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Background/Objectives: Hemodialysis-induced myocardial stunning (HIMS) is a frequent complication in patients undergoing maintenance hemodialysis, characterized by transient left ventricular dysfunction due to ischemic episodes. Mitochondrial dysfunction and fluctuations in key ions such as potassium (K+) and calcium (Ca2+) are implicated in the pathogenesis of HIMS. This study aims to investigate the role of mitochondrial dysfunction and the protective potential of mitochondrial ATP-sensitive potassium channels (mitoKATP) in mitigating HIMS. Methods: A 5/6 nephrectomy rat model was established to mimic chronic kidney disease and the subsequent HIMS. The effects of mitoKATP channel modulators were evaluated by administering diazoxide (DZX), a mitoKATP opener, and 5-hydroxydecanoate (5-HD), a mitoKATP blocker, before hemodialysis. Mitochondrial function was assessed by measuring membrane potential, ATP synthase activity, and intramitochondrial Ca2+ levels. Myocardial function was evaluated using speckle tracking echocardiography. Results: Rats undergoing hemodialysis exhibited significant reductions in left ventricular strain and synchrony. DZX administration significantly improved mitochondrial function and reduced myocardial strain compared to controls. Conversely, 5-HD worsened mitochondrial swelling and disrupted myocardial function. Higher K+ and Ca2+ concentrations in the dialysate were associated with improved mitochondrial energy metabolism and myocardial strain. Conclusions: Mitochondrial dysfunction and ion imbalances during hemodialysis are key contributors to HIMS. The activation of mitoKATP channels provides mitochondrial protection and may serve as a potential therapeutic strategy to mitigate HIMS. [ABSTRACT FROM AUTHOR]

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 β‐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 β‐blockers with their different β‐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 β‐blockers, with the non‐selective inhibitor having a more favourable impact. This is the first investigation to demonstrate that β‐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 β‐receptor blocker, ameliorated adverse metabolic remodelling compared to metoprolol, a selective β1‐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 β‐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. [ABSTRACT FROM AUTHOR]

Purpose: In a preclinical study using a swine myocardial infarction (MI) model, a delayed enhancement (DE)-multi-detector computed tomography (MDCT) scan was performed using a hybrid system alongside diagnostic invasive coronary angiography (ICA) without the additional use of a contrast agent, and demonstrated an excellent correlation in the infarct area compared with histopathologic specimens. In the present investigation, we evaluated the feasibility and diagnostic accuracy of a myocardial viability assessment by DE-MDCT using a hybrid system comprising ICA and MDCT alongside diagnostic ICA without the additional use of a contrast agent. Materials and Methods: We prospectively enrolled 13 patients (median age: 67 years) with a previous MI (>6 months) scheduled to undergo ICA. All patients underwent cardiac magnetic resonance (CMR) imaging before diagnostic ICA. MDCT viability scans were performed concurrently with diagnostic ICA without the use of additional contrast. The total myocardial scar volume per patient and average transmurality per myocardial segment measured by DE-MDCT were compared with those from DE-CMR. Results: The DE volume measured by MDCT showed an excellent correlation with the volume measured by CMR (r=0.986, p <0.0001). The transmurality per segment by MDCT was well-correlated with CMR (r=0.900, p<0.0001); the diagnostic performance of MDCT in differentiating non-viable from viable myocardium using a 50% transmurality criterion was good with a sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of 87.5%, 99.5%, 87.5%, 99.5%, and 99.1%, respectively. Conclusion: The feasibility of the DE-MDCT viability assessment acquired simultaneously with conventional ICA was proven in patients with chronic MI using DE-CMR as the reference standard. [ABSTRACT FROM AUTHOR]

Background/Objectives: Hemodialysis-induced myocardial stunning (HIMS) is a frequent complication in patients undergoing maintenance hemodialysis, characterized by transient left ventricular dysfunction due to ischemic episodes. Mitochondrial dysfunction and fluctuations in key ions such as potassium (K+) and calcium (Ca2+) are implicated in the pathogenesis of HIMS. This study aims to investigate the role of mitochondrial dysfunction and the protective potential of mitochondrial ATP-sensitive potassium channels (mitoKATP) in mitigating HIMS. Methods: A 5/6 nephrectomy rat model was established to mimic chronic kidney disease and the subsequent HIMS. The effects of mitoKATP channel modulators were evaluated by administering diazoxide (DZX), a mitoKATP opener, and 5-hydroxydecanoate (5-HD), a mitoKATP blocker, before hemodialysis. Mitochondrial function was assessed by measuring membrane potential, ATP synthase activity, and intramitochondrial Ca2+ levels. Myocardial function was evaluated using speckle tracking echocardiography. Results: Rats undergoing hemodialysis exhibited significant reductions in left ventricular strain and synchrony. DZX administration significantly improved mitochondrial function and reduced myocardial strain compared to controls. Conversely, 5-HD worsened mitochondrial swelling and disrupted myocardial function. Higher K+ and Ca2+ concentrations in the dialysate were associated with improved mitochondrial energy metabolism and myocardial strain. Conclusions: Mitochondrial dysfunction and ion imbalances during hemodialysis are key contributors to HIMS. The activation of mitoKATP channels provides mitochondrial protection and may serve as a potential therapeutic strategy to mitigate HIMS.

Background and aimsIschemic preconditioning (IPC), i.e., brief periods of ischemia, protect the heart from subsequent prolonged ischemic injury, and reduces infarction size. Myocardial stunning refers to transient loss of contractility in the heart after myocardial ischemia that recovers without permanent damage. The relationship between IPC and myocardial stunning remains incompletely understood. This study aimed primarily to examine the effects of IPC on the relationship between ischemia duration, stunning, and infarct size in an ischemia-reperfusion injury model. Secondarily, this study aimed to examine to which extent the phosphoproteomic changes induced by IPC relate to myocardial contractile function.Methods and resultsRats were subjected to different durations of left anterior descending artery (LAD) occlusion, with or without preceding IPC. Echocardiograms were acquired to assess cardiac contraction in the affected myocardial segment. Infarction size was evaluated using triphenyl tetrazolium chloride staining. Phosphoproteomic analysis was performed in heart tissue from preconditioned and non-preconditioned animals. In contrast to rats without IPC, reversible akinesia was observed in a majority of the rats that were subjected to IPC and subsequently exposed to ischemia of 13.5 or 15 min of ischemia. Phosphoproteomic analysis revealed significant differential regulation of 786 phosphopeptides between IPC and non-IPC groups, with significant associations with the sarcomere, Z-disc, and actin binding.ConclusionIPC induces changes in phosphosites of proteins involved in myocardial contraction; and both accentuates post-ischemic myocardial stunning and reduces infarct size.

Objective: Neurogenic myocardial stunning is a type of stress-induced cardiomyopathy thought to be a result of dysregulation of the autonomic nervous system. Heart rate variability (HRV) analysis is a potential method for understanding the underlying mechanisms of autonomic dysfunction in ischemic stroke. The aim of the study was to investigate HRV in stroke patients in accordance with troponin levels. Patients and Methods: Sixty-six patients (mean age 65 ± 13 years; 39 male) presenting with acute ischemic stroke were consecutively included. High-sensitive cardiac troponin I (hs-cTnI) levels were accepted as elevated when> 0.04 ng/mL. All patients underwent ambulatory electrocardiographic (ECG) monitoring within the first seven days to obtain time-domain and frequency-domain measures of HRV. Results: Twenty patients (30.3 %) had elevated hs-cTnI. Patients with high troponin levels had significantly lower left ventricular ejection fraction (LVEF), higher ST-segment-T wave changes, and higher N terminal pro-brain natriuretic peptide (NT-proBNP) levels. Low-frequency/high-frequency (LF/HF) value was significantly higher in the troponin-positive group, but other ambulatory ECG monitoring parameters such as SDNN, SDANN, RMSSD, and pNN50 were similar among patients. Conclusion: Neurogenic myocardial damage presenting with high troponin levels can be seen in ischemic stroke patients and may be associated with sympathetic overactivity. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is the leading cause of end-stage kidney disease in many countries. The management of diabetic patients who receive dialysis can be challenging. Diabetic dialysis patients have higher rates of cardiovascular events and mortality due to metabolic factors and accelerated vascular calcification. Diabetic haemodialysis patients have high rates of haemodynamic instability which leads to organ ischaemia and end organ damage; autonomic dysfunction seems to play an important role in haemodynamic instability and abnormal organ perfusion during haemodialysis. Poor glycaemic control contributes to fluid overload and worse cardiovascular outcome. Xerostomia and thirst are the main drivers for fluid overload in haemodialysis patients and in peritoneal dialysis a chronic state of hyperhydration that is related to absorption of glucose from the PD fluids, protein loss and malnutrition contributes to fluid overload. Glycaemic control is of great importance and adjustments to diabetic agents are required. In haemodialysis, a reduction in insulin dose is recommended to avoid hypoglycaemia whereas in peritoneal dialysis an increase in insulin dose is often required. Foot ulcers and infection are more common in diabetic dialysis patients compared to non-diabetic dialysis patients or diabetic patients with normal renal function and regular surveillance for early identification is important. Ultimately, a multi-disciplinary approach which includes diabetologist, nephrologist, dietitians, microbiologist, vascular surgeon, interventional radiologist is required to address the complicated aspects of diabetic patient care on dialysis.

The prognosis of cardiac arrest (CA) is dismal despite the ongoing progress in cardiopulmonary resuscitation (CPR). ginsenoside Rb1 (Gn-Rb1) has been verified to be cardioprotective in cardiac remodeling and cardiac ischemia/reperfusion (I/R) injury, but its role is less known in CA. After 15 min of potassium chloride-induced CA, male C57BL/6 mice were resuscitated. Gn-Rb1 was blindly randomized to mice after 20 s of CPR. We assessed the cardiac systolic function before CA and 3 h after CPR. Mortality rates, neurological outcome, mitochondrial homeostasis, and the levels of oxidative stress were evaluated. We found that Gn-Rb1 improved the long-term survival during the post-resuscitation period but did not affect the ROSC rate. Further mechanistic investigations revealed that Gn-Rb1 ameliorated CA/CPR-induced mitochondrial destabilization and oxidative stress, partially via the activation of Keap1/Nrf2 axis. Gn-Rb1 improved the neurological outcome after resuscitation partially by balancing the oxidative stress and suppressing apoptosis. In sum, Gn-Rb1 protects against post-CA myocardial stunning and cerebral outcomes via the induction of the Nrf2 signaling pathway, which may offer a new insight into therapeutic strategies for CA. [ABSTRACT FROM AUTHOR]

IntroductionThe life-sustaining treatment of hemodialysis (HD) induces recurrent and cumulative systemic circulatory stress resulting in cardiovascular injury. These recurrent insults compound preexisting cardiovascular sequalae leading to the development of myocardial injury and resulting in extremely high morbidity/mortality. This is largely a consequence of challenged microcirculatory flow within the myocardium (evidenced by detailed imaging-based studies). Currently, monitoring during HD is performed at the macrovascular level. Non-invasive monitoring of organ perfusion would allow the detection and therapeutic amelioration of this pathophysiological response to HD. Non-invasive percutaneous perfusion monitoring of the skin (using photoplethysmography—PPG) has been shown to be predictive of HD-induced myocardial stunning (a consequence of segmental ischemia). In this study, we extended these observations to include a dynamic assessment of skin perfusion during HD compared with directly measured myocardial perfusion during dialysis and cardiac contractile function.MethodsWe evaluated the intradialytic microcirculatory response in 12 patients receiving conventional HD treatments using continuous percutaneous perfusion monitoring throughout HD. Cardiac echocardiography was performed prior to the initiation of HD, and again at peak-HD stress, to assess the development of regional wall motion abnormalities (RWMAs). Myocardial perfusion imaging was obtained at the same timepoints (pre-HD and peak-HD stress), utilizing intravenous administered contrast and a computerized tomography (CT)-based method. Intradialytic changes in pulse strength (derived from PPG) were compared with the development of HD-induced RWMAs (indicative of myocardial stunning) and changes in myocardial perfusion.ResultsWe found an association between the lowest pulse strength reduction (PPG) and the development of RWMAs (p = 0.03) and also with changes in global myocardial perfusion (CT) (p = 0.05). Ultrafiltration rate (mL/kg/hour) was a significant driver of HD-induced circulatory stress [(associated with the greatest pulse strength reduction (p = 0.01), a reduction in global myocardial perfusion (p = 0.001), and the development of RWMAs (p = 0.03)].DiscussionPercutaneous perfusion monitoring using PPG is a useful method of assessing intradialytic hemodynamic stability and HD-induced circulatory stress. The information generated at the microcirculatory level of the skin is reflective of direct measures of myocardial perfusion and the development of HD-induced myocardial stunning. This approach for the detection and management of HD-induced cardiac injury warrants additional evaluation.

Cardiac arrest (CA) causes high mortality due to multi-system organ damage attributable to ischemia-reperfusion injury. Recent work in our group found that among diabetic patients who experienced cardiac arrest, those taking metformin had less evidence of cardiac and renal damage after cardiac arrest when compared to those not taking metformin. Based on these observations, we hypothesized that metformin's protective effects in the heart were mediated by AMPK signaling, and that AMPK signaling could be targeted as a therapeutic strategy following resuscitation from CA. The current study investigates metformin interventions on cardiac and renal outcomes in a non-diabetic CA mouse model. We found that two weeks of metformin pretreatment protects against reduced ejection fraction and reduces kidney ischemia-reperfusion injury at 24 h post-arrest. This cardiac and renal protection depends on AMPK signaling, as demonstrated by outcomes in mice pretreated with the AMPK activator AICAR or metformin plus the AMPK inhibitor compound C.At this 24-h time point, heart gene expression analysis showed that metformin pretreatment caused changes supporting autophagy, antioxidant response, and protein translation. Further investigation found associated improvements in mitochondrial structure and markers of autophagy. Notably, Western analysis indicated that protein synthesis was preserved in arrest hearts of animals pretreated with metformin. The AMPK activation-mediated preservation of protein synthesis was also observed in a hypoxia/reoxygenation cell culture model. Despite the positive impacts of pretreatment in vivo and in vitro, metformin did not preserve ejection fraction when deployed at resuscitation. Taken together, we propose that metformin's in vivo cardiac preservation occurs through AMPK activation, requires adaptation before arrest, and is associated with preserved protein translation.

Takotsubo syndrome (TTS) is a clinical condition characterized by temporary regional wall motion anomalies and dysfunction that extend beyond a single epicardial vascular distribution. Various pathophysiological mechanisms, including inflammation, microvascular dysfunction, direct catecholamine toxicity, metabolic changes, sympathetic overdrive-mediated multi-vessel epicardial spasms, and transitory ischemia may cause the observed reversible myocardial stunning. Despite the fact that TTS usually has an acute coronary syndrome-like pattern of presentation, the absence of culprit atherosclerotic coronary artery disease is often reported at coronary angiography. However, the idea that coronary artery disease (CAD) and TTS conditions are mutually exclusive has been cast into doubt by numerous recent studies suggesting that CAD may coexist in many TTS patients, with significant clinical and prognostic repercussions. Whether the relationship between CAD and TTS is a mere coincidence or a bidirectional cause-and-effect is still up for debate, and misdiagnosis of the two disorders could lead to improper patient treatment with unfavourable outcomes. Therefore, this review seeks to provide a profound understanding of the relationship between CAD and TTS by analyzing potential common underlying pathways, addressing challenges in differential diagnosis, and discussing medical and procedural techniques to treat these conditions appropriately.

All the developed techniques of myocardial protection found their places and time, as none of them disappeared. However, until now cardioplegic arrest remains a golden standard of myocardial protection. Over time, the methods of myocardial protection are constantly improved and the palette of cardioplegic solutions becomes increasingly richer. Today modern cardiosurgery possesses numerous alternative options in choosing an appropriate cardioplegic protection. Despite its almost universal usage, cardioplegy, in its current form, is associated with potential disadvantages which makes these cardioprotective schemes less effective in certain clinical situations and certain patient groups. As a result of the need of a safe method of protection of the myocardium various variants of cardioplegic solutions continue to be developed. The main aim set to myocardial protection is the improvement and extension of its lifetime. Unfortunately, a perfect cardioplegic solution is still not designed and due to this, the choice of an appropriate protection remains an individual choice of each cardiosurgeon. [ABSTRACT FROM AUTHOR]

Takotsubo syndrome (TTS) can result in acute heart failure and lead to a potentially life-threatening complication of aneurysmal subarachnoid hemorrhage (aSAH). The incidence of TTS in aSAH is less than 10% of all patients with aSAH, with a preponderance of postmenopausal women. Early indicators of TTS include elevated serum troponin levels and electrocardiographic abnormalities. The key finding is left ventricular wall motion abnormality. Echocardiography and coronary angiography help to establish the diagnosis. Vasopressors, milrinone, levosimendan, insulin, and anticoagulation may be required. The value of beta-blockers is a matter of controversy. TTS must not delay the treatment of a ruptured aneurysm. The clinical outcome in patients with aSAH and TTS is mostly determined by the aSAH and not the TTS.

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

Stress-induced cardiomyopathy, in contrast to acute myocardial infarction, is a type of acute heart failure characterized by reversible left ventricular dysfunction. Cardiac imaging primarily reveals left ventricle myocardial stunning, 81.7% of which is apical type. Emotional or psychological stress usually precedes the onset of stress-induced cardiomyopathy, which is increasingly being recognized as a unique neurogenic myocardial stunning disease. To distinguish between acute myocardial infarction and acute viral or auto-immune myocarditis, this review summarizes specific mechanisms of myocardial stunning in stress-induced cardiomyopathy, such as calcium disorders, metabolic alterations, anatomical and histological variations in different parts of the left ventricle, and microvascular dysfunction. [ABSTRACT FROM AUTHOR]

Background: The effectiveness of percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) is still uncertain, especially for patients with ischemic left ventricular dysfunction. This study aimed to assess hibernating myocardium (HM), as determined by single-photon emission computed tomography (SPECT) and 18 F-FDG positron emission tomography (PET), and to compare the benefits of PCI and optimal medical therapy (OMT)., Methods: A retrospective study collected data from 332 patients with CTO and ischemic left ventricular dysfunction. The study compared patients who underwent PCI or OMT via propensity score matching (PSM) analysis which was performed with a 1:2 matching protocol using the nearest neighbour matching algorithm. The primary endpoint of the study was the occurrence of major adverse cardiac events (MACE), defined as a composite of cardiac death, readmission for worsening heart failure (WHF), revascularization and myocardial infarction (MI)., Results: After PSM, there were a total of 246 individuals in the PCI and OMT groups. Following Cox regression, hibernating myocardium/total perfusion defect (HM/TPD) was identified as an independent risk factor (hazard ratio (HR): 1.03, 95% confidence interval (CI): 1.008-1.052, p = .007). The cut-off value of HM/TPD was 38%. The results of the subgroup analysis suggest that for patients with HM/TPD >38%, the OMT group had a greater risk of MACE (p = .035). A sensitivity analysis restricting patients with single-vessel CTO lesions, HM/TPD remained an independent predictor (HR 1.025, 95% CI 1.008-1.043, p = .005)., Conclusion: HM/TPD is an independent predictor of MACE, and for patients with HM/TPD > 38%, CTO-PCI had a lower risk of MACE compared with OMT. However, further validation is still needed through large-scale studies., (© 2024 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.)

BackgroundMyocardial infarction (MI) is a major cause of heart failure. Left ventricular adverse remodeling is common post-MI. Several studies have demonstrated a correlation between reduced myocardial strain and the development of adverse remodeling. Cardiac magnetic resonance (CMR) with fast-strain encoding (fast-SENC) or feature tracking (FT) enables rapid assessment of myocardial deformation. The aim of this study was to establish a head-to-head comparison of fast-SENC and FT in post-ST-elevated myocardial infarction (STEMI) patients, with clinical 2D speckle tracking echocardiography (2DEcho) as a reference.MethodsThirty patients treated with primary percutaneous coronary intervention for STEMI were investigated. All participants underwent CMR examination with late gadolinium enhancement, cine-loop steady-state free precession, and fast-SENC imaging using a 1.5T scanner as well as a 2DEcho. Global longitudinal strain (GLS), segmental longitudinal strain (SLS), global circumferential strain (GCS), and segmental circumferential strain (SCS) were assessed along with the MI scar extent.ResultsThe GCS measurements from fast-SENC and FT were nearly identical: the mean difference was 0.01 (2.5)% (95% CI – 0.92 to 0.95). For GLS, fast-SENC values were higher than FT, with a mean difference of 1.8 (1.4)% (95% CI 1.31–2.35). Tests of significance for GLS did not show any differences between the MR methods and 2DEcho. Average strain in the infarct-related artery (IRA) segments compared to the remote myocardium was significantly lower for the left anterior descending artery and right coronary artery culprits but not for the left circumflex artery culprits. Fast-SENC displayed a higher area under the curve for detecting infarcted segments than FT for both SCS and SLS.ConclusionGLS and GCS did not significantly differ between fast-SENC and FT. Both showed acceptable agreement with 2DEcho for longitudinal strain. Segments perfused by the IRA showed significantly reduced strain values compared to the remote myocardium. Fast-SENC presented a higher sensitivity and specificity for detecting infarcted segments than FT.

The prognosis of cardiac arrest (CA) is dismal despite the ongoing progress in cardiopulmonary resuscitation (CPR). ginsenoside Rb1 (Gn-Rb1) has been verified to be cardioprotective in cardiac remodeling and cardiac ischemia/reperfusion (I/R) injury, but its role is less known in CA. After 15 min of potassium chloride-induced CA, male C57BL/6 mice were resuscitated. Gn-Rb1 was blindly randomized to mice after 20 s of CPR. We assessed the cardiac systolic function before CA and 3 h after CPR. Mortality rates, neurological outcome, mitochondrial homeostasis, and the levels of oxidative stress were evaluated. We found that Gn-Rb1 improved the long-term survival during the post-resuscitation period but did not affect the ROSC rate. Further mechanistic investigations revealed that Gn-Rb1 ameliorated CA/CPR-induced mitochondrial destabilization and oxidative stress, partially via the activation of Keap1/Nrf2 axis. Gn-Rb1 improved the neurological outcome after resuscitation partially by balancing the oxidative stress and suppressing apoptosis. In sum, Gn-Rb1 protects against post-CA myocardial stunning and cerebral outcomes via the induction of the Nrf2 signaling pathway, which may offer a new insight into therapeutic strategies for CA.

The C-terminal region of cardiac troponin I (cTnI) is known to be important in cardiac function, as removal of the last 17 C-terminal residues of human cTnI has been associated with myocardial stunning. To investigate the C-terminal region of cTnI, three C-terminal deletion mutations in human cTnI were generated: Δ1 (deletion of residue 210), Δ3 (deletion of residues 208-210), and Δ5 (deletion of residues 206-210). Mammalian two-hybrid studies showed that the interactions between cTnI mutants and cardiac troponin C (cTnC) or cardiac troponin T (cTnT) were impaired in Δ3 and Δ5 mutants when compared to wild-type cTnI. Troponin complexes containing 2-[4'-(iodoacetamido) anilino] naphthalene-6-sulfonic acid (IAANS) labeled cTnC showed that the troponin complex containing cTnI Δ5 had a small increase in Ca(2+) affinity (P

Copyright of Clinical Neuroscience / Ideggyógyászati Szemle is the property of LifeTime Media Kft. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Takotsubo syndrome (TTS) can result in acute heart failure and lead to a potentially life-threatening complication of aneurysmal subarachnoid hemorrhage (aSAH). The incidence of TTS in aSAH is less than 10% of all patients with aSAH, with a preponderance of postmenopausal women. Early indicators of TTS include elevated serum troponin levels and electrocardiographic abnormalities. The key finding is left ventricular wall motion abnormality. Echocardiography and coronary angiography help to establish the diagnosis. Vasopressors, milrinone, levosimendan, insulin, and anticoagulation may be required. The value of beta-blockers is a matter of controversy. TTS must not delay the treatment of a ruptured aneurysm. The clinical outcome in patients with aSAH and TTS is mostly determined by the aSAH and not the TTS. [ABSTRACT FROM AUTHOR]

Cardiac abnormalities are frequently reported in acute subarachnoid hemorrhage (SAH) patients. However, frank ST-elevation and myocardial dysfunction mimicking acute coronary syndrome is a rare occurrence. Systemic and local catecholamine release mediate myocardial injury and may explain raised troponin levels, concordant regional wall motion abnormalities and systolic dysfunction. These findings can pose a significant problem in the acute setting where “time-is-muscle” paradigm can rush clinicians towards a “rule-in” diagnosis of acute myocardial infarction.

Background: Pediatric (especially preadolescent) asphyxiation secondary to near hanging is a seldom reported entity and tends to be predominantly accidental in nature. Objective: The objective of the study was to assess and report the course during the intensive care unit (ICU) stay and the unique problems that are pertinent to pediatric near-hanging injuries. Methodology: A 10-year retrospective analysis (2009–2019) was conducted after obtaining ethical approval. Results: Eleven patients presented to our pediatric ICU over the past 10 years, with pediatric asphyxiation secondary to near hanging. Among these children, most of them had saree swing as the mode of hanging; this subgroup had a higher morbidity and mortality. They tend to have higher markers of myocardial ischemia (high troponin T and creatine kinase). About half of the patients required fluid boluses, inotropic requirement, and ventilation at admission. Patients with pulmonary edema tended to have low oxygen saturation (SpO2), even without respiratory distress at admission, and higher ventilator and inotropic requirement. Only half of the patient population admitted were discharged with good neurological outcome (Glasgow Coma Scale: 15/15 at discharge). Conclusion: The nature of complications secondary to hanging necessitates ICU monitoring, with pediatric ENT and anesthesia backup. The presence of low SpO2at admission in this setting should alert the clinician to possibility of pulmonary edema. Parents should be made aware that saree swing can lead to accidental asphyxiation. It is important to raise awareness to prevent this entity as it is associated with poor outcome.

Takotsubo cardiomyopathy (TCM) is a transient wall motion abnormality of the left ventricular apex associated with emotional or physical stress. In the setting of diabetic ketoacidosis (DKA), it is thought to be caused by the compound effect of a catecholamine surge and the noxious effect of acidosis and ketones leading to myocardial stunning. In this report, the first of its kind in the Middle East, we describe the case of a 71-year-old comatose patient, who was being treated for DKA and hypernatremia and was incidentally diagnosed with TCM. We also review 15 case reports of DKA-induced TCM published to date in the literature, many of which had an atypical presentation and good outcomes. Furthermore, we discuss possible risk factors for TCM in our case and supporting literature. It is recommended to maintain increased vigilance and attempt early identification of such conditions in acutely ill patients to prevent life-threatening complications., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, AlShehabi et al.)

Hemodialysis (HD)-induced myocardial stunning, characterized by transient left ventricular systolic dysfunction during HD, has been reported to be common and associated with a poor prognosis. However, the pathophysiology is not fully understood. We herein report a case of HD-induced myocardial stunning without obstructive coronary artery disease complicated by coronary microvascular dysfunction (CMD), suggesting that CMD plays a crucial role in the pathophysiology of this disease.

Patients with end-stage kidney disease on haemodialysis (HD) have an elevated risk of cardiovascular disease (CVD). These patients also experience high levels of physical deconditioning and programmes of rehabilitation have been tested in a variety of forms with variable success. It has been suggested that programmes of exercise rehabilitation have a role to play in improving the physical condition of patients on HD and in addressing the traditional and non-traditional risk factors that drive CVD for this population. Intradialytic exercise has often been suggested as a convenient way of delivering rehabilitation for patients on HD, as it makes use of otherwise dead time, but there are legitimate concerns about this group of at-risk patients undertaking exercise at a time when their myocardium is already vulnerable to the insults of demand ischaemia from the processes of dialysis and ultrafiltration. A study in this issue of Clinical Kidney Journal provides reassuring data, showing that cycling during dialysis potentially reduces evidence of demand ischaemia (episodes of myocardial stunning). Together with the safety and quality of life data, we expect from the multicentre PrEscription of Intra-Dialytic Exercise to Improve quAlity of Life in Patients With Chronic Kidney Disease study (the protocol for which is published concurrently), rehabilitation programmes that include intradialytic exercise are perhaps closer than ever for patients on HD. [ABSTRACT FROM AUTHOR]

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Purpose: In a preclinical study using a swine myocardial infarction (MI) model, a delayed enhancement (DE)-multi-detector computed tomography (MDCT) scan was performed using a hybrid system alongside diagnostic invasive coronary angiography (ICA) without the additional use of a contrast agent, and demonstrated an excellent correlation in the infarct area compared with histopathologic specimens. In the present investigation, we evaluated the feasibility and diagnostic accuracy of a myocardial viability assessment by DE-MDCT using a hybrid system comprising ICA and MDCT alongside diagnostic ICA without the additional use of a contrast agent., Materials and Methods: We prospectively enrolled 13 patients (median age: 67 years) with a previous MI (>6 months) scheduled to undergo ICA. All patients underwent cardiac magnetic resonance (CMR) imaging before diagnostic ICA. MDCT viability scans were performed concurrently with diagnostic ICA without the use of additional contrast. The total myocardial scar volume per patient and average transmurality per myocardial segment measured by DE-MDCT were compared with those from DE-CMR., Results: The DE volume measured by MDCT showed an excellent correlation with the volume measured by CMR (r=0.986, p <0.0001). The transmurality per segment by MDCT was well-correlated with CMR (r=0.900, p <0.0001); the diagnostic performance of MDCT in differentiating non-viable from viable myocardium using a 50% transmurality criterion was good with a sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of 87.5%, 99.5%, 87.5%, 99.5%, and 99.1%, respectively., Conclusion: The feasibility of the DE-MDCT viability assessment acquired simultaneously with conventional ICA was proven in patients with chronic MI using DE-CMR as the reference standard., Competing Interests: The authors have no potential conflicts of interest to disclose., (© Copyright: Yonsei University College of Medicine 2024.)

Background and Aims: Ischemic preconditioning (IPC), i.e., brief periods of ischemia, protect the heart from subsequent prolonged ischemic injury, and reduces infarction size. Myocardial stunning refers to transient loss of contractility in the heart after myocardial ischemia that recovers without permanent damage. The relationship between IPC and myocardial stunning remains incompletely understood. This study aimed primarily to examine the effects of IPC on the relationship between ischemia duration, stunning, and infarct size in an ischemia-reperfusion injury model. Secondarily, this study aimed to examine to which extent the phosphoproteomic changes induced by IPC relate to myocardial contractile function., Methods and Results: Rats were subjected to different durations of left anterior descending artery (LAD) occlusion, with or without preceding IPC. Echocardiograms were acquired to assess cardiac contraction in the affected myocardial segment. Infarction size was evaluated using triphenyl tetrazolium chloride staining. Phosphoproteomic analysis was performed in heart tissue from preconditioned and non-preconditioned animals. In contrast to rats without IPC, reversible akinesia was observed in a majority of the rats that were subjected to IPC and subsequently exposed to ischemia of 13.5 or 15 min of ischemia. Phosphoproteomic analysis revealed significant differential regulation of 786 phosphopeptides between IPC and non-IPC groups, with significant associations with the sarcomere, Z-disc, and actin binding., Conclusion: IPC induces changes in phosphosites of proteins involved in myocardial contraction; and both accentuates post-ischemic myocardial stunning and reduces infarct size., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Elmahdy, Shekka Espinosa, Kakaei, Pylova, Jha, Zulfaj, Krasnikova, Al-Awar, Sheybani, Sevastianova, Berger, Nejat, Molander, Andersson, Omerovic, Hussain and Redfors.)

Subarachnoid hemorrhage (SAH) is a devastating cerebral event caused by an aneurysmal rupture. In addition to neurological injury, SAH has significant effects on cardiac function and the peripheral microcirculation. Since these peripheral complications may exacerbate brain injury, the prevention and management of these peripheral effects are important for improving the overall clinical outcome after SAH. In this investigation, we examined the effects of SAH on cardiac function and vascular reactivity in a well-characterized blood injection model of SAH. Standard echocardiographic and blood pressure measurement procedures were utilized to assess cardiac function and hemodynamic parameters in vivo; we utilized a pressure myography approach to assess vascular reactivity in cremaster skeletal muscle resistance arteries ex vivo. We observed that elevated catecholamine levels in SAH stun the myocardium, reduce cardiac output and augment myogenic vasoconstriction in isolated cremaster arteries. These cardiac and vascular effects are driven by beta- and alpha-adrenergic receptor signaling, respectively. Clinically utilized adrenergic receptor antagonists can prevent cardiac injury and normalize vascular function. We found that tumor necrosis factor (TNF) gene deletion prevents the augmentation of myogenic reactivity in SAH: since membrane-bound TNF serves as a mechanosensor in the arteries assessed, alpha-adrenergic signaling putatively augments myogenic vasoconstriction by enhancing mechanosensor activity.

Background: There is significant uncertainty regarding the timing of onset of cardiovascular stunning after cardiac surgery. Cardiovascular stunning is affecting both contractility (Ees) and arterial load. Arterial load may be represented by arterial elastance (Ea) and participates in ventriculo-arterial coupling through the Ea/Ees ratio, giving information on efficiency and performance. An alternative approach to ventriculo-arterial interaction is oscillatory power fraction (OPF). The aim of this study was to investigate the immediate beat-to-beat effects of on-pump coronary artery bypass graft (CABG) surgery on contractility, cardiac power parameters, arterial load and ventriculo-arterial coupling as well as classical haemodynamic parameters.Methods: We included 41 patients scheduled for fast-track CABG surgery. Measurements were taken before and after cardiopulmonary bypass. A flow and pressure curve were recorded from transoesophageal pulsed wave Doppler and a radial artery catheter, respectively. This enabled the calculation of stroke work, total cardiac energy delivery, OPF and Ea/Ees ratio. Routine haemodynamic monitoring provided the classical haemodynamic parameters.Results: Immediately after cardiopulmonary bypass there was no firm evidence for alterations in contractility, stroke work, stroke volume or arterial elastance. Ea/Ees ratio and OPF remained unchanged.Conclusions: There was no evidence for clinically relevant cardiac stunning or altered arterial load immediately after cardiopulmonary bypass for CABG surgery. The unchanged Ea/Ees ratio and OPF are indicating unchanged cardiac efficiency before and after cardiopulmonary bypass. This indicates that in elective CABG patients cardiovascular stunning is perhaps a phenomenon of inflammation and not immediate ischaemia-reperfusion injury or mechanical handling. [ABSTRACT FROM AUTHOR]

Background: Cardiac injury and myocarditis have been described in adults with coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in children is typically minimally symptomatic. We report a series of febrile pediatric patients with acute heart failure potentially associated with SARS-CoV-2 infection and the multisystem inflammatory syndrome in children as defined by the US Centers for Disease Control and Prevention.Methods: Over a 2-month period, contemporary with the SARS-CoV-2 pandemic in France and Switzerland, we retrospectively collected clinical, biological, therapeutic, and early outcomes data in children who were admitted to pediatric intensive care units in 14 centers for cardiogenic shock, left ventricular dysfunction, and severe inflammatory state.Results: Thirty-five children were identified and included in the study. Median age at admission was 10 years (range, 2-16 years). Comorbidities were present in 28%, including asthma and overweight. Gastrointestinal symptoms were prominent. Left ventricular ejection fraction was <30% in one-third; 80% required inotropic support with 28% treated with extracorporeal membrane oxygenation. Inflammation markers were suggestive of cytokine storm (interleukin-6 median, 135 pg/mL) and macrophage activation (D-dimer median, 5284 ng/mL). Mean BNP (B-type natriuretic peptide) was elevated (5743 pg/mL). Thirty-one of 35 patients (88%) tested positive for SARS-CoV-2 infection by polymerase chain reaction of nasopharyngeal swab or serology. All patients received intravenous immunoglobulin, with adjunctive steroid therapy used in one-third. Left ventricular function was restored in the 25 of 35 of those discharged from the intensive care unit. No patient died, and all patients treated with extracorporeal membrane oxygenation were successfully weaned.Conclusions: Children may experience an acute cardiac decompensation caused by severe inflammatory state after SARS-CoV-2 infection (multisystem inflammatory syndrome in children). Treatment with immunoglobulin appears to be associated with recovery of left ventricular systolic function. [ABSTRACT FROM AUTHOR]