European Journal of Cardiovascular Medicine

Takotsubo syndrome (TTS) can be described as an acute, transiently occurring form of heart failure with dysfunction of the left ventricle (LV). Intense physical and emotional stress has been identified as the most common trigger factor [1, 2]. A fear about upcoming surgical procedure, the operation itself or the administration of drugs that mimic stress hormones may cause this syndrome [2, 3]. In this case, we will present a case of severe takotsubo syndrome related to haemodynamic consequences of cardiac tamponade and rescue procedures

A 69-year-old woman with biatrial-ventricular pacemaker (BiA DDD) implanted 19 years ago due to tachy-brady syndrome with Morgagni Adams Stokes syndrome in the course of atrial fibrillation was admitted to the hospital because of leads dysfunction. One year before she underwent pacemaker replacement due to battery depletion. Other diagnosed diseases include hypertension and moderate tricuspid regurgitation. The patient was qualified for transvenous lead extraction procedure (TLE) with the use of polypropylene unpowered Byrd’s dilator sheaths (Cook Medical®). Continuous monitoring of TLE procedure with transesophageal echocardiography (TEE) was a standard procedure in the centre.

Preoperative risk of lead extraction was estimated. The sum of age of three leads was 57y (19y each lead). It is well documented in the literature, that the sum of the leads age > 50y means high risk of major TLE complication (cardiac tamponade or TV damage). Available official risk score calculators confirmed high risk of planned TLE procedure: LECOM (probability of a difficult extraction procedure was 40, 48%) [4], SAFeTY TLE (risk of major complications 3, 75%) [5]. Patient’s risk factors are the following: female gender, three very old leads (the risk is cumulative), loop of lead in ventricular or adhesions between leads [6].

The TEE before lead extraction showed sectionally thickened leads and the extensive adhesion of all three leads in the superior vena cava with the presence of connective tissue around the leads. Moreover, the loop of ventricle lead interfered with tricuspid valve causing moderate tricuspid regurgitation. Left ventricular ejection fraction (LVEF) was normal (60%).

A fluoroscopic examination confirmed the presence of lead loop in the right ventricle. Venography revealed the occlusion of subclavian, brachiocephalic veins and superior vena cava with well-developed collateral circulation.

Figure 1: Venography – occlusion of subclavian, brachiocephalic veins and superior vena cava (A). Lead loop in the right ventricle in fluoroscopy (blue arrow) (B). Removal of the atrial lead, visible polypropylene Byrd dilator sheath with the atrial lead inside (yellow arrow) (C). The fragment of the lead left in the right ventricle (red arrow) (D)

As the patient was pacemaker-dependent, temporary pacing was provided conventionally throught the femoral venous approach.

At the beginning of the procedure one of the atrial lead and right ventricle lead were removed uneventfully. After removal of second atrial lead, TEE showed an increase in pericardial fluid with simultaneous significant drop in blood pressure. The diagnosis of acute cardiac tamponade was established. Immediate sternotomy was performed - cardiac tamponade was confirmed and blood was removed from the pericardial sac. The site of perforation in the right atrial appendage was revealed and promptly sutured. In the meantime, due to an additional drop in blood pressure, the anesthesiology team administered norepinephrine and adrenaline to the patient. After removal of cardiac tamponade and administration of drugs mentioned above, the blood pressure temporarily raised to 250/150 mm Hg and after a few minutes depression of cardiac contractility was observed. TEE revealed generalized severe hypokinesis of the left ventricular walls with preserved contractility of the parabasal segments.

Because of cardiogenic shock with low cardiac output syndrome the patient was connected to cardio-pulmonary bypass pump (CPB). Being on cardiopulmonary bypass surgical team decided to stop the heart and remove remaining lead fragments from right ventricle and right atrium (Figure 2). First attempts to wean from CPB were unsuccessful due to poor contractility of left ventricle. As the procedure took place in hybrid room, an emergency coronary angiography was performed. The examination did not reveal any significant changes in the coronary arteries, which allowed to exclude coronary artery disease as the cause of cardiogenic shock. However, constriction of the main coronary arteries was visible.

The continuous infusion of milrinone and dobutamine was administered. An intra-aortic balloon pump (IABP) was inserted through the left femoral artery. External pacing was initiated with use of two epicardial temporary leads placed on cardiac wall.

After 155 minutes of extracorporeal circulation the contractility of left ventricle was partially restored, so thanks to support with the intra-aortic balloon pump and high doses of catecholamines it was finally possible to disconnect the patient from CPB.

Immediately after surgery, the troponin level was 17.8 ng/ml. The next day it dropped to 3.88 ng/ml and normalized in the following days.

During the procedure and in the perioperative period, a total of 13 units of packed red blood cells, 2 units of fresh frozen plasma and 1 packed platelet were administered.

In the following days, the gradual hemodynamic stabilization was observed. After 3 days the intra-aortic ballon was removed and the administration of catecholamines was discontinued. Seven days after the surgery, a new DDD pacemaker was implanted under local anesthesia through the right subclavian vein. The follow-up TTE revealed a 20x7mm thrombus near the right atrium, without fluid in the pericardium. LVEF returned to the initial value of 60%. On 20th day after surgery, the patient was discharged home in a good condition, without any disabilities.

Figure 2: Removed leads with visible damage (A). One of the removed atrial lead with epicardial fatty tissue (B). TEE , 2D, frame from a video recording. Cardiac tamponade after extraction of atrial lead, visible fluid in the pericardial sac (red arrows) and fragment of a thickened lead in the right ventricle (RV) (yellow line). Left atrium (LA), right atrium (RA). (C). Surgical removal of lead fragments (D).

Perforation of the right atrium with subsequent acute cardiac tamponade, emergency sternotomy, loss of large amounts of blood and administration of catecholamines resulted in acute heart failure (cardiogenic shock) lasting several days. Patient required urgent circulatory support with cardiopulmonary bypass (CPB) first, than with an intra-aortic ballon pump (IABP) and catecholamines subsequently to allow the heart to restore contractility. TEE showed severe but fortunately reversible LV contractility reduction with preserved contractility of the basal segments. This course of the disease allowed to recognize takotsubo cardiomyopathy (takotsubo syndrome – TTS). What is also characteristic of this syndrome, usually left ventricular contractility and LVEF returns to normal after a few weeks or months [1, 2].

TTS can be provoked by various triggers. It should be differentiated from acute coronary syndrome [7]. Therefore, urgent coronary angiography was performed and significant changes in the coronary vessels were excluded.

Perioperative TTS is an increasing condition defined in the setting of emotional and physiological stressors imposed by surgery [8]. However, TTS during the procedure may be caused by various factors such as pain or the administration of catecholamines such as adrenaline [1-3, 7, 8]

In our opinion, in this particular case, sudden administration of high dose of catecholamines (adrenaline and noradrenaline) in the first minutes of acute cardiac tamponade was a trigger of takostubo syndrome. The direct cause of the observed blood pressure drop was mechanical - diastolic heart failure caused by acute tamponade. The administration of catecholamines in a high dose to a patient with normal left ventricular systolic function may result in acute severe heart failure. The suggested correct solution to the above-described problem should be rapid decompression of the tamponade without the administration of positive inotropic drugs.

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