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Z Kardiol 94:474478 (2005) DOI 10.

1007/s00392-005-0251-0

CASE REPORT

M. Krivokuca C. Behrmann M. Sievert K. Werdan R. Prondzinsky

Thromboembolic cerebral ischaemic attack complicating cardiac catheterization


Successful local thrombolytic therapy with reduced dose rt-PA

Thromboembolischer zerebraler Insult whrend einer Herzkatheteruntersuchung Erfolgreiche lokale Lysetherapie mit rt-PA

Received: 13 December 2004 Accepted: 8 February 2005

Dr. med. Mirko Krivokuca ()) Department of Medicine III University Hospital Martin-Luther-University Halle-Wittenberg 06097 Halle, Germany Tel.: +49-345/557 30 77 Fax: +49-345/557 20 72 E-Mail: mirko.krivokuca@medizin.uni-halle.de Karl Werdan Roland Prondzinsky Department of Medicine III Martin-Luther-University Halle-Wittenberg Halle, Germany Curd Behrmann Department of Radiology University Hospital Martin-Luther-University Halle-Wittenberg Halle, Germany Maike Sievert Department of Neurology University Hospital Martin-Luther-University Halle-Wittenberg Halle, Germany

n Zusammenfassung Thromboembolische zerebrovaskulre Ischmieereignisse sind eine mgliche Komplikation diagnostischer und interventioneller Herzkatheteruntersuchungen. In diesem Fallbericht werden die notwendigen diagnostischen Schritte und eine erfolgreiche Behandlungsstrategie am Beispiel einer Patientin mit symptomatischer zerebraler Ischmie im Rahmen einer Herzkatheteruntersuchung aufgezeigt. Im Anschluss an eine initiale CT-Untersuchung zum Ausschluss einer zerebralen Blutung erfolgte eine angiographische Darstellung der zerebralen Gefe unter Verwendung der Herzkatheterschleuse in der A. femoralis. Dabei konnte ein intrakranieller Verschluss der rechten A. carotis interna kurz vor ihrer Bifurkation demonstriert werden. Es erfolgte eine lokale Lysetherapie mit einer reduzierten rt-PADosis von 34 mg. Die nachfolgende Angiographie zeigte eine Reperfusion des verschlossenen Gefes verbunden mit einer deutlichen Besserung der Symptomatik. n Schlsselwrter Herzkatheteruntersuchung thromboembolische Komplikationen zerebrale Ischmie lokale Thrombolyse

n Summary Cerebral ischaemia caused by thromboembolism is a possible complication of diagnostic and interventional cardiac catheterization. In this case report we describe the diagnostic steps and successful treatment strategy in the management of a patient who suffered from cerebral ischaemia during cardiac catheterization. Initial CT scanning to exclude cerebral haemorrhage was followed by angiography through the cardiac catheterization sheath in the right femoral artery. Occlusion just before the intracranial bifurcation of the right internal carotid artery was found and local thrombolysis given with a reduced dose of 34 mg rt-PA. The subsequent angiogram showed restored perfusion in the affected vessel after completion of thrombolytic therapy and resolution of neurological symptoms. n Key words Cardiac catheterization thromboembolic complications cerebral ischaemia local thrombolysis

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Introduction
Non-haemorrhagic cerebrovascular ischaemic disease is a major cause of disability and mortality. Acute thromboembolic occlusion of cerebral vessels during catheter procedures is a rare complication and occurs in approximately 0.11% of cardiac catheterizations [10]. The implications to an individuals health and life quality are enormous, however, since frequently disability or death result.

Case report
We report the case of a 60-year old woman who was admitted to the hospital with increasing dyspnoea over a few weeks and 5 days of severe dyspnoea and orthopnoea at rest. The medical history revealed no previous cardiovascular illness or, more importantly, no history of cerebrovascular ischaemic events. A clinical diagnosis of severe congestive cardiac failure was made.

n Clinical examination
Gross peripheral oedema, pulmonary rales and anasarca were noted. A 2/6 mitral incompetence murmur was found.

Left ventriculogram: Calculated ejection fraction was 35% and third degree mitral regurgitation was noted. Coronary angiography was then performed using a 5 French (F) Judkins L4 catheter for the left coronary artery. Immediately following intubation of the left coronary ostium the patients blood pressure dropped to 80/55 mmHg, followed by immediate withdrawal of the catheter by the examiner. The investigation was discontinued since clinical examination found a left facial nerve palsy, right sided gaze and left upper limb palsy. Rapid circulatory support was established by infusion of 500 ml of electrolyte solution and oxygen was administered via a nasal probe. An urgent cranial CT scan was achieved 15 minutes after the initial symptoms to exclude cerebral haemorrhage (Fig. 1). Following this, a cerebral angiography was immediately performed through the right femoral arterial sheath using an EnvoyTM multipurpose catheter in the right internal carotid artery. Occlusion close to the right sided intracranial internal carotid bifurcation was demonstrated (Fig. 2). Insertion of a TrackerTM microcatheter into the occlusion site was followed by infusion of 20 mg rt-PA as a bolus dose followed by continuous infusion of a further 14 mg through the catheter close to the occlusion site (Fig. 3). A total dose of 34 mg rtPA and 6000 units of heparin were infused over one hour to achieve reperfusion of the internal carotid occlusion (Fig. 4). There was angiographic evidence,

n Investigations
The ECG showed right axis deviation and regular sinus rhythm with no evidence of acute ischaemia. Transthoracic and transoesophageal echocardiography demonstrated left atrial (52 mm) and left ventricular dilatation (78 mm). Left ventricular ejection fraction was severely impaired and degenerative mitral valve disease and severe mitral regurgitation was found. There was no evidence of intracardiac thrombi. Spontaneous echo contrast was present in the left atrium, and grade II sessile plaques were noted in the thoracic aorta. Carotid ultrasound showed no evidence of plaque structures or relevant stenosis. Following completion of non-invasive diagnostic procedures and after stabilization of the patients clinical condition a cardiac catheterization was undertaken: Haemodynamics during left and right heart catheterization (pressures in mm Hg): Right atrium: 13; Right ventricle: 40/14; Pulmonary artery: 40/27/33; Pulmonary capillary wedge mean 25. Aorta: 100/72/ 83; left ventricle: 97/22 mmHg. Cardiac output: 3.52 l/min; cardiac index: 1.68 l/(min m2).

Fig. 1 Cranial computer tomography (CCT) immediately after the cerebral ischaemic event (day 0): No evidence of haemorrhage or infarction

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Fig. 2 Carotid artery angiography showing occlusion of the intracranial internal carotid artery prior to the bifurcation into anterior and middle cerebral artery (black arrow)

Fig. 4 Carotid artery angiography showing successful reperfusion of both anterior (black arrow) and middle (white arrow) cerebral artery

Fig. 3 Carotid artery angiography showing a TrackerTM catheter at the occlussion site (black arrow)

Fig. 5 CCT on day 2 shows a 5 mm hypodense lesion in the central area of the right internal capsule consistent with a small area of infarction (white arrow)

however, of a persisting occlusion in the pericallosal artery. The clinical symptoms resolved completely. Six hours later, the right femoral sheath was removed and a compression bandage applied. The patient was heparinized for a further 24 hours. After initial monitoring in the stroke unit, the patient was

transferred the following day to the medical observation ward. CT scanning 48 hours after the event demonstrated a hypodense lesion in the central area of the right internal capsule consistent with a small area of infarction (Fig. 5).

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Discussion
Despite the low incidence of clinically apparent cerebral ischaemic events during cardiac catheterization, it is still a major complication of this procedure with limited therapeutic options. There are a number of possible causes of cerebral ischaemia during cardiac catheterization: The majority of cases are due to thromboembolic events. Non-ionic contrast agents used during the investigation can occasionally cause neurological symptoms with time delays of many hours, sometimes non-specific, such as, visual disturbance or more significantly, cortical blindness [14]. Air embolism is another rare cause of cerebral ischaemic events and may be due to air trapping in the contrast agent pump used for aortography and left ventriculogram. Treatment with hyperbaric oxygen should be considered in these cases. Cerebral thromboembolic ischaemic complications do occur despite preventive measures such as saline injections into catheters prior and after their use, short intravascular contact times of guide wires, avoiding unnecessary catheter manipulations in the ascending aorta and the aortic arch and appropriate hydration prior to the procedure [12]. These complications are found in both diagnostic and interventional procedures. However, the majority of patients suffer only mild, transient symptoms and only a minority have prolonged ischaemia. In addition to catheter derived thrombi, emboli can also result from aortic atheroma or from the left ventricle due to previous or acute myocardial infarction and impaired left ventricular function. A review by Sheikhzadeh et al. [13] was recently published in this journal indicating the increased risk of systemic and cerebral embolism in patients with atheromatous disease of the thoracic aorta. Catheterization of occluded bypass grafts and the left internal mammary artery are also sources of thromboembolic events. The risk of cerebral ischaemia is increased in these patients and has to be considered additionally to the catheterization procedural risk. Recent evidence suggests a higher risk for thromboembolic complications in patients with haematological diseases such as Polycythaemia Rubra Vera [11]. The Cooperative Study found cerebral thromboembolic complications in 0.2% using transbrachial vascular access and 0.231.1% in transfemoral access for coronary angiography [2]. Current complication registries have documented event rates of around 0.07 to 0.11% in cardiac catheterization with coronary angiography [10, 15]. Fuchs [5] reported a stroke incidence of 0.38% (both, ischaemic and haemorrhagic) and a 0.12% incidence of transient ischaemic attacks in patients undergoing percutaneous coronary interventions.

Fig. 6 Algorithm for the management of acute cerebrovascular thromboembolic ischaemic events in the cardiac catheterization laboratory. (*) Glycoprotein IIb/IIIa receptor antagonists

In 2003, Omran [7] reported focal diffusion-imaging abnormalities consistent with acute cerebral embolic events in MRI scans of 22 out of a total of 101 patients who underwent retrograde catheterization of a stenosed aortic valve. Clinically apparent neurological deficits were reported in three patients. Overall, the risk of cerebral thromboembolic events is closely related to vascular risk factors. Asymptomatic embolic events are more frequent then clinically detected, as demonstrated by transcranial Doppler ultrasound studies [8]. Current treatment options for acute ischaemic stroke include both local and systemic thrombolytic therapy and mechanical thrombus disruption [9]. Since publication of the PROACT trials in 1998 and 1999 [3, 6] local intra-arterial thrombolysis is of specific interest due to higher doses of thrombolytics at the occlusion site, potentially higher reperfusion rates and fewer systemic side effects. There is, however, no trial to date directly comparing local vs. systemic thrombolysis in acute ischaemic stroke [4]. In a more recent study of 100 patients with stroke due to middle cerebral artery occlusion undergoing local intra-arterial thrombolysis with urokinase, intracerebral haemorrhages occurred in 7% and puncture site complications in 3% [1]. Therefore, low dose local rt-PA treatment is of special interest since systemic thrombolytic effects and local bleeding complications at the arterial puncture site of catheterization are potential adverse events of higher systemic doses. Accordingly, despite the poor prognosis reported for these patients in the literature [4], our patient achieved appropriate reperfusion in the occluded intracranial carotid artery bifurcation with clinical re-

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solution of symptoms when given the lowest possible rt-PA dose. Cerebral ischaemia caused by thromboembolism is a rare but severe and life-threatening complication

of cardiac catheterization. Its severely disabling consequences can, however, often be prevented by an emergency thrombolytic approach according to a standardized management algorithm (Fig. 6).

References
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