ABSTRACT
Left ventricular assist devices (LVAD) are used in the treatment of advanced left ventricular heart failure. LVAD can serve as a bridge to orthotopic heart transplantation or as a destination therapy in cases where orthotopic heart transplantation is contraindicated. Ventricular arrhythmias are frequently observed in patients with LVAD. This problem is further compounded as a result of diagnostic difficulties arising from presently available electrocardiographic methods. Due to artifacts from LVAD-generated electromagnetic fields, it can be challenging to assess the origin of arrhythmias in standard ECG tracings. In this article, we will review and discuss common mechanisms, diagnostics methods, and therapeutic strategies for ventricular arrhythmia treatment, as well as numerous problems we face in LVAD implant patients.
Subject(s)
Heart Failure , Heart-Assist Devices , Humans , Arrhythmias, Cardiac/diagnosis , Arrhythmias, Cardiac/therapy , Heart Failure/diagnosis , Heart Failure/therapy , Heart Ventricles , ElectrocardiographyABSTRACT
AIMS: Inflammatory state is considered a risk factor of atrial fibrillation (AF) occurrence. The aim of this study was a prospective evaluation of the inflammation parameters in patients with different forms of AF without structural heart disease. METHODS AND RESULTS: One hundred fifty-eight patients with paroxysmal/persistent AF (87; 55.1% men, mean age 65.8±9.6 years) without structural heart disease were enrolled in the study. Inflammatory parameters: WBC, ESR, hs-CRP, IL-6, IL-15 and TNF-alpha were measured at baseline and after one year follow-up. Despite frequent AF episodes median values of WBC, ESR and C-reactive protein at baseline and after follow up were within normal ranges. There were no significant differences between WBC, ESR and hs-CRP regarding AF types. In patients who developed permanent AF form (n=14) hs-CRP concentrations were higher at baseline: 0.35 (IQR1: 0.09 IQR: 0.61) vs 0.15 (IQR1: 0.07 IQR: 0.29), p<0.01. Nevertheless, after one year's observation these differences were not significant. Among all cytokines were studied only IL-15 was significantly correlated with the number of AF episodes (r=0.26), mean (IQ1-IQ3): 10 (3-30) vs 60 (50-100), p=0.00681. CONCLUSION: Basic inflammatory markers were not changed in patients with refractory atrial fibrillation episodes in prospective one year's observation. Only cytokine IL-15 was correlated to numbers of AF episodes. It's potential role as a marker of arrhythmia deserves further evaluation.
