Neurogenic Stress Cardiomyopathy Research Articles

A Case of Aneurysmal Sub Arachnoid Hemorrhage Complicated by Nstemi and Acute Pulmonary Edema

Aneurysmal SAH is a life threatening event which can cause permanent disability, the mortality and morbidity will be increased with associated complications like ACS and Acute pulmonary edema, which are rare complications of aneurysmal SAH. The combination of these three conditions imposes important treatment dilemmas. These patients tend to have electrocardiographic changes along with elevated cardiac biomarkers and neurogenic stress cardiomyopathy and pulmonary edema.

Prevalence of Neurogenic Stress Cardiomyopathy in Acute Ischemic Stroke and Relationship with Leukocytosis (P14-5.026)

<h3>Objective:</h3> Describe incidence of neurogenic stress cardiomyopathy (NSC) in acute ischemic stroke (AIS) and determine if there is an association between leukocytosis and development of NSC. <h3>Background:</h3> NSC is a syndrome of cardiac impairment following an acute neurologic injury. Cardiac impairment is identified by reduced left ventricular ejection fraction (LVEF), ventricular wall motion abnormalities, and elevated cardiac troponin and brain natriuretic peptide (BNP). Limited studies have found troponin elevations in 17–20% of stroke patients, but NSC is not well described. Inflammation is one of the proposed potential mechanisms of stroke-induced cardiac injury. Inflammation in AIS may correlate with development of NSC, but this has not been well studied. <h3>Design/Methods:</h3> Retrospective review of 688 adult patients admitted to a single tertiary care center with AIS from 2018 to 2021. NSC was defined by at least one of the following: reduced LVEF, ventricular wall motion abnormalities, elevated troponin, or elevated BNP within first 24 hours of admission. Leukocytosis was defined as white blood cell (WBC) count &gt; 12.0 × 10⁹/L. <h3>Results:</h3> NSC was observed in 267 (39%) of the 688 patients with AIS. Mean age was 67 years old and 46% female. Mean NIHSS in those with NSC was 10. Mean length of hospital stay was 8 days. Leukocytosis was observed 12% of patients with NSC and in 8% of patients without NSC. Mean WBC in patients with NSC was 8.63 × 10⁹/L. Mean WBC in patients without NSC was 8.07 × 10⁹/L. Analysis via two-tailed T-test revealed no significant difference between groups (<i>p</i>&gt;0.5). <h3>Conclusions:</h3> We found a high incidence of NSC, when compared to previous reports. There was no statistically significant difference in leukocytosis between groups. Further research is needed to identify risk factors of NSC, including other markers of inflammation, that may better elucidate the underlying mechanism. <b>Disclosure:</b> Dr. Wolf has nothing to disclose. Dr. Shah has nothing to disclose. Mr. Coleman has nothing to disclose. Dr. Mullen has received publishing royalties from a publication relating to health care. Dr. Koffman has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant for Law Firm.

The Heart Is at Risk: Understanding Stroke-Heart-Brain Interactions with Focus on Neurogenic Stress Cardiomyopathy-A Review.

In recent years, it has been convincingly demonstrated that acute brain injury may cause severe cardiac complications-such as neurogenic stress cardiomyopathy (NSC), a specific form of takotsubo cardiomyopathy. The pathophysiology of these brain-heart interactions is complex and involves sympathetic hyperactivity, activation of the hypothalamic-pituitary-adrenal axis, as well as immune and inflammatory pathways. There have been great strides in our understanding of the axis from the brain to the heart in patients with isolated acute brain injury and more specifically in patients with stroke. On the other hand, in patients with NSC, research has mainly focused on hemodynamic dysfunction due to arrhythmias, regional wall motion abnormality, or left ventricular hypokinesia that leads to impaired cerebral perfusion pressure. Comparatively little is known about the underlying secondary and delayed cerebral complications. The aim of the present review is to describe the stroke-heart-brain axis and highlight the main pathophysiological mechanisms leading to secondary and delayed cerebral injury in patients with concurrent hemorrhagic or ischemic stroke and NSC as well as to identify further areas of research that could potentially improve outcomes in this specific patient population.

Hemorrhagic Cerebral Insults and Secondary Takotsubo Syndrome: Findings in a Novel In Vitro Model Using Human Blood Samples.

Intracranial hemorrhage results in devastating forms of cerebral damage. Frequently, these results also present with cardiac dysfunction ranging from ECG changes to Takotsubo syndrome (TTS). This suggests that intracranial bleeding due to subarachnoid hemorrhage (SAH) disrupts the neuro–cardiac axis leading to neurogenic stress cardiomyopathy (NSC) of different degrees. Following this notion, SAH and secondary TTS could be directly linked, thus contributing to poor outcomes. We set out to test if blood circulation is the driver of the brain–heart axis by investigating serum samples of TTS patients. We present a novel in vitro model combining SAH and secondary TTS to mimic the effects of blood or serum, respectively, on blood–brain barrier (BBB) integrity using in vitro monolayers of an established murine model. We consistently demonstrated decreased monolayer integrity and confirmed reduced Claudin-5 and Occludin levels by RT-qPCR and Western blot and morphological reorganization of actin filaments in endothelial cells. Both tight junction proteins show a time-dependent reduction. Our findings highlight a faster and more prominent disintegration of BBB in the presence of TTS and support the importance of the bloodstream as a causal link between intracerebral bleeding and cardiac dysfunction. This may represent potential targets for future therapeutic inventions in SAH and TTS.

Relation between brain natriuretic peptide and delayed cerebral ischemia in patients with aneurysmalsubarachnoid hemorrhage

BackgroundBrain natriuretic peptide (BNP), often used to evaluate degree of heart failure, has been implicated in fluid dysregulation and inflammation in critically-ill patients. Twenty to 30% of patients with aneurysmal subarachnoid hemorrhage (aSAH) will develop some degree of neurogenic stress cardiomyopathy (NSC) and in turn elevation of BNP levels. We sought to explore the association between BNP levels and development of delayed cerebral ischemia (DCI) in patients with aSAH. MethodsWe retrospectively evaluated the records of 149 patients admitted to the Neurological Intensive Care Unit between 2006 and 2015 and enrolled in an existing prospectively maintained aSAH database. Demographic data, treatment and outcomes, and BNP levels at admission and throughout the hospital admission were noted. ResultsOf the 149 patients included in the analysis, 79 developed DCI during their hospital course. We found a statistically significant association between DCI and the highest recorded BNP (OR 1.001, 95% CI-1.001–1.002, p = 0.002). The ROC curve analysis for DCI based on BNP showed that the highest BNP level during hospital admission (AUC 0.78) was the strongest predictor of DCI compared to the change in BNP over time (AUC 0.776) or the admission BNP (AUC 0.632). ConclusionOur study shows that DCI is associated not only with higher baseline BNP values (admission BNP), but also with the highest BNP level attained during the hospital course and the rapidity of change or increase in BNP over time. Prospective studies are needed to evaluate whether routine measurement of BNP may help identify SAH patients at high risk of DCI.

Incidence and Outcomes of Registry-Based Acute Myocardial Infarction After Aneurysmal Subarachnoid Hemorrhage.

Acute myocardial infarction (AMI) is the rarest and least studied cardiac complication of aneurysmal subarachnoid hemorrhage (aSAH). Precise estimates of the incidence of AMI after aSAH are unavailable. Our goal was to estimate the incidence of registry-based AMI (rb-AMI) after aSAH and determine its association with clinical outcomes. Adult patients with aSAH in the National Inpatient Samples from 2002 to 2014 were included in the study. We evaluated risk factors for rb-AMI using univariate and multivariate regression models. Clinical outcomes that were assessed included functional status at discharge, in-patient mortality, length of stay, and total hospitalization cost, adjusting for patient demographics and cardiovascular risk factors through an inverse probability weighted analysis. Subgroup analyses were further performed stratified by rb-AMI type (ST-segment elevation myocardial infarction [STEMI] vs. non-STEMI [NSTEMI]). A total of 139,734 patients with aSAH were identified, 3.6% of whom had rb-AMI. NSTEMI was the most common type of rb-AMI occurring after aSAH (71% vs. 29% for NSTEMI vs. STEMI, respectively). Patient characteristics associated with higher odds of rb-AMI included age, female sex, poor aSAH grade, and various cardiovascular risk factors. Rb-AMI was also associated with poor functional status at discharge, higher in-hospital mortality, and a longer and more costly hospital stay. Rb-AMI occurs in 3.6% of patients with aSAH and is associated with poor functional status at discharge, higher in-patient mortality, and a longer and more costly hospitalization. Differentiating between different types of rb-AMI would be important in optimizing the management of patients with aSAH. Our definition of rb-AMI likely includes patients with neurogenic stress cardiomyopathy, which may confound the results.

The Use of Levosimendan in the Treatment of Neurogenic Stress Cardiomyopathy in a Patient with Nontraumatic Subarachnoid Hemorrhage (Case Report)

We present a case of cardiogenic shock due to neurogenic stress cardiomyopathy (NSC) in a patient with nontraumatic subarachnoid hemorrhage caused by a ruptured aneurysm of the right pericallosal artery. Due to the catecholamine-resistant shock, levosimendan was administered under advanced hemodynamic control, including transpulmonary thermodilution and echocardiography. This resulted in an improved cardiac contractility and reduced demand for catecholamines. Full stabilization of hemodynamic parameters was achieved by day 5. In the discussion section we reviewed available published case reports of using levosimendan in stress cardiomyopathy treatment.

Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage

Cerebral hypoperfusion is a key factor for determining the outcome after subarachnoid hemorrhage (SAH). A subset of SAH patients develop neurogenic stress cardiomyopathy (NSC), but it is unclear to what extent cerebral hypoperfusion is influenced by cardiac dysfunction after SAH. The aims of this study were to examine the association between cardiac function and cerebral perfusion in a murine model of SAH and to identify electrocardiographic and echocardiographic signs indicative of NSC. We quantified cortical perfusion by laser SPECKLE contrast imaging, and myocardial function by serial high-frequency ultrasound imaging, for up to 7 days after experimental SAH induction in mice by endovascular filament perforation. Cortical perfusion decreased significantly whereas cardiac output and left ventricular ejection fraction increased significantly shortly post-SAH. Transient pathological ECG and echocardiographic abnormalities, indicating NSC (right bundle branch block, reduced left ventricular contractility), were observed up to 3 h post-SAH in a subset of model animals. Cerebral perfusion improved over time after SAH and correlated significantly with left ventricular end-diastolic volume at 3, 24, and 72 h. The murine SAH model is appropriate to experimentally investigate NSC. We conclude that in addition to cerebrovascular dysfunction, cardiac dysfunction may significantly influence cerebral perfusion, with LVEDV presenting a potential parameter for risk stratification.

Prospective Analysis of Role of hsTnT and NT-proBNP in Prediction of Neurogenic Stress Cardiomyopathy in Patients with Aneurysmal Subarachnoid Haemorrhage.

Neurogenic stress cardiomyopathy (NSC), also known as stress-induced cardiomyopathy (SIC), is a significant complication of aneurysmal subarachnoid hemorrhage and an important contributor to morbidity mortality. This prospective observational study assessed whether the high sensitive troponin T (hsTnT) and N-terminal pro-B-type natriuretic peptide (NTproBNP) helps in the prediction of NSC after SAH. The consecutive patients with aSAH without any cardiac history were included prospectively over 12 months. Neurological assessment for the grade of SAH (Hunt & Hess and WFNS grade), electrocardiogram, and echocardiography done at admission. The serial measurements of serum hsTnT and NTproBNP for consecutive 7 days done. The NSC is defined as transient hypokinesia of the ventricular wall on echocardiography. The study included 69 patients, and 7 (10.1%) were diagnosed with NSC. The NSC had a positive correlation with Hunt and Hess grade (P = 0.010), and the serum levels of hsTnT and NTproBNP were higher in patients with NSC in comparison to without NSC over all 7 days. The peak levels of hsTnT and NTproBNP were significantly higher in patients with cardiomyopathy (P = 0.000 and 0.032, respectively). The best cut-off level of peak hsTnT was 0.032 pg/dl to predict cardiomyopathy with sensitivity and specificity of 100% and 80%, respectively, and NTproBNP was 430.6 ng/dL with sensitivity and specificity of 86% and 73%, respectively. The peak levels of hsTnT and NTproBNP with abnormal ECG and echocardiography at admission help identify NSC in the early phase of aSAH.

Fragile Endothelium and Brain Dysregulated Neurochemical Activity in COVID-19.

Immune system and renin-angiotensin-aldosterone system dysregulation with associated cytokine release syndrome may be a key feature of early stage of SARS-CoV-2 organotropism and infection. Following viral mediated brain injury, dysregulated neurochemical activity may cause neurogenic stress cardiomyopathy, which is characterized by transient myocardial dysfunction and arrhythmias. Cardiomyopathy along with acute acute inflammatory thromboembolism and endotheliitis (fragile endothelium) might at least partially explain the underlying mechanisms of rapidly evolving life-threatening COVID-19. Further studies are clearly required to explore these complex pathologies.

MISCODED: AN IMITATOR OF A CODE STEMI

Neurogenic stress cardiomyopathy (NSC) is associated with troponin and ST-segment elevation that can mimic MI. NSC is seen with hemorrhagic or ischemic stroke, traumatic brain injury, or subarachnoid hemorrhage. Rarely, it may be observed in patients with cerebral metastatic disease. 33-year-old

Neurogenic Stress Cardiomyopathy Following Subarachnoid Hemorrhage Is Associated with Vagal Complex Degeneration: First Experimental Study

Neurogenic stunned myocardium (NSM) is a devastating complication of subarachnoid hemorrhage (SAH). The most widely accepted mechanism in the pathogenesis of NSM and takotsubo cardiomyopathy is catecholamine-mediated direct myocardial injury. The aim of this study is to examine if there is any effect of sympathetic overactivity of the stellate ganglions on myocardial tissues, secondary to vagal complex degeneration in SAH-induced NSM. This study was conducted on 25 New Zealand female rabbits. After the examination, all animals were assigned into 3 groups randomly: a control group (n= 5), a sham group (n= 5), and a study group (n= 15) that was subjected to experimental SAH with double injection of blood into the cisterna magna. After 7 animals exhibited NSM, all animals were killed. Their brains, vagal complexes, stellate ganglions, and hearts were extracted and examined by histopathologic methods. Degenerated nodose ganglion neurons and stellate ganglion neuron densities were compared with degenerated myocardial tissue/normal myocardial tissue ratios, and the results were analyzed with the Mann-Whitney U test. Three rabbits in the study group died immediately after the second injection of blood. NSM developed in 7 animals after 1 to 5 days, which was diagnosed with transthoracic echocardiography. Interestingly, the animals that developed NSM had more stellate ganglia neurons and more degenerated neuron densities of nodose ganglia (P<0.001). NSM and takotsubo cardiomyopathy may be induced by vagal complex degeneration and sympathetic overactivity, which originated from more neurons, including stellate ganglia and more degenerated neuron densities of nodose ganglia.

Neurogenic stress cardiomyopathy following aneurysmal subarachnoid haemorrhage: a literature review

Summary Neurogenic stress cardiomyopathy (NSC) is defined as transient cardiac dysfunction occurring after primary brain injury, such as aneurysmal subarachnoid haemorrhage, and characterised by left ventricular systolic dysfunction with reduced ejection fraction and abnormalities of regional wall motion. It may also be suspected if elevated levels of cardiac biomarkers and ECG abnormalities are present. It is a reversible condition with favourable long-term prognosis if diagnosed and treated timely, however, NSC is associated with higher rates of early mortality and complications, including pulmonary oedema, cardiogenic shock, delayed cerebral ischaemia. Early diagnosis of the NSC is important in order to prevent these complications and reduce mortality. Management of the NSC is complicated and a multidisciplinary approach is usually required.

Transcranial Doppler Waveforms During Intra-aortic Balloon Pump Counterpulsation for Vasospasm Detection After Subarachnoid Hemorrhage.

Transcranial Doppler ultrasound is a standard screening tool for vasospasm after subarachnoid hemorrhage. Prevention of vasospasm-induced delayed cerebral ischemia after subarachnoid hemorrhage depends on optimization of cerebral perfusion pressure, which can be challenged by neurogenic stress cardiomyopathy. Intra-aortic balloon pumps have been utilized to augment cerebral perfusion, but they change the transcranial Doppler waveform, altering its interpretability for vasospasm screening. To assess the features of the transcranial Doppler waveform that correlate with vasospasm. We retrospectively reviewed cases of subarachnoid hemorrhage that underwent same-day transcranial Doppler ultrasound and angiography. Transcranial Doppler waveforms were assessed for mean velocity, peak systolic velocity, balloon pump-augmented diastolic velocity, and a novel feature, "delta velocity" (balloon pump-augmented velocity - systolic velocity). Relationship of flow velocity features to vasospasm was estimated by generalized estimating equation models using a Gaussian distribution and an exchangeable correlation structure. There were 31 transcranial Doppler and angiography pairings (12 CT angiography/19 digital subtraction angiography) from 4 patients. Fourteen pairings had proximal vasospasm by angiography. Delta velocity was associated with proximal vasospasm (coefficient -6.8 [95% CI -9.8 to -3.8], P<.001). There was no significant correlation with proximal vasospasm for mean velocity (coefficient -13.0 [95% CI -29.3 to 3.4], P=.12), systolic velocity (coefficient -8.7 [95% CI -24.8 to 7.3], P=.29), or balloon pump-augmented velocity (coefficient -15.3 [95% CI -31.3 to 0.71], P=.06). Delta velocity, a novel transcranial Doppler flow velocity feature, may reflect vasospasm in patients with subarachnoid hemorrhage and intra-aortic balloon pumps.

Poster 270: Neurogenic Stress Cardiomyopathy Associated with Subarachnoid Hemorrhage: A Case Report

Poster 270: Neurogenic Stress Cardiomyopathy Associated with Subarachnoid Hemorrhage: A Case Report

Neurogenic stress cardiomyopathy: What do we need to know

The interaction between the heart and brain is complex and integral to the maintenance of normal cardiovascular function. Even in the absence of coronary disease, acute neuronal injury can induce a variety of cardiac changes. Recent neuroimaging data revealed a network including the insular cortex, anterior cingulate gyrus, and amygdala playing a crucial role in the regulation of central autonomic nervous system. Damage in these areas has been associated with arrhythmia, myocardial injury, higher plasma levels of brain natriuretic peptide, catecholamines, and glucose. Some patients after brain injury may die due to occult cardiac damage and functional impairment in the acute phase. Heart failure adversely influences acute stroke mortality. Troponin and NT-proBNP are elevated in acute brain injury patients, in response to the activated renin–angiotensin–aldosterone system and other neurohumoral changes, as a protective mechanism for sympathoinhibitory activity. Such patients have been shown to be associated with higher short- and long-term mortality. While thrombolysis, neuroprotection, and other measures, alone or in combination, may limit the cerebral damage, attention should also be directed toward the myocardial protection. Early administration of cardioprotective medication aimed at reducing increased sympathetic tone may have a role in myocardial protection in stroke patients. For a full understanding of the brain–heart control, the consequences of disruption of this control, the true incidence of cardiac effects of stroke, and the evidence-based treatment options further research are needed.

Reversible Stress Cardiomyopathy Secondary to Aneurysmal Subarachnoid Hemorrhage: A Case Report

BackgroundAcute cerebral incidents have been correlated with cardiac manifestations. Specifically, subarachnoid hemorrhage has been correlated with a syndrome described as neurogenic stress cardiomyopathy and mimics acute coronary syndrome. Case ReportA 55-year-old woman presented at the Emergency Department of our hospital complaining of vomiting and headache of sudden onset. Computed tomography angiography revealed a ruptured aneurysm at the tip of the basilar artery and the patient underwent a successful complete embolism of the sac of the aneurysm. During hospitalization, the patient developed electrocardiographic alterations and elevation of cardiac biomarkers, and echocardiography showed an impairment of left ventricular systolic function. The patient was diagnosed with neurogenic stress cardiomyopathy and she was treated conservatively. Why Should an Emergency Physician Be Aware of This?Clinicians should be aware of neurogenic stress cardiomyopathy because early diagnosis and treatment are the cornerstones for achieving a better outcome.

Brain-Heart Interaction: Cardiac Complications After Stroke.

Neurocardiology is an emerging specialty that addresses the interaction between the brain and the heart, that is, the effects of cardiac injury on the brain and the effects of brain injury on the heart. This review article focuses on cardiac dysfunction in the setting of stroke such as ischemic stroke, brain hemorrhage, and subarachnoid hemorrhage. The majority of post-stroke deaths are attributed to neurological damage, and cardiovascular complications are the second leading cause of post-stroke mortality. Accumulating clinical and experimental evidence suggests a causal relationship between brain damage and heart dysfunction. Thus, it is important to determine whether cardiac dysfunction is triggered by stroke, is an unrelated complication, or is the underlying cause of stroke. Stroke-induced cardiac damage may lead to fatality or potentially lifelong cardiac problems (such as heart failure), or to mild and recoverable damage such as neurogenic stress cardiomyopathy and Takotsubo cardiomyopathy. The role of location and lateralization of brain lesions after stroke in brain-heart interaction; clinical biomarkers and manifestations of cardiac complications; and underlying mechanisms of brain-heart interaction after stroke, such as the hypothalamic-pituitary-adrenal axis; catecholamine surge; sympathetic and parasympathetic regulation; microvesicles; microRNAs; gut microbiome, immunoresponse, and systemic inflammation, are discussed.

Acute Brain Diseases as Triggers for Stress Cardiomyopathy: Clinical Characteristics and Outcomes

To determine the clinical characteristics and outcomes of patients with neurogenic stress cardiomyopathy (NSC) among patients admitted to our neuroscience intensive care unit (NICU). Following institutional review board approval, consecutive adult patients admitted to the NICU between 2009 and 2013 with definite and possible NSC were included. Data on patient demographics, baseline clinical information, cardiac function, and laboratory values were collected. Outcomes included length of stay, modified Rankin Scale (mRS) at discharge and long-term follow-up. Continuous variables were compared using a student's t test, and categorical variables were compared using a Chi-square test. Among 34 patients included in the study, the most common presenting symptom was dyspnea (17 patients, 50%). Subarachnoid hemorrhage (SAH) was the most common neurological inciting event (11 patients, 32.4%), but two-thirds of this cohort had other neurological triggers. The most common electrocardiogram changes were QT-interval prolongation (30 patients, 88.2%) and T-wave inversion (22 patients, 64.7%). The most common echocardiographic pattern was the apical variant (14 patients, 41.2%), and 26% of patients had right ventricular involvement (P=0.03) which was a predictor of poor outcome along with inotropic support (P=0.006). Functional outcome was poor (mRS>3) in 53% of patients at discharge, but function improved over time in most survivors. NSC is most common after SAH, but can result from a wide spectrum of acute brain insults. Requirement of inotropic support was the strongest indicator of prognosis at last follow-up. Patients with NSC often have poor function at discharge but many improve over time.

Cardiac injury in severe head trauma: a review of literature

Neurogenic stress cardiomyopathy (NSC) is a stress induced cardiomyopathy reported in various neurological disorders. The most widely accepted theory for the mechanism of NSC is the “catecholamine hypothesis”. The available evidence suggests the presence of NSC in patients with severe TBI. The presence of cardiac injury could be a poor prognostic finding in patients with TBI. The possible cardiac injury in TBI patients would make the critical care physicians more cautious with hemodynamic management of these patients. Larger studies with more sophisticated asessment would help to confirm the presence of cardiac injury in these patients.