FFR) for diagnosing myocardial ischemia in coronary artery disease (CAD). A systematic literature search was performed in the Web of Science Core Collection for publications from 2015 to 2025, using an expanded strategy combining CT-FFR terms with synonyms for myocardial ischemia and CAD. Bibliometric data visualization and analysis were conducted using CiteSpace and VOSviewer to examine publication trends, national/institutional contributions, collaborative networks, core journals, keyword co-occurrence, and citation bursts. From an initial retrieval of 730 records, 582 eligible publications (405 articles, 117 reviews) were included. Annual publication output showed sustained growth with a compound annual growth rate (CAGR) of 6.4%. The United States led in publication volume (n = 231) and total citations, followed by China in output (n = 143), though with lower average citation impact. International collaboration was prominent, with the US, China, and Italy forming central hubs.JACC: Cardiovascular Imagingwas the leading journal in both output and influence. Keyword analysis confirmed "Fractional Flow Reserve," "Coronary Artery Disease," and "Diagnostic Performance" as core themes. Burst detection revealed a clear evolution: early research (2015-2018) focused on technical validation (e.g., "dual source ct"), while recent trends (2022-2025) shifted towards clinical integration, with strong bursts for "stable chest pain," "diagnosis," and "coronary computed tomography angiography." This bibliometric analysis delineates a dynamic and growing CT-FFR research field, marked by a transition from technological exploration to clinical guideline-directed application. The findings highlight distinct geographic patterns of productivity and influence, and clarify the evolution of research priorities towards personalized, ischemia-guided patient management. Future research is anticipated to focus on multimodal integration with plaque and perfusion imaging, artificial intelligence-driven workflow solutions, and evidence generation in complex patient cohorts to solidify clinical adoption.

Intraoperative hypotension (IOH) can affect patient outcomes following craniotomy. The Hypotension Prediction Index (HPI) can predict IOH in advance, enabling early, proactive management. We evaluated whether an HPI-integrated hemodynamic management protocol reduces IOH during brain tumor surgery. This single-center, parallel-group randomized controlled trial was registered prospectively with the Clinical Trial Registry-India (CTRI/2024/07/069939, dated 04/07/2024) and funded by the Indian Council of Medical Research. Consenting adult patients undergoing brain tumor decompression were randomized 1:1 to HPI-guided (n=90) or conventional care (control) (n=90) hemodynamic management. The primary outcome was duration of IOH (MAP<65mmHg). Secondary outcomes included time-weighted average (TWA) of IOH, episodes, severity, and timing of IOH, vasopressor use, myocardial ischemia, acute kidney injury, delirium, intensive care unit (ICU) stay, and hospital stay. Of 180 enrolled patients, 176 were analyzed (HPI n=86; control n=90). HPI guidance significantly reduced IOH duration (MAP<65mmHg: 600 [180 to 960] vs. 1820 [420 to 4620] s; P <0.001), TWA of MAP <65mmHg (0.10 [0.03 to 0.22] vs. 0.32 [0.07 to 1.01] mmHg; P <0.001), and number of hypotensive episodes (4 [2 to 7] vs. 6 [2 to 13]; P =0.004). TWA of MAP<60mmHg and <55mmHg was also significantly lower in the HPI group ( P <0.001). The IOH duration was lesser in the HPI group than in the control group during both presurgical and surgical phases. Postoperative outcomes did not differ between groups. HPI-guided hemodynamic management significantly reduced the burden of IOH during brain tumor surgery.

Hypoxia preconditioning enhances the cardioprotective effects of induced regulatory T cells after myocardial infarction through HIF-1α-mediated mechanisms.

Dipyridamole stress cardiac 99mTc-SPECT (DS-SPECT) is commonly used to detect myocardial ischemia. Blunted heart rate response (BHRR) during pharmacologic stress has been associated with adverse outcomes. This study evaluated the significance of BHRR in an unselected real-world DS-SPECT cohort and compared it with routine imaging findings. In this single-center retrospective cohort study, all adult patients who underwent dipyridamole stress SPECT without adjunct exercise between 2014 and 2017 were included. Clinical data were obtained from the electronic medical record and structured pre-test interviews, and patients were followed through September 2020. Study population consisted of 388 patients, 227 (58.5%) had normal imaging results, and 245 (63.1%) exhibited BHRR. During a mean follow-up of four years, multivariable analysis found association of BHRR with cardiovascular death (HR 8.09, 95% CI:1.06-61.91, p < 0.05). Patients with abnormal DS-SPECT imaging and BHRR had a nearly fourfold increased risk of adverse cardiovascular events (HR 3.79, 95% CI: 1.24-11.63, p < 0.05). Moreover, individuals demonstrating both abnormal imaging results and BHRR experienced the highest rate of all-cause mortality (HR 2.93, 95% CI: 1.1-7.7, p < 0.01). Overall, BHRR significantly correlated with increased all-cause and cardiovascular mortality. In unselected patients referred to DS-SPECT, BHRR was associated with cardiovascular mortality. Moreover, in our population group, when combined with abnormal imaging results, BHRR significantly increases the association with DS-SPECT for cardiovascular morbidity and all-cause mortality. These findings may support future inclusion of BHRR in DS-SPECT studies.

Chimeric antigen receptor-T cell therapy-induced cardiotoxicity: Pathophysiological mechanisms and pharmacological intervention strategies.

Microvascular dysfunction and neurovascular signalling impairment in diabetic silent myocardial ischemia.

Myocardial infarction (MI) remains a leading cause of death and disability worldwide, yet the molecular mechanisms underlying cardiomyocyte death during ischemic injury are not fully understood. Here, we identify disulfidptosis-a recently described form of regulated cell death-as a novel contributor to myocardial ischemic injury. In ischemia-mimetic models, glucose and oxygen deprivation lead to NADPH depletion and excessive disulfide bond accumulation in cardiomyocytes, accompanied by F-actin cytoskeletal collapse, a defining feature of disulfidptosis. Mechanistically, impairment of the NADPH/thioredoxin (Trx) system amplifies disulfide stress, while calcium overload-induced activation of calpains disrupts cytoskeletal protein conformation, removing steric constraints that normally prevent aberrant disulfide bonding. The synergistic effect of these two processes creates favorable oxidative and spatial structural conditions for the occurrence of disulfidptosis. Inhibition of Trx activity promotes disulfide death; pharmacological inhibition of calpainthe or blockade of calcium overload significantly reduces disulfide accumulation and preserves cytoskeletal integrity, confirming their crucial role in ischemia-induced disulfidptosis. Based on the above findings, this study confirms that disulfidptosis represents a previously unrecognized mechanism of cardiomyocyte death in myocardial ischemia, revealing the mechanistic link between metabolic stress, redox imbalance, and cytoskeletal collapse; and proposing a novel pathological remodeling process of disulfide bonds characterized by "Cleavage-Fragmentation-Mismatch". These insights provide new conceptual and therapeutic perspectives for cardioprotection.