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Management of Dysrhythmias during Coronary AngioJet

David Antoniucci, MD Author Affiliations: From the Division of Cardiology, Careggi Hospital, Florence, Italy. The author reports no conflicts of interest regarding the content herein. Address for correspondence: David Antoniucci, MD, Careggi Hospital, Viale Morgagni, Florence, I-50134, Italy. E-mail: david.antoniucci@virgilio.it
August 2008

How to Minimize the Need for Temporary Pacemaker during Rheolytic Thrombectomy

ABSTRACT: Background. Whatever the mechanism or mechanisms involved in the genesis of bradyarrhythmias during rheolytic thrombectomy (RT), the severity and duration of bradycardia are related to vessel location and the duration of the activation of the RT catheter. The latter implies that procedural variables may have a role in the prevention or attenuation of bradycardia and subsequent minimization of the need for temporary pacemaker insertion. Methods. From January 2004 to December 2007, 396 patients with ST-segment elevation acute myocardial infarction received RT using the single-pass anterograde technique. All but 2 patients had RT without temporary pacemaker support. The 2 patients with temporary pacemakers received the electrical support before arriving in the cath lab. Results. No major clinical adverse events related to bradyarrhythmias occurred. Conclusion. The single-pass anterograde RT technique minimizes the need for temporary pacemaker insertion and is safe and effective. J INVASIVE CARDIOL 2008;20:22A–24A Bradycardia during rheolytic thrombectomy (RT), generally due to atrial standstill or less frequently to atrioventricular block, is a common occurrence and may be the result of adenosine release by hemolysis during use of the AngioJet® Rheolytic™ Thrombectomy System (Possis Medical, Inc., Minneapolis, Minnesota) in treating lesions in the right coronary artery or dominant circumflex artery. It is likely that another mechanism related to vagal chemoceptor and baroceptor stimulation is involved in the genesis or worsening of bradycardia during RT into the right coronary artery or a left dominant circumflex artery, and the activation of an acetylcholine-mediated process seems to be confirmed by the frequent diffuse spasm of the epicardial vessel after RT. Whatever the mechanism or mechanisms involved in the single case, the severity and duration of bradycardia are related to vessel location and the duration of the activation of the RT catheter. The latter implies that procedural variables may have a role in the prevention or attenuation of bradycardia and subsequent minimization of the need for a temporary pacemaker. Obviously, a temporary pacemaker is effective in preventing bradycardia, but this effect is obtained at the cost of an unavoidable lengthening of the procedure and a substantial risk of right ventricular perforation and cardiac tamponade. In the AiMI trial, the incidence of cardiac tamponade in the RT arm was 0.8%, and in this study, temporary pacemakers were routinely used in right coronary artery or circumflex artery RT as recommended by the study protocol according to the approved label use of the device.1 The single-pass anterograde RT technique minimizes the need for a temporary pacemaker. A single pass of the RT catheter is sufficient to remove a fresh large thrombus in most patients (Figures 1 and 2). The RT catheter should be activated at least 1 cm proximal to the thrombus to create a suction vortex prior to advancing the device. Thrombectomy is initiated by advancing the RT catheter slowly (1 mm/second–3 mm/second) to and through the thrombosed segment. Typically, the RT catheter can cross the lesion without difficulty and it should be advanced as far as possible according to lesion location and the length of the vessel distal to the occlusion. Thrombectomy is restarted at the end of the proximal-to-distal pass, with a distal-to-proximal pullback at the same velocity. After the first proximal-to-distal pass, the device is retrieved into the guide catheter. An angiographic check is performed to assess restoration of flow. In the large majority of cases,2 a thrombolysis in myocardial infarction (TIMI) grade 3 flow is restored without more evidence of residual thrombus, and treatment with the RT catheter should be stopped at this point. In the event of persistent occlusive thrombosis, a second pass with the RT catheter should be performed. Such persistence of thrombus is generally due to old, partially organized thrombus in an aneurysmatic vessel. In this situation, a second pass with the RT catheter may be only partially effective, and placement of a noncovered or covered stent should be considered in order to decrease the risk of distal embolization. In some cases, treatment with the RT catheter may result in the persistence of TIMI grade 0 or 1 flow. In such cases, “no reflow” may be due to occlusive epicardial spasm or exceptionally to microvessel spasm. Intracoronary administration of vasodilatory agents (e.g., nitrate-nitroglycerin, isosorbide dinitrate, nipride and/or verapamil or diltiazem) may resolve the spasm in a few seconds. If spasm is apparent after the first pass with the RT catheter, subsequent passes should not be made until the spasm is resolved and then only if there is evidence of residual thrombus. If no reflow persists, it is mandatory to understand the underlying cause before any other attempt with the RT catheter or a balloon catheter or before adjunctive pharmacologic therapy is administered. An effective diagnostic approach is an ultraselective injection of contrast medium beyond the occlusion using a dual lumen catheter. This method will allow assessment of the wire position within the lumen and the diagnosis of persistent microvessel spasm, persistent massive thrombosis or an incorrect position of the wire (dissection or perforation). In cases of no reflow distal to the occlusion, repeat administration of intracoronary vasodilatory drugs should be performed. This precautionary policy may avoid not only severe bradycardia during the RT procedure but also other major complications, such as extensive dissection, coronary perforation and cardiac tamponade. Some operators use a distal-to-proximal pullback pass, but the retrograde technique should not be performed as the initial thrombectomy run. Any catheter, even a conventional 0.014" guidewire, may produce embolism while crossing the lesion. No reflow due to distal embolization not only may decrease the effectiveness of reperfusion but also may increase the risk of reflex bradycardia. If bradycardia occurs during the RT procedure, it is sufficient to stop the activation of the device in most cases: after very few seconds from device deactivation, spontaneous supraventricular or ventricular escape beats, or those elicited by cough or atropine, break off the bradycardia. Thus, in some cases the single-pass procedure may be done with multiple device activation for very short periods. Assessing the Efficacy of RT before Direct Infarct Artery Stent Implantation The Florence-AngioJet randomized trial was the first study that assessed the efficacy of RT before direct infarct artery stent implantation in patients who underwent percutaneous coronary intervention (PCI) for acute myocardial infarction.3 This study was based on a sample of 100 patients with a first acute myocardial infarction. Endpoints of the study were early ST-segment elevation resolution, the corrected TIMI frame count and the infarct size as assessed by technetium-99m sestamibi scintigraphy at 1 month. All endpoints were reached. Patients randomized to thrombectomy before direct stenting had a higher incidence of early ST-segment elevation resolution (90% vs. 72%, p = 0.022), lower corrected TIMI frame counts (18.2 ± 7.7 vs. 22.5 ± 11.0, p = 0.032) and smaller infarcts (13.0 ± 11.6% vs. 21.2 ± 18.0%, p = 0.010) as compared to patients randomized to direct stenting alone. By multivariate analysis, the only variables related to the early ST-segment resolution were randomization to thrombectomy (OR 3.56, 95% CI 1.11 to 11.42, p = 0.032) and diabetes mellitus (OR 0.24, 95% CI 0.07 to 0.86, p = 0.029). No patients had temporary pacemaker insertion, and no major adverse events related to bradyarrhythmias occurred. After the conclusion of the study, our center routinely performed RT with the anterograde single-pass technique before direct stent implantation in patients with acute ST-segment elevation myocardial infarction and angiographic evidence of thrombus after infarct artery wiring associated with the restoration of a TIMI grade 2 or 3 flow (TIMI thrombus grade 2 to 4)4 or with a persistent occluded vessel after wiring (TIMI thrombus grade 5). From January 2004 to December 2007, 396 patients with ST-segment elevation acute myocardial infarction received RT. Table 1 summarizes baseline clinical, angiographic and procedural characteristics of this series of patients. In all but 2 patients, RT was performed without temporary pacemaker insertion. The 2 patients with temporary pacemakers received the electrical support before arriving in the cath lab due to prolonged asystolia after DC shock of a ventricular fibrillation in one case and to severe bradycardia due to complete atrioventricular block in the other case. Again, no major clinical adverse events related to bradyarrhythmias occurred. Conclusion The single-pass anterograde procedure without temporary pacemaker insertion is safe and effective. Temporary pacemaker before rheolytic thrombectomy increases the risk of ventricle perforation, lengthens the procedure time and increases costs.

1. Ali A, Cox D, Dib N, et al. Rheolytic thrombectomy with percutaneous coronary intervention for infarct size reduction in acute myocardial infarction: 30-day results from a multicenter randomized study. J Am Coll Cardiol 2006;48:244–252.
2. The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group. N Engl J Med 1985;312:932–936.
3. Antoniucci D, Valenti R, Migliorini A, et al. Comparison of rheolytic thrombectomy before direct infarct artery stenting versus direct stenting alone in patients undergoing percutaneous coronary intervention for acute myocardial infarction. Am J Cardiol 2004;93:1033–1035.
4. Early effects of tissue-type plasminogen activator added to conventional therapy on the culprit coronary lesion in patients presenting with ischemic cardiac pain at rest. Results of the Thrombolysis in Myocardial Ischemia (TIMI IIIA) Trial. Circulation 1993;87:38–52.

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