Transient ST-Segment Elevation during Transseptal Catheterization for Atrial Fibrillation Ablation

Abstract

For the treatment of refractory left atrial tachyarrhythmias, including atrial fibrillation, transseptal catheterization is often performed in order to achieve pulmonary vein isolation and left atrial substrate ablation. Herein, we report an unexpected ST-segment elevation in a 71-year-old man during a Brockenbrough transseptal catheterization procedure for atrial fibrillation ablation. The results of immediate coronary angiography were normal.

The few reports of similar observations have not yielded a definite conclusion about the underlying pathophysiology of this electrocardiographic phenomenon. We reviewed the medical literature and hypothesize that manipulation of the intraseptal and left atrial ganglion plexuses by the transseptal needle and sheath causes an imbalance in autonomic innervation, which leads to coronary artery spasm and ST-segment elevation. Nonetheless, coronary artery air embolism during the transseptal approach should also be considered in the differential diagnosis. If the elevation is transient and there is no evidence of acute myocardial infarction, we believe that careful monitoring and evaluation are more appropriate than immediate termination of the ablation procedure.

Transseptal catheterization is often performed to achieve pulmonary vein isolation and left atrial (LA) substrate ablation in the treatment of refractory LA tachyarrhythmias, including atrial fibrillation (AF). Herein, we present the unusual case of a patient who experienced unexpected ST-segment elevation in the inferior leads during the Brockenbrough transseptal catheterization procedure for AF ablation. We review the medical literature and discuss the potential underlying mechanisms.

Case Report

In September 2009, a 71-year-old man with a history of hypertension presented with frequent, symptomatic paroxysmal AF. The AF did not respond to flecainide therapy, and amiodarone caused a dermatologic reaction. The patient was referred for AF ablation by means of pulmonary vein isolation. Before the procedure, a transesophageal echocardiogram showed a left ventricular ejection fraction of 0.60 and a normal LA appendage flow velocity without thrombus. The interatrial septum was grossly intact, and results of an agitated saline bubble study were negative for an intracardiac shunt. A transthoracic echocardiogram of the LA revealed a volume index of 33 mL/m² and a diameter of 3.9 cm. Computed tomographic angiography showed normal anatomy of the 4 pulmonary veins.

The patient was placed under general anesthesia. By use of the modified Seldinger technique, three 7F sheaths were inserted into the right femoral vein, and 7F and 9F sheaths were inserted into the left femoral vein. All the sheaths were flushed. A coronary sinus decapolar electrode catheter was placed into the coronary sinus, and 2 lamp sheaths were exchanged for the 7F sheaths by use of an over-the-wire technique in the right femoral vein. After a baseline electrophysiologic study, double transseptal punctures were performed without technical difficulty with use of a Brockenbrough 1 transseptal needle kit (BRK1™; St. Jude Medical; St. Paul, Minn). The punctures were guided by intracardiac echocardiography (ACUSON AcuNav® 8F catheter; Siemens Medical Solutions USA, Inc; Mountain View, Calif). The patient was given 5,000 units of heparin, followed by an infusion of 1,000 units/hr immediately after the successful transseptal procedure. After the 2nd puncture and during the first 2 minutes of the passage and manipulation of the 7F transseptal sheath, a 3-mm ST-segment elevation was noted in the inferior leads on the electrocardiographic (ECG) monitor (Fig. 1). Shortly thereafter, the patient developed sinus bradycardia at 40 beats/min and hypotension that responded to intravenous fluids and a 120-µg bolus injection of phenylephrine. Right atrial pacing was initiated to support the heart rate. An intracardiac echocardiogram showed good left ventricular systolic function and no evidence of pericardial effusion. Levels of cardiac enzymes during and after the procedure did not suggest an acute myocardial infarction.

Fig. 1 Electrocardiogram (recording speed, 25 mm/s) shows ST-segment elevation in leads II, III, and aVF during the passage and manipulation of two 7F transseptal sheaths through the atrial septum.

Coronary artery angiography, performed less than 30 minutes after the patient's condition became stable, showed Thrombolysis in Myocardial Infarction (TIMI)-3 blood flow to all 3 major coronary arteries. The angiogram showed no significant flow-limiting lesion, coronary vasospasm, thromboembolus, or air embolus (Fig. 2). The ST-segment elevation returned to ECG baseline in 4 minutes, without any intervention. The 4 pulmonary veins were then isolated uneventfully. The patient was discharged from the hospital the next day without symptoms or ECG changes.

Fig. 2 Coronary angiography in A) left and B) right anterior oblique projections show no significant coronary artery blockage or spasm. The linear displacement of contrast medium in the proximal segment of the right coronary artery is due to contrast streaming.

A = Judkins right 4 catheter; B = quadripolar electrophysiologic catheter at the high right atrium; C = two 7F sheaths; D = right coronary artery; E = left anterior descending coronary artery; F = decapolar electrophysiologic catheter in the coronary sinus; G = left circumflex coronary artery; H = Judkins left 4 catheter

Discussion

Atrial fibrillation is the most common cardiac arrhythmia that clinicians encounter. This arrhythmia can be managed through rate or rhythm control. Atrial fibrillation ablation by means of pulmonary vein isolation is a common alternative method of treating patients who are refractory to pharmacologic therapy or who cannot tolerate it.¹ As with other invasive procedures, AF ablation can result in sequelae of its own, such as cerebral thromboembolism, pulmonary vein stenosis, pericardial effusion, cardiac tamponade, esophageal–atrial fistula, and phrenic nerve paralysis.¹ However, sequelae other than those directly associated with the ablation can also occur. In our patient, we observed a rare and noteworthy transient ST-segment elevation during transseptal catheterization for pulmonary vein isolation.

The few reports of similar observations^2–9 have yielded no definite conclusion about the underlying mechanism of the ST-segment elevation. Some authors have proposed that autonomic imbalance-mediated coronary spasm is the mechanism behind the phenomenon,3,5–7,9 whereas others have suggested thrombus² or air embolism^9,10 as the cause. After reviewing the medical literature, we believe that autonomic imbalance (probably via enhanced parasympathetic stimulation) and mediated coronary spasm is the most likely cause of this unique complication. Even the definitive pathogenesis of coronary spasm is debatable: Endo and colleagues¹¹ and Athanassopoulos and Maroutsos¹² suggested that the autonomic nervous system plays an important role in causing coronary artery spasm. Yasue and associates¹³ concluded that the parasympathetic nervous system may participate in the mechanism of coronary spasm.

ST-Segment elevation with normal coronary angiographic results has occurred during patent foramen ovale closure.^14,15 Rigatelli and colleagues¹⁴ reported hypotension and ST-segment elevation in leads II, III, and aVL when a patent foramen ovale was crossed with a standard 4F multipurpose diagnostic catheter. However, coronary air embolism and thrombus were not detected on a coronary angiogram. Ludman and colleagues¹⁵ reported similar ECG changes shortly after atrial septal puncture and passage of the Inoue balloon in 8 patients who were undergoing percutaneous mitral valvuloplasties. All of the patients' transesophageal echocardiograms were normal before the procedure. Both reports^14,15 suggest that intraseptal and LA manipulation caused increased parasympathetic stimulation, which resulted in vessel spasm and the associated ECG abnormality.

We found 8 reports of 16 patients with ST-segment elevation when transseptal LA catheterization was used during AF ablation procedures (Table I).^2-9 The elevations occurred during intraseptal and LA manipulation, transseptal punctures, transseptal catheter passage, or pulmonary vein isolation. Two patients developed ST-segment elevation during transseptal puncture,^3,9 as did 2 after transseptal puncture but before pulmonary vein isolation.^2,9 Of note, in all but 1 case, the elevation occurred exclusively in the inferior leads while coronary angiography showed no obstruction. The observations raise the question of why the myocardial injury pattern in the form of ST-segment elevation predominantly occurred in the inferior leads, which typically correspond with the myocardium that is supplied by the right coronary artery (RCA) or sometimes by the left circumflex coronary artery (LCx). The chance of myocardial injury caused by embolism is almost identical in the right or left coronary artery system.

TABLE I. Characteristics of 17 Patients with Transient ST-Segment Elevation during Atrial Fibrillation Ablation with Use of the Transseptal PVI Procedure

The selective location of the ST-segment injury pattern may indicate a link between the atrial septum, the LA, and the RCA or LCx territory. An intricate intracardiac nervous system has been identified in animal and human hearts.^16,17 Atrial ganglionated plexuses were found on the superior surface of the left and right atria, the posterior medial surface of the LA, the inferior and lateral aspects of the posterior LA, and the interatrial septum. Hence, it is plausible that manipulation of the atrial septum and the LA causes selective activation of right cardiac parasympathetic nerve stimulation to the inferior or posterior myocardial region that is supplied by the RCA or LCx.

In earlier reports, the ST-segment elevation usually resolved within 4 to 6 minutes after the procedure was halted. When an immediate coronary angiogram yields normal results, catheter-associated coronary thrombus and air embolism would most likely not account for the transient ECG injury pattern. Furthermore, in our patient, both the absence of catheter exchange and the intraprocedural infusions of heparin reduced the probability of thrombus formation. Tada and colleagues⁶ reported 2 cases of chest pain and transient ST-segment elevation hours and days postprocedurally, with normal coronary angiographic results. In 1 patient, the 1st elevation occurred at midnight on postprocedural day 1, followed by 2 episodes that resolved without intervention. The 2nd patient experienced angina on postprocedural day 3 and again on days 8, 12, and 13. On day 13, ST-segment elevation was detected. The authors concluded that the chest pain and ST-segment elevation resulted from vessel spasm. Thrombus or air embolism would not repeatedly occur postprocedurally if the coronary arteries were normal.

Although we propose that coronary vasospasm was the mechanism of ST-segment elevation in our patient, we cannot entirely exclude coronary air embolism as another potential cause. Coronary air embolism is a recognized complication of the transseptal procedure for the catheter ablation of left free-wall accessory pathways,¹⁰ coronary angiography,¹⁸ coronary angioplasty,¹⁹ off-pump bypass,²⁰ and balloon mitral valvuloplasty.²¹ Lesh and co-authors¹⁰ described a case wherein several air bubbles obstructed flow to the distal RCA, which led to marked ST-segment elevation in the inferior leads during catheter-based transseptal ablation. Coronary angiography was performed within 3 minutes of the ECG changes. Nitroglycerin, oxygen, and forceful injections of contrast medium were administered. After several minutes, the ST-segment elevation and air embolism resolved. In most situations, air embolism resolves on its own and has no substantial sequelae. However, it may cause irreversible myocardial damage.²² As in our case, the abovementioned patient developed bradycardia and hypotension when the ST-segment elevation occurred.¹⁰

Our patient's profound sinus bradycardia and hypotension could be the result of a Bezold-Jarisch–like reflex, as in 2 cases reported by Arita and associates.⁴ Bradycardia and hypotension resolved upon atropine injection with norepinephrine infusion in 1 patient, and upon atropine injection in the other patient. The authors concluded that the transient complications were due to catheter manipulation that caused vagal stimulation-induced RCA dilation. In addition, they believed that the ST-T changes in the inferior leads were caused by RCA dilation, not spasm. This Bezold-Jarisch reflex was also reported in patients who sustained myocardial infarction and myocardial ischemia.^23,24 Experimental evidence suggests that this cardiac reflex results from the activation of inhibitory cardiac receptors with vagal afferents that are located predominantly in the inferoposterior wall of the left ventricle.²⁵ As a result, we cannot rule out the possibility that our patient's bradycardia and hypotension were related to a Bezold-Jarisch reflex.

Conclusion

We have reported a rare occurrence of ST-segment elevation during transseptal catheterization for the performance of pulmonary vein isolation to treat paroxysmal AF. On the basis of our medical literature review and the nature of our patient's case, we believe that sheath manipulation across the atrial septum and in the LA causes autonomic nervous imbalance with activation of the right cardiac parasympathetic nerve and leads to coronary vasospasm. Our patient's bradycardia and hypotension may have been partially related to a Bezold-Jarisch reflex. However, coronary artery air embolism should always be part of the differential diagnosis. Our experience and that of others suggests that ST-segment elevation should not preclude continuing the ablation procedure after careful monitoring and evaluation of the patient.