Coronary angiography and cardiac catheterization have become the gold standard for the diagnosis and management of coronary artery disease. Acute ischemic stroke during or after cardiac catheterization or percutaneous cardiac intervention (PCI) is a rare but catastrophic complication with significant morbidity and mortality.1 Stroke occurs in 0.05-0.10% of diagnostic catheterizations and in 0.18-0.44% of patients undergoing PCI.2 These risks are higher when coronary interventions are performed on an emergent basis.
In another large, retrospective study that evaluated 47,000 patients undergoing PCI, stroke was seen in 0.40% of the total population, of which 0.30% of patients had an elective PCI and 0.60% of patients had an emergent PCI for acute coronary syndrome.3 The procedure, equipment used, and operative technique can also have impact on the risk of stroke. Procedural risk features such as the use of larger caliber catheters and longer fluoroscopic time can also increase risk of stroke. For emergent cardiac catheterization, the procedure time is often of longer duration, greater contrast is used, and aggressive anticoagulation is used. The risk of stroke during coronary intervention is also increased due to conditions associated with significant hemodynamic compromise such as the presence of coronary artery thrombus, use of intra-aortic balloon pump, interventions of previous bypass grafts, and retrograde catheterization of the left ventricle in patients with aortic stenosis.4,5 Stroke is frequently associated with comorbidities such as hypertension, diabetes mellitus, heart disease, renal failure, and advanced age. Previously, high risk patients with severe comorbidities were excluded from cardiac catheterization and PCI, whereas now these patients routinely undergo such procedures. Here, we present a case report where a patient developed an acute ischemic stroke while undergoing cardiac catheterization for an abnormal pharmacological stress test, after presenting with substernal chest pain.
A 66-year-old Caucasian male with a past medical history of coronary artery disease, status post coronary artery bypass for multivessel disease, peripheral arterial disease, status post bilateral stents of common iliac arteries, chronic diastolic congestive heart failure, insulin-dependent diabetes mellitus, hypertension, hyperlipidemia, chronic obstructive pulmonary disease, obstructive sleep apnea, depression, and tobacco abuse was admitted to community hospital for evaluation of substernal chest pain associated with shortness of breath. The electrocardiogram was noted for normal sinus rhythm 69 beats per minute, left ventricular hypertrophy, and nonspecific ST/T changes without any ischemic changes. Initial troponin was negative. Pharmacological nuclear stress test with Lexiscan was noted for inferior wall pharmacological-induced ischemia and diminished left ventricular ejection fraction (LVEF) of 37%. Transthoracic echocardiogram had LVEF 45-50%, mild concentric left ventricular hypertrophy, and akinesis of basal to mid inferior and inferoseptal walls. A plan was made to perform coronary angiography with left heart catheterization to rule out acute coronary syndrome.
The next day, the procedure was performed using a right femoral access introduction of a 6 French sheath. The patient was noted to have diffuse disease in the posterior descending artery and mild disease in the mid and distal left anterior descending artery, with patent grafts. During the procedure, the patient was noted to have an acute change in mental status, with aphasia and right-sided weakness. The procedure was immediately aborted and a stroke alert was called. The patient did not have any complications such as bleeding at the right femoral access site. Stat brain computed tomography (CT) was negative for acute intracranial abnormality, including hemorrhage. Neurosurgery was immediately consulted and recommended a CT of the brain and neck angiogram, which did not show any stenosis of the vessels. There was a concern for acute embolic stroke from suspected coronary intervention. Tissue plasminogen activator (tPA) was advised and immediately administered. The patient was subsequently transferred to the intensive care unit for management of suspected acute stroke status post tPA administration. He was noted to have bleeding at the right femoral access site. A FemoStop (Abbott Vascular) was subsequently placed. Vascular surgery was consulted after the patient developed a right groin hematoma. A CT of the abdomen and pelvis was immediately ordered and showed increased soft tissue density along the right rectus abdominis muscle, extending into the anterior right thigh with high suspicion of hematoma and active bleeding. The FemoStop was immediately removed and manual compression pressure was applied for bleeding. Hemoglobin dropped from 13.3 g/dL to 10.5 g/dL, and the patient was transfused with 1 unit of packed red blood cells. Later, during the evening, the patient became minimally responsive and desaturated in the low 70s on 5L O2. He was immediately intubated for acute respiratory failure and altered mental status. His blood pressure was also 74/56 mmHg and he was given 1 L of normal saline bolus. Postintubation chest x-ray was negative for any active disease in the lungs. Arterial blood gas at that time had pH=7.0, pCO2=29, pO2 >500, HCO3=7, and O2 saturation=99. The patient was given sodium bicarbonate 100 mEq IV ×1 and started on a sodium bicarbonate drip at 150 mls/hr. Two hours later, the patient became hypotensive and bradycardic, and had a cardiac arrest. He was coded for 10 minutes before return of spontaneous circulation was achieved. The patient subsequently coded three more times. He could not be resuscitated during the last code and expired.
Neurologic complications are infrequently associated with cardiac catheterization or PCI. The incidence of acute ischemic stroke in this patient population is low, ranging from 0.2% to 0.4%.1,6 A previous study from a large volume center by Dukkipati et al6 showed that stroke occurred in 0.44% of 20,679 consecutive patients who underwent PCI. Cerebral infarction after angioplasty could be attributed to the following artery distributions: 56% in middle cerebral, 2% in anterior cerebral, 37% in posterior cerebral, 5% in superior cerebellar, 5% in posterior inferior cerebellar, and 7% in basilar.6 A large, retrospective study evaluated over 426,000 patients undergoing PCI between 2007 and 2012 in the British Cardiovascular Intervention Society database, and found stroke as a complication in 0.13% of the total cohort.7 Multivariate analysis has shown that the occurrence of stroke was more frequently associated with older age, hypertension, diabetes mellitus, heart disease, renal failure, severity of coronary artery disease, and history of stroke. Studies have also shown increased incidence of stroke with procedural risk factors such as emergent cardiac catheterization, longer procedure time, retrograde catheterization of the left ventricle in patients with aortic stenosis, greater contrast use, interventions of previous bypass grafts, presence of coronary artery thrombus, and use of an intra-aortic balloon pump.4,5,8 One possible explanation for stroke includes less care in advancing the catheter through the aorta during urgent cardiac catheterization, which can dislodge aortic plaques and result in subsequent embolization of debris to the brain. Dislocation of aortic atheroma during catheter manipulation, thrombus formation in the catheter, or air embolism are the main embolic sources triggering ischemic stroke during cardiac catheterization or PCI. Patients with coronary artery disease have an increased risk of stroke at baseline. These patients can have severe atheroma in the aortic arch and descending aorta that increases the risk of cerebral embolism during coronary catheterization.9
Most strokes related to cardiac catheterization present during the procedure or within the first 24 hours after the procedure.6,10 Ischemic stroke often manifests with symptoms of visual disturbance, hemiparesis, aphasia, or altered mental status. Ischemic strokes as a result of invasive cardiac intervention are often embolic. Previous research has shown that a disproportionate number of ischemic strokes related to cardiac catheterization involve the vertebrobasilar circulation.11 In addition to focal neurologic deficits, ischemic strokes from diffuse bilateral cerebral embolization can also manifest as a non-focal presentation with altered mentation and somnolence. Currently, no standard therapy for ischemic stroke exists. Intravenous thrombolytic therapy with recombinant tissue plasminogen activator has shown benefit if given up to 4.5 hours in the general stroke population. There have been no clear benefits of thrombolytic therapy for ischemic strokes contributed to cardiac catheterization. Periprocedural ischemic stroke complicating cardiac catheterization has no clear management strategy. De Marco et al reported six cases of periprocedural ischemic stroke that were successfully managed with immediate cerebral angiography.12 Cerebral angiography in this population has shown promising results, as it allows identification of the occluded vessel and offers reperfusion by local thrombolysis or mechanical means, with a greater success than with the use of intravenous thrombolysis.13,14 Cerebral angiography confirms the diagnosis of embolic stroke and treatment can be immediately given at that time. Selective intra-arterial thrombolysis is superior to intravenous thrombolysis in the setting of strokes complicating cardiac catheterization, as most of these patients have already been given full-dose anticoagulation and an antiplatelet regimen that predisposes them to a higher risk of bleeding.
Acute ischemic stroke is an iatrogenic complication of cardiac catheterization. It carries a high morbidity and mortality burden if not rapidly diagnosed and acted upon. Institutions offering cardiac catheterization services should implement a protocol for its management, and interventional cardiologists must be made familiar with the diagnosis and management protocols. Cardiac interventions must be performed in institutions that have a stroke team. In an event of periprocedural stroke, neurologists and stroke teams must be immediately available, become involved early on, and assist in making collaborative decisions. This case describes a rare complication of ischemic stroke requiring intravenous thrombolytic therapy in a patient who underwent cardiac catheterization for an abnormal stress test after presenting with substernal chest pain. After intravenous thrombolysis, our case was complicated by a large, right groin, actively bleeding hematoma and subsequent cardiac arrest resulting in death. Therefore, use of intravenous thrombolysis in acute ischemic stroke as a complication of periprocedural cardiac catheterization should be based on a careful individual risk assessment. Further randomized, controlled trials are necessary to assess safety, efficacy, and utilization of this treatment.
1Department of Internal Medicine, Nazareth Hospital, Philadelphia, Pennsylvania; 2Department of Internal Medicine, East Tennessee State University, Johnson City, Tennessee; 3Department of Medicine, Shifa College of Medicine, Islamabad, Pakistan; 4Department of Cardiology, Nazareth Hospital, Philadelphia, Pennsylvania
Disclosure: The authors report no conflicts of interest regarding the content herein.
Dr. Sheharyar Minhas can be contacted at firstname.lastname@example.org.
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