Ventricular tachycardia in the setting of rheumatoid arthritis (CROSBI ID 583531)
Prilog sa skupa u zborniku | sažetak izlaganja sa skupa
Podaci o odgovornosti
Škerk, Vedrana ; Manola, Šime ; Radeljić, Vjekoslav ; Radić, Berislav ; Pintarić, Hrvoje ; Delić-Brkljačić, Diana
engleski
Ventricular tachycardia in the setting of rheumatoid arthritis
Background: Ventricular tachycardia (VT) predominantly occurs in ischemic surrounding, via re-entry mechanism. Studies researching endothelial dysfunction have raised the question of its effects to the heart. Some of the endothelial dysfunction (ED)markers are belived to have significant role in acute coronary syndromes and cardiomyopathies. However, there are not many studies researching ED linked to arrhythmias. Rheumatoid arthritis (RA) presents a chronic inflammation, vasculitis and thus ED. Here we present a patient with a longstanding RA, on chronic therapy with non-steroidal anti-inflammatory drugs and aminosalicylates, that has developed hemodinamically stable sustained VT. Methods: The patient\'s sinus rhythm was restored, in deep sedation, by a single direct current (DC) shock. Laboratory findings (RBC, WBC, Fe, UIBC, thyroid hormones, HBA1c, SE, CRP, electrolytes, creatinine, aminotransferases, urine) were normal. Noninvasive and invasive cardiology tests were performed. Results: The initial electrocardiogram (ECG) presented monomorphic LBBB VT. Following ECGs, after DC shock, demonstrated no pathology. Echocardiographic finding manifested normal ejection fraction, mild concentric hypertrophy, delayed relaxation and almost intact valves. Treadmill test was negative to coronary artery disease. The patient underwent coronarography that displayed no significant pathology. Electrophysiologic (EP) study was performed and no arrhythmias were induced. Conclusions: The patient presented with a minimally symptomatic (palpitations) hemodinamically stable VT. There are few possible underlying mechanims of VT in this particular patient, like RA induced vasculitis and/ or ED storm, or RA therapeutic agents. Presumably, all of the mentioned contributed to the developement of VT in this case. Further investigations are required in order to enhance the understanding of the mechanism of VT in patients with chronic inflammatory diseases. We find this case report a reminder of a possible etiology of a non-inducible VT.
Ventricular tachycardia; rheumatoid arthritis
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
Podaci o prilogu
2011.
objavljeno
Podaci o matičnoj publikaciji
Cardiology Update 2011
Podaci o skupu
Cardiology Update 2011
poster
13.02.2011-18.02.2011
Davos, Švicarska