Fulminant Myocarditis: Brief Review

Fulminant myocarditis (FM) is a rare disease characterized by acute hemodynamic impairment and ventricular arrhythmias due to severe myocardial inflammation. It is typically preceded by a viral infection but any of multiple other toxic and infective agents may also be the inciting agent. Diagnosis is based on biomarkers and/or cardiac imaging, but endomyocardial biopsy is the standard test for confirming the diagnosis. FM usually requires therapeutic support of cardiac function and treatment of malignant arrhythmias. Contrary to prior concepts, recent evidence has revealed that patients with FM are more likely to die or need heart transplantation than those with the nonfulminant form of the disease. Early recognition and aggressive management are essential for favorable outcomes.

Abstract 141: Early Cytokine Profile in Selectively Vulnerable Brain Regions, Heart and Serum After Asphyxial Cardiac Arrest vs. Ventricular Fibrillation Cardiac Arrest in Rats

Background: Currently, post-resuscitative care for survivors of cardiac arrest (CA) is independent of the etiology of CA. We have previously reported that asphyxial CA (ACA) results in different injury pattern vs. ventricular fibrillation CA (VFCA). Exploration of the early inflammatory response could identify insult-specific targets for future therapies. We hypothesized that the early systemic and regional neuroinflammatory cytokine response could differ between ACA vs. VFCA. Methods: Adult male rats were subjected to a 10 min ACA, or 10 min VFCA (n=12/group). Naives (n=12) and shams (n=12) subjected to anesthesia and instrumentation but not CA served as controls. Serum, heart and regional brain cytokine signatures were assessed in selectively vulnerable brain regions: cerebellum, cortex, hippocampus and striatum at 3 h. NSE, S100b and troponin T were also assessed. Results: Asphyxiation produced an ~4 min period of severe hypoxemia followed by a no-flow duration of ~ 6±1 min. VF immediately induced no-flow. Brain cytokines in naïve rats were low or undetectable. Shams had a modest effect on selected cytokines. Both ACA and VFCA resulted in robust selected cytokine responses in serum, heart and brain (Fig. 1) with significant regional differences in brain that identified striatum as a selective neuroinflammatory target. No significant differences in cytokines between CA models were observed. NSE, S100b and troponin T were similarly increased after ACA and VFCA vs. naives and/or shams. Conclusions: Both models of CA resulted in marked systemic, heart and brain cytokine response. Biomarkers of organ injury were also comparable. Contrasting prior studies showing greater oxidative stress and brain injury in ACA, but greater hemodynamic impairment after VFCA, systemic and brain cytokine profiles revealed similar increases across insults, suggesting that the cytokine response may not mediate key secondary injury differences between these two CA phenotypes.

Isolated Bilateral Internal Carotid Artery Stenosis and Recurrent Ischemic Strokes in a Patient with Suspected Giant Cell Arteritis

Giant cell arteritis (GCA) is a common type of vasculitis and may present various forms. Ischemic stroke is one of the complications and sometimes the first symptom of this disease. We want to present the case of a 58-year-old female patient with suspected GCA who suffered from recurrent ischemic strokes due to progressive stenosis of the internal carotid arteries. This site of manifestation is rare but indicative of GCA. The patient was first treated with corticosteroids and methotrexate later with tocilizumab. Facing progressive hemodynamic impairment, an extra-intracranial-bypass-surgery was performed. Although inflammatory activity was reduced, new strokes occurred.