Neurogenic Stunned Myocardium in Severe Neurological Injury.

PURPOSE OF REVIEW: Neurogenic stunned myocardium (NSM) is a poorly recognized cardiac manifestation of neurological illness. This review addresses the contemporary understanding of NSM pathophysiology, epidemiology, diagnosis, and clinical management. RECENT FINDINGS: While the precise pathophysiology and diagnosis remain unclear, NSM is phenotypically atypical stress cardiomyopathy that can be partially attributed to excess catecholaminergic toxicity. NSM is a diagnosis of exclusion where electrocardiography, echocardiography, and cardiac biomarkers are frequently abnormal. Clinical expertise is crucial to evaluate and differentiate NSM from acute coronary syndrome and in the evaluation of potential cardiac transplantation donors after unsalvageable severe neurological injury. Neurogenic stunned myocardium is a relatively common and clinically impactful condition. More research is needed, particularly to refine clinical prognostication of NSM and rule out intrinsic cardiac injury in order to optimize donor candidacy in the event of brain death.

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.

Association of Central Venous Oxygen Saturation Variability and Mortality in Hemodialysis Patients.

BACKGROUND: Central venous oxygen saturation (ScvO2) is correlated with cardiac output. In most patients, ScvO2 declines during hemodialysis (HD) due to factors such as reduced preload, myocardial stunning, and intermittent arrhythmias. Previous research has shown that low ScvO2 is associated with higher mortality in chronic HD patients. In this research, we tested the hypothesis that ScvO2 variability is associated with all-cause mortality. METHODS: We conducted a retrospective study in 232 chronic HD patients with central venous catheter as vascular access. ScvO2 was recorded 1× per minute during dialysis using the Crit-Line monitor. A 6-month baseline comprising at least 10 dialysis treatments with ScvO2 recordings preceded a follow-up period of up to 3 years. The coefficient of variation (CV) of ScvO2 (100 times the ratio of the standard deviation and mean of ScvO2) served as a measure of ScvO2 stability during baseline. Patients were stratified by median population CV of ScvO2 during baseline, and survival during follow-up was compared between the 2 groups by Kaplan Meier and multivariate Cox analysis. The association between CV of ScvO2 and all-cause mortality during follow-up was further assessed by Cox analysis with a spline term for CV of ScvO2. RESULTS: The mean CV ± standard deviation of ScvO2 in our population was 6.1 ± 2.7% and the median was 5.3%. Univariate Kaplan-Meier analysis (p = 0.043) and multivariate Cox analysis (hazard ratio [HR] 1.16; p = 0.0005) indicated that a CV of ScvO2 > 5.3% was significantly associated with increased mortality. In Cox analysis with spline term, a CV of ScvO2 >  11% was associated with a significantly increased HR for all-cause mortality. CONCLUSION: High ScvO2 variability during dialysis is associated with increased all-cause mortality.

Identifying and Managing Hibernating Myocardium: What's New and What Remains Unknown?

PURPOSE OF REVIEW: Hibernation is an important and reversible cause of myocardial dysfunction in ischaemic heart failure. RECENT FINDINGS: Hibernation is an adaptive process that promotes myocyte survival over maintaining contractile function. It is innate to mammalian physiology, sharing features with physiological hibernation in other species. Advanced imaging methods have reasonable accuracy in identifying hibernating myocardium. Novel superior hybrid methods may provide diagnostic potential. New evidence supports the role of surgical revascularisation in ischaemic heart failure, but the role of viability tests in planning such procedures remains unclear. Research to date has exclusively involved patients with ambulatory heart failure: Investigating the role of hibernation in ADHF is a key avenue for the future. Whilst our understanding of hibernation pathophysiology has improved dramatically, the clinical utility of identifying and targeting hibernation remains unclear.

Acute Cardiac Complications in Critical Brain Disease.

Acute cardiac complications in critical brain disease should be understood as a clinical condition representing an intense brain-heart crosstalk and might mimic ischemic heart disease. Two main entities (neurogenic stunned myocardium [NSM] and stress cardiomyopathy) have been better characterized in the neurocritically ill patients and they portend worse clinical outcomes in these cases. The pathophysiology of NSM remains elusive. However, significant progress has been made on the early identification of neurocardiac compromise following acute critical brain disease. Effective prevention and treatment interventions are yet to be determined.

Baicalein Rescues Delayed Cooling via Preservation of Akt Activation and Akt-Mediated Phospholamban Phosphorylation.

Cooling reduces the ischemia/reperfusion (I/R) injury seen in sudden cardiac arrest (SCA) by decreasing the burst of reactive oxygen species (ROS). Its cardioprotection is diminished when delay in reaching the target temperature occurs. Baicalein, a flavonoid derived from the root of ScutellariabaicalensisGeorgi, possesses antioxidant properties. Therefore, we hypothesized that baicalein can rescue cooling cardioprotection when cooling is delayed. Two murine cardiomyocyte models, an I/R model (90 min ischemia/3 h reperfusion) and stunning model (30 min ischemia/90 min reperfusion), were used to assess cell survival and contractility, respectively. Cooling (32 °C) was initiated either during ischemia or during reperfusion. Cell viability and ROS generation were measured. Cell contractility was evaluated by real-time phase-contrast imaging. Our results showed that cooling reduced cell death and ROS generation, and this effect was diminished when cooling was delayed. Baicalein (25 µM), given either at the start of reperfusion or start of cooling, resulted in a comparable reduction of cell death and ROS production. Baicalein improved phospholamban phosphorylation, contractility recovery, and cell survival. These effects were Akt-dependent. In addition, no synergistic effect was observed with the combined treatments of cooling and baicalein. Our data suggest that baicalein may serve as a novel adjunct therapeutic strategy for SCA resuscitation.

[New thoughts in mechanism research of acupuncture for myocardial stunning from κ-opioid receptor signaling pathway].

By reviewing the literature regarding the development mechanism of myocardial stunning, effects of acupuncture on myocardial ischemic injury, and correlation between acupuncture and κ-opioid receptor, it was suggested that acupuncture was highly likely to act on κ-opioid receptor in myocardial cells, and directly treated myocardial malfunction induced by myocardial stunning through κ-opioid receptor and its signaling pathway. In addition, acupuncture could inhabit the signaling pathway of adrenoceptor ß1, one of the main functional receptors, to indirectly improve myocardial ischemic injury. From κ-opioid receptor signaling pathway, the action mechanism of acupuncture for prevention and treatment of myocardial stunning was discussed in this paper, hoping to provide new ideas for possible mechanism of acupuncture for myocardial ischemic injury.