Sunday, May 28, 2023
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A 69-year-old man received a dual-chamber implantable cardioverter defibrillator (ICD). He was diagnosed with a myocardial infarction (MI) 6 years ago and suffered cardiac arrest 3 years ago. He also has severe bradycardia. To date, he has had no detectable device therapies.
He presents to the office for device evaluation following a recent episode of near syncope. Device interrogation showed the following intracardiac tracings occurring around the time of his near syncopal event.
Figure 1. Intracardiac tracings occurring around the time of near syncope.
Possible causes of this patient's near syncope include:
As shown in the tracings, the most likely cause of this patient's near syncope is EMI and its consequences on ICD function. EMI is most prominently seen on the 2 ventricular leads and more subtly on the atrial lead.
It was unclear from the patient's history as to why this occurred, and exposure to obvious EMI sources was not immediately evident. The EMI was identified by the ICD as ventricular fibrillation/tachycardia, and atrial pacing was discontinued. This is normal ICD function.
In this patient with severe sinus node dysfunction, lack of atrial pacing resulted in asystole and near syncope. Demonstration of spontaneous "noise" on both atrial and ventricular leads makes it highly unlikely that there is a ventricular lead fracture. Additional ICD testing was performed and no problems were identified.
The patient has continued follow-up for the past 12 months and no EMI has been detected. There have also not been any atrial or ventricular lead abnormalities.
A 79-year-old man presents with previous MI and left ventricular ejection fraction 25%. Three years ago, he underwent ICD implantation for documented sustained ventricular tachycardia, and he has required amiodarone 200 mg/day to prevent recurrent ICD shocks. The patient is also on an angiotensin converting enzyme inhibitor, statin, and a low-dose beta-blocker. The patient's device antitachycardia pacing (ATP) feature is programmed 'on.'
ICD interrogation demonstrated 83 successful ATP therapies over the course of the past 4 months. Figure 2 shows the intracardiac electrograms recorded prior to successful ATP therapy.
Figure 2. Intracardiac electrograms prior to successful ATP therapy.
The top tracing demonstrates a supraventricular tachycardia with characteristics similar to those of atrial flutter, which was followed later by the onset of ventricular tachycardia, noted on the middle and bottom tracings. This patient had many such episodes that were asymptomatic, and ATP treatment successfully terminated all of them.
In terms of the next appropriate course of treatment, at this time, it was believed that a change in antiarrhythmic drug treatment was not necessary. However, an arrhythmia that was likely atrial flutter was detected. Careful analysis of other episodes also revealed periods of a similar atrial arrhythmia.
Since the risk of stroke appears similar in patients with atrial flutter compared with atrial fibrillation, this patient would likely benefit from warfarin therapy unless a contraindication was present. He has numerous conditions that put him at high risk for stroke, including his age, coronary artery disease, and left ventricular dysfunction. Warfarin therapy was instituted in this patient, and no complications have been reported during follow-up.
