Clinical story of a 55-year-old man who survived a heart attack only to be thrown into a relentless cycle of life‑threatening heart rhythms. This article walks you through the case in detail—what happened, why the conventional treatments sometimes fail, and how an advanced surgical strategy, a VATS-guided bilateral sympathectomy, ultimately stopped the cycle of ventricular tachycardia (VT) and restored the patient’s quality of life.

My goal in telling this case is to share not just the timeline of events but to explain the medical reasoning at each step, demystify the procedures involved, and highlight the real-world impact of modern electrophysiology and cardiac surgery working together. If you or a loved one are facing complex arrhythmias, this article will help you understand the options and the rationale behind them.

Outline

  • Introduction to the case and immediate clinical presentation
  • Initial emergency care: cardiac arrest, resuscitation, and primary PCI
  • Post-infarct complications: heart block, reduced LV function, and recurrent ventricular tachycardia
  • Standard antiarrhythmic approaches: medications, implantable cardioverter-defibrillator (ICD), and catheter ablation
  • When standard therapy isn’t enough: electrical storm and repeated ICD shocks
  • The role of the sympathetic nervous system in arrhythmias
  • VATS-guided bilateral sympathectomy: what it is, why it works, how it’s done
  • Patient outcome and follow-up
  • Clinical lessons and decision-making points
  • Frequently asked questions (FAQ)

Case Presentation: A Sudden Cascade

A 55-year-old man arrived at our emergency department with chest pain suspicious for an acute coronary syndrome. Based on his presentation and initial evaluation, we planned to move him to the catheterization laboratory for a primary percutaneous transluminal coronary angioplasty (PTCA), commonly known as primary PCI, to reopen the blocked coronary artery responsible for his heart attack.

Before the transfer could be completed, he suffered a sudden cardiac arrest. Prompt cardiopulmonary resuscitation and advanced cardiac life support measures restored his circulation, but his rhythm then deteriorated into a complete heart block. Given the acute coronary event and conduction abnormality, we expedited his transfer to the cath lab and performed primary PCI.

Following revascularization, his immediate condition stabilized. However, echocardiography showed that his left ventricular (LV) function was markedly depressed. Over the next six weeks he developed ventricular tachycardia (VT), a rapid and potentially lethal heart rhythm originating from the heart’s ventricles. VT in the setting of a recently infarcted and poorly functioning left ventricle is a high-risk situation.

First-Line Treatments: Medications and Device Therapy

We started antiarrhythmic medications and implanted a device to protect the patient from sudden cardiac death caused by recurrent VT. In the transcript I refer to “ACD,” but the intended meaning here is an implantable cardioverter-defibrillator (ICD). An ICD continuously monitors heart rhythm and delivers therapies—antitachycardia pacing or shocks—when dangerous arrhythmias occur.

For months after ICD implantation the patient’s life was disrupted by recurrent VT producing multiple ICD shocks. Repeated shocks are physically painful and emotionally traumatizing and indicate that the arrhythmia substrate remains active despite medications and device therapy.

Catheter Ablation: When the Trigger Needs to Be Eliminated

After recurrent shocks, we proceeded with catheter-based VT ablation. During VT ablation, electrophysiologists map the electrical circuits responsible for the arrhythmia and deliver energy (usually radiofrequency) to destroy the small areas of abnormal tissue that sustain VT.

The patient had a period of relief for about two months after the ablation, which is not uncommon. Ablation can significantly reduce arrhythmia burden and ICD therapies, but in some patients—particularly those with severely scarred hearts after infarction—the substrate for VT is large and dynamic. This can result in recurrence even after technically successful ablation.

Electrical Storm: Recurrent Shocks and the Need for a Different Strategy

When the patient returned with repeated shocks again despite medications, an ICD, and prior ablation, we were facing an “electrical storm”—a term used for sustained, recurrent ventricular arrhythmias requiring repeated ICD therapies within a short time frame. Electrical storm is a medical emergency associated with high morbidity and mortality. It is also profoundly destabilizing for patients: each ICD shock can worsen sympathetic activation, which itself can provoke more arrhythmias, creating a vicious cycle.

Standard escalation steps include optimizing antiarrhythmic drugs, repeat ablation if feasible, hemodynamic support, and general anesthesia to suppress sympathetic tone during mapping and ablation. However, when those measures fail or are not sufficient, we consider adjunctive or alternative therapies. One such option is surgical sympathetic denervation.

Understanding the Sympathetic Nervous System’s Role in VT

To understand why sympathetic denervation can help, it’s important to review the role of the autonomic nervous system—specifically the sympathetic arm—in ventricular arrhythmias. The sympathetic nervous system increases heart rate, contractility, and electrical excitability. After a myocardial infarction, surviving myocytes in the scar border zones are more sensitive to catecholamines (adrenaline, noradrenaline). Excess sympathetic stimulation can increase dispersion of electrical recovery and trigger or sustain ventricular tachyarrhythmias.

In some patients with recurrent VT or electrical storm, reducing cardiac sympathetic input can markedly decrease arrhythmia burden. This can be achieved temporarily by medications that blunt sympathetic effects (beta-blockers) or by nerve blocks. For a longer-term effect, surgical or chemical denervation targets the cervical and thoracic sympathetic chain supplying the heart. The stellate ganglion, located at the lower part of the neck, contributes significantly to cardiac sympathetic innervation; its removal or disruption can reduce arrhythmia susceptibility.

VATS-Guided Bilateral Sympathectomy: The Definitive Step

Given the patient’s ongoing shocks despite prior interventions, we referred him for surgical management. Our thoracic surgery team performed a video-assisted thoracoscopic surgery (VATS)-guided bilateral sympathectomy. Let’s break down what that means and why we chose bilateral rather than unilateral denervation.

What is VATS-guided sympathectomy?

VATS stands for video-assisted thoracoscopic surgery. It is a minimally invasive surgical technique that uses small incisions, a thoracoscope (camera), and specialized instruments to access the chest cavity without the need for a large open thoracotomy. For cardiac sympathetic denervation, the surgeon identifies and divides or removes the lower half of the stellate ganglion (on each side) and the thoracic sympathetic chain at levels that supply the heart (typically T2 to T4).

Why bilateral sympathectomy?

Historically, unilateral left-sided cardiac sympathetic denervation was used for refractory ventricular arrhythmias because the left sympathetic chain more strongly influences ventricular arrhythmogenesis. However, in severe or refractory cases—especially when arrhythmias recur after left-sided interventions—bilateral sympathectomy can offer additional benefit by reducing sympathetic input from both sides. Bilateral denervation may be more effective in patients with electrical storm or persistent VT despite prior therapies.

Mechanism of action

By interrupting sympathetic fibers that project to the heart, sympathectomy reduces the release of catecholamines at the myocardial level and lowers local sympathetic tone. This decreases excitability and heterogeneity in the ventricular electrophysiologic substrate, reducing the likelihood of VT initiation and maintenance. In many patients, sympathectomy results in fewer arrhythmias and dramatically reduces ICD therapies.

The Operation and Immediate Outcome

The thoracic surgeon performed a VATS-guided bilateral sympathectomy. The minimally invasive approach allowed precise visualization and interruption of the sympathetic chain with shorter recovery time compared with open surgery.

Following surgery, the patient experienced a sustained period without arrhythmia or ICD shocks. For the past four months he has been completely asymptomatic—no VT episodes and no ICD interventions. This outcome underscores how surgical sympathectomy can be life-saving and life-changing for select patients with refractory ventricular arrhythmias.

Why This Approach Was Appropriate for This Patient

Several features of this case made bilateral sympathectomy a reasonable and ultimately successful option:

  • Ischemic cardiomyopathy with markedly reduced LV function, creating a diffuse and arrhythmogenic substrate.
  • Recurrent VT episodes despite guideline-directed therapy: antiarrhythmic drugs and an ICD.
  • Temporary response to VT ablation, but recurrence shortly afterward, indicating an aggressive or multifocal substrate not fully amenable to catheter ablation alone.
  • Repeated painful and psychologically traumatic ICD shocks, constituting an electrical storm and severely impacting quality of life.
  • Availability of a thoracic surgical team experienced in VATS sympathectomy and multidisciplinary support for the patient.

Alternatives and Complementary Therapies

While sympathectomy can be key in selected refractory cases, it’s part of a broader array of options. These include:

  • Optimized antiarrhythmic therapy (e.g., amiodarone, sotalol, mexiletine)—often tried first or continued alongside other therapies.
  • Repeat or extended catheter ablation sessions—sometimes multiple procedures are needed to control complex VT.
  • Mechanical circulatory support (e.g., intra-aortic balloon pump, Impella, extracorporeal membrane oxygenation) during acute electrical storm when hemodynamic instability is present.
  • Left cardiac sympathetic denervation (LCSD) as a unilateral option—used especially in inherited arrhythmia syndromes like long QT or catecholaminergic polymorphic VT.
  • Heart transplantation in end-stage heart failure with refractory arrhythmias—considered when LV dysfunction is severe and other therapies fail or are unsuitable.

Risks and Considerations of Sympathectomy

No procedure is risk-free. Specific considerations for bilateral sympathectomy include:

  • Horner’s syndrome: When the stellate ganglion is damaged or removed, patients can develop partial Horner’s syndrome (drooping eyelid, small pupil, reduced facial sweating) on the affected side. The risk is higher with cervical extension of the resection; careful surgical technique aims to minimize this.
  • Compensatory hyperhidrosis: Some patients experience increased sweating in other areas of the body after sympathectomy.
  • Pain, bleeding, infection, and general risks associated with anesthesia and thoracic surgery.
  • Punctate or incomplete relief—sympathectomy may not completely eliminate all arrhythmias in every patient.

In this patient, the benefits—cessation of repeated life‑threatening arrhythmias and elimination of repeated ICD shocks—far outweighed the risks. He recovered uneventfully and has been asymptomatic for months.

Patient Perspective and Quality of Life

ICD shocks are not just clinically significant; they carry a major psychological burden. Patients often describe shocks as feeling like a sudden, sharp kick or even an explosion in the chest. Recurrent shocks can cause anxiety, depression, and withdrawal from normal activities. Stopping the cycle of shocks profoundly improves quality of life.

In this case, following sympathectomy the patient reported no arrhythmias and was free of shocks for months. This outcome highlights the importance of considering patient-centered goals—reducing suffering and restoring daily life—when deciding on advanced therapies.

Follow-Up and Long-Term Care

After surgical sympathectomy, close follow-up is essential. This includes:

  • Regular cardiology and electrophysiology visits to monitor LV function, device interrogation, and medication adjustments.
  • Rehabilitation and lifestyle counseling: cardiac rehabilitation, exercise prescription according to LV function, dietary guidance, and smoking/alcohol cessation if applicable.
  • Mental health support: counseling or therapy for patients who have experienced prolonged ICD shocks or cardiac arrest episodes.
  • Device checks: Even if arrhythmias are suppressed, the ICD remains an important safety net and needs periodic interrogation and battery management.

Key Takeaways and Clinical Lessons

  • Ischemic cardiomyopathy can lead to recurrent ventricular tachycardia, even after successful revascularization.
  • ICDs are life-saving but can cause physical and psychological harm when delivering frequent shocks; they treat the arrhythmia but do not prevent it.
  • Catheter ablation is an effective and minimally invasive intervention for many VTs, but scar-related and multifocal VT can recur.
  • The sympathetic nervous system plays a central role in arrhythmogenesis. In refractory cases, surgical cardiac sympathetic denervation can be a decisive therapy.
  • VATS-guided bilateral sympathectomy provides a minimally invasive route to achieve denervation and can stop electrical storms when other therapies fail.
  • Multidisciplinary care—cardiology, electrophysiology, thoracic surgery, anesthesiology, and rehabilitation—is essential for complex arrhythmia management.

FAQ

Q: What is ventricular tachycardia (VT)?

A: Ventricular tachycardia is a rapid heart rhythm that originates in the ventricles (the lower chambers of the heart). It can be sustained or nonsustained, and when sustained it can impair cardiac output and progress to ventricular fibrillation, which causes sudden cardiac death without immediate treatment.

Q: How does an ICD work?

A: An implantable cardioverter-defibrillator (ICD) continuously monitors heart rhythm. When it detects a dangerous ventricular arrhythmia, it can deliver pacing therapies to terminate the rhythm or deliver an electric shock to restore normal rhythm. ICDs have saved countless lives but do not prevent arrhythmias from occurring in the first place.

Q: What is catheter ablation for VT?

A: Catheter ablation uses specialized catheters and mapping systems to identify the precise regions of the ventricle responsible for initiating or sustaining VT. Radiofrequency energy is delivered to eliminate those areas, reducing or preventing recurrence. Success depends on the complexity and extent of the arrhythmogenic substrate.

Q: Why would VT recur after ablation?

A: Recurrence can occur because the arrhythmogenic substrate is extensive, new circuits form over time, or the original ablation did not eliminate every critical pathway. Scar-related VT is particularly challenging due to the diffuseness and heterogeneity of damaged myocardium.

Q: What is a VATS-guided bilateral sympathectomy?

A: It is a minimally invasive surgical procedure that interrupts the thoracic sympathetic chain on both sides using video-assisted thoracoscopic techniques. This reduces sympathetic input to the heart and can lower the propensity for ventricular arrhythmias.

Q: Who is a candidate for sympathectomy?

A: Patients with life-threatening, recurrent ventricular arrhythmias (electrical storm) that are refractory to medications, ICD therapy, and catheter ablation may be candidates. Decisions are individualized based on the overall clinical picture, comorbidities, and the patient’s wishes.

Q: What are the risks of sympathetic denervation?

A: Risks include surgical complications like bleeding and infection, anesthesia-related risks, potential Horner’s syndrome if the stellate ganglion is disrupted high in the neck, and compensatory hyperhidrosis. The balance of benefits and risks should be discussed carefully with the surgical team.

Q: Does sympathectomy cure the underlying heart disease?

A: No. Sympathectomy treats the arrhythmogenic influence of the sympathetic nervous system but does not reverse the underlying ischemic damage to the heart. Ongoing management of heart failure, coronary artery disease, and other cardiac conditions remains essential.

Q: How long does it take to recover from VATS sympathectomy?

A: Recovery from a minimally invasive VATS procedure is typically faster than from open surgery. Many patients can resume light activities within days and more vigorous activities within a few weeks, depending on overall health and recovery. Hospital stay is usually short, often one to a few days.

Q: Will I still need my ICD after sympathectomy?

A: In most cases, yes. The ICD remains an important safety net because sympathectomy reduces but does not eliminate the risk of arrhythmia entirely. Continued device follow-up is essential.