Multiple sclerosis (MS) has been suggested to be an autoimmune demyelinating disease of the central nervous system (CNS), whose primary target is either myelin itself, or myelin-forming cells, the oligodendrocytes. Although axonal damage occurs in MS, it is regarded as a secondary event to the myelin damage. Here, the lesion develops from the myelin (outside) to the axons (inside) "Outside-In model". The Outside-In model has been supported by an autoimmune model for MS, experimental autoimmune (allergic) encephalomyelitis (EAE). However, recently, (1) EAE-like disease has also been shown to be induced by immune responses against axons, and (2) immune responses against axons and neurons as well as neurodegeneration independent of inflammatory demyelination have been reported in MS, which can not be explained by the Outside-In model. Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease (TMEV-IDD) is a viral model for MS. In TMEV infection, axonal injury precedes demyelination, where the lesion develops from the axons (inside) to the myelin (outside) "Inside-Out model". The initial axonal damage could result in the release of neuroantigens, inducing autoimmune responses against myelin antigens, which potentially attack the myelin from outside the nerve fiber. Thus, the Inside-Out and Outside-In models can make a "vicious" immunological cycle or initiate an immune cascade.

BACKGROUND/AIM Acute heart failure (AHF) is one of the most common diseases in emergency medicine, associated with poor prognosis and high in-hospital and long-term mortality. The aim of this study was to investigate characteristics, outcomes and one year mortality of patients with AHF in the local population. METHODS This prospective study consisted of 64 consecutive unselected patients treated in the Coronary Care Unit of the Emergency Centre (Clinical Center of Serbia, Belgrade) and were followed for one year after the discharge. RESULTS Mean age of the patients was 63.6 +/- 12.6 years and 59.4% were males. Acute congestion (43.8%) and pulmonary edema (39.1%) were the most common presentations of AHF. Mean left ventricular ejection fraction (LVEF) was 39.7% +/- 9.25%, while 44.4% of the patients had LVEF > or = 50%. At discharge, 55.9% of the patients received therapy with P-blockers, 94.9% diuretics, out of which 47.7% spironolactone, 94.9% patients were given ACE-inhibitors or angiotensin receptor blockers (ARB). The 12-month all-cause mortality was 26.5%. Independent predictors of one year mortality were previous hospitalization due to heart disease, reduced LVEF, reduced fraction of shortening (FS) and a higher tricuspid velocity. CONCLUSION One year mortality of our patients with AHF was high, similar to the known European studies. Independent predictors of one year mortality were previous hospitalization due to heart disease, reduced LVEF and LVFS and a higher tricuspid velocity.