There is a concern about the
There is a concern about the possibility that some patients with WPW syndrome who have LV dyssynchrony and atypical delta waves, as in the present case, may be diagnosed with DCM. In these WPW syndrome patients, although medical therapy might not improve LV dysfunction, RFCA of the AP might improve the LV dysfunction . Before making a diagnosis of DCM accompanied by LV dyssynchrony, we should exclude WPW syndrome with atypical delta waves. Furthermore, atypical delta waves in a 12-lead ECG should be evaluated without depending on an ECG auto-analysis.
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Introduction Sarcoidosis is a multisystem granulomatous disease of unknown etiology. In autopsy studies, cardiac involvement has been reported in 40–50% of patients .
Case report The patient was a 60-year-old man who experienced palpitations for the past 6 months. During a medical clinic visit, atrial tachycardia (AT) was suggested on 12-lead electrocardiography (ECG) with a cytoskeleton rate of 75beats/min and 3–5:1 atrioventricular conduction. The Holter ECG recorded the AT and frequent ventricular tachycardia (VT) episodes of 3–18 beats (Fig. 1A). Because the AT and VT were drug-refractory, he was referred to our hospital for an electrophysiologic study and catheter ablation. Echocardiography revealed dilatation of the right and left atria and a mildly reduced left ventricular (LV) systolic function with an aneurysm on the basal posterior LV wall. Blood examination results were normal, including angiotensin converting enzyme levels. Chest radiography and computed tomography (CT) revealed cardiac dilatation, but lung parenchyma lymph nodes were not swollen. Contrast-enhanced magnetic resonance imaging (MRI) revealed delayed enhancement of the aneurysm. The coronary angiogram was normal. The 18F-fluorodeoxyglucose positron emission tomography (PET)–CT revealed extensive hypermetabolic activity in the basal posterior septum and LV posterolateral wall. Together, these findings suggested the presence of cardiac sarcoidosis. A voltage map obtained during the electrophysiologic study revealed low-voltage areas in the high anterior and lateral portions of the right atrium. Atrial activation during the AT occurred in the counterclockwise direction around the tricuspid valve. Pacing from the cavotricuspid isthmus exhibited concealed entrainment; therefore, typical atrial flutter (AFL) was diagnosed. The AFL was terminated by ablation of the cavotricuspid isthmus. Thereafter, sustained monomorphic VT, with the morphology of a right-bundle branch block and superior axis, was induced by programmed right ventricular stimulation. An LV voltage map obtained during sinus rhythm revealed a low-voltage area with delayed potentials in the posterior LV aneurysm. The activation map during VT revealed a focal reentrant pattern with a clockwise rotation in the posterior LV aneurysm, where a mid-diastolic potential was recorded (Fig. 1B). Pacing from this site demonstrated concealed entrainment (Fig. 1C). These findings strongly suggested that the mechanism of the VT was reentry. The VT terminated 7.8s after commencing radiofrequency ablation, and was no longer inducible by programmed ventricular pacing.
Discussion Ventricular arrhythmias are the most well-known and feared cardiac manifestations of cardiac sarcoidosis. However, AFL is relatively rare, with a reported prevalence of 5% . In this case, MRI and 18F-FDG PET–CT strongly supported a diagnosis of cardiac sarcoidosis, and the patient had typical AFL; however, the morphology showed an atypical AT on ECG. This case of cardiac sarcoidosis was rare, not only because of the supraventricular tachyarrhythmia but also because of the double tachycardias, i.e., simultaneous VT and AFL. The etiology of these tachyarrhythmias remains unknown. Previous cases of cardiac sarcoidosis with ATs were associated with systemic hypertension, diastolic dysfunction, and LA enlargement. Further, atrial fibrillation was the most common clinical manifestation . Their results suggested that ATs could be related to atrial dilatation secondary to LV dysfunction. In fact, arrhythmias may be less commonly caused by direct granulomatous involvement of the atria [3–5]. However, this case had a typical AFL with right-sided dominant atrial dilatation and scar formation, suggesting a different mechanism. For example, noncaseating granulomas may favor involvement of specific regions of the septum and basal ventricle, but eventually become widespread, and may even involve the atria as well. Although a pathological examination failed to finalize the underlying mechanism of these double tachyarrhythmias, this case highlights the fact that in some cases of cardiac sarcoidosis, the ventricles as well as the atria may be involved in producing arrhythmias of not only a ventricular but also an atrial origin.