Oxygen Supply-demand Mismatch Research Articles

Abstract 4138376: A Machine Learning Approach to Predict Percutaneous Coronary Intervention in Patients with Critical Illness and Signs of Myocardial Injury

Background: Critically ill patients frequently experience multi-organ dysfunction and unstable vital signs, increasing their risk of myocardial injury and elevated serum troponin levels. Myocardial injury from oxygen supply-demand mismatch, whether due to systemic disease or obstructive coronary artery disease (CAD), often leads to patients undergoing an invasive coronary angiogram (ICA) and potentially percutaneous coronary intervention (PCI) if obstructive CAD is identified. However, this procedure carries significant risks for critically ill patients. To address this challenge, we aimed to develop a machine learning (ML) model to predict the need for PCI in critically ill patients with myocardial injury. Methods: The study cohort included critically ill patients with elevated serum troponin levels who underwent ICA during their hospitalization at a single institution from 2012 to 2022. We defined critical illness as a life-threatening condition requiring intensive support for vital sign instability. Patients with atherothrombosis identified during ICA were excluded from the study, focusing only on patients with type 2 MI. We utilized Matplotlib to analyze patient data, including demographics, lab results, vital signs, and comorbidities. We then used XGBoost, a supervised ML algorithm, for binary classification tasks. An ensemble of decision trees was employed, with gradient boosting to correct errors from previous trees. XGBoost iteratively adjusted predictions, creating a model to predict which patients required PCI. Results: Out of 765 patients, 173 (22.6%) underwent PCI. The cohort had a mean age of 60.5 ± 13.5 years, with 41.7% being female. The ML model accurately identified non-PCI candidates at 75% and PCI candidates at 64%, achieving an overall accuracy of 73%. The three most important features identified by the model were a history of diabetes, diastolic heart failure, and whether the patient received a blood transfusion during hospitalization. Conclusion: A ML approach using XGBoost demonstrated moderate accuracy in predicting the need for PCI in critically ill patients with signs of myocardial injury. This prediction holds clinical significance due to the heightened risks associated with ICA in these patients. Given that PCI occurred in only 22.6% of the cohort, future models should include a higher proportion of patients who underwent PCI to improve the robustness and true positive accuracy of the model.

Triggers of type 2 myocardial infarction: implications for long-term prognosis

Abstract Background Type 2 myocardial infarction (T2MI) is characterized by a mismatch between myocardial oxygen supply and demand, unrelated to acute coronary thrombosis. This discrepancy arises from triggers, which may or may not be of cardiac origin. Common cardiac triggers include coronary artery spasm, coronary embolism, and arrhythmias, whereas non-cardiac triggers encompass factors such as anemia, hypertension/hypotension, sepsis, renal damage, and respiratory failure. However, identifying these triggers isn't always straightforward. Aim Our study aimed to identify, whenever possible, the triggers contributing to the oxygen supply-demand mismatch in T2MI cases, as defined by the Fourth Universal Definition of Myocardial Infarction. Additionally, we sought to explore the correlation between these triggers and patient prognosis. Methods We enrolled all consecutive patients diagnosed with non-ST-segment elevation myocardial infarction (NSTEMI) who met the criteria for T2MI and underwent coronary angiography within 72 hours of diagnosis. Patients were categorized into three groups based on the trigger causing T2MI: cardiac, non-cardiac, and unidentified. The primary endpoint was the occurrence of major adverse cardiovascular events (MACEs), including all-cause mortality, new myocardial infarction, hospitalization for heart failure, and ischemic stroke, during long-term follow-up. We estimated MACE-free survival using Kaplan-Meier curves and compared it among the three groups using the log-rank test. Multivariable logistic regression analysis was performed to identify independent predictors of MACE. Results The final cohort comprised 598 T2MI patients, with 308 having a cardiac trigger, 147 having a non-cardiac trigger, and 143 with an unidentified trigger. The mean age of the overall population was 69.6±13.1 years, with a median follow-up time of 25 (13-49) months. Kaplan-Meier curves demonstrated statistically significant differences in MACEs based on the trigger causing T2MI (p<0.001). Specifically, patients with an unidentified trigger exhibited a better prognosis, while those with a non-cardiac trigger had a worse prognosis during long-term follow-up. Multivariable logistic regression analysis confirmed that not having an identified trigger is an independent protective factor for MACEs (HR 0.63, 95% CI 0.45-0.89, p=0.009, unidentified trigger vs cardiac + non-cardiac trigger). Conclusions T2MI is prevalent in clinical practice, yet reliable outcome predictors remain elusive. Our findings indicate a relationship between the type of trigger precipitating T2MI and patient prognosis, notably demonstrating that the absence of a specific identifiable trigger is linked to a more favorable long-term outcome. Further studies are needed to better define the prognostic stratification of these patients.MACE-free survival Kaplan Meier

Evaluation of troponinI serum levels in patients with arrhythmias with and without coronary artery disease.

Elevated levels of cardiac enzymes in the blood are an indicator of ongoing cardiac ischemia. Persistent tachycardia may lead to myocardial ischemia due to oxygen supply-demand mismatch. We sought to evaluate the probability of underlying coronary artery disease (CAD) in patients with symptomatic supraventricular (SVT) or ventricular tachyarrhythmias (VT) based on cardiac enzyme level fluctuation. Troponin I (TNI) levels were measured twice and coronary angiography was also performed in patients without a history of cardiovascular disease and symptomatic SVT or VT. Of the 114 (group A: CAD (n = 40), group B: no CAD (n = 74)) patients eligible for the study, 34patients in group A and 64patients in group B had SVT, while 6patients in group A and 10 patients in group B had VT. All patients with underlying CAD developed a significantly elevated TNI level compared to baseline, irrespective of arrhythmia type (2.02 ± 7.98 ng/ml vs. 5.64 ± 13.38, p = 0.031). In patients without CAD, TNI level was not significantly elevated compared to the baseline level, irrespective of arrhythmia type (0.34 ± 1.38 ng/ml vs. 0.48 ± 1.48 ng/ml, p = 0.158). Most patients with normal TNI levels (46 of 47 patients; 98 %) had SVT. CAD was present in 13 of 47 patients (27 %) with tachycardia, despite normal TNI levels. Elevated TNI levels are not helpful to discriminate between SVT and VT. An increase in TNI level in repeated blood sampling can help identify patients with higher probability of underlying CAD. Patients with VT demonstrated higher increases in TNI levels, compared to patients with SVT.

Histopathologic Validation of Stress T1 Mapping in Myocardial Ischemia: Another Step toward Clinical Translation?

Histopathologic Validation of Stress T1 Mapping in Myocardial Ischemia: Another Step toward Clinical Translation?

The bidirectional association between atrial fibrillation and myocardial infarction.

Atrial fibrillation (AF) is associated with an increased risk of myocardial infarction (MI) and vice versa. This bidirectional association relies on shared risk factors as well as on several direct and indirect mechanisms, including inflammation, atrial ischaemia, left ventricular remodelling, myocardial oxygen supply-demand mismatch and coronary artery embolism, through which one condition can predispose to the other. Patients with both AF and MI are at greater risk of stroke, heart failure and death than patients with only one of the conditions. In this Review, we describe the bidirectional association between AF and MI. We discuss the pathogenic basis of this bidirectional relationship, describe the risk of adverse outcomes when the two conditions coexist, and review current data and guidelines on the prevention and management of both conditions. We also identify important gaps in the literature and propose directions for future research on the bidirectional association between AF and MI. The Review also features a summary of methodological approaches for the study of bidirectional associations in population-based studies.

Angina in 2022: Current Perspectives.

Angina is the main symptom of ischemic heart disease; mirroring a mismatch between oxygen supply and demand. Epicardial coronary stenoses are only responsible for nearly half of the patients presenting with angina; whereas in several cases; symptoms may underlie coronary vasomotor disorders; such as microvascular dysfunction or epicardial spasm. Various medications have been proven to improve the prognosis and quality of life; representing the treatment of choice in stable angina and leaving revascularization only in particular coronary anatomies or poorly controlled symptoms despite optimal medical therapy. Antianginal medications aim to reduce the oxygen supply-demand mismatch and are generally effective in improving symptoms; quality of life; effort tolerance and time to ischemia onset and may improve prognosis in selected populations. Since antianginal medications have different mechanisms of action and side effects; their use should be tailored according to patient history and potential drug-drug interactions. Angina with non-obstructed coronary arteries patients should be phenotyped with invasive assessment and treated accordingly. Patients with refractory angina represent a higher-risk population in which some therapeutic options are available to reduce symptoms and improve quality of life; but robust data from large randomized controlled trials are still lacking.

Abstract 14372: Case Series: Non-Lipid Plaque Formation as the Mechanism for Ponatinib-Induced Vascular Toxicity Using Operator-Assisted Virtual Histology Optical Coherence Tomography

Introduction: The third-generation tyrosine kinase inhibitor ponatinib approved for treating chronic myeloid leukemia (CML) rendered drug resistant with a threonine-315-isoleucine (T315I) mutation is associated with increased incidence of vascular adverse events (VAEs). This case series sought to elucidate the mechanism of these VAEs. Methods: Two patients with CML and two patients with Philadelphia chromosome positive acute lymphocytic leukemia (Ph+ ALL) on at least one year of ponatinib therapy were imaged with optical coherence tomography (OCT) after presenting with angina. An additional four patients from an institutional OCT database were matched across clinical parameters (age, sex, diabetes, prior coronary artery disease (CAD) history, prior congestive heart failure (CHF) history, hypertension, and family history of CAD) to serve as controls. Plaque composition was assessed using operator-assisted virtual histology OCT (vOCT). Results: Clinical presentations included 2 cases of NSTEMI, 1 case of unstable angina, and 1 case of stable angina pectoris among the 4 ponatinib patients. Atherosclerosis was composed primarily of calcium and fibrous tissue with minimal lipid presence (0 ± 0°) compared to the matched controls. The matched controls had a mean non-zero lipid content of 48.43 ± 18.36°, ( P < 0.05) (Table 1). Three of the four patients had cardiovascular risk factors. Conclusions: Ponatinib causes VAEs through non-lipid plaque formation driving a symptomatology consistent with an oxygen supply-demand mismatch. This mechanism is distinct from traditional pathways of excess lipid and plaque instability causing coronary artery disease and merits further investigation.

MASSIVE PULMONARY ARTERY ANEURYSM: AN UNCOMMON CAUSE OF MYOCARDIAL ISCHEMIA

MASSIVE PULMONARY ARTERY ANEURYSM: AN UNCOMMON CAUSE OF MYOCARDIAL ISCHEMIA

High-sensitivity Cardiac Troponin T in Sepsis:Prognostic Value and Risk Factors of Its Elevation

Objective To explore the prognostic value of high-sensitivity cardiac troponin T (hs-cTnT) in predicting mortality within 28 days among sepsis patients,and to investigate the risk factors of hs-cTnT elevation. Methods The clinical and laboratory data of patients with sepsis or septic shock who were hospitalized at the Second Affiliated Hospital of Chongqing Medical University from December 2017 to September 2021 were collected and retrospectively analyzed.The patients were assigned into a hs-cTnT elevated group (hs-cTnT>0.1 ng/ml) and a hs-cTnT non-elevated group (hs-cTnT≤0.1 ng/ml).The prognosis was compared between the two groups and the risk factors of hs-cTnT elevation were determined. Results A total of 225 patients were included in this study,including 49 in hs-cTnT elevated group (21.8%) and 176 in hs-cTnT non-elevated group (78.2%).The receiver operating characteristic curve showed that maximum hs-cTnT had predictive value for death within 28 days (P<0.001).The maximum hs-cTnT showed the area under the receiver operating characteristic curve of 0.767 (95%CI=0.699-0.835),the sensitivity of 62.5%,and the specificity of 79.9%.The mortality within 28 days of hs-cTnT elevated group was higher than that of hs-cTnT non-elevated group (53.1% vs. 17.0%, χ2=26.595, P<0.001).Multivariate Logistic regression analysis revealed that the independent predictors of hs-cTnT elevation were age ≥75.5 years (OR=5.990, 95%CI=2.143-16.742, P=0.001),lactate ≥4.05 mmol/L (OR=4.982,95%CI=1.433-17.315,P=0.012),oxygenation index ≤169.15 mmHg (OR=5.052, 95%CI=1.888-13.514, P=0.001),B-type brain natriuretic peptide precursor ≥6 687.0 pg/ml (OR=5.991, 95%CI=2.226-16.128, P<0.001),fibrinogen ≤2.87 g/L (OR=3.325,95%CI=1.175-9.404, P=0.024),and International Society on Thrombosis and Haemostasis overt disseminated intravascular coagulation score ≥5.5 (OR=7.631, 95%CI=1.157-50.338, P=0.035). Conclusions hs-cTnT showed good performance in predicting mortality within 28 days among the patients with sepsis.Coagulation disorder,microthrombus formation,and myocardial oxygen supply-demand mismatch may be the risk factors of myocardial injury in sepsis.

Mechanisms of Myocardial Ischemia in Cancer Patients: A State-of-the-Art Review of Obstructive Versus Non-Obstructive Causes.

In patients with cancer, myocardial infarction (MI) has distinct features and mechanisms compared to the non-oncology population. Triggers of myocardial ischemia specific to the oncology population have been increasingly identified. Coronary plaque disruption, coronary vasospasm, coronary microvascular dysfunction, spontaneous coronary artery dissection, and coronary oxygen supply-demand mismatch are all causes of MI that have been shown to have specific triggers related to either the treatments or complications of cancer. MI can occur in the presence or absence of atherosclerotic coronary artery disease (CAD). MI with nonobstructive CAD (MINOCA) is a heterogeneous syndrome that has distinct pathophysiology and different epidemiology from MI with significant CAD (MI-CAD). Recognition and differentiation of MI-CAD and MINOCA is essential in the oncology population, due to unique etiology and impact on diagnosis, management, and overall outcomes. There are currently no reports in the literature concerning MINOCA as a unified syndrome in oncology patients. The purpose of this review is to analyze the literature for studies related to known triggers of myocardial ischemia in cancer patients, with a focus on MINOCA. We propose that certain cancer treatments can induce MINOCA-like states, and further research is warranted to investigate mechanisms that may be unique to certain cancer states and types of treatment.

Recurrent myocardial injury is a strong predictor of ICU mortality in COVID-19

Abstract Funding Acknowledgements Type of funding sources: None. Background Myocardial injury is common in COVID-19, and has been linked to disease severity and mortality.1 Its pathophysiology is not fully elucidated and suggested mechanisms include cytokine damage, endotheliitis, myocarditis, ferroptosis, acute coronary syndrome, oxygen supply-demand mismatch and pulmonary embolism.2-3 Elevated serum cardiac troponin (cTn) – as surrogate marker of myocardial injury – at admission and during hospitalisation is associated with poor outcome.4-5 Comparison of available trial data, however, is unfeasible, because of variable definition and sampling timing/intervals/assays.6 Peculiarly, prognostic cut-off cTn values are often – retrospectively – set much lower than recommended by the guidelines.6-8 Furthermore, robust intensive care unit (ICU) outcome data regarding cTn evolution over time is lacking. Purpose The aim of this study is to critically explore the correlation between myocardial injury and mortality in a tertiary ICU population, using both standard and high cTn cut-off values, and to scrutinise the impact of timing and recurrence. Methods All adult COVID-19 patients admitted to our tertiary ICU between 06/03/2020 and 27/09/2021 were enrolled in this large, retrospective, single centre, cohort study. Patients requiring extracorporeal membrane oxygenation (n=29) were excluded. Myocardial injury was defined – as per ESC guidelines - as high-sensitive cardiac troponin I (hs-cTnI) peak &amp;gt;45ng/L (99th percentile upper reference limit) and ‘major’ myocardial injury was defined as hs-cTnI &amp;gt;135ng/L (3x upper limit of normal).6-7 Recurrent myocardial injury was considered if a new hs-cTnI peak above cut-off point occurred after normalisation. Patients were categorised according to peak (‘standard’ &amp;gt;45ng/L vs ‘high’ &amp;gt;135ng/L), onset (‘on admission’ vs ‘during hospitalisation’) and recurrence (‘single’ vs ‘multiple’) of hs-cTnI rise. Statistical analysis was done by logistic regression, using IBM SPSS version 28. Results A total of 193 COVID-19 ICU patients were included. Patient characteristics, disease severity indices and treatment details are summarised in Table 1. The mean age was 62 years and ICU mortality was 22%. Myocardial injury overall occurred in 51% (n=99) and major myocardial injury occurred in 39% (n=75) of patients. Obtained results were consistent across standard (&amp;gt;45ng/L) and high (&amp;gt;135ng/L) hs-cTnI cut-off groups. Myocardial injury only present at ICU admission was not correlated with mortality in our cohort, contradicting prior (mostly non-ICU) trials. Single hs-cTnI peak during ICU hospitalisation, however, and, especially recurrent hs-cTnI peaks were strong predictors of ICU mortality. The respective incidence, odds ratio, 95% confidence intervals and p-values are displayed in Table 2. Conclusion Myocardial injury occurring during ICU hospitalisation and, especially, recurrent myocardial injury is strongly correlated with ICU mortality in COVID-19 patients.

Emerging Role of Platelet-Endothelium Interactions in the Pathogenesis of Severe SARS-CoV-2 Infection-Associated Myocardial Injury.

Cardiovascular dysfunction and disease are common and frequently fatal complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, from early on during the SARS-CoV-2 virus pandemic it was recognized that cardiac complications may occur, even in patients with no underlying cardiac disorders, as part of the acute infection, and that these were associated with more severe disease and increased morbidity and mortality. The most common cardiac complication is acute cardiac injury, defined by significant elevation of cardiac troponins. The potential mechanisms of cardiovascular complications include direct viral myocardial injury, systemic inflammation induced by the virus, sepsis, arrhythmia, myocardial oxygen supply-demand mismatch, electrolyte abnormalities, and hypercoagulability. This review is focused on the prevalence, risk factors and clinical course of COVID-19-related myocardial injury, as well as on current data with regard to disease pathogenesis, specifically the interaction of platelets with the vascular endothelium. The latter section includes consideration of the role of SARS-CoV-2 proteins in triggering development of a generalized endotheliitis that, in turn, drives intense activation of platelets. Most prominently, SARS-CoV-2–induced endotheliitis involves interaction of the viral spike protein with endothelial angiotensin-converting enzyme 2 (ACE2) together with alternative mechanisms that involve the nucleocapsid and viroporin. In addition, the mechanisms by which activated platelets intensify endothelial activation and dysfunction, seemingly driven by release of the platelet-derived calcium-binding proteins, SA100A8 and SA100A9, are described. These events create a SARS-CoV-2–driven cycle of intravascular inflammation and coagulation, which contributes significantly to a poor clinical outcome in patients with severe disease.

Type 2 Myocardial Infarction: CURRENT CONCEPTS AND OUR EXPERIENCE WITH CARDIAC REHABILITATION.

Type 2 myocardial infarction (T2MI) is commonly encountered in clinical practice, yet little is known about this challenging condition. Outpatient cardiac rehabilitation (CR) is an integral component in the care of patients with MI. However, specific recommendations for CR, information on the feasibility of participation, and outcome measures for patients with T2MI are lacking. The frequency of T2MI is markedly variable and depends on the studied population, disease definition, adjudication process, cardiac troponin assays, and cutoff values used to make the diagnosis of T2MI. Clinically, it is difficult to distinguish T2MI from type 1 MI or myocardial injury. Type 2 myocardial infarction occurs due to myocardial oxygen supply-demand mismatch without acute atherothrombotic plaque disruption and is associated with adverse short- and long-term prognoses. Currently, there are substantial gaps in knowledge regarding T2MI and there are no clear guidelines for the optimal management of these patients. In this article, we present important current concepts surrounding T2MI including the definition, pathophysiology, epidemiology, diagnosis, prognosis, and management. We also discuss referral patterns to CR and participation rates and provide our experience with a case series of 17 patients. Very few patients with T2MI are referred to and participate in CR. Our small case series indicated that patients with T2MI respond favorably to CR and that exercise training following standard guidelines appears safe and is well tolerated.

Mechanisms and management of prothrombotic state in COVID-19 disease.

The novel severe acute respiratory syndrome viral disease outbreak due to SARS-CoV-2 is a rapidly evolving disease and represents one of the greatest medical challenges in recent times. It is believed that SARS-CoV-2 has migrated from bats to an intermediate host and then to humans. This article aims at the mechanism and management of prothrombotic state in COVID-19 positive patients. We tried to present how the SARS-CoV-2 virus can induce thromboembolic events and the incidence of these thromboembolic events. We also tried to depict anticoagulation management in these patients as well as postdischarge plan and follow-up. Invasion of type 2 pneumocytes by the SARS-CoV-2 virus is critical in the course of illness because it results in activation of immune cells leading to elevation of cytokines. The subsequent activation of T cells and macrophages infiltrates the infected myocardial cells causing direct myocardiocyte toxicity and development of arrhythmia. Hypoxia or hypotension during the clinical course causes a mismatch between myocyte oxygen supply and workload demand resulting in cardiac distress. SARS-CoV-2 affects endothelial cells and pericytes that lead to severe micro and macrovascular dysfunction, and together with oxygen supply-demand mismatch, immune hyperresponsivity can potentially cause destabilization and plaque rupture causing acute coronary syndromes. Other mechanisms of injury include myocarditis, pericarditis, stress cardiomyopathy, vasculitis, and DIC (Disseminated intravascular coagulation)/microthrombi. SARS-CoV-2 enters the cells by the Spike protein S whose surface unit, S1, binds to the ACE2 receptor on the host cell. The type II transmembrane serine proteases TMPRSS2 and histone acetyltransferases (HAT) are host cell proteases that are recruited by the virus to cleave ACE2 surface protein S which facilitates the viral entry. Therefore, TMPRSS2 and HAT could be targeted for potential drugs against SARS-CoV-2. SARS-CoV-2 uses an RNA-dependent RNA polymerase for proliferation, which is targeted by remdesivir that is currently approved for emergency use by Food and Drug Administration (FDA). We need to adopt a multifaceted approach when combating SARS-CoV-2 because it presents several challenges including medical, psychological, socioeconomic, and ethical. COVID-19 is the biggest calamity during the 21st century, we need to have a keen understanding of its pathophysiology and clinical implications for the development of preventive measures and therapeutic modalities.

Cardiovascular Co-morbidity in COVID-19 Pandemic

At present, we are in the middle of a global pandemic due to COVID 19 disease caused by SARS-CoV-2 viral infection. It has now spread virtually to every corner of the globe. Medical professionals are faced with the challenge of managing diverse clinical manifestations and multisystem involvement of this infection. Although respiratory system is mainly involved COVID-19 disease, there have been diverse manifestations within the cardiovascular (CV) system that posing unique therapeutic challenges. Clinically, a patient may have features of myocarditis, heart failure, acute myocardial infarction, arrhythmia, and vascular thrombosis. Of these manifestations, the most common mechanism implicated is direct myocardial injury, whereas systemic inflammation, oxygen supply-demand mismatch, plaque rupture have also been suggested. Furthermore, current available data suggest cardiovascular related manifestations lead to increased morbidity and mortality. Also, patients with underlying cardiac conditions are more prone for severe disease and death. Although there are limited treatment options available for COVID-19 currently, it is imperative that the potential cardiovascular implications of these therapies are to be considered in these patients. There is need to review current available information regarding the implication of cardiovascular co-morbidity in COVID-19 disease so that we have uptodate and better understanding in this global problem. This review highlights the manifestations, pathophysiological mechanisms for cardiovascular manifestations of COVID-19 and address specific concerns of cardiac patients regarding medications and further management.

Sympathetic reactivity and inflammation: another joint problem in rheumatoid arthritis?

Sympathetic reactivity and inflammation: another joint problem in rheumatoid arthritis?

Using near-infrared spectroscopy myocardial oximetry to monitor myocardial oxygen balance in a swine model of cardiac surgery: a descriptive study.

Monitoring of the adequacy of myocardial protection with cardioplegia is nearly non-existent in clinical cardiac surgical practice and instead relies on well-defined protocols for delivery of cardioplegia often resulting in inadequate protection. We hypothesized that Near Infrared Spectroscopy technology could be useful in the monitoring of the myocardial oxygen state by attaching the monitors to the epicardium in a porcine model of cardiac surgery. The experiments were conducted with 3 different protocols of 2 pigs each for a total of 6 pigs. The objective was to induce episodic, oxygen supply-demand mismatch. Methods for decreased supply included decreasing coronary blood flow, coronary blood hypoxemia, coronary occlusion, hypovolemia, and hypotension. Methods for increase demand included rapid ventricular pacing and the administration of isoproterenol. Changes in myocardial tissue oximetry were measured and this measurement was then correlated with blood hemoglobin saturations of oxygen from coronary sinus blood samples. We found that decreases in myocardial oxygen supply or increases in demand due to any of the various experimental conditions led to decreases in both myocardial tissue oximetry and hemoglobin oxygen saturation of coronary sinus blood with recovery when the conditions were returned to baseline. Correlation between myocardial tissue oximetry and hemoglobin oxygen saturation of coronary sinus blood was moderate to strong under all tested conditions. This may have translational applications as a monitor of adequacy of myocardial protection and the detection of coronary occlusion.

The effect of SGLT2 inhibitors on silent myocardial ischemia

Abstract Background In large cardiovascular (CV) outcome trials, sodium-glucose co-transporter 2 (SGLT2) inhibitors reduced the development of heart failure (HF) in patients with type 2 diabetes (T2DM). Also it reduced CV death and worsening HF events in HFrEF patients. It is unknown whether SGLT2 inhibitors work through glucose-dependent mechanism or it could have other effects not related to glucose on cardiovascular morbidity and mortality in diabetic patients. Its effect on silent ambulatory myocardial ischemia (SAMI) has not been reported yet. In this study we report the effect of SGLT2 inhibitors on (SAMI). Treating silent myocardial ischemia has a prognostic effect and may improve long term mortality of chronic ischemic heart disease (CIHD). Methods We enrolled 44 type 2 diabetic patients with proven stable coronary artery disease (CAD) and at least one episode of on silent ambulatory myocardial ischemia (SAMI) on ambulatory ECG monitoring. All of them were receiving optimal therapy for CIHD and type 2 DM. 22 patients were randomized to receive Dapagliflozin 5mg qd and the other 22 patients received placebo. Ambulatory monitoring was repeated after 4 to 6 months of therapy. The two groups were comparable with respect to baseline characteristics, number of episodes of ST-segment depression, HgbA1c level, and baseline serum cholesterol levels. Holters were read by a blinded cardiologist. Results The Dapagliflozin group experienced a significant reduction in the number of episodes of ST-segment depression compared with the placebo group. ST-segment depression completely resolved in 8 of 22 patients (36%) in the Dapagliflozin group versus 3 of 22 (13%) in the placebo group and the Dapagliflozin group exhibited a highly significant reduction in (SAMI) (P&amp;lt;0.001). By logistic regression, treatment with Dapagliflozin was an independent predictor of (SAMI) resolution. Conclusions Therapy with SGLT2 inhibitors in type2 DM patients results in reduction or resolution of (SAMI) recorded as episodes of ST-segment depression in ambulatory monitoring of the ECG. A larger study is required to confirm this theory and to see the effect of SAMI reduction on long term mortality of CIHD in diabetics. Possible mechanisms for this beneficial effects of SGLT2i includes: Reduction in oxygen supply-demand mismatch, improvement in cardiac microvascular function, modulation of cardiac energy metabolism, reduction in glucotoxicity, reduction in sympathetic nervous system activation and reduction in blood pressure. Funding Acknowledgement Type of funding source: None

The peak levels of highly sensitive troponin I predicts in-hospital mortality in COVID-19 patients with cardiac injury: a retrospective study.

AimsTo investigate the association between levels of highly sensitive troponin I (hs-troponin I) and mortality in novel coronavirus disease 2019 (COVID-19) patients with cardiac injury.Methods and resultsWe retrospectively reviewed the medical records of all COVID-19 patients with increased levels of hs-troponin I from two hospitals in Wuhan, China. Demographic information, laboratory test results, cardiac ultrasonographic findings, and electrocardiograms were collected, and their predictive value on in-hospital mortality was explored using multivariable logistic regression. Of 1500 patients screened, 242 COVID-19 patients were enrolled in our study. Their median age was 68 years, and (48.8%) had underlying cardiovascular diseases. One hundred and seventy-six (72.7%) patients died during hospitalization. Multivariable logistic regression showed that C-reactive protein (>75.5 mg/L), D-dimer (>1.5 μg/mL), and acute respiratory distress syndrome were risk factors of mortality, and the peak hs-troponin I levels (>259.4 pg/mL) instead of the hs-troponin I levels at admission was predictor of death. The area under the receiver operating characteristic curve of the peak levels of hs-troponin I for predicting in-hospital mortality was 0.79 (95% confidence interval, 0.73–0.86; sensitivity, 0.80; specificity, 0.72; P < 0.0001).ConclusionOur results demonstrated that the risk of in-hospital death among COVID-19 patients with cardiac injury can be predicted by the peak levels of hs-troponin I during hospitalization and was significantly associated with oxygen supply-demand mismatch, inflammation, and coagulation.

Severe cardiac complications of extended pleurectomy and decortication: a case report

Introduction Extended pleurectomy and decortication is a specialised procedure performed typically in elderly patients with comorbidities (1). The nature of surgery presents significant physiological stress to the cardiovascular system. Here we report an an unexplained complication of EPD that occurred in our operating theatre. Methods A 70 year-old underwent an EPD for mesothelioma, following neoadjuvant chemotherapy. He was an ex-smoker with moderate chronic obstructive airways disease, hypertensive and hyperlipidemic, and a normal preoperative electrocardiogram and echocardiogram. He had an uneventful induction of anaesthesia and the airway was secured with 41 French left double lumen tube, and maintained with desflurane and intermittent boluses of 0.25% levobupivacaine through a thoracic epidural (T4/T5 space). Routine and invasive arterial and central venous pressure monitoring were used. Surgery was uneventful with a blood loss of 250 mls and minimal dysrrhythmias during pericardectomy. At the closure of thoracotomy, sudden marked ST elevation noted was on the five-lead ECG and posterolateral ischaemic changes on a 12-lead recording (see figure 1A), associated with hypotension requiring boluses of adrenaline. No obvious precipitating event was noted. An adrenaline infusion of 0.15microg/kg/min was started to provide cardiovascular stability. Results Once transferred for angiography, the ST segments had normalized (figure 1B) and his adrenaline requirements dropped. A stable plaque in the left anterior descending artery with no flow limitation was detected. A transoesophageal echocardiogram was normal. The patient was extubated the following day on the ICU. A troponin rise (table) and persistent T wave changes (figure 1C) were detected. Discussion Intra-operative dysrhythmias are not uncommon during EPD whilst the pericardium is manipulated but rarely seen at the end of surgery (1-3), but sudden unexplained ST elevation has not to our knowledge previously been reported. Multiple breeches to the visceral pleura occur during surgery, and we speculate a small gas embolus to a coronary artery or sudden hypotension-related myocardial oxygen supply-demand mismatch may explain the severe but transient clinical and electrocardiographic findings and type two myocardial infarction, given the normal coronary angiography and post-operative echocardiography.