Unifocal premature ventricular complex ablation for recurrent ventricular fibrillation in a post–myocardial infarction patient with acquired long QT

Key Teaching Points.

• •QT-prolonging drugs can trigger malignant arrhythmias: Azithromycin-induced corrected QT prolongation led to premature ventricular complex (PVC)-triggered ventricular fibrillation (VF) in this patient with structural heart disease.
• •Overdrive pacing is a lifesaving bridge: temporary pacing at 120 beats per minute suppressed recurrent PVCs and VF when antiarrhythmics failed.
• •Catheter ablation + implantable cardioverter-defibrillator (ICD) ensures long-term survival: Ablation of fascicular PVCs reduced arrhythmic burden, and ICD implantation provided secondary prevention.

Introduction

Premature ventricular complexes (PVCs) can trigger life-threatening ventricular arrhythmias in structural heart disease.¹ This case highlights the importance of recognizing PVC-triggered ventricular fibrillation (VF) in high-risk patients with structural heart disease. In patients with structural heart disease and recurrent VF from unifocal PVCs, catheter ablation has been proven to be a safe, effective, and potentially lifesaving option.1, 2, 3

Case report

History of presentation

A 53-year-old gentleman presented to the emergency room with complaints of shortness of breath and epigastric discomfort for 3 days. He also reported a history of fever and cough 3 days prior, for which he received oral treatment on an outpatient visit. Upon arrival, his vital signs were as follows: blood pressure of 160/82 mm Hg, heart rate of 102 beats per minute (bpm), respiratory rate of 36 breaths per minute, and oxygen saturation of 98% on 4 L of oxygen. Examination revealed no jugular venous distention, a Glasgow coma scale score of 15/15, bilateral crackles up to the midzones, normal S1 and S2 heart sounds without additional sounds, and no edema. An electrocardiogram (ECG) performed on arrival is shown in Figure 1.

Figure 1.

Represents a 12-lead electrocardiogram with a normal sinus rhythm, small Q waves in inferior leads (II, III, aVF), subtle ST-segment depression in leads V5–V6 and a corrected QT by Bazett’s formula of 495 ms.

Medical history

His comorbidities included diabetes mellitus for 20 years, hypertension, and non-hemodialysis-dependent chronic kidney disease, with a baseline creatinine level of 3.0 mg/dL.

Differential diagnosis

The initial clinical impression was acute coronary syndrome, complicated by an acquired prolonged QT interval. The patient was subsequently admitted with a primary diagnosis of non-ST-elevation myocardial infarction (NSTEMI). Additional diagnoses included congestive heart failure, anemia of chronic disease, acute kidney injury superimposed on chronic kidney disease, and a lower respiratory tract infection, for which he received azithromycin in the outpatient facility.

Investigations

Laboratory investigations revealed the following: hemoglobin of 8.3 g/dL, white blood cell count of 8.4 × 10³/μL with 79% neutrophils, platelets of 271 × 10³/μL, blood urea nitrogen of 42 mg/dL, creatinine of 4.5 mg/dL, serial troponins of 1880 ng/L and 2157 ng/L, pro-B-type natriuretic peptide of 43,000 pg/mL, and C-reactive protein of 19 mg/L.

An echocardiogram revealed an ejection fraction of 25% with severe global hypokinesia, grade 2 diastolic dysfunction, and mild mitral regurgitation.

Management

He was treated with dual antiplatelet therapy, and heparin, antibiotics (piperacillin/tazobactam), and intravenous (IV) diuretics (furosemide) for heart failure. 5 days later, after his heart failure was stabilized and the contrast-induced nephropathy risk was considered, a coronary angiogram was done. It showed moderate blockage in the left circumflex artery and a severe 99% blockage in the proximal right coronary artery (RCA). He had a stent placed in the proximal RCA (percutaneous coronary intervention [PCI] with drug-eluting stent). Post-PCI ECG is shown in Figure 2.

Figure 2.

Represents a 12-lead electrocardiogram after percutaneous coronary intervention. No new changes were observed, and corrected QT was 494 ms by Bazett’s formula.

9 hours after PCI, the patient developed VF arrest. After cardioversion and subsequent cardiopulmonary resuscitation for a total of 6 minutes, a return of spontaneous circulation was achieved. Post–return of spontaneous circulation ECG revealed no ST-T changes; however, frequent unifocal premature ventricular contractions (PVCs) were noted along with a prolonged corrected QT (QTc) interval of 542 ms (Figure 3).

Figure 3.

Represents a 12-lead electrocardiogram with unifocal premature ventricular complexes likely originating from the left posterior fascicle, a (relatively shorter) coupling interval of 400 ms, and a corrected QT of 542 ms.

Morphology of PVC revealed right bundle branch block pattern, biphasic I, aVL, and superior axis with a QRS width of 120 ms (likely originating from the left posterior fascicle). The patient was electively intubated and given an IV lidocaine bolus followed by an infusion. Despite lidocaine infusion, the patient again developed polymorphic ventricular tachycardia (PMVT) owing to the long-short phenomenon, which was secondary to frequent monomorphic PVCs with a short coupling interval and prolonged QT, deemed secondary to azithromycin (Figure 4). A repeat left heart catheterization revealed no new changes, with a patent stent in the proximal RCA without compromising any visible side branch.

Figure 4.

Represents a 12-lead electrocardiogram showing unifocal premature ventricular complexes and a long-short sequence leading to ventricular fibrillation in the later part of the strip.

Owing to ongoing VF secondary to PVCs, overdrive pacing was started using a temporary pacemaker placed in the right ventricle (RV) at 110 bpm, which was later increased to 120 bpm to control recurrent PMVT/VF. When the temporary pacemaker lead dislodged, the patient developed PMVT again, progressing to VF, but was successfully resuscitated. Given the recurrent PMVT, and normal AV conduction, a temporary-permanent pacemaker was placed using a right atrial lead connected to an external generator via the right internal jugular vein. The patient remained dependent on pacing, with PMVT returning within seconds of stopping. Owing to worsening kidney function, he required multiple dialysis sessions with ultrafiltration. Once QTc shortened to <470 ms, various antiarrhythmics (lidocaine, amiodarone, and beta-blockers) were tried, but PMVT recurred whenever the pacing rate dropped below 120 bpm.

Given that the PVCs were unifocal, ablation was planned. The procedure was done using standard techniques, with access through the right femoral vein and artery. A retrograde aortic root access was gained because it provides adequate access to the left ventricular (LV) septum that we suspected to be our targeted area. A catheter was placed in the RV, and another was passed into the LV through the aortic valve. An irrigated tip catheter (BLAZER II) was used for ablation. ECG suggested the PVCs were coming from the LV inferoseptal wall or left posterior fascicle, matching the clinical PVCs. An activation mapping technique was performed for PVC localization, looking for the site of earliest activation. The PVC was difficult to map because of repeatedly deteriorating into VF after following a similar long-short sequence by PVCs (Figure 5). Similarly, pace mapping was not performed owing to triggering of VF secondary to pacing maneuver; therefore, we located the area of the left posterior fascicle under fluoroscopy guidance (Figure 6) and an electrical mapping system.

Figure 5.

Intracardiac electrogram showing ventricular bigeminy at different coupling intervals of 320 and 300 ms, respectively.

Figure 6.

Fluoroscopy with an anteroposterior view showing the location of the ablation catheter tip at the lower third of the left posterior fascicle inside the left ventricle via aortic route, an active fixation lead in the right atrium, and a quadripolar catheter in the right ventricle.

We then decided to ablate the earliest Purkinje potentials in the area of the lower third of the posterior fascicle; therefore, we proceeded with anatomic localization of the likely culprit area (left posterior fascicle), and no abnormal Purkinje potentials/signals or scar was evident (Figure 7). We performed 18 ablation burns at 35 W for a total duration of 14 minutes. No tachycardia or PVCs were inducible after ablation with 600 ms and 400 ms drive train with up to 5 extras, with catheter manipulation at the LV apex or with dobutamine use. After that, we waited for 1 hour after the procedure without pacing with no recurrence of PVCs. No complications were observed. During the procedure, cardioversion was performed approximately 18 times. The flow map for the mapping during the EP study is depicted in Figure 8.

Figure 7.

Intracardiac electrogram showing radiofrequency ablation at the earliest potentials at the distal tip of the ablation catheter (labeled at HIS d).

Figure 8.

The management cycle performed during the EP study and ablation. The team consisted of a consultant electrophysiologist, an EP fellow, a cardiology resident, and a trained EP technician. bpm = beats per minute; Defib = defibrillator; EGM = electrogram; EP = electrophysiology; PMVT = polymorphic ventricular tachycardia; PPM = permanent pacemaker; PVC = premature ventricular complex; VT = ventricular tachycardia.

Postprocedure PVCs again returned but with a reduced frequency, and the patient did not develop VF episodes related to those PVCs. Postprocedure ECG is shown in Figure 9, which reveals settling of PVCs with no change in the QRS morphology compared with preprocedure ECG.

Figure 9.

Postprocedure 12-lead electrocardiogram without premature ventricular complexes and corrected QT of 465 ms.

While looking at the QTc trend, it revealed on arrival QTc by Bazett’s formula of 495 ms (Figure 1), post-PCI QTc was 494 ms by Bazett’s formula (Figure 2), and later on it increased to 542 ms associated with PVC-induced VF (Figure 3) and then after ablation went down to QTc of 465 ms (Figure 9). Ventilator support was gradually weaned, and after a successful weaning trial 13 days after intubation, the patient was extubated. The temporary-permanent pacing lead was removed. Renal parameters started to improve. Subsequently, an implantable cardioverter-defibrillator (ICD) was implanted before discharge planning. The beta-blocker on discharge was switched to metoprolol (50 mg twice daily). In addition, the patient was prescribed amiodarone 400 mg once daily, with a plan to taper it off during clinic follow-up. The remainder of the treatment included dual antiplatelet therapy (aspirin and clopidogrel), along with apixaban owing to extensive LV PVC ablation, as well as atorvastatin, furosemide, and a hydralazine and nitrate combination for heart failure.

Outcome and follow-up

Over the subsequent 3-month follow-up, no further episodes of VT were noted on device interrogation, and the patient achieved baseline functionality as before the hospitalization. Postablation outcome after 1 year patient remains well with no ICD shocks and need for hospitalization.

Discussion

Ventricular arrhythmias, from simple PVCs to sustained VT and VF, are a major cause of illness and death.¹ PVCs are common and usually harmless, but, in some cases, they can cause symptoms, heart dysfunction, or trigger VF. Catheter ablation is a safe and effective first-line treatment in such cases.² Haïssaguerre et al first reported using ablation for PVC-triggered VF in patients with normal heart structure.⁴ These PVCs, occurring during the heart’s vulnerable period (R-on-T), can lead to VT or VF, and ablation may prevent VF.³ Ablation works better than medications for reducing PVCs and is recommended in cases of severe symptoms, PVC-induced cardiomyopathy, or VF.²

We presented a unique case of post-PCI recurrent VF triggered by PVCs originating from the LV endocardial inferoseptal wall in a patient with NSTEMI, congestive heart failure, CKD and probable acquired long QT syndrome. This case shows how complex heart conditions and certain drugs, such as azithromycin, can interact. The patient had several health issues, including a lung infection treated with azithromycin, which likely led to acquired long QT syndrome. Macrolides, especially azithromycin, are known to cause QT prolongation and raise the risk of torsades de pointes.⁵ Although torsades de pointes was first suspected as the cause of the cardiac arrest, the patient developed VF triggered by unifocal PVCs, even after the QT interval had returned to normal.

VF is a dangerous arrhythmia often triggered by a PVC during the heart’s vulnerable repolarization phase.⁶ Schnur et al⁷ reported VF or sustained VT after PCI in only 0.4% of patients with NSTEMI, mostly in those with multivessel disease, poor LV function, or significant hypertrophy; none died within a year. Our case adds to the limited data on VF in patients with NSTEMI, especially those with acquired long QT and frequent unifocal PVCs. Myocardial electrical storm is a life-threatening condition with repeated episodes of ventricular arrhythmias needing frequent defibrillation.⁸ It often requires more than medications, such as deep sedation, overdrive pacing, or mechanical support, but these measures may offer only short-term control.⁸ In our case, despite multiple therapies, the arrhythmia remained uncontrolled until catheter ablation was done, which successfully stopped the arrhythmia. Ablation of PVC triggers has shown success in cases including post–myocardial infarction (MI), normal hearts, and channelopathies.³ Monomorphic PVCs from Purkinje-like fibers are known to trigger VF by causing electrical instability, making them an important focus in preventing sudden cardiac arrest.¹

In patients with structural heart disease, frequent PVCs raise the risk of death, often owing to reentry arrhythmias.⁶ Catheter ablation targeting PVCs is a key and growing treatment for VF. Although removing PVC triggers is the main goal, targeting scar tissue has also been explored, although with limited data.⁹ Successful ablation requires pinpointing the PVC origin using intracardiac mapping methods such as activation and pace mapping.² In structural heart disease, Purkinje fibers, more resistant to damage, often trigger VF, especially from the border of scarred cardiac tissue after MI.³ Singleton et al¹⁰ reported a case of VF storm after MI, resistant to treatment, but successfully controlled with ablation of a unifocal PVC.

Our patient had successful revascularization and stable electrolytes. Ahlers et al¹¹ reported a similar case where VF was triggered by a Purkinje-like PVC from the inferoseptal LV near the posterior fascicle, close to the RV moderator band. These areas, including the left posterior fascicle and RV moderator band, can trigger VF even without scarring. Ablation targeting Purkinje-like PVCs near the posterior fascicle has been effective, even in patients without structural heart disease.¹¹

Conclusion

This case shows the difficulty of treating recurrent VF caused by unifocal PVCs in a high-risk patient. After failed drug therapy and pacing, radiofrequency ablation successfully stopped the PVCs. A secondary prevention ICD was implanted, preventing further episodes. This highlights the importance of personalized treatment, early intervention, and long-term follow-up in managing refractory arrhythmias.

Take-home messages

• •Catheter-based radiofrequency ablation can effectively treat recurrent VF triggered by unifocal PVCs when conventional therapies fail.
• •Early recognition, personalized treatment, and the use of an ICD for secondary prevention are crucial for improving outcomes in high-risk patients.

Disclosures

The authors have no conflicts of interest to disclose.