Cerebellar Haemorrhage Leading to Sudden Cardiac Arrest

IntroductionIntracranial haemorrhage (ICH) is a known, but a rare cause of out of hospital cardiac arrest (OHCA). It results in the development of non-shockable rhythms such as asystole or pulseless electrical activity (PEA).Case ReportA 77- years old male had an OHCA without any prodrome. An emergency medical services (EMS) team responded to an emergency call and intubated the patient at the site before transporting him to the Acute Care Hospital, New Brunswick, New Jersey, USA. On admission, a non-contrast computed tomography scan of the head revealed a large cerebellar haemorrhage. Non-traumatic ICH is a rare cause of OHCA. Although subarachnoid haemorrhage causing cardiac arrest has been described in the literature, cerebellar haemorrhage leading to cardiac arrest is rare. The mechanism by which ICH patients develop cardiac arrest is likely explained by a massive catecholamine surge leading to cardiac stunning.ConclusionA non-shockable rhythm in the seting of a sudden cardiac arrest should raise alarms for a primary non-cardiac ethology, especially a primary cerebrovascular event. The absence of brainstem reflexes increases the likelihood of an intracranial process.

Cardiac stunning during haemodialysis: the therapeutic effect of intra-dialytic exercise

Background Cardiovascular risk is elevated in end-stage renal disease. Left ventricular (LV) dysfunction is linked to repetitive transient ischaemia occurring during haemodialysis (HD). Cardiomyocyte ischaemia results in ‘cardiac stunning’, evidenced by regional wall motion abnormalities (RWMAs). Ischaemic RWMA have been documented during HD resulting in maladaptive cardiac remodelling and increased risk of heart failure. Intra-dialytic exercise is well tolerated and can improve quality of life and functional capacity. It may also attenuate HD-induced cardiac stunning. Methods This exploratory study aimed to assess the effect of intra-dialytic cycle ergometry on cardiac stunning. Twenty exercise-naïve participants on maintenance HD (mean ± SD, 59 ± 11 years) underwent resting echocardiography and maximal cardiopulmonary exercise testing. Subsequently, cardiac stunning was assessed with myocardial strain-derived RWMAs at four time points during (i) standard HD and (ii) HD with 30 min of sub-maximal intra-dialytic cycle ergometry at a workload equivalent to 90% oxygen uptake at the anaerobic threshold (VO2AT). Central haemodynamics and cardiac troponin I were also assessed. Results Compared with HD alone, HD with intra-dialytic exercise significantly reduced RWMAs after 2.5 h of HD (total 110 ± 4, mean 7 ± 4 segments versus total 77 ± 3, mean 5 ± 3, respectively; P = 0.008). Global cardiac function, intra-dialytic haemodynamics and LV volumetric parameters were not significantly altered with exercise. Conclusions Intra-dialytic exercise reduced cardiac stunning. Thirty minutes of sub-maximal exercise at 90% VO2AT was sufficient to elicit acute cardio-protection. These data potentially demonstrate a novel therapeutic effect of intra-dialytic exercise.

Cardiac stunning as first manifestation of multiple sclerosis: A case report reminding us not to overlook cardiovascular autonomic dysfunction in multiple sclerosis

Autonomic dysfunction is common but frequently overlooked in multiple sclerosis (MS) patients. The case of a Tako-Tsubo cardiomyopathy on which this commentary is based shows that centrally triggered autonomic dysfunction may be the first life-threatening manifestation of MS.

Congestive Heart Failure (CHF) During Induction In ACUTE Promyelocytic Leukemia (APL) Patients

Background APL is a highly curable malignancy with cure rates of greater than 90% in most co-operative group trials. Population-based studies show that the survival is only about 65-70% with up to 30% early deaths. The most common reasons of early deaths are bleeding, differentiation syndrome (DS) and infection. Differentiation syndrome is very peculiar to this disease and potentially fatal unless recognized early. The wide variety of clinical presentations associated with DS might lead to delay in diagnosis in some patients which may lead to poorer outcomes. European Leukemia Net recommendations suggest that congestive heart failure (CHF) is one of the presenting features of DS and most of the reports on cardiac abnormalities focus on pericardial effusion. Cardiac stunning is only briefly reported in the literature. Cardiac stunning might be a result of cytokine storm attributable to tumor lysis in addition to being part of the DS. Here we report the incidence of CHF in patients undergoing induction for APL. Methods We performed a retrospective chart review on patients diagnosed with APL who received induction between December 1, 2004 and July 31, 2013 at Georgia Regents University and also patients who were referred to us from surrounding treatment centers with whom we co-manage these patients. Baseline and follow up ejection fractions (EF) were recorded by echocardiogram or nuclear medicine scan. We evaluated patients who had a drop in EF during the induction period. Results 41 consecutive patients with APL with normal ejection fraction at diagnosis were evaluated. 1 patient refused treatment and was excluded. 38/40 patients received idarubicin and ATRA remission induction and 2 patients received Arsenic and ATRA. There were seven deaths during induction phase of treatment In the surviving patients, 10 patients had a repeat ECHO during the first 30 days of induction phase for suspected cardiomyopathy. 5 patients (15.1% of surviving patients) demonstrated a decrease in EF and all five were in the anthracycline group. The age range of patients with drop in EF was 30-75 years. Absolute drop in EF was between 10- 35%. Only one patient had mild elevation in troponins while others had no elevation. 3 out of the 5 patients had significant DS. Of the surviving patients, 4 out of 5 patients recovered their EF completely with one patient recovering partially to 45-50% (from 20-25%). Conclusions Anthracyclines, along with ATRA, are still the mainstay of treatment for this curable malignancy. Although the incidence of cardiac abnormalities is described with repeated courses of anthracyclines, a single dose of anthracyclines can also play a role in cardiac injury. The highly inflammatory state present during the early treatment of APL might also play a role in cardiac injury resulting in higher number of patients with decreased EFs. DS clinical presentation most commonly involves dyspnea and edema, which are also symptoms of heart failure. Prompt cardiac evaluation should be undertaken to rule out congestive heart failure as an early start to therapy will lead to improved outcomes. Disclosures: Awan: Lymphoma Research Foundation: Research Funding; Spectrum Pharmaceuticals Inc.: Speakers Bureau. Jillella:Lymphoma Leukemia society: Research Funding. Kota:Teva: Speakers Bureau; Ariad: Advisory board, Advisory board Other.

Upregulation of CaMKIIδ during ischaemia–reperfusion is associated with reperfusion-induced arrhythmias and mechanical dysfunction of the rat heart: involvement of sarcolemmal Ca2+-cycling proteins

Although Ca2+/calmodulin-dependent protein kinase II delta (CaMKIIδ) has been implicated in development of different phenotypes of myocardial ischaemia–reperfusion injury, its involvement in arrhythmogenesis and cardiac stunning is not sufficiently elucidated. Moreover, the mechanisms by which CaMKIIδ mediates disturbances in excitation–contraction coupling, are not exactly known. To investigate this, KN-93 (0.5 µmol/L), a CaMKII inhibitor, was administered before induction of global ischaemia and reperfusion in isolated Langendorff-perfused rat hearts. Expression of CaMKIIδ and the sarcollemal Ca2+-cycling proteins, known to be activated during reperfusion, was analyzed using immunoblotting. KN-93 reduced reperfusion-induced ectopic activity and the incidence of ventricular fibrillation. Likewise, the severity of arrhythmias was lower in KN-treated hearts. During the pre-ischaemia phase, neither inotropic nor chronotropic effects were elicited by KN-93, whereas post-ischaemic contractile recovery was significantly improved. Ischaemia–reperfusion increased the expression of CaMKIIδ and sodium–calcium exchanger (NCX1) proteins without any influence on the protein content of alpha 1c, a pore-forming subunit of L-type calcium channels (LTCCs). On the other hand, inhibition of CaMKII normalized changes in the expression of CaMKIIδ and NCX1. Taken together, CaMKIIδ seems to regulate its own turnover and to be an important component of cascade integrating NCX1, rather than LTCCs that promote ischaemia–reperfusion-induced contractile dysfunction and arrhythmias.

Neurogenic stunned myocardium after acute hydrocephalus

Neurogenic stunned myocardium (NSM) is a syndrome of cardiac stunning after a neurological insult. It is commonly observed after aneurysmal subarachnoid hemorrhage but is increasingly being reported after other neurological events. The underlying mechanism of NSM is believed to be a hypothalamic-mediated sympathetic surge causing weakened cardiac contractility and even direct cardiac myocyte damage. The authors report 2 cases of NSM in pediatric patients after acute hydrocephalus. Both patients experienced severe cardiac dysfunction in the acute phase but ultimately had a good neurological outcome and a full cardiac recovery. The identification, treatment, and outcome in 2 rare pediatric cases of NSM are discussed, and the history of the brain-cardiac connection is reviewed.