Several studies have reported that periprocedural dual antiplatelet therapy lowers the incidence of thromboembolic complications (TEC) associated with coiling of unruptured aneurysms. We hypothesized that preprocedural administration of dual antiplatelet agents (aspirin and cilostazol) for 7days may reduce the risk of complications associated with diagnostic cerebral digital subtraction angiography (DSA).
We retrospectively reviewed the records of patients who underwent diagnostic cerebral DSA between September 2015 and April 2018. Of the 419 patients included (149 men, 270 women, mean age 58.5 years), 221 (72 men, 149 women, mean age 57.8 years) who underwent cerebral DSA between September 2015 and June 2016 were not premedicated with antiplatelet therapy. The remaining 198 (77 men, 121 women, mean age 59.4 years) who underwent cerebral DSA between July 2016 and April 2018 were premedicated with dual antiplatelet therapy (aspirin and cilostazol). We defined ischemic stroke as a cerebral DSA-induced complication identified on magnetic resonance imaging (MRI) among patients with neurological symptoms.
Of the 221 patients who did not receive antiplatelet therapy, 210 (95.0%) showed no neurological symptoms; however, 11 (5.0%) developed neurological symptoms with MRI-proven ischemic stroke, which represents a TEC. Of the 198 patients who received dual antiplatelet therapy, 196 patients (99.0%) showed no evidence of TEC. The remaining 2 (1.0%) developed diplopia and motor weakness each, and MRI confirmed acute ischemic stroke (p=0.019).
The use of dual antiplatelet agents (aspirin and cilostazol) for 7 days before DSA may reduce the risk of cerebral DSA-induced TEC.
Following the availability of novel technology, cerebral digital subtraction angiography (DSA) is commonly used clinically to diagnose cerebrovascular abnormalities
Among the various complications of cerebral DSA including nausea, vomiting, transient hypotension, anaphylaxis, and groin hematoma
Antiplatelet and anticoagulant therapy effectively reduces the risk of thromboembolism
We retrospectively reviewed the records of 419 patients who underwent diagnostic cerebral DSA between September 2015 and April 2018 (
Cerebral DSA was performed via the transfemoral arterial approach using a dedicated biplane neuroangiography unit (RF-1000-125, Artis Zee biplane, Siemens Healthineer, Berlin, Germany) with the help of 1 type of guidewire (Terumo®, 0.035 inch, Tokyo, Japan) and 3 types of catheters—Taper (Cook, Bloomington, IN, USA), Imager (Boston Scientific, Marlborough, MA, USA), Simmons I (AngioDynamics, Queensbury, NY, USA). A non-ionic contrast medium (lomeron 300 [iomeprol 612.4 mg/mL], Bracco S.p.A., Milan, Italy) was used for all procedures with automatic machine injection of the contrast medium followed by a saline flush after each injection. The FemoSeal®, vascular closure device, was used for hemostasis at the site of vascular access. All procedures in this series were performed by a single neurovascular surgeon (the author of this study).
Patients who underwent DSA between July 2016 and April 2018 received aspirin and cilostazol (both 100 mg/day) for 7 days. All antiplatelet therapy was discontinued post-procedure in premedicated patients who underwent cerebral DSA but did not develop TEC.
Comparison between two groups was performed using Fisher's exact test, chi-square test and independent t tests (signigicant level 0.05). Statistical analysis was performed using the SPSS software, version 19 (IBM SPSS Statistics, IBM Corp., Armonk, NY). A p-value<0.05 was considered statistically significant.
We analyzed the complication ratio based on risk factors including hypertension, diabetes mellitus, hyperlipidemia, history of stroke, smoking, heart disease such as heart failure or arrhythmia, chronic kidney disease, and others that can affect the vascular status. Our analysis showed that these risk factors did not significantly affect the incidence of DSA-induced TEC (
There was a significant difference in the incidence of TEC between patients who took dual antiplatelet therapy and those who did not, which is consistent with our hypothesis. Of the 221 patients who did not receive antiplatelet therapy, 210 patients (95.0%) did not report neurological symptoms; however, 11 patients (5.0%) reported various neurological symptoms including motor weakness and showed MRI-proven ischemic stroke (
Cerebral DSA and noninvasive cerebrovascular imaging modalities have shown steady improvement over the past several decades. Presently, diagnostic cerebral DSA is commonly performed for treatment planning of endovascular or open surgical procedures
Diagnostic cerebral DSA may result in local complications such as access-site hematoma formation and systemic complications including headache, nausea, vomiting, and/or transient hypotension, nephropathy, and neurological deficits
Thromboembolism is the most common cause of ischemic stroke, which can cause transient or permanent neurological deficit including hemiparesis, aphasia, visual symptoms, and a diminished level of consciousness, among others
Presently, the key concern is to minimize diagnostic cerebral DSA-related complications and identify strategies to effectively manage those that have already occurred.
The risk factors for ischemic stroke after cerebral DSA include hypertension, diabetes mellitus, dyslipidemia, cardiac disorders like heart failure or arrhythmia, a history of smoking, chronic kidney disease, the number of catheters used, types of catheters used, and the volume of contrast agent used
An ischemic stroke may occur during the cerebral DSA procedure secondary to vascular spasm or neurovascular dissection following severe vascular stenosis or occlusion. However, most instances of ischemic stroke following cerebral DSA may be associated with distal embolization of air or particulate matter
Several studies have reported that the dual antiplatelet therapy compared to single antiplatelet therapy could significantly lower numerical or clinical findings associated with platelet aggregation that cause thrombus
Aspirin, an irreversible inhibitor of cyclooxygenase, inhibits the conversion of arachidonic acid to thromboxane A2 and prevents vasospasm and platelet aggregation
Cilostazol inhibits phosphodiesterase 3, which is strongly expressed in platelets and vascular smooth muscle cells
This study suggests that preprocedural dual antiplatelet therapy can significantly reduce the cerebral DSA-induced TEC rate. However, there are some limitations on this study. First, considering the effect of learning curve of operator is the limitation of this paper, further reevaluation will be needed in the future. Second, although our population is the perfect representation of our center, we could not determine whether this population was representative of the entirety of population who were performed cerebral DSA. Third, this study was retrospective and consisted only of the available data at a single institution. A better designed randomized controlled trial would be needed.
The use of dual antiplatelet agents (aspirin and cilostazol) over a week before the procedure may reduce the risks of cerebral DSA-induced complications.
This work was supported by a grant from the Chunma medical research foundation, Korea, 2019.
Diffusion-weighted magnetic resonance imaging scan obtained in a woman who developed right-sided motor weakness immediately after diagnostic cerebral digital subtraction angiography for an unruptured aneurysm. An acute ischemic stroke involving the left thalamus and both occipital lobes was confirmed as a thromboembolic complication. Of note, she had not been administered premedication.
Image shows a man who was premedicated with dual antiplatelet therapy and was diagnosed with an acute ischemic stroke involving the right pretectal region. He complained of a diplopia.
Without premedication | With Premedication | Total | |
---|---|---|---|
Number of patients | 221 | 198 | 419 |
Male | 72 | 77 | 149 |
Female | 149 | 121 | 270 |
Mean age (years) | 57.8 (21-80) | 59.4 (19-80) | 58.6 (19-80) |
Cases in premedication | Number |
---|---|
Unruptured aneurysm | 338 (80.67%) |
Intervention evaluation | 51 (12.17%) |
Arteriovenous malformation | 9 (2.15%) |
Carotid carvernous fistula | 5 (1.19%) |
Moyamoya | 2 (0.48%) |
Stenosis/occlusion/dissection | 13 (3.10%) |
Atherosclerosis | 1 (0.24%) |
Total | 419 |
Risk factor\Thromboembolic complication | NO | YES | p-value | |
---|---|---|---|---|
Hypertension | No | 110 | 7 | 0.466 |
Yes | 100 | 4 | ||
Diabetes mellitus | No | 180 | 9 | 0.720 |
Yes | 30 | 2 | ||
Hyperlipidemia | No | 191 | 10 | 0.996 |
Yes | 19 | 1 | ||
Stroke history | No | 171 | 10 | 0.426 |
Yes | 39 | 1 | ||
heart disease | No | 195 | 11 | 0.359 |
Yes | 15 | 0 | ||
Smoking | No | 185 | 9 | 0.535 |
Yes | 25 | 2 | ||
Chronic kidney disease | No | 204 | 11 | 0.57 |
Yes | 6 | 0 | ||
Number of vessel Examined | 1 | 35 | 0 | 0.212 |
2 | 9 | 0 | ||
3 | 90 | 4 | ||
4 | 76 | 7 | ||
5 | 0 | 0 |
Risk factor\Thromboembolic complication | NO | YES | p-value | |
---|---|---|---|---|
Hypertension | No | 109 | 1 | 0.874 |
Yes | 87 | 1 | ||
Diabetes mellitus | No | 168 | 1 | 0.155 |
Yes | 28 | 1 | ||
Hyperlipidemia | No | 169 | 2 | 0.572 |
Yes | 27 | 0 | ||
Stroke history | No | 160 | 1 | 0.167 |
Yes | 29 | 1 | ||
heart disease | No | 188 | 2 | 0.771 |
Yes | 8 | 0 | ||
Smoking | No | 181 | 2 | 0.684 |
Yes | 15 | 0 | ||
Kidney disease | No | 194 | 2 | 0.919 |
Yes | 1 | 0 | ||
Number of vessel Examined | 1 | 4 | 0 | 0.989 |
2 | 8 | 0 | ||
3 | 116 | 1 | ||
4 | 66 | 1 | ||
5 | 1 | 0 | ||
Type of catheter | Taper | 159 | 1 | 0.358 |
Imager | 9 | 0 | ||
Simmon | 28 | 1 |
Premedication\Thromboembolic complication | No | Yes | Total | p-value |
---|---|---|---|---|
No | 210 (95.0%) | 11 (5.0%) | 221 | 0.019 |
Yes (aspirin+cilostazol) | 196 (99.0%) | 2 (1.0%) | 198 | |
Total | 406 (96.9%) | 13 (3.1%) | 419 |
Symptoms as thromboembolic complication\Premedication | No | Yes |
---|---|---|
Motor weakness | 6 (46.2%) | 1 (7.7%) |
Ocular symptom | 3 (23.0%) | 1 (7.7%) |
Dysarthria | 1 (7.7%) | 0 (0.0%) |
Paresis | 1 (7.7%) | 0 (0.0%) |
Total | 11 (84.6%) | 2 (15.4%) |