Stroke after cardiac catheterization

INTRODUCTION — Stroke resulting from cardiac catheterization is relatively common due to the high volume of cardiac procedures performed worldwide. This topic will review periprocedural stroke in the setting of cardiac catheterization, which includes diagnostic and interventional procedures. Other aspects of acute stroke are discussed elsewhere. (See "Initial assessment and management of acute stroke" and "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use".)

MECHANISMS — Patients may experience either ischemic or hemorrhagic stroke in the setting of cardiac catheterization.

Ischemic stroke — In most cases, the mechanism of ischemic stroke is directly related to cardiac catheterization itself, which initially involves advancing catheters over wires into the aorta, generally using either transfemoral or transradial access. Catheter or wire manipulation may dislodge debris made up of thrombus, calcific material, or cholesterol particles from atherosclerotic plaques within the aortic arch and the proximal carotid and vertebral arteries [1-4]. In addition, fresh thrombus material may form at the catheter and guidewire tips. Most cases of ischemic stroke related to cardiac catheterization are caused by such thromboemboli. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

The mechanism of ischemic stroke is similar between diagnostic and interventional procedures. However, interventional catheters are on average larger than diagnostic catheters and the procedures are often longer and thus there may be a theoretical increase in risk.

Ultimately, one or more catheters end up in one of the cardiac chambers or in the coronary arteries. Catheterization across a degenerated aortic valve may lead to thromboembolism and the risk of stroke may be particularly high in patients with significant valvular aortic stenosis (AS) who undergo retrograde catheterization of the aortic valve [5,6]. This was demonstrated in a study of 152 patients with AS (mean age 71 years) who were randomly assigned to cardiac catheterization with or without catheter passage through the valve [5]. The following findings were noted:

●Brain magnetic resonance imaging (MRI) obtained before and after the catheterization demonstrated focal lesions consistent with cerebral emboli in 22 percent of those who underwent retrograde catheterization of the aortic valve, but in none of the patients who did not.

●Detailed neurologic examination done before and after the catheterization demonstrated clinically apparent deficits in 3 percent of those who underwent retrograde catheterization, but in none of the other patients.

As a result, catheterization across a degenerated aortic valve should be performed with caution in patients with severe calcific AS and only when the information sought cannot be reliably obtained noninvasively [6].

Less common causes of ischemic stroke related to cardiac catheterization include air embolism, thromboembolism from clot in the left ventricle, periprocedural hypotension, arterial dissection, and fractured guidewire [7,8].

Hemorrhagic stroke — Patients having cardiac catheterization are at increased risk for hemorrhagic stroke because of acquired hemostatic abnormalities induced by thrombolytic, anticoagulant, and/or antiplatelet regimens used in the periprocedural time period [9]. (See "Periprocedural complications of percutaneous coronary intervention", section on 'Anticoagulation-associated bleeding'.)

INCIDENCE

Ischemic and hemorrhagic stroke — Mainly retrospective data suggest that stroke (within 36 hours) occurs at a rate of 0.1 to 0.6 percent in patients undergoing diagnostic cardiac catheterization [10-13]. The higher estimate (0.6 percent) comes from a meta-analysis of studies that performed systematic neurologic evaluation and brain magnetic resonance imaging (MRI) [13]. Among those undergoing percutaneous coronary (artery) intervention (PCI), the rate ranges from 0.07 to 0.96 percent [12,14-20].

Hemorrhagic stroke, most often intracerebral hemorrhage, has accounted for 8 to 46 percent of stroke related to cardiac catheterization in the few registries that distinguish between ischemic and hemorrhagic stroke types [9,12,15,18,19,21]. Subarachnoid hemorrhage following cardiac catheterization is probably uncommon if not rare, with only a few cases reported in the literature [9,22]. However, most studies of invasive cardiac procedures reporting the incidence of intracranial hemorrhage do not distinguish intracerebral hemorrhage from subarachnoid hemorrhage. The risk of hemorrhagic stroke is probably increased for patients undergoing acute coronary interventions because of the intense antithrombotic regimens that are used [9,23].

Compared with procedures on the coronary arteries, the incidence of periprocedural stroke is somewhat higher after aortic valvuloplasty or radiofrequency catheter ablation for atrial fibrillation. (See "Atrial fibrillation: Catheter ablation", section on 'Periprocedural embolic events' and "Transcatheter aortic valve implantation: Complications", section on 'Stroke and subclinical brain injury'.)

Asymptomatic embolism — Asymptomatic cerebral embolism is much more common than clinically manifest stroke, as illustrated by the findings of a 2017 systematic review and meta-analysis of studies reporting brain infarcts on diffusion-weighted MRI in patients undergoing cardiac procedures [13]. All included studies performed neurologic examinations and brain MRI both pre-and post-procedure. Among 833 patients who had diagnostic cardiac catheterization, the incidence of asymptomatic (silent) radiographic brain infarcts was 8 percent (95% CI 4.1-12), while the incidence of clinically symptomatic events (ischemic stroke and transient ischemic attack) was 0.6 percent (95% CI 0.1-1.1).

Transcranial Doppler ultrasonography studies reveal an even higher prevalence (up to 100 percent) of microemboli during cardiac catheterization procedures [24-27]. The majority of these microemboli occur during contrast injection, while a smaller number are observed with movement of the catheter/guide wire. Most of the signals that are seen with injection of solutions have profiles consistent with gaseous origin (eg, air bubbles) and are thought to be of no clinical consequence, whereas the microembolic signals that occur during catheter and guide wire manipulation have signal profiles consistent with particulate origin (eg, atheromatous debris), and could result in transient or persistent ischemic brain injury. Nevertheless, most patients are asymptomatic. These observations suggest that catheter manipulation in the diseased aortic root releases small pieces of atherosclerotic debris more commonly than suspected, based upon the low incidence of clinically apparent stroke. (See 'Mechanisms' above.)

RISK FACTORS — Patient-related risk factors for stroke with cardiac catheterization and PCI include the following [3,9,10,12,15,17,18,20,21,28-30]:

●Older age (>75 to 80 years)

●Hypertension

●Diabetes mellitus

●History of stroke

●Kidney failure

●Heart failure

●Severe coronary artery atherosclerotic disease, including the presence of triple vessel disease

●Coronary artery thrombus

●Carotid artery disease

Procedural risk factors for stroke include the following [5,9,10,12,15,17,18,20,21,29-31]:

●Emergency procedure, including acute coronary syndrome

●Longer procedure time

●Greater contrast use

●Retrograde catheterization of the left ventricle in patients with aortic stenosis

●Interventions at bypass grafts

●Use of an intra-aortic balloon pump

Additional risk factors for hemorrhagic stroke include the use of anticoagulation or thrombolytic agents for acute myocardial infarction, age ≥75 years, female sex, systolic blood pressure ≥160 mmHg, Black race, and low body weight (table 1) [32].

PREVENTION — Meticulous attention to technical factors such as wire and catheter exchanges is mandatory in all patients, regardless of risk factors. (See "Complications of diagnostic cardiac catheterization".)

For patients undergoing percutaneous coronary intervention, there is some evidence that radial artery catheterization may be associated with a lower risk of stroke compared with femoral artery catheterization. This evidence is reviewed elsewhere. (See "Periprocedural complications of percutaneous coronary intervention", section on 'Radial artery access' and "Percutaneous arterial access techniques for diagnostic or interventional procedures", section on 'Radial artery'.)

CLINICAL PRESENTATION — Most strokes related to cardiac catheterization present during the procedure or within the first 24 hours after the procedure [21,33].

Frequent manifestations of ischemic stroke and intracerebral hemorrhage include visual disturbance, aphasia, dysarthria, hemiparesis, and altered mental status. In contrast, subarachnoid hemorrhage usually presents with headache and global neurologic deficits, mainly altered level of consciousness. A maximal deficit at onset or a fluctuating course suggest ischemic stroke, while gradual worsening of neurologic deficits over minutes to hours and signs of elevated intracranial pressure suggest hemorrhage. However, clinical features alone do not reliably distinguish brain ischemia from hemorrhage, necessitating neuroimaging.

The symptoms and signs of acute ischemic stroke often correspond to recognized stroke syndromes with focal neurologic deficits attributable to ischemia within a vascular territory affecting the cerebral cortex (eg, aphasia and left hemiparesis related to embolic occlusion within the left middle cerebral artery territory), brainstem, or cerebellum. (See "Clinical diagnosis of stroke subtypes".) Monocular visual loss may be caused by retinal embolism [34,35]. Some data suggest that a disproportionate number of ischemic strokes related to cardiac catheterization affect the vertebrobasilar circulation [29,36,37], but other reports suggest that the rate of posterior circulation ischemic stroke is close to 20 percent [15], as might be expected given the percentage of blood that the posterior circulation supplies to the brain. In addition to focal deficits, a nonfocal presentation of ischemic stroke with reduced alertness and encephalopathy can occur because of diffuse bilateral cerebral embolization.

EVALUATION AND DIAGNOSIS — The evaluation of the patient who is undergoing or who has recently undergone cardiac catheterization and who is suspected of an acute stroke is presented briefly here. Acute stroke evaluation is discussed in detail separately. (See "Initial assessment and management of acute stroke".)

Important aspects of the evaluation of any patient with periprocedural neurologic deterioration suggestive of stroke include:

●Rapid activation of the stroke team.

●Stabilization of airway, breathing, and circulation.

●Checking serum glucose, as symptoms of hypoglycemia may mimic stroke; low serum glucose (<60 mg/dL [<3.3 mmol/L]) should be corrected rapidly.

●Platelet count and coagulation studies if there is suspicion for thrombocytopenia or coagulopathy.

●Determining symptom onset time or the last time the patient was known to be neurologically normal. In a sedated patient, this time would be when the patient was last alert enough to be assessed.

●A focused history and examination will help in the development of a differential diagnosis.

●Emergency brain imaging with noncontrast computed tomography (CT) or magnetic resonance imaging (MRI), and concurrent neurovascular imaging with CT angiogram or magnetic resonance (MR) angiogram.

●CT or MR perfusion imaging, if the clinical diagnosis of stroke is uncertain (eg, high suspicion for a seizure with a postictal state and no arterial occlusion visualized on CT angiogram). However, caution should be taken not to delay stroke treatment (if indicated) in order to obtain additional tests, weighing the risk of treating a mimic with intravenous thrombolysis with the benefit of more rapid treatment. Perfusion studies or MRI may also be useful in patients with unknown time of onset or more than 4.5 hours from last known well.

We recommend brain imaging with CT or MRI to rule out hemorrhage as a standard approach. In contrast, some experts have advocated immediate angiography followed by intra-arterial thrombolysis rather than obtaining a head CT or MRI after an acute stroke from cardiac catheterization, because the time needed for brain imaging may significantly delay treatment of a vessel occlusion [38]. However, this approach would require a high level of confidence that intracranial hemorrhage is not causing the stroke symptoms, that any identified vessel occlusion is acute and responsible for the symptoms, and that the risk of hemorrhagic transformation of the acute ischemic stroke is low (eg, the diagnostic procedure was done without the use of full-dose anticoagulation and/or glycoprotein IIb/IIIa inhibitors).

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of acute stroke after cardiac catheterization includes seizure, migraine, encephalopathy, and toxic-metabolic disturbances such as hypoglycemia. In some cases, the recognition of stroke deficits can be confounded by altered mentation caused by sedative medications used for the procedure or by comorbid medical or neurologic conditions.

●Transient cortical blindness – An additional but rare consideration in the periprocedural period is that of contrast-induced transient cortical blindness [39-42], which can occur with ionic and nonionic contrast media. Onset is seen within minutes to hours after the procedure, typically beginning with blurred vision that rapidly progresses to complete blindness, usually associated with headache. Additional symptoms may include vomiting, confusion, aphasia, memory impairment, and limb weakness or ataxia. On head computed tomography (CT) performed without additional contrast, there is often enhancement from contrast administered during cardiac catheterization affecting the cortex, particularly the parieto-occipital lobes, as well as the deep gray structures, brainstem, and/or cerebellum. Symmetrical white matter edema in the posterior cerebral hemispheres is another frequent finding. In one affected patient evaluated with brain magnetic resonance imaging (MRI), hyperintense signal on T2-weighted sequences was seen in the occipital lobes, thalami, and cerebellum [41].

In nearly all cases, the neurologic impairments and neuroimaging abnormalities gradually resolve over days. Although the mechanism is uncertain, a transient vasculopathy with disruption of the blood-brain barrier is postulated, suggesting that this is a form of posterior reversible encephalopathy syndrome (PRES), also called reversible posterior leukoencephalopathy syndrome [40,43,44]. (See "Reversible posterior leukoencephalopathy syndrome".)

●Contrast extravasation – In addition to being associated with the signs and symptoms described above, extravasation of contrast after coronary angiography can sometimes radiographically mimic the appearance of subarachnoid hemorrhage [45] and intracerebral hemorrhage [46] on noncontrast head CT scan. When in doubt, an acute MRI may be helpful to distinguish contrast from intracerebral hemorrhage.

●Bilateral occipital lobe infarction – Although visual loss after cardiac catheterization has usually been related to contrast, and therefore reversible, bilateral occipital lobe infarction may present in a similar manner and must be considered [47].

ISCHEMIC STROKE TREATMENT — Treatment of acute ischemic stroke is dependent on the time elapsed from stroke onset, which is considered to be the time the patient was last known well. The standard management of acute ischemic stroke is discussed in greater detail separately. (See "Initial assessment and management of acute stroke".)

Intravenous thrombolysis — For eligible patients (table 2) with acute ischemic stroke related to cardiac catheterization, we suggest intravenous thrombolytic therapy, provided that treatment is initiated within 4.5 hours of the time last known well; we consider treatment beyond 4.5 hours (algorithm 1) for selected patients based on advanced imaging (those with an ischemic brain lesion on magnetic resonance imaging [MRI] diffusion-weighted imaging but no corresponding hyperintensity on fluid-attenuated inversion recovery [FLAIR], an imaging mismatch that correlates with a stroke onset time of 4.5 hours or less). Intravenous thrombolysis is discussed in greater detail elsewhere, including the management of blood pressure before and during intravenous thrombolysis administration (table 3). (See "Approach to reperfusion therapy for acute ischemic stroke" and "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use".)

●Risk of bleeding – The risk of bleeding with intravenous thrombolytic therapy is relatively high in these patients compared with the broad population of patients with ischemic stroke if aggressive antithrombotic therapy was used during the procedure. There is the potential to worsen groin site complications resulting from the catheterization access procedure; these risks are typically manageable, as demonstrated by trials of catheter-based thrombectomy after intravenous thrombolysis for stroke. However, the exception is suspected retroperitoneal hemorrhage, based on unexplained hypotension or back pain with or without ecchymosis, which would be an absolute contraindication [48]. The benefits and risks of intravenous thrombolytic therapy after cardiac catheterization need to be weighed carefully in potential candidates, considering any unique risks in each case (eg, concern for retroperitoneal hemorrhage as a complication of cardiac catheterization).

An issue of particular importance to the treatment of patients in the peri- or post-catheterization setting is the use of anticoagulants and antiplatelet agents:

•A normal aPTT should be documented prior to administration of intravenous thrombolysis for ischemic stroke if heparin was administered within 48 hours. Protamine sulfate can be used to reverse the effect of heparin in the setting of hemorrhagic stroke. (See 'Hemorrhagic stroke treatment' below.)

For patients with a prolonged aPTT, mechanical thrombectomy is the preferred treatment option for eligible patients [49].

•The degree to which glycoprotein IIb/IIIa inhibitor therapy may increase the risk of hemorrhagic complications with intravenous thrombolysis for ischemic stroke is unknown, although preliminary data suggest safety [50-52]. Endovascular interventions are the preferred treatment option in this setting as well.

•Single or dual antiplatelet therapy is not a contraindication to intravenous thrombolysis.

●Clot composition – Stroke caused by embolization of fresh thrombus forming on the catheter or guidewire would seem to be ideally suited to thrombolytic treatment. However, theoretical concerns about the utility of thrombolytic therapy for ischemic stroke after cardiac catheterization are based upon the possible composition of some other types of thrombi causing stroke in this setting [53]. For example, dislodged debris from aortic atherosclerotic plaque might consist primarily of calcific material, which may not be responsive to thrombolysis. Alternatively, calcific thrombus might undergo partial lysis leading to distal migration of calcific fragments [54]. In addition, air embolism and metallic fragments would be impervious to thrombolytic agents.

●Efficacy – Despite concerns about bleeding and clot composition, data from a retrospective, multicenter, observational study evaluating ischemic stroke after cardiac catheterization suggest that intravenous thrombolysis is safe and efficacious in this setting [53]. Among 66 consecutive cases of ischemic stroke after cardiac catheterization, 12 patients were treated acutely with thrombolysis (7 with intravenous 5 with intra-arterial recombinant tissue plasminogen activator), while 54 received no thrombolysis. Patient demographics (age, medical comorbidities, and cardiac procedure characteristics) were similar between the thrombolysis and no thrombolysis groups. Eleven of these 12 treated patients had received periprocedural heparin, and two of the seven who received intravenous thrombolysis had prolonged activated partial thromboplastin time (aPTT). The following observations were made [53]:

•There was a significant improvement in stroke symptoms by predefined end points in patients who received thrombolysis compared with those who did not, including change in the National Institutes of Health Stroke Scale (NIHSS) score from baseline to 24 hours (-6 versus 0) and change in NIHSS score from baseline to seven days (-6.5 versus -1.5).

•There were no significant differences between groups in mortality or bleeding events, including symptomatic intracranial hemorrhage, hemopericardium, and other systemic bleeding causing hemodynamic instability or requiring transfusions.

Additional case reports and case series, while potentially limited by publication bias, also suggest reasonable safety and efficacy of thrombolysis for patients with acute ischemic stroke related to cardiac catheterization [36,55-61].

Mechanical thrombectomy — Patients with acute ischemic stroke caused by a large vessel occlusion may be eligible for mechanical thrombectomy if they can be treated within 24 hours of the time they were last known to be well (algorithm 2), irrespective of whether the patient was treated with intravenous thrombolysis. Details of mechanical thrombectomy for acute ischemic stroke are reviewed separately. (See "Mechanical thrombectomy for acute ischemic stroke".)

Rapid treatment — Regardless of reperfusion therapy modality, it is imperative to minimize the time to treatment. Longer times to reperfusion translate to lower likelihoods of good clinical outcome.

HEMORRHAGIC STROKE TREATMENT — For patients with hemorrhagic stroke (ie, intracerebral hemorrhage or subarachnoid hemorrhage), urgent management issues involve reversal of anticoagulation when feasible, blood pressure control, and treatment of elevated intracranial pressure. The management following cardiac catheterization follows the same principles as the management of hemorrhagic stroke in other settings. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis" and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Nonaneurysmal subarachnoid hemorrhage", section on 'Management and prognosis'.)

All anticoagulant and antiplatelet drugs should be discontinued acutely and should not be used until cessation of bleeding is documented by neuroimaging (and possibly longer depending on risk-benefit profile).

●Anticoagulant reversal – Anticoagulant effect should typically be reversed immediately with appropriate agents, while considering the potential for risk (metal heart valve and other higher hypercoagulability risk) versus benefit (early, small bleed that may be prevented from devastating expansion).

•For patients with unfractionated heparin-associated intracerebral hemorrhage, protamine sulfate is recommended for urgent treatment. Protamine sulfate can be administered by slow intravenous infusion (not greater than 20 mg/min and no more than 50 mg over any 10-minute period). The appropriate dose of protamine sulfate depends on the dose of heparin given and the time elapsed since that dose. For patients with low-molecular weight (LMW) heparin-associated intracranial bleeding, andexanet alfa or protamine sulfate can be used for anticoagulant reversal. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Unfractionated heparin' and "Reversal of anticoagulation in intracranial hemorrhage", section on 'LMW heparin' and "Heparin and LMW heparin: Dosing and adverse effects", section on 'Reversal'.)

•For patients taking warfarin, aggressive and rapid use of intravenous vitamin K, unactivated prothrombin complex concentrate (PCC), and other factors may be necessary. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Warfarin'.)

•Antidotes to oral factor Xa and direct thrombin inhibitors are discussed elsewhere. (See "Management of bleeding in patients receiving direct oral anticoagulants", section on 'Dabigatran reversal' and "Management of bleeding in patients receiving direct oral anticoagulants", section on 'Factor Xa inhibitors' and "Reversal of anticoagulation in intracranial hemorrhage", section on 'Reversal strategy for specific anticoagulants'.)

●Blood pressure control – Severe elevations in blood pressure may worsen intracerebral hemorrhage (ICH). Labetalol, nicardipine, esmolol, enalapril, hydralazine, nitroprusside, and nitroglycerin are useful intravenous agents for controlling blood pressure. Specific recommendations for managing elevated blood pressure in patients with acute intracerebral hemorrhage are reviewed in detail separately. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Blood pressure management'.)

●Elevated ICP – Initial management of elevated intracranial pressure (ICP) includes elevating the head of the bed to 30 degrees and use of analgesia and sedation. Suggested intravenous agents for sedation are propofol, etomidate, or midazolam. Suggested agents for analgesia and antitussive effect are morphine or alfentanil.

More aggressive therapies for reducing elevated ICP include osmotic diuretics (eg, mannitol), ventricular catheter drainage of cerebrospinal fluid, neuromuscular blockade, and hyperventilation. We suggest continuous monitoring of ICP and arterial blood pressure when using these aggressive therapies, with the goal of maintaining cerebral perfusion pressure above 70 mmHg. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Intracranial pressure management'.)

●Need for surgical intervention – For patients with a cerebellar hemorrhage >3 cm in diameter with clinical deterioration, brainstem compression, and/or hydrocephalus due to ventricular obstruction, we recommend surgical evacuation of hemorrhage. Surgery for supratentorial ICH is controversial; standard craniotomy might be considered only for those who have lobar clots within 1 cm of the surface. The routine evacuation of supratentorial ICH in the first 96 hours is not recommended. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Blood pressure management'.)

SUPPORTIVE CARE — Important acute stroke management issues, some already mentioned above, include the following:

●Assessing swallowing and preventing aspiration. (See "Initial assessment and management of acute stroke", section on 'Swallowing assessment' and "Complications of stroke: An overview", section on 'Dysphagia'.)

●Optimizing head of bed position; for patients in the acute phase of stroke who are at risk for elevated intracranial pressure, aspiration, cardiopulmonary decompensation, or oxygen desaturation, we suggest keeping the head in neutral alignment with the body and elevating the head of the bed to 30 degrees; for patients in the acute phase of stroke who are not at risk for elevated intracranial pressure, aspiration, or worsening cardiopulmonary status, we suggest keeping the head of bed flat (0 to 15 degree head-of-bed position). (See "Initial assessment and management of acute stroke", section on 'Head and body position'.)

●Managing blood pressure:

•For patients with acute ischemic stroke who will receive thrombolytic therapy or mechanical thrombectomy, antihypertensive treatment is recommended so that systolic blood pressure is ≤180 mmHg and diastolic blood pressure is ≤105 mmHg during and after treatment (table 3). This issue is discussed in detail separately. (See "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use", section on 'Management of blood pressure'.)

•For patients with acute ischemic stroke who are not treated with thrombolytic therapy, we suggest treating high blood pressure only if the hypertension is extreme (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg), or if the patient has another clear indication (active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, acute kidney failure, or preeclampsia/eclampsia). When treatment is indicated, we suggest cautious lowering of blood pressure by approximately 15 percent during the first 24 hours after stroke onset. (See "Initial assessment and management of acute stroke", section on 'Blood pressure goals in ischemic stroke'.)

•In both ICH and subarachnoid hemorrhage (SAH), the approach to blood pressure lowering must account for the potential benefits (eg, reducing further bleeding) and risks (eg, reducing cerebral perfusion). Recommendations for blood pressure management in acute ICH and SAH are discussed in detail separately. (See "Initial assessment and management of acute stroke", section on 'Blood pressure in acute hemorrhagic stroke' and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Blood pressure management' and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Blood pressure control'.)

●Treating hypoglycemia and hyperglycemia. (See "Initial assessment and management of acute stroke", section on 'Hypoglycemia' and "Initial assessment and management of acute stroke", section on 'Hyperglycemia'.)

●Evaluating and treating the source of any fever; for patients with acute stroke, we suggest maintaining normothermia for at least the first several days after an acute stroke. (See "Initial assessment and management of acute stroke", section on 'Fever'.)

●Preventing deep venous thrombosis and pulmonary embolism. (See "Prevention and treatment of venous thromboembolism in patients with acute stroke", section on 'Approach to VTE prevention'.)

PROGNOSIS — Stroke after cardiac catheterization is associated with a high in-hospital and 30-day mortality rate [10,15,17-19,21]. In the largest of these studies, the 30-day mortality rate after percutaneous coronary interventions was 19 percent for patients who experienced an ischemic stroke and 50 percent for those who had a hemorrhagic stroke, versus 2 percent in those without stroke [19]. Few data are available for long-term outcomes among survivors, but among 69 patients with stroke or transient ischemic attack who survived hospitalization in one report, transfers to inpatient rehabilitation, nursing home, or assisted living made up 31 percent of discharges [21]. The high morbidity and mortality associated with these strokes justifies aggressive preventive strategies during the catheterization procedure (see "Complications of diagnostic cardiac catheterization", section on 'Atheroembolism') and aggressive, rapid treatment strategies when the stroke occurs. (See 'Ischemic stroke treatment' above and 'Hemorrhagic stroke treatment' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".)

SUMMARY AND RECOMMENDATIONS

●Stroke types and incidence – Diagnostic and interventional cardiac catheterization may lead to either ischemic or hemorrhagic stroke. The overall incidence of clinically apparent stroke during or after cardiac catheterization is well under 1 percent in most studies, but may be higher with certain interventional procedures, particularly with aortic valvuloplasty. (See 'Mechanisms' above and 'Incidence' above.)

●Manifestations – Most strokes related to cardiac catheterization present during the procedure or within the first 24 hours after the procedure. Frequent manifestations of ischemic stroke and intracerebral hemorrhage (ICH) include visual disturbance, aphasia, dysarthria, hemiparesis, and altered mental status. (See 'Clinical presentation' above.)

●Evaluation – Important aspects of the management of any patient with periprocedural neurologic deterioration suggestive of stroke include stabilization of airway, breathing, and circulation; stroke team activation; urgent brain and neurovascular imaging; determination of time last known well; and laboratory tests such as serum glucose and measures of hemostasis. (See 'Evaluation and diagnosis' above.)

●Differential – The differential diagnosis of acute stroke includes transient ischemic attack, seizure, migraine, encephalopathy, and other conditions such as hypoglycemia. An additional consideration in the periprocedural period is that of contrast-induced transient cortical blindness. (See 'Differential diagnosis' above.)

●Ischemic stroke treatment – For eligible patients with ischemic stroke who can be treated within 4.5 hours of time last known well, and selected patients with unknown time of onset and favorable imaging (algorithm 1), we suggest intravenous thrombolytic therapy (table 2) (Grade 2C). Compared with intravenous thrombolysis for acute ischemic stroke in the general population, intravenous thrombolysis after cardiac catheterization may have an increased bleeding risk and lower efficacy, as discussed above. (See 'Ischemic stroke treatment' above and "Approach to reperfusion therapy for acute ischemic stroke" and "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use".)

Patients with acute ischemic stroke caused by a large artery occlusion who can be treated within 24 hours of the time they were last known to be at their neurologic baseline should be evaluated for mechanical thrombectomy (algorithm 2), irrespective of whether the patient was treated with intravenous thrombolysis. Details of mechanical thrombectomy for acute ischemic stroke are reviewed separately. (See "Mechanical thrombectomy for acute ischemic stroke".)

●Hemorrhagic stroke treatment – For patients with ICH or SAH, urgent management issues involve reversal of anticoagulation, blood pressure control, and treatment of elevated intracranial pressure. (See 'Hemorrhagic stroke treatment' above.)

●Prognosis – Stroke after cardiac catheterization is associated with a high morbidity and mortality rate. (See 'Prognosis' above.)