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"UNUSUAL" ATRIAL FLUTTER: A CASE REPORT
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Abstract
A 64–years old male patient was admitted in the Emergency Department with signs of heart failure in a setting of dilated hypokinetic cardiomyopathy with severe depression of left ventricular ejection fraction and no severe coronary artery disease. In the previous medical history: systemic arterial hypertension, obesity, dysthyroidism due to amiodarone, history of atrial fibrillation treated by transcatheter ablation in the left atrium with pulmonary veins isolation (PVI) and the creation of an anterior line in 2010. The ECG documented an atrial flutter rhythm 2:1 probably typical (Fig. 1). An indication was therefore made for hospitalization in Cardiology. After the restoration of a good hemodynamic state, given the persistence of the atrial tachyarrhythmia, an indication for transcatheter ablation was formulated. The electrophysiological study highlighted an activation sequence suggestive of typical common flutter (cranial–caudal right atrial activation; proximal–distal left atrial activation). We then proceeded to ablate the cavo–tricuspid isthmus without interrupting the arrhythmia. Therefore, left and right atrial electroanatomical mapping was performed which confirmed the right isthmic block and documented the left origin of the flutter, showing conduction gaps in the ostia of the pulmonary veins and in the previous anterior ablation line between the mitral annulus and the right superior pulmonary vein (RSPV) (Fig 2,3). Ablation of these gaps effectively stopped the arrhythmia. At the end of the procedure, after stimulation via atrial bursts of up to 200 msec there was no induction of arrhythmias. One month after the procedure, there was an improvement in the contractile function of the left ventricle. Discussion: This clinical case offers us an example of how the analysis of the surface ECG alone is not sufficient to adequately describe the complexity of the arrhythmic substrate characterizing an arrhythmia such as atrial flutter or atrial fibrillation. The electrophysiological study through electroanatomical reconstruction of endocavitary activation proves indispensable for the correct identification and consequent treatment of these complex arrhythmias, with clear clinical benefits for the patient.
Oxford University Press (OUP)
Title: "UNUSUAL" ATRIAL FLUTTER: A CASE REPORT
Description:
Abstract
A 64–years old male patient was admitted in the Emergency Department with signs of heart failure in a setting of dilated hypokinetic cardiomyopathy with severe depression of left ventricular ejection fraction and no severe coronary artery disease.
In the previous medical history: systemic arterial hypertension, obesity, dysthyroidism due to amiodarone, history of atrial fibrillation treated by transcatheter ablation in the left atrium with pulmonary veins isolation (PVI) and the creation of an anterior line in 2010.
The ECG documented an atrial flutter rhythm 2:1 probably typical (Fig.
1).
An indication was therefore made for hospitalization in Cardiology.
After the restoration of a good hemodynamic state, given the persistence of the atrial tachyarrhythmia, an indication for transcatheter ablation was formulated.
The electrophysiological study highlighted an activation sequence suggestive of typical common flutter (cranial–caudal right atrial activation; proximal–distal left atrial activation).
We then proceeded to ablate the cavo–tricuspid isthmus without interrupting the arrhythmia.
Therefore, left and right atrial electroanatomical mapping was performed which confirmed the right isthmic block and documented the left origin of the flutter, showing conduction gaps in the ostia of the pulmonary veins and in the previous anterior ablation line between the mitral annulus and the right superior pulmonary vein (RSPV) (Fig 2,3).
Ablation of these gaps effectively stopped the arrhythmia.
At the end of the procedure, after stimulation via atrial bursts of up to 200 msec there was no induction of arrhythmias.
One month after the procedure, there was an improvement in the contractile function of the left ventricle.
Discussion: This clinical case offers us an example of how the analysis of the surface ECG alone is not sufficient to adequately describe the complexity of the arrhythmic substrate characterizing an arrhythmia such as atrial flutter or atrial fibrillation.
The electrophysiological study through electroanatomical reconstruction of endocavitary activation proves indispensable for the correct identification and consequent treatment of these complex arrhythmias, with clear clinical benefits for the patient.
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