Ventricular Fibrillation after Elective Percutaneous Coronary Intervention

Case Description:

A 60 year old with past medical history of tobacco abuse was admitted for evaluation of chest pain without significant electrocardiogram (ECG) changes, electrolyte abnormalities or troponin elevation. Stress test revealed fixed inferolateral defects with EF44% and associated hypokinesis. Interestingly, an echocardiogram revealed an EF 55-60% with no regional wall motion abnormalities. Catheterization revealed an obstructive lesion in the PDA that had drug eluting stent successfully placed. Approximately one hour after stent placement routine ECG did not reveal any significant acute changes and patient was asymptomatic (see Figure 1). Approximately 150min after stent placement, the patient had an episode of ventricular fibrillation (VF) that required an external DC cardioversion (see Figure 2). Repeat cardiac catheterization did not reveal stent thrombosis or spasm. The patient underwent an uncomplicated single chamber defibrillator placement the following day.

Figure 1.  EKG Prior to VF Arrest


Figure 2.  Telemetry Strip Showing the VF Arrest



VF arrest during PCI has been reported to have an incidence of 2.1% with higher incidence of VF during right coronary artery PCI. (HUA02) VF arrest during PCI is most commonly precipitated by contrast, ischemia from coronary dissection, embolism, spasm, or catheter manipulation and occurs during the cardiac catheterization. (NIS84) VF arrest after elective percutaneous coronary intervention (PCI) is uncommon. Indeed, an examination of 19,497 patients undergoing PCI revealed a 0.84% incidence of VF and no episodes of VF arrest temporally unrelated to vessel injection were reported. (ADD05) Survivors of VF arrest in the setting of myocardial infarction (MI) have similar mortality to those not experiencing VF arrest during acute MI. (DEJ09) In contrast, mortality in survivors of in-hospital cardiac arrest has been reported as high as 47% during a median followup of 1.3 years. (HEL11) It is unclear if the mechanism of VF arrest in our patient is secondary to PCI or rather a primary VF arrest. There is a prior report of delayed three vessel coronary spasm in a patient receiving paclitaxel drug-eluting stents however, coronary spasm was demonstrated on repeat catheterization in that report. (KIM05) Our patient did not report any ischemic symptoms preceding his VF arrest (though his EKG had subtle ST changes suggesting possible ischemia) nor did his repeat catheterization reveal vessel thrombosis, spasm, or dissection. Additionally, peri- and post-procedural myocardial injury from slow coronary flow, microvascular embolization, and elevated levels of troponin causing reperfusion tissue damage and cardiac dysfunction leads to worse long-term prognosis than those without myocardial injury (ISH08); our patient did not have significantly elevated pre- or post-procedure troponin levels. The time course of ischemia-induced reperfusion changes is likely less than 30minutes based upon prior experimental models of ischemia. (WIL08) Five minutes of coronary artery occlusion avoids increased risk of ventricular arrhythmias in animals and 30 minutes is appropriate for adequate reperfusion. (DAV81,DAV82,RUF79,WIL08) When the left anterior descending artery is transiently occluded in dogs, there is an initial (t=0-2minutes) small decrease in peak R wave amplitude and conduction velocity followed by a large increase in these indices over the ensuing 1-2minutes. (HOL76) There is a rapid return to baseline when occlusion is released and reperfusion occurs. This biphasic response has also been documented in dogs undergoing circumflex artery occlusions lasting 5minutes. (DAV81,DAV82) However, Ruffy et al (RUF79) found that LAD occlusions for 5 minutes in the dog resulted in a decrease in electrogram R wave amplitudes with no biphasic response. The progressive decrease in R wave amplitude (with the subsequent increase in amplitude) has been demonstrated in isolated rabbits hearts during global ischemia over 10 minutes (KAB89), isolated pig hearts during LAD occlusions for 5 minutesJAN86, and humans subject to 60minutes of unresolved ischemia. (VAI94) Of note, these electrical alterations were rapidly reversible upon reperfusion. (HOL76,RUF79,KAB89,JAN86) In summary then, our patient experienced a VF arrest 150min after elective PCI without conclusive evidence of procedural-related ischemia and well outside the conventional 30min window of reperfusion electrical alterations seen in experimental models. The role of defibrillator implantation as secondary prevention in patients like this is unclear.


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