Metabolomics of repetitive myocardial stunning in chronic multivessel coronary artery stenosis: Effect of non-selective and selective ß1-receptor blockers.

Chronic coronary artery stenosis can lead to regional myocardial dysfunction in the absence of myocardial infarction by repetitive stunning, hibernation or both. The molecular mechanisms underlying repetitive stunning-associated myocardial dysfunction are not clear. We used non-targeted metabolomics to elucidate responses to chronically stunned myocardium in a canine model with and without ß-adrenergic blockade treatment. After development of left ventricular systolic dysfunction induced by ameroid constrictors on the coronary arteries, animals were randomized to 3 months of placebo, metoprolol or carvedilol. We compared these two ß-blockers with their different ß-adrenergic selectivities on myocardial function, perfusion and metabolic pathways involved in tissue undergoing chronic stunning. Control animals underwent sham surgery. Dysfunction in stunned myocardium was associated with reduced fatty acid oxidation and enhanced ketogenic amino acid metabolism, together with alterations in mitochondrial membrane phospholipid composition. These changes were consistent with impaired mitochondrial function and were linked to reduced nitric oxide and peroxisome proliferator-activated receptor signalling, resulting in a decline in adenosine monophosphate-activated protein kinase. Mitochondrial changes were ameliorated by carvedilol more than metoprolol, and improvement was linked to nitric oxide and possibly hydrogen sulphide signalling. In summary, repetitive myocardial stunning commonly seen in chronic multivessel coronary artery disease is associated with adverse metabolic remodelling linked to mitochondrial dysfunction and specific signalling pathways. These changes are reversed by ß-blockers, with the non-selective inhibitor having a more favourable impact. This is the first investigation to demonstrate that ß-blockade-associated improvement of ventricular function in chronic myocardial stunning is associated with restoration of mitochondrial function. KEY POINTS: The mechanisms responsible for the metabolic changes associated with repetitive myocardial stunning seen in chronic multivessel coronary artery disease have not been fully investigated. In a canine model of repetitive myocardial stunning, we showed that carvedilol, a non-selective ß-receptor blocker, ameliorated adverse metabolic remodelling compared to metoprolol, a selective ß1-receptor blocker, by improving nitric oxide synthase and adenosine monophosphate protein kinase function, enhancing calcium/calmodulin-dependent protein kinase, probably increasing hydrogen sulphide, and suppressing cyclic-adenosine monophosphate signalling. Mitochondrial fatty acid oxidation alterations were ameliorated by carvedilol to a larger extent than metoprolol; this improvement was linked to nitric oxide and possibly hydrogen sulphide signalling. Both ß-blockers improved the cardiac energy imbalance by reducing metabolites in ketogenic amino acid and nucleotide metabolism. These results elucidated why metabolic remodelling with carvedilol is preferable to metoprolol when treating chronic ischaemic left ventricular systolic dysfunction caused by repetitive myocardial stunning.

Determination of viable myocardium through delayed enhancement cardiac magnetic resonance imaging combined with 18F-FDG PET myocardial perfusion/metabolic imaging before CABG.

PURPOSE: Study aims to investigate the consistency of delayed enhancement cardiac magnetic resonance imaging (DE-CMR) and 18F-FDG PET myocardial imaging in evaluating myocardial viability before CABG. METHODS: The study analyzed data from 100 patients who were examined with DE-CMR, PET imaging, and echocardiography before and after CABG. All subjects were followed up for 6-12 month post- CABG. RESULTS: DE-CMR and PET imaging have high consistency (90.1%; Kappa value = 0.71, p < 0.01) in determining myocardial viability. The degree of delayed enhancement was negatively correlated with the improvement in myocardial contractile function in this segment after revascularization (P < 0.001). The ratio of scarred myocardial segments and total DE score was significantly lower in the improvement group than non-improvement group. Multivariate regression identified that hibernating myocardium (OR = 1.229, 95%CI: 1.053-1.433, p = 0.009) was influencing factor of LVEF improvement after CABG. CONCLUSION: Both imaging techniques are consistent in evaluating myocardial viability. Detecting the number of hibernating myocardium by PET is also important to predict the left heart function improvement after CABG.

Hematomyelia Presenting with Neurogenic Stunned Myocardium.

Various neurological disorders and emotional stress may cause left ventricular dysfunction, known as a neurogenic stunned myocardium. A previously healthy 71-year-old woman collapsed immediately after experiencing left arm numbness and pain. Thereafter, the patient complained of anterior chest pain and became comatose. An electrocardiogram showed ST-segment elevation of I, aVL, and V2-3 and depression of II, III, and aVF. Echocardiography revealed anteroseptal hypokinesis of the left ventricle. Emergency coronary angiography revealed no significant stenosis in the coronary arteries; however, left ventriculography revealed obvious anteroseptal hypokinesis. When the patient regained consciousness the following day, tetraplegia was observed. Spinal computed tomography and magnetic resonance imaging revealed an intramedullary spinal cord hemorrhage from the medulla to the conus. The cardiac function recovered, but the patient remained tetraplegic with poor spontaneous respiration. Although its incidence is extremely rare, hematomyelia should be recognized as a potential cause of neurogenic stunned myocardium.

Cardiac patterns for differentiation of neurogenic stunned myocardium in aneurysmal subarachnoid hemorrhage versus acute ischemic stroke.

AIMS: Neurogenic stunned myocardium (NSM) has heterogeneous presentations for acute ischemic stroke (AIS) and aneurysmal subarachnoid hemorrhage (SAH). We sought to better define NSM and differences between AIS and SAH by evaluating individual left ventricular (LV) functional patterns by speckle tracking echocardiography (STE). METHODS: We evaluated consecutive patients with SAH and AIS. Via STE, LV longitudinal strain (LS) values of basal, mid, and apical segments were averaged and compared. Different multivariable logistic regression models were created by defining stroke subtype (SAH or AIS) and functional outcome as dependent variables. RESULTS: One hundred thirty-four patients with SAH and AIS were identified. Univariable analyses using the chi-squared test and independent samples t-test identified demographic variables and global and regional LS segments with significant differences. In multivariable logistic regression analysis, when comparing AIS to SAH, AIS was associated with older age (OR 1.07, 95% CI 1.02-1.13, p = 0.01), poor clinical condition on admission (OR 7.74, 95% CI 2.33-25.71, p < 0.001), decreased likelihood of elevated admission serum troponin (OR .09, 95% CI .02-.35, p < 0.001), and worse LS basal segments (OR 1.18, 95% CI 1.02-1.37, p = 0.03). CONCLUSION: In patients with neurogenic stunned myocardium, significantly impaired LV contraction by LS basal segments was found in patients with AIS but not with SAH. Individual LV segments in our combined SAH and AIS population were also not associated with clinical outcomes. Our findings suggest that strain echocardiography may identify subtle forms of NSM and help differentiate the NSM pathophysiology in SAH and AIS.

ATP-Sensitive Potassium Channel Opener Diazoxide Reduces Myocardial Stunning in a Porcine Regional With Subsequent Global Ischemia Model.

Background ATP-sensitive potassium channels are inhibited by ATP and open during metabolic stress, providing endogenous myocardial protection. Pharmacologic opening of ATP potassium channels with diazoxide preserves myocardial function following prolonged global ischemia, making it an ideal candidate for use during cardiac surgery. We hypothesized that diazoxide would reduce myocardial stunning after regional ischemia with subsequent prolonged global ischemia, similar to the clinical situation of myocardial ischemia at the time of revascularization. Methods and Results Swine underwent left anterior descending occlusion (30 minutes), followed by 120 minutes global ischemia protected with hyperkalemic cardioplegia±diazoxide (N=6 each), every 20 minutes cardioplegia, then 60 minutes reperfusion. Cardiac output, time to wean from cardiopulmonary bypass, left ventricular (LV) function, caspase-3, and infarct size were compared. Six animals in the diazoxide group separated from bypass by 30 minutes, whereas only 4 animals in the cardioplegia group separated. Diazoxide was associated with shorter but not significant time to wean from bypass (17.5 versus 27.0 minutes; P=0.13), higher, but not significant, cardiac output during reperfusion (2.9 versus 1.5 L/min at 30 minutes; P=0.05), and significantly higher left ventricular ejection fraction at 30 minutes (42.5 versus 15.8%; P<0.01). Linear mixed regression modeling demonstrated greater left ventricular developed pressure (P<0.01) and maximum change in ventricular pressure during isovolumetric contraction (P<0.01) in the diazoxide group at 30 minutes of reperfusion. Conclusions Diazoxide reduces myocardial stunning and facilitates separation from cardiopulmonary bypass in a model that mimics the clinical setting of ongoing myocardial ischemia before revascularization. Diazoxide has the potential to reduce myocardial stunning in the clinical setting.

Neurogenic stunned myocardium resulting from surgical brainstem handling during resection of paediatric recurrent medulloblastoma-a possible brain heart interaction.

BACKGROUND: Neurogenic stunned myocardium (NSM) is characterised by an acute onset cardiac dysfunction following an acute neurological insult which mimics acute coronary syndrome. CASE DETAILS: A 12-year-old male child was admitted to the neuro-intensive care unit (NICU) following midline suboccipital craniotomy and resection of recurrent medulloblastoma. Postoperatively, in NICU, he developed tachycardia and hypotension, which was unresponsive to fluid challenge requiring norepinephrine infusion. Intraoperatively, during tumour resection from the dorsal medulla, episodes of hypertension and bradycardia were observed. Intraoperative blood loss was adequately managed with a stable hemodynamic profile without postoperative anaemia. An electrocardiogram showed sinus tachycardia with T wave inversion, and blood investigation revealed elevated cardiac troponin T levels. Point of care ultrasound (POCUS) of heart and lung showed features of NSM. Infusion dobutamine was added to achieve a target mean arterial pressure of 65 mm Hg with concomitant furosemide infusion and fluid restriction. Daily POCUS assessment of cardiac contractility and volume status was done. The patient was weaned from vasoactive drugs and ventilator following improvement of cardiac function and was discharged from NICU after 17 days. CONCLUSION: NSM results from the excessive release of catecholamines following stimulation of trigger zones in the brain. To date, a handful of cases of pediatric NSM following primary brain tumour are reported where hydrocephalus resulted in trigger zone activation. In this presented case, direct brain stem stimulation during tumour resection might have triggered NSM. Irrespective of the cause, timely diagnosis and execution of supportive management in our patient resulted in a positive outcome.

Neurogenic stunned myocardium in acute ischemic stroke.

BACKGROUND AND PURPOSE: Neurogenic myocardial injury occurs as a result of dysregulation of autonomic nervous system. The aim of this study was to explore the frequency of elevated troponin and dynamic ST segment/T wave changes and their relation with left ventricular (LV) systolic functions in acute ischemic stroke patients. METHODS: One hundred and twenty-five patients (mean age: 65.1±15.2years, 76 male) presenting with acute ischemic stroke were consecutively included. 12-lead electrocardiogram was taken to assess dynamic ST segment/T wave changes, conventional transthoracic echocardiography to determine LV ejection fraction (LVEF). High-sensitive cardiac troponin I (hs-cTnI) level>0.04ng/mL was accepted as elevated. RESULTS: Twenty-seven patients (21.6%) had elevated hs-cTnI and 60 patients (48%) had dynamic ST segment/T wave changes. The stroke patients with elevated hs-cTnI had significantly higher NT-proBNP values (2302±3450pg/mL vs 799±2075pg/mL p<0.001) and higher frequency of ST segment/T wave changes (85.2% vs 37.8% p<0.001), and lower LVEF (52.2±13.6% vs 61.0±8.5% p=0.002) compared to patients with normal troponin levels. The patients with ST segment/T wave changes had significantly higher frequencies of hyper-lipidemia (31.7% vs 15.4% p=0.031) and coronary artery disease (CAD) (43.3% vs 13.8% p<0.001), hs-cTnI (0.19±0.55ng/mL vs 0.02±0.01ng/mL p<0.001) and NT-proBNP levels (1430±2564pg/mL vs 842±2425pg/mL p=0.016), and lower LVEF (56.1±11.7% vs 61.9±8.3% p=0.009). Linear regression analysis revealed presence of CAD, but not ST segment/T wave changes as an independent predictor of hs-cTnI (p=0.034). LVEF was independently associated with hs-cTnI (p=0.003) and presence of CAD (p=0.009) when adjusted by age, sex and presence of ST segment/T wave changes. CONCLUSION: Troponin elevation and ST segment/T wave changes occurring in patients suffering acute ischemic stroke, especially in those with CAD, may be a sign of neurogenic stunned myocardium.

Changes in Global Left Ventricular Myocardial Work Indices and Stunning Detection 3 Months After ST-Segment Elevation Myocardial Infarction.

Global left ventricular (LV) myocardial work (MW) indices (GLVMWI) are derived from speckle tracking echocardiographic strain data in combination with non-invasive blood pressure measurements. Changes in global work index (GWI), global constructive work (GCW), global wasted work (GWW) and global work efficiency (GWE) after ST-segment elevation myocardial infarction (STEMI) have not been explored. The aim of present study was to assess the evolution of GLVMWI in STEMI patients from baseline (index infarct) to 3 months' follow-up. Three-hundred and fifty patients (265 men; mean age 61 ± 10 years) with STEMI treated with primary percutaneous coronary intervention (PCI) and guideline-based medical therapy were retrospectively evaluated. Clinical variables, conventional echocardiographic measures and GLVMWI were recorded at baseline within 48 hours post-primary PCI and 3 months' follow-up. LV ejection fraction (from 54 ± 10% to 57 ± 10%, p < 0.001), GWI (from 1449 ± 451 mm Hg% to 1953 ± 492 mm Hg%, p < 0.001), GCW (from 1624 ± 519 mm Hg% to 2228 ± 563 mm Hg%, p < 0.001) and GWE (from 93% (interquartile range (IQR) 86%-95%) to 95% (IQR 91%-96%), p < 0.001) improved significantly at 3 months' follow-up with no significant difference in GWW (from 101 mm Hg% (IQR 63-155 mm Hg%) to 96 mm Hg% (IQR 64-155 mm Hg%); p = 0.535). On multivariable linear regression analysis, lower values of troponin T at baseline, increase in systolic blood pressure and improvement in LV global longitudinal strain were independently associated with higher GWI and GCW at 3 months' follow-up. In conclusion, the evolution of GWI, GCW and GWE in STEMI patients may reflect myocardial stunning, whereas the stability in GWW may reflect permanent myocardial damage and the development of non-viable scar tissue.

Extracorporeal Membrane Oxygenation for Hemodynamic Support.

Extracorporeal membrane oxygenation was first successfully achieved in 1975 in a neonate with meconium aspiration. Neonatal extracorporeal membrane oxygenation has expanded to include hemodynamic support in cardiovascular collapse before and after cardiac surgery, medical heart disease, and rescue therapy for cardiac arrest. Advances in pump technology, circuit biocompatibility, and oxygenators efficiency have allowed extracorporeal membrane oxygenation to support neonates with increasingly complex pathophysiology. Contraindications include extreme prematurity, extremely low birth weight, lethal chromosomal abnormalities, uncontrollable hemorrhage, uncontrollable disseminated intravascular coagulopathy, and severe irreversible brain injury. The future will involve collaboration to guide and evolve evidence-based practices for this life-sustaining therapy.

Better characterization of dipyridamole-induced myocardial stunning by systolic wall thickening. A gated perfusion SPECT study.

AIM AND PATIENTS: The aim of the present study was to assess the additional value of systolic wall thickening to myocardial perfusion in diagnosing myocardial stunning induced by dipyridamole infusion. We selected 52 ischemic patients (43 males; mean age 65.5 ± 7.64), with CAD documented by angiography. Ischemia was defined as a summed difference score ≥ 5. All patients underwent a 2-day gated perfusion SPECT protocol. The patients received a dose of 740 MBq of 99mTc-tetrofosmin after stress and at rest. RESULTS: The post-stress LVEF was significantly lower than rest LVEF (48.3% ± 14.5% vs. 50.7% ± 15%; P = 0.0001). The wall thickening summed difference score was 3.97 ± 3.84 (P = 0.0001). At a multivariate regression analysis, only WT-SDS as independent variable was significantly correlated with myocardial ischemia (SDS) (P = 0.001). We divided patients according to SDS in those with mild (SDS < 8) and severe (SDS ≥ 8) ischemia. WT-SDS, but not ∆LVEF, was significantly different between groups. CONCLUSIONS: WT-SDS showed a better correlation with the degree of ischemia than the depression in the global function of the left ventricle. It allowed to better identify the stunning phenomenon in patients submitted to pharmacological stress.

The clinical usefulness of phase analysis in detecting coronary artery disease using dipyridamole thallium-201-gated myocardial perfusion imaging with a cadmium-zinc-telluride camera.

BACKGROUND: Previous studies have demonstrated left ventricular mechanical dyssynchrony (LVMD) in patients with severe coronary artery disease (CAD) with ≥ 70% stenosis. The aim of this study was to evaluate the clinical usefulness of stress/rest LVMD in the diagnosis of CAD with ≥ 50% stenosis using dipyridamole thallium-201 (Tl-201) myocardial perfusion imaging (MPI) with a cadmium-zinc-telluride camera. METHODS AND RESULTS: A total of 476 patients without known CAD who underwent dipyridamole Tl-201 MPI and coronary angiography within 6 months were retrospectively reviewed. LVMD parameters including phase standard deviation and phase histogram bandwidth, phase skewness and phase kurtosis, as well as myocardial perfusion and myocardial stunning were assessed in post-stress and rest MPI. Relationships between the presence of CAD on coronary angiography and single photon emission computerized tomography (SPECT) parameters were evaluated. The presence of perfusion abnormalities was the best diagnostic tool in detecting CAD. Although less left ventricular synchrony was observed post-stress in the CAD group compared to the non-CAD group, no significant dyssynchrony was noted. CONCLUSIONS: The addition of phase analysis to help diagnose CAD in Tl-201-gated SPECT with dipyridamole stress may have limited value in patients with CAD with ≥ 50% stenosis.

Chemical chaperones improve the functional recovery of stunned myocardium by attenuating the endoplasmic reticulum stress.

AIM: Myocardial ischaemia/reperfusion (I/R) produces structural and functional alterations depending on the duration of ischaemia. Brief ischaemia followed by reperfusion causes reversible contractile dysfunction (stunned heart) but long-lasting ischaemia followed by reperfusion can result in irreversible injury with cell death. Events during I/R can alter endoplasmic reticulum (ER) function leading to the accumulation of unfolded/misfolded proteins. The resulting ER stress induces activation of several signal transduction pathways, known as unfolded protein response (UPR). Experimental evidence shows that UPR contributes to cell death in irreversible I/R injury; however, there is still uncertainty for its occurrence in the stunned myocardium. This study investigated the ER stress response and its functional impact on the post-ischaemic cardiac performance of the stunned heart. METHODS: Perfused rat hearts were subjected to 20 minutes of ischaemia followed by 30 minutes of reperfusion. UPR markers were evaluated by qRT-PCR and western blot. Post-ischaemic mechanical recovery was measured in absence and presence of two chemical chaperones: tauroursodeoxycholic acid (TUDCA) and 4-phenylbutyric acid (4-PBA). RESULTS: Analysis of mRNA and protein levels of various ER stress effectors demonstrated that different UPR signalling cascades, involving both pro-survival and pro-apoptotic pathways, are activated. Inhibition of the UPR with chemical chaperones improved the post-ischaemic recovery of cardiac mechanical function without affecting the I/R-induced increase in oxidative stress. CONCLUSION: Our results suggest that prevention of ER stress by chemical chaperones could be a therapeutic tool to limit deterioration of the contractile function in clinical settings in which the phenomenon of myocardial stunning is present.

Neurogenic Stunned Myocardium: A Case Report and Brief Review.

BACKGROUND: Neurogenic stunned myocardium (NSM) is a condition in a group of stress cardiomyopathies with evolving nomenclature that includes Takotsubo cardiomyopathy. It manifests through electrocardiogram changes, cardiac enzyme elevation, and regional or global kinetic wall motion abnormalities. CASE REPORT: We present a 43-year-old female with a subarachnoid hemorrhage who developed persistent hypotension and tachycardia secondary to neurogenic stress cardiomyopathy. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: It is important to consider NSM in any patient with neurologic pathology and undifferentiated shock. Early recognition in the emergency department setting can yield valuable data to guide the treatment and improve clinical outcomes in these patients.

Predictors of left atrial appendage stunning after electrical cardioversion in patients with atrial fibrillation.

The transient left atrial appendage (LAA) dysfunction after electrical cardioversion (CV), which is called as LAA-stunning, was found to be an important etiology of thrombus formation. The aim of the present study was to investigate the risk factors of LAA-stunning. This study included 134 patients who underwent catheter ablation for non-paroxysmal, non-valvular, and symptomatic atrial fibrillation (AF). Internal-CV was performed, and LAA emptying fraction (LAA-EF) was assessed using LAA-angiogram before and just after CV. LAA-stunning (defined as 10% reduction of LAA-EF after CV) was observed in 45/134 patients (34%). Patients in LAA-stunning group had longer duration of AF prior to CV, higher brain natriuretic peptide (BNP), higher prevalence of patients taking calcium blocker, larger left atrial (LA) diameter, elevated E wave, and larger LA volume than those in non LAA-stunning group. Multivariate analysis showed that longer duration of AF prior to CV (p = 0.015, OR 1.033 for 1 month extend, 95% CI 1.006-1.073) and elevated BNP (p = 0.038, OR 1.041 for each 10 pg/mL increase, 95% CI 1.001-1.009) were associated with LAA-stunning. In addition, all patients were divided into four groups based on the combination between duration of AF prior to CV and BNP; group 1 (low BNP/short-lasting AF), group 2 (high BNP/short-lasting AF), group 3 (low BNP/long-lasting AF), and group 4 (high BNP/long-lasting AF). The rate of LAA-stunning was the highest in the group 4 (55.6%). Elevated BNP and long duration of AF were associated with LAA stunning after electrical cardioversion.

Hydrocephalus-induced neurogenic stunned myocardium and cardiac arrest in a child: completely reversed with CSF diversion.

Neurogenic stunned myocardium (NSM) is a potentially fatal cause of sudden cardiogenic dysfunction due to an acute neurological event, most commonly aneurysmal subarachnoid hemorrhage in adults. Only two pediatric cases of hydrocephalus-induced NSM have been reported. Here the authors report a third case in a 14-year-old boy who presented with severe headache, decreased level of consciousness, and shock in the context of acute hydrocephalus secondary to fourth ventricular outlet obstruction 3 years after standard-risk medulloblastoma treatment. He was initially stabilized with the insertion of an external ventricular drain and vasopressor treatment. He had a profoundly reduced cardiac contractility and became asystolic for 1 minute, requiring cardiopulmonary resuscitation when vasopressors were inadvertently discontinued. Over 1 week, his ventricles decreased in size and his cardiac function returned to normal. All other causes of heart failure were ruled out, and his impressive response to CSF diversion clarified the diagnosis of NSM secondary to hydrocephalus. He was unable to be weaned from his drain during his time in the hospital, so he underwent an endoscopic third ventriculostomy and has remained well with normal cardiac function at more than 6 months' follow-up. This case highlights the importance of prompt CSF diversion and cardiac support for acute hydrocephalus presenting with heart failure in the pediatric population.

The spectrum of acute cardiopulmonary events associated with multiple sclerosis exacerbations.

Diverse acute neurological injuries may cause acute cardiopulmonary events including neurogenic pulmonary edema (NPE) and neurogenic stunned myocardium (NSM). The mechanism is probably mediated by sympathetic nervous system activation. Focal central nervous system (CNS) lesions, such as demyelinating lesions in multiple sclerosis (MS), may also cause cardiopulmonary disturbances. We aim to review the acute cardiopulmonary events associated with MS relapses. We performed a literature search using PubMed, and selected case reports of acute cardiac and/or pulmonary events related to MS exacerbations. We grouped these events into three categories: 1) NPE with normal cardiac function; 2) NSM and Takotsubo cardiomyopathy (TTC); 3) coexisting myocardial dysfunction and pulmonary edema. In some cases, cardiac and pulmonary symptoms preceded the onset of neurological symptoms. The majority of cases were associated with acute demyelinating lesions located in the medulla. Acute brainstem MS relapses, with demyelinating lesions affecting the medulla, may cause acute cardiac and pulmonary events presumably secondary to sympathetic hyperstimulation. Specific regions in the medulla that regulate cardiac function, systemic blood pressure and pulmonary hydrostatic pressure seem to be responsible for these events.

Intradialytic exercise preconditioning: an exploratory study on the effect on myocardial stunning.

BACKGROUND: Exercise preconditioning provides immediate protection against cardiac ischemia in clinical/preclinical studies in subjects without chronic kidney disease. In individuals requiring renal replacement therapy, hemodialysis (HD) results in significant circulatory stress, causing acute ischemia with resultant recurrent and cumulative cardiac injury (myocardial stunning). Intradialytic exercise (IDE) has been utilized to improve functional status in individuals receiving HD. The objective of this study was to explore the role of IDE as a preconditioning intervention and assess its effect on HD-induced myocardial stunning. METHODS: We performed a single-center cross-sectional exploratory study in adults on chronic HD participating in a clinical IDE program. HD-induced cardiac stunning was evaluated over two HD sessions within the same week: a control visit (no exercise) and an exposure visit (usual intradialytic cycling). Echocardiography was performed at the same three time points for each visit. Longitudinal strain values for 12 left ventricular segments were generated using speckle-tracking software to assess the presence of HD-induced regional wall motion abnormalities (RWMAs), defined as a ≥20% reduction in strain; two or more RWMAs represent myocardial stunning. RESULTS: A total of 19 patients were analyzed (mean age 57.2 ± 11.8 years, median dialysis vintage 3.8 years). The mean number of RWMAs during the control visit was 4.5 ± 2.6, falling to 3.6 ± 2.7 when incorporating IDE (a reduction of -0.95 ± 2.9; P = 0.17). At peak HD stress, the mean number of RWMAs was 5.8 ± 2.7 in the control visit versus 4.0 ± 1.8 during the exposure visit (a reduction of -1.8 ± 2.8; P = 0.01). CONCLUSION: We demonstrated for the first time that IDE is associated with a significant reduction in HD-induced acute cardiac injury.