Stroke Complicating Cardiac Catheterization — A Preventable and Treatable Complication

Stroke Complicating Cardiac Catheterization — A Preventable and Treatable Complication
Stroke Complicating Cardiac Catheterization — A Preventable and Treatable Complication
Author(s): 

Rajiv Sankaranarayanan, MBBS MRCP(UK), Adel Msairi, MB BCh MRCP(UK), Gershan K. Davis, MBBS, MD, FRACP, FRCP, FACC, FESC

Incidence
Coronary angiography has been and currently remains the gold standard for the diagnosis of coronary artery disease. It is an invasive procedure and is thus associated with various risks such as vascular and hemodynamic complications, contrast reaction, arrhythmias, myocardial infarction, stroke and death.1
Cardiac catheterization-related stroke has an incidence of 0.03% to 0.3% for diagnostic procedures2–4 and 0.3–0.4% for percutaneous coronary intervention (PCI).5,6 In patients undergoing percutaneous interventions, stiff, large-bore guiding catheters are used. These design characteristics can be more traumatic to the aorta than diagnostic catheters, which are more flexible and have smaller lumens and tapered tips.

Causes of and Predisposing Factors for Stroke
Patients with ischemic coronary artery disease often have generalized atherosclerosis. The use of guidewires and catheters may, therefore, cause fragmentation of atherosclerotic plaques with subsequent embolization.3,5,7,8 Other causes include air or cholesterol embolism and thrombus formation at the catheter tip.9,10
Some patient characteristics have been shown to increase the risk of a stroke due to cardiac catheterization. These include female gender, left ventricular hypertrophy,2 hypertension, diabetes mellitus, renal insufficiency and previous stroke.2,3,5,6,8 Large atherosclerotic burden, such as in those patients with advanced coronary artery disease, prior coronary artery bypass grafting (CABG), or extensive plaque on transesophageal echocardiography2,4 may also increase risk. Depressed ejection fraction has also been shown to increase risk, possibly by dislodgement of apical thrombus during left ventriculography.2 These patients should therefore be identified prior to the cardiac catheterization procedure as high risk for cerebrovascular complications.
The procedure, equipment used and operative technique can also have an impact on the risk of stroke. Two recognized procedural risk features are longer fluoroscopic time3 and the use of larger-caliber catheters.11 Judkins left and Multipurpose guiding catheters have been shown to more frequently dislodge atheromatous debris from the aorta than other catheters. This is possibly because they are more traumatic to the aorta due to their long second-curve design. The use of smaller guiding catheters is recommended to avoid the risk of vascular embolization.11 Efforts should be made, especially in high-risk patients, to avoid prolonged fluoroscopy and to use catheters less likely to dislodge thrombi. Prolonged fluoroscopy may be a reflection of more complex or difficult procedures with the use of more interventional equipment.
Microemboli have been frequently detected during invasive cardiovascular procedures.12,13 Solid microemboli are most likely due to mechanical fragmentation of atherosclerotic plaques or clots from the tip of the catheter. Gaseous emboli are usually caused by the entry of microbubbles during the injection of contrast and saline. While the majority (92%) of microemboli are gaseous, solid emboli have been more associated with cerebral injury.14 It has been shown, however, that larger volumes of intra-arterial air may also disturb brain metabolism.12
Vascular access through the radial artery instead of the femoral artery is being used increasingly for cardiac catheterization. The transradial approach gives rise to a higher number of solid cerebral microemboli than transfemoral catheterization, but there is no evidence showing whether these lead to cerebrovascular symptoms.14 When introduced from the right arm, the guidewire has to pass the apertures of the right vertebral and the right common carotid arteries. The guidewire may, at least in some cases, cause some mechanical force upon atherosclerotic plaques located near these apertures. Solid emboli generated during guidewire advancement from the femoral artery will be carried in the bloodstream to the abdominal viscera or the lower limbs. One study has shown that none of the patients who underwent brachial catheterization had an embolic event compared to 17% of patients who underwent femoral catheterization.7 The influence of the route of access on symptomatic embolization during coronary angiography has not been definitively established. Cerebral microemboli are predominantly detected during catheter advancement, catheter flushing, contrast injection and ventriculography.14 There is also a significant correlation between the number of microemboli and the volume of contrast used.14
Various studies have tried to estimate the significance of atherosclerotic aortic debris on cardiac catheterization. Atherosclerotic plaques of the thoracic aorta, as detected by transesophageal echocardiography, are a common finding in patients with coronary artery disease.15 These patients are at increased risk for catheter-related stroke or peripheral embolism, particularly in the presence of mobile atherosclerotic debris.7 The strongest clinical predictors of atherosclerotic aortic debris are advanced age and peripheral vascular disease.7 Karalis et al7 recommended the brachial approach instead of transfemoral cardiac caheterization in patients with mobile aortic plaque in order to prevent stroke or peripheral embolization.
In summary, patients at risk for cerebrovascular complications of cardiac catheterization should be identified in advance. It also merits consideration whether transesophageal echocardiography should be used to identify at-risk patients who have mobile atherosclerotic plaques. Once these patients are identified, further measures should be undertaken to ensure that they are well hydrated prior to the procedure, as well as adopting techniques during the catheterization itself to minimize the chances of a stroke occurring. These include the use of atraumatic catheters, avoiding prolonged fluoroscopy time and not performing ventriculography if possible, especially if echocardiographic information is available.

Clinical Features
Pericoronary angiography strokes often occur during or immediately after the procedure when the femoral artery sheath is still in place,9 but the diagnosis can be delayed up to 36 hours in some cases.3 Common symptoms include visual disturbance, motor weakness, aphasia and altered mental status. There is vertebrobasilar involvement in almost half of the cases.2,3,5,6 Asymptomatic cerebral infarction following cardiac catheterization has been shown to occur in about 15% of patients.16
A 37-month study2 of about 6,500 patients who underwent invasive cardiac procedures such as left heart catheterization, balloon angioplasty and valvuloplasty, had an overall 0.4% incidence of neurological complications. The most common symptoms were visual disturbances (26%), hemiparesis (26%) and facial droop (26%). Deficits were localizable to the posterior circulation in 36% of patients and anterior in 64%. Al-Mubarak et al showed that most of the embolic strokes during catheterization procedures are associated with an embolus located in either the common carotid bifurcation or the proximal middle cerebral artery.17 In a recent 1-year study of pericoronary angiography strokes,10 the occluded vessel was the middle cerebral artery (MCA) in 24% of patients, the posterior cerebral artery in 19%, the basilar artery in 5%, the vertebral artery in 10% and occlusion in 2 anterior circulation branches (MCA, anterior cerebral artery, or both) in 43% patients. In another study of strokes complicating 20,900 cardiac catheterization procedures, the posterior circulation was affected in 21 of the 39 infarcts.3
The majority of patients who had a stroke following cardiac catheterization had an unfavorable outcome with a Rankin score of 3–6, i.e., moderate disability to coma, with a high inpatient mortality rate.3 The Rankin score is a measure of post-stroke handicap. Patients with large-vessel strokes tended to do worse.3

Investigations
Computed tomography (CT) or magnetic resonance imaging (MRI), or both, have been performed in various studies investigating stroke post-cardiac catheterization. The contrast resolution of MRI is significantly higher than CT, making it far more sensitive than CT, especially in early cerebral ischemia.18 Diffusion-weighted (DWI) MRI is very sensitive for detecting cerebral ischemia within minutes after its onset, far exceeding any other imaging method available today.19 Studies using this imaging modality have shown that new cerebral lesions may be detected immediately after catheterization of stenotic aortic valves and CABG.20 Omran et al20 also found, after catheterization of stenotic aortic valves, that every acute cerebral DWI lesion was still present as a similar low-intensity lesion on conventional MRI sequences 3 months later. This strongly suggests that they represented irreversible ischemic injury. DWI with MRI has also shown multiple acute lesions (often tiny, cortical and in different vascular territories) distinct from the symptomatic lesion. This is consistent with a shower of embolic material.3 CT is still the most widely-used imaging option mainly to rule out hemorrhagic stroke. Transcranial Doppler (TCD) is also an established noninvasive method which can be used to detect cerebral microemboli.21 If the femoral sheath is still in place, however, cerebral angiography is a quicker and more sensitive investigative modality.
Diagnostic cerebral angiography in patients with acute stroke can better define the thrombus morphology, degree of occlusion by the offending thrombus and presence or absence of collateral pathways.22 This investigation requires involvement of an interventional neuroradiologist. It may become necessary for cardiologists to develop this skill, in view of the fact that many cardiac centers do not have access to an interventional neuroradiologist. The degree of vessel occlusion has been classified by using the thrombolysis in myocardial infarction (TIMI) score. TIMI 0 is complete occlusion, TIMI 1 is contrast material passage through the clot with minimal perfusion, TIMI 2 is partial flow and/or recanalization, and TIMI 3 is complete flow and/or recanalization.23 A “TICI score” in stroke studies specifies “cerebral” rather than “myocardial” perfusion with corresponding grade definitions. Although cerebral angiography carries a finite risk of complications due to the procedure itself, the relative risk is considered to be low in the setting of acute stroke.24


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