Thursday, March 8, 2012
Methodist Institute for Technology, Innovation & Education (MITIESM)
The Methodist Hospital
Houston, Texas
. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Stroke is a devastating event. With a rapid response, focused and advanced imaging and open and percutaneous intervention, a stroke service will save brain tissue, preserve function and rescue quality of life. This year, the Methodist DeBakey Heart & Vascular Center and Methodist Neurological Institute have collaborated to provide a cutting-edge curriculum for physicians, nurses and technologists in cerebrovascular diagnosis management and treatment, from the arch of the aorta to the terminal branches of the cerebral vessels. Methodist is proud of its multidisciplinary stroke teams and the stroke Network that provides remote viewing and triage of patients while their stroke is in evolution. Linked to this symposium, we have a noninvasive imaging course and hands-on skills workshop to allow the participants to see, feel, interpret and treat cerebrovascular disease.
Conflict of Interest Disclosure: The authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest, and the following were reported: Dr. Lumsden is a consultant for Boston Scientific Corporation, VNUS Medical Technologies, Inc., W.L. Gore & Associates, Inc., Abbott Laboratories, MAQUET, Siemens Healthcare, and Medtronic, Inc.; is on the speakers bureau for Boston Scientific, W.L. Gore & Associates, Inc., and Medtronic, Inc.; is a shareholder in Hatch Medical, NorthPoint Domain, and Embrella Cardiovascular, Inc.; and receives research funding from Nycomed, Hansen Medical, W.L. Gore & Associates, Inc., Harvest Technologies, Boston Scientific, Lombard Medical Technologies, and Bolton Medical, Inc.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Intravenous tissue plasminogen activator (tPA) remains the only effective reperfusion therapy to reverse ischemic stroke. Its timely delivery to all eligible patients should be a priority in the development of stroke treatment centers and ambulance delivery systems. Its augmentation with ultrasound will be discussed below.
Despite lower revascularization rates with respect to endovascular thrombectomy, patients treated with systemic thrombolysis achieve good functional outcomes likely due to earlier treatment initiation. Currently, no evidence exists that primary intra-arterial revascularization could be any better than systemic tPA within the 3-hour time window.
Systemic tPA administration remains the fastest way to initiate treatment for acute ischemic stroke. Since tPA works by induction of partial recanalization of large thrombi, early augmentation of fibrinolysis to improve recanalization is desirable. This augmentation is feasible and can be safely achieved at the bedside with transcranial doppler (TCD) or sonothrombolysis. In the CLOTBUST trial all patients received systemic tPA as standard of care, and 73% of patients achieved any recanalization (46% complete, 27% partial) with tPA + TCD versus 50% recanalization (17% complete, 33% partial) with tPA alone within 2 hours of treatment (p<0.001). Sustained complete recanalization at 2 hours was 38% vs. 13%, respectively (p=0.03). A recent meta-analysis of 6 randomized and 3 non-randomized clinical studies of sonothrombolysis showed that any diagnostic ultrasound monitoring can at least double the chance of early complete arterial recanalization with no increase in the risk of symptomatic intracerebral hemorrhage. Transcranial ultrasound delivery in an operator-independent and dose-controlled manner was successfully tested in phase I-II clinical studies in stroke-free volunteers and stroke patients treated with systemic tPA. A novel operator-independent device for sonolysis (Cerevast therapeutics, inc.) is now being tested in a pivotal phase III clinical trial (CLOTBUSTER, NCT01098981).
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Transcranial color-coded doppler sonography (TCCD) allows the insonation of intracranial cerebral arteries, veins and cerebral parenchyma. This investigation is mainly performed through the temporal and the foraminal bone windows, and the detection rate of intracranial vessels can be significantly increased by the administration of ultra-sound contrast agents. TCCD offers the vascular neurologist a unique non-invasive real-time neuroimaging modality for the evaluation of characteristics of blood flow velocities in both arterial and venous systems, adding important physiological and pathophysiological information to the structural image of the brain at the bedside of the patient. In conjunction with extracranial ultrasound investigation, TCCD plays a key role in the diagnostic stage of patients with acute ischemic stroke, since it helps to identify intracranial vessel narrowing and occlusion, and collateral flow due to extracranial vessel occlusion. Extended applications such as emboli monitoring, right-to-left shunt detection, and vasomotor reactivity testing help the vascular neurologist ascertain stroke mechanisms at bedside, plan and monitor treatment, and determine prognosis. The unique role of TCCD is best seen in the monitoring phase, since it allows real-time identification of vessel recanalization or reocclusion, be it spontaneous or post-thrombolysis. It is very well known that the clinical benefit derived from thrombolysis is directly correlated to an early recanalization; however, in up to 60% of patients receiving systemic thombolysis, recanalization is a slow and incomplete process. The enhancement of thrombolysis by ultrasound energy, sonothrombolysis, is a new application; it has been demonstrated that ultrasound enhances the effect of recombinant tissue plasminogen activator (rt-PA), and there is evidence that the addition of microbubbles at low dosages increases this effect even further, making recanalization faster and more complete. However, the safety of ultrasound exposure of the brain for therapeutic purposes is still an ongoing issue, especially when TCCD is used.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Non-embolic ischemic pathologies are the most common cause of vertebral artery posterior circulation symptoms. These lesions, such as external compression due to osteophytes or occlusive atherosclerotic plaques, often cause transient ischemia. Other pathologies affecting the vertebral arteries include vasculidities, trauma, dissection, aneurysm, and thromboembolic disease. Posterior circulation strokes are the result of thromboembolic atherosclerotic vertebral artery disease in 20% of cases. Such strokes are generally associated with higher mortality than anterior circulation strokes. Despite the recent upsurge of interest in vertebral artery pathology, optimal treatment is unclear and based on relatively small case series and consensus statements. Medical management has no role in external compression syndromes of the vertebral arteries such as postural stenosis at the atlanto-occipital or atlanto-axial level (Bow Hunter’s Syndrome) or with vertebral osteophytes. However, medical management is critical to good outcomes in other pathologies.
Atherosclerotic risk factor management is the mainstay for asymptomatic vertebral disease and includes smoking cessation, control of hypertension and hyperlipidemia. Aspirin with or without extended-release dipyridamole is effective for secondary prevention in patients with previous transient ischemic attack (TIA) or stroke. Clopidogrel is an acceptable alternative in patients unable to tolerate aspirin. The risk of bleeding outweighs the benefit of combination aspirin and clopidogrel. There is no known benefit with oral anticoagulants in such patients.
Symptomatic acute thromboembolic ischemia with evidence of thrombus in the vertebral arteries can be due to trauma or atherosclerotic disease. Thrombolytic agents can be considered and anticoagulation is recommended for at least 3 months. Patients with posterior circulation strokes and atherosclerotic vertebral disease without evidence of luminal thrombus should receive antiplatelet therapy, statins, and antihypertensive agents. Patients with traumatic dissections even without symptoms should also be considered for anticoagulation or antiplatelet therapy.
Patients with recurrent vertebral thromboembolic symptoms despite optimal medical therapy should be referred for endovascular or open surgery. Since no randomized trials comparing medical, surgical, or endovascular therapies exist, the best treatment remains unclear for patients with symptomatic atherosclerotic vertebral artery disease.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest, and the following were reported: the author receives research funding from Cook Medical and is a consultant for C.R. Bard, Inc.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Atherosclerotic intracranial arterial stenosis is an important cause of stroke, accounting for 5% to 10% of ischemic strokes among whites and an even higher proportion of strokes among blacks, asians, and hispanics. The WASID trial previously showed that standard medical management of symptomatic high-grade intracranial stenosis is associated with a high risk of stroke recurrence. The SAMMPRIS trial compares percutaneous transluminal angioplasty and stenting (PTAS) with medical management in a randomized clinical study.
SAMMPRIS randomly assigned patients who had a recent transient ischemic attack (TIA) or stroke attributed to stenosis of 70% to 99% of the diameter of a major intracranial artery (internal carotid artery, middle cerebral artery, vertebral artery, or basilar artery) to aggressive medical management alone versus aggressive medical management plus PTAS with the use of the Wingspan stent system. The primary endpoint was stroke or death within 30 days after enrollment or revascularization procedure, or stroke in the territory of the qualifying artery beyond 30 days.
Enrollment was stopped after 451 patients underwent randomization, because the 30-day rate of stroke or death was 14.7% in the PTAS group (nonfatal stroke 12.5%, fatal stroke 2.2%) and 5.8% in the medical management group (nonfatal stroke 5.3%, fatal stroke 0.4%) (P=0.002). Beyond 30 days, stroke in the same territory occurred in 13 patients in each group, with a mean duration of follow-up, which is ongoing, of 11.9 months. The primary endpoint event rate differed significantly between the two treatment groups (P=0.009), with 1-year rates of 20.0% in the PTAS group and 12.2% in the medical management group.
In patients with intracranial arterial stenosis, aggressive medical management was superior to PTAS with the use of the Wingspan stent system, both because the risk of early stroke after PTAS was high and because the risk of stroke with aggressive medical therapy alone was lower than projected by prior natural history studies.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Transcranial Doppler (TCD) was first introduced by Rune Aaslid in 1982 to assess cerebral hemodynamics. Power-motion mode Doppler (PMD) was later added (Mark Moehring) and has simplified the TCD examination by making vessel location easier and faster. Parameters measured by TCD include: mean cerebral arterial blood flow velocities (MFV), pulsatility index (PI), and relative change in mean peak systolic velocity (PSV) over time (delta % change). Changes in these parameters and spectral analysis evaluation allow us to decide whether hemodynamically significant deviations from baseline are present.
It is important to understand proper patient and transducer positioning, anatomic landmarks, and appropriate scale settings. The patient is typically in a recumbent position. The head is straight for the ophthalmic and siphon interrogation, and is turned slightly away from the transducer for the remaining windows. There are four “windows” for insonation of the cerebral arteries, which consist of the orbital, temporal, sub-occipital, and submandibular. A typical diagnostic TCD exam would interrogate the ophthalmic artery (OA) and siphon from the transorbital approach at 10% power. The power should then be increased to 100% and the transtemporal approach would be used to assess the middle cerebral artery (MCA), anterior cerebral artery (ACA), posterior cerebral artery (PCA), and the collateral vessels [the anterior communicating artery (AcomA) and posterior communicating artery (PcomA)] if present and detectable. The suboccipital approach is then used to insonate the vertebral arteries and basilar artery through the foramen magnum. The submandibular approach is used to obtain the internal carotid artery velocities as the artery enters the skull. The depth, direction of flow, and resistance (DDR) are the key points in assessing these arteries. Direction of flow in each artery is in relation to the transducer probe position and the course of the vessel being interrogated. Each waveform has its own unique signature. TCD images are stored on the machine and can be transferred to digital storage, CD, or flash drive after completion of the exam. A report can be generated from the machine or entered into a digital system.
TCD can also be used for monitoring vasospasm and brain death, detection of emboli using a fixed head frame, detection of patent foramen ovale using bubble injection, measuring vasomotor reactivity for vasomotor reserve, and operating room monitoring during vascular and cardiovascular surgeries.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
It is estimated that approximately 2 million people living in North America and Europe have asymptomatic extracranial carotid artery stenosis that could be considered for treatment. In the United States, cerebrovascular disease is the third leading cause of death. Despite the proven benefit of carotid endarterectomy or stenting in patients harboring significant carotid stenosis, with and without neurologic symptoms, and the fact that the majority of strokes occur in asymptomatic patients, screening of asymptomatic patients for extracranial carotid artery disease has not been recommended by the United States Preventive Service Task Force (USPSTF), claiming the evidence was insufficient to recommend for or against screening of asymptomatic patients. Others have claimed that screening is not cost-effective.
There are many who do not agree with the recommendations of the USPSTF regarding carotid screening. In fact, multiple specialty societies have provided comprehensive and timely evidence-based multispecialty practice guidelines on screening for asymptomatic carotid artery stenosis in the general population and selected subsets of patients. We will review the recommendations of these societies so as to better identify the subset of patients who would most likely have the highest prevalence of carotid stenosis and, thus, would benefit from carotid artery screening. In addition, we will describe a protocol utilizing a quick carotid scan (QCS) that is rapid, accurate, and cost effective in screening to prevent stroke.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Carotid ultrasound is an essential tool in stroke screening and diagnosis, but it is technically demanding. The first element of any protocol is identification of the patient and explanation of the procedure. The next element is to position the patient and label the record for future use. Once these tasks are performed, a carotid study can be performed. An essential carotid protocol starts with a scan from the lowest cervical portion of the common carotid to the most cephalad segment of the internal carotid artery in the neck on both sides. Longitudinal and transverse imaging should be employed. Color shift should be noted. Waveforms in the common, internal, and external carotid arteries should be noted. Abnormal inflow and outflow should be identified early as this impacts any interpretations. Peak systolic velocity and end diastolic velocity measurements at 3 points in each vessel and at the site of maximum stenosis where color shift is maximal are determined and recorded. Post stenotic turbulence should be documented. Appropriate power, filter, and angle controls should be used throughout the study. The operator should also categorize plaque composition and plaque surface characteristics as needed based on the findings during the study. At the end of the study, review the data and labeling to ensure the correct number and type of images have been collected and to do a preliminary interpretation. If there is diagnostic uncertainty or technical issues, ask for a second opinion before allowing the patient to leave the scanning area. The final task of any protocol is to input the data into the reporting system and provide preliminary interpretations before assigning the study for physician interpretation.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Carotid stenting has been shown to have equivalence to carotid endarterectomy and has distinct benefits in high-risk anatomic and physiological patients. Carotid ultrasound can provide the location of the bifurcation and can also provide information on the composition of the plaque to be treated. In primary lesions, the number and size of captured particulate correlated with greyscale median and with the combined ultrasound findings of echogenicity, heterogenicity, and luminal irregularity/ulceration. However, none of these ultrasound factors correlated independently with embolic particulate. Duplex imaging of the stented carotid should follow the same protocol as a normal carotid study with additional attention paid to the position of the stent, its apposition to the wall, and the internal contours of the stent surface. An un-stented carotid artery is likely to have a more elastic vessel wall than a stented one, even if stenosis is present. Therefore, duplex ultrasound cut-off criteria for the degrees of an in-stent stenosis, based on blood velocity parameters, are different from the established cut-offs used for un-stented arteries. Routine criteria cannot be applied to stented arteries, and several new criteria have been established (Table).
The peak systolic velocity of the stented artery is a better predictor for in-stent restenosis than the end-diastolic velocity or the internal carotid artery (ICA) to common carotid artery (CCA) ratio. Carotid duplex is an effective way to follow the patency and healing of a carotid stent.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
| Stenosis | Peak Systolic Velocity | Sensitivity | Specificity | Positive Predictive Value | Negative Predictive Value |
| 0-29% | <154 cm/s | 99% | 89% | 96% | 97% |
| ≥30-50% | ≥154cm/s | 99% | 89% | 99% | 97% |
| ≥51-80% | ≥224 cm/s | 99% | 90% | 99% | 90% |
| ≥81% | ≥325 cm/s | 100% | 99% | 100% | 88% |
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
In this review, a summary is provided of the neurocognitive outcomes of carotid revascularization and coronary artery bypass graft (CABG) surgeries with an emphasis on predictors of postsurgical cognitive impairments. Neurocognitive and behavioral changes occur in a subset of patients after carotid endarterectomy (CEA), carotid artery stenting (CAS), and CABG surgeries. Both impairments and improvements have been reported in the extant literature. Improvements in cognitive function are attributed to increased cerebral blood flow and improved general health. Different studies have offered varying rates of cognitive decline after CEA surgery ranging from 4-47%. For CAS, rates of decline vary from 0-36%. For CABG surgery, rates of decline can be as high as 53% immediately after surgery to 42% five years after surgery. Depending on the type of surgery, risk of cognitive decline is dependent on several factors including surgery characteristics, disease characteristics, and patient demographic characteristics. Surgery-related issues include procedure-related hypoperfusion, emboli released during surgery (even with the use of embolic protection devices), and use of cardiopulmonary bypass leading to postperfusion syndrome. Several ongoing studies are comparing neurocognitive outcomes between CAS and CEA. Preliminary reports show no definitive answer to the question of whether or not one surgery has a better cognitive outcome compared to the other. For any of these surgeries, older age predicts poorer cognitive outcome, possibly reflecting reduced patient compensatory reserve or greater risk of stroke. Diabetes mellitus is found to be a risk factor for cognitive impairment, stroke or death in CEA, but not CAS. Monocyte chemoattractant protein-1, a hypothesized marker of pre-existing small vessel vascular disease, has also been found to predict short-term cognitive decline after CEA surgery. Presurgical identification of Mild Cognitive impairment (a hypothesized prodromal stage to dementia) is a predictor of postsurgical confusion. For CABG surgery, established predictors of cognitive decline include impaired left ventricular function, peripheral vascular disease, elevated presurgical creatinine levels, and pre-existing neurologic illness (e.g., previous stroke). Methodological differences exist among previous research that increase or decrease the likelihood of identifying postsurgical cognitive impairments including type of neuropsychological tasks used (e.g., less sensitive global measures versus domain specific tests), patient selection criteria (e.g., strict exclusion of sicker patients), follow-up testing interval (shorter intervals confounded by general medical problems and their effects on cognition, and longer intervals confounded by typical age-related cognitive changes), and statistical methodology (arbitrary definition of what defines an adverse cognitive event; reporting of group means versus individual rates of decline). Review of the literature suggests that there is some risk of cognitive decline involved in any of these surgeries. Identifying risk factors associated with cognitive decline is important to the presurgical selection process and helps clinicians more effectively consider the risks versus benefits of different surgeries.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Diffusion-weighted imaging (DWI) provides image contrast that is dependent on the molecular motion of water. This method was introduced into clinical practice in the mid-1990s. Because ultrafast magnetic resonance imaging (MRI) sequences such as echo planar imaging (EPI) can be used, DWI is highly sensitive (81–100%) and specific (86–100%) for detection of acute ischemia within the first 12 hours after stroke symptom onset, with sensitivities and specificities in the 90–100% range at specialized stroke centers. DWI can demonstrate acute ischemic lesions as early as 11 minutes after symptom onset. DWI is superior to conventional MRI and computed tomography (CT) in the first 6 hours because there is usually an insufficient increase in tissue water for the reliable detection of hypoattenuation on CT and hyperintensity on T2 and fluid-attenuated inversion recovery (FLAIR) MR images.
Although infarcts are usually identifiable on CT, T2, and flair images after 6 hours, DWI can also be valuable at later time points because of its higher contrast-to-noise ratio. CT is widely used to exclude hemorrhage prior to thrombolytic therapy in the emergency room, but follow-up imaging by MRI provides more information.
DWI is fairly resistant to patient motion, with imaging times ranging from a few seconds to 2 minutes. DWI is the most reliable method for the early detection of cerebral ischemia, definition of infarct core, and differentiation of acute ischemia from other disease processes that mimic stroke.
Although DWI has been useful in research and the clinical management of stroke, diffusion tensor imaging (DTI) and diffusion kurtosis imaging (DKI) may offer additional diagnostic information on the microstructural status of tissue. This is because diffusion in tissue is affected by the presence of semipermeable membranes and oriented microstructures in the intracellular, extracellular, and vascular compartments that result in the preferential movement of water parallel to these obstacles. This directional dependence of diffusion is known as anisotropy. In the brain, white matter has relatively high anisotropy because diffusion is much greater parallel than perpendicular to major white matter tracts. Gray matter, alternatively, has relatively low anisotropy. Heterogeneity of the diffusion environment from compartmentalization also results in non-Gaussian probability distribution of water diffusion, which can be quantified by kurtosis. The purpose of this review is to discuss the development and applications of DWI, DTI, and DKI in acute and chronic ischemia.
The term diffusion refers to the general transport of matter whereby molecules or ions mix through normal agitation in a random way. When describing the mixing of different liquids or gases, diffusion is described in terms of a concentration gradient of the diffusing substance. In biologic tissues, the driving force is the motion of water within water, driven by thermal agitation and commonly referred to as Brownian motion.
All DWIS (linearly T2-weighted and exponentially diffusion-weighted) should be reviewed with apparent diffusion coefficient (ADC) maps (linearly diffusion-weighted, without a T2 component) and/or exponential images (exponentially diffusion-weighted, without a T2 component). The use of the ADC map and/or exponential image is essential for proper interpretation of DWIS because areas of diminished and increased diffusion can both appear bright on DWIS. In acute ischemic lesions with restricted diffusion, the T2 and diffusion effects both cause increased signal on DWI, and the DWI has the highest contrast-to-noise ratio. Lesions with restricted diffusion also appear hyperintense on exponential images, but they appear less hyperintense compared with the DWI because there is no T2 effect. Lesions with restricted diffusion appear dark on the ADC map. Conversely, areas of increased diffusion may appear hyperintense, isointense, or hypoin-tense to normal brain parenchyma on DWI, depending on the strength of the T2 and diffusion components, but are hyper-intense on the ADC map and hypointense on the exponential image. When a lesion is hyperintense on both the DWI and the ADC map and hypointense on the exponential image, the phenomenon is referred to as T2 shine-through and may be seen with late subacute infarcts or chronic ischemic lesions.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Stenosis of the subclavian or vertebral artery (VA) can be found in patients who have widespread atherosclerosis. Steal manifests as various forms of alternating flow signal in one of the VAs at rest or can be augmented during a hyperemia cuff test. Blood pressure differences measured between the two arms are also objective clues for proper diagnosis. Although subclavian steal is rarely symptomatic, most patients have antegrade low-resistance flow in the basilar artery (BA) despite flow reversal in one of the terminal VAs. The low-resistance flow in the BA comes from the donor VA that feeds the brain and contralateral arm. Lee and colleagues examined the vertebral arteries using transcranial Doppler (TCD) to determine if potential collaterals that feed the stealing vertebral-subclavian system were present, hypoplastic, or atretic.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Transcranial Doppler (TCD) is the “doctor’s stethoscope for the brain”. It is a non-invasive, safe, and cost-effective bedside test for evaluating the cerebrovascular circulation in real time. TCD shows the spectral flow waveforms, blood flow direction and velocities in the intracerebral vessels, adding physiologic information to the anatomical images obtained with other imaging modalities. TCD can also detect collaterals through the ophthalmic, anterior communicating, and posterior communicating arteries caused by hemodynamically significant carotid stenosis or vertebrobasilar lesions. TCD remains the only method for detecting cerebral vessel embolization among other pathologies. TCD provides essential, real time, hemodynamic information about the intracranial circulation that is complementary to “static” brain imaging modalities.
After the spectral waveform has been sampled and its type recognized from the single gate display, spectral measurements are used to calculate the mean flow velocity (MFV) and pulsatility index (PI) values, parameters that describe cerebral circulation and form the quantitative basis for diagnosis of a particular circulatory abnormality. Although velocity does not equate to flow volume, it correlates well with vessel patency and the degree of an arterial stenosis. The PI is an indirect measure of peripheral resistance. Post-stenotic blunted waveforms have a low-resistance PI (<0.6). Normotensive patients that are breathing room air should have a PI between 0.6 and 1.2 in all normal diameter vessels. The ophthalmic arteries normally have high-resistance PI values (>1.2). Patients with chronic hypertension will also have an elevated PI. The spectral waveform shows a peaked systolic upstroke but has a decreased velocity during diastole.
In an effort to develop a method of rapid TCD evaluation and interpretation, a fast track insonation protocol was developed. Using such a protocol, emergency room TCD studies could be completed and interpreted within minutes at the bedside by the treating clinician, nurse, or technologist.
In addition to identifying changes in intracranial blood flow velocity, TCD detection of embolic particulate matter as well as gas bubbles have been well validated in laboratory and animal models. The intensity of the Doppler signal of an embolus traveling in blood depends on the size and acoustic impedance. The minimum detectable diameter of gaseous emboli has been reported at 10 μm, while particulate emboli can be detected from 40 μm. If microembolic signals (MES) are seen on both the side of the carotid stenosis or revascularization procedure and the contralateral side, the origin of the embolus may be from a central source (e.g., the heart or aorta). Unilateral MES more likely result from catheter movement, manipulation, or selective injection in the ipsilateral carotid system. However, emboli can cross the mid-line through collateral pathways and enter the contralateral middle cerebral artery (MCA) even with two patent internal carotid arteries (ICAs). Over 10% of embolic lesions detected on post-procedural testing occur on the contralateral side to the intervention. Monitoring bilateral MCAS during carotid interventions also helps differentiate MES from artifacts and determine changes related to blood pressure or cardiac output.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Transcranial doppler (TCD) is the “doctor’s stethoscope for the brain”. It is a non-invasive, safe, and cost-effective bedside test for evaluating the cerebrovascular circulation. TCD can also detect potential collateral flow signals in the ophthalmic, anterior communicating, and posterior communicating arteries caused by hemodynamically significant carotid stenosis. TCD remains the only method to detect asymptomatic embolization but does even more. TCD provides essential “real time”, hemodynamic information about the intracranial circulation compared to “static” brain imaging modalities.
Neurological complications related to carotid interventions are usually due to perioperative hypoperfusion, hyper-perfusion, or, most commonly, thrombosis and embolism. In addition to symptomatic thromboembolic events, silent subclinical cerebroembolism occurs at an even higher rate. Monitoring for, and real time detection of such events with TCD are critical to prevent, diagnose, and reverse procedure-related complications. TCD monitoring of the middle cerebral artery (MCA) during carotid artery stenting (CAS) is a valuable tool that quickly alerts clinicians to these complications. Monitoring bilateral MCAs also helps differentiate micro-embolic signals (MES) from artifacts and determine changes related to blood pressure, catheter manipulation, or cardiac output. Fewer MES were detected by TCD with the use of covered stents. Flow reversal techniques further reduces Mes during stent deployment.
TCD monitoring of carotid endarterectomy (CEA) can identify patients that develop ischemia during surgery. Cerebral blood flow measurements, electroencephalography (EEG), evoked potentials, cerebral oximetry, direct stump pressure measurements, and ultrasound can be used for this purpose. If CEA is performed under local anesthesia, patient status also can be monitored with repeat clinical examinations. EEG and cerebral oximetry are very sensitive to the development of cerebral ischemia, even before clinical changes become apparent; however, these methods can miss ischemia, particularly with general anesthesia, and are limited in their ability to determine the mechanism by which ischemia develops. Ultrasound can be “too” sensitive to detect microembolization and cerebral ischemia; however, it can demonstrate in real time the mechanism by which ischemia has developed (i.e., embolism, hypoperfusion, thrombosis, or hyperperfusion).
In summary, after either the CAS or CEA procedure, improved intracranial flow is an important sign of a job well done. On the other hand, the lack of velocity improvement or abnormal signals could prompt the initiation of rescue therapy.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
There are approximately 750,000 cases of stroke reported annually in the united states with 30% to 40% of unknown etiology. It has been reported that 56% of cryptogenic stroke patients 55 years old or younger have a patent foramen ovale (PFO). The PFO is a feature of the fetal heart configuration that permits flow of placental oxygenated blood from the right to the left atrium. In some individuals this channel, which usually seals during early childhood, remains patent as a functional atrial septal defect that allows flow under certain circumstances. There is evidence that shows an association between a PFO and ischemic stroke, particularly with cryptogenic stroke. Migraines have also been associated with a PFO.
The diagnosis of PFO is made through several methods including transthoracic echocardiography (TTE), transesophageal echocardiography (TEE), and cardiac catheterization. Transcranial doppler (TCD) offers a sensitive and minimally invasive method for the detection and grading of the PFO by accurately detecting and counting microbubble-induced embolic signals within the intracranial arteries.
There are pitfalls and advantages inherent to TCD in the detection of PFO. When performed correctly, in conjunction with standard echocardiography, TCD can improve the accuracy of the diagnostic work-up of the patient suspected to have a PFO.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Computational simulations of the hemodynamics in cerebral aneurysm is an active field of research motivated by its potential for virtual treatment planning, for visualizing flow changes during aneurysm growth, and for assessing rupture risk through quantification of hemodynamic parameters. In particular, wall shear stress (WSS), a force exerted parallel to the aneurysmal wall by the flowing blood, has been associated with aneurysm rupture. It has been suggested that WSS modulates the endothelial cell phenotype and that a WSS magnitude of less than 1.5 Pascal (Pa) may lead to the degeneration of the arterial wall.
Due to the lack of a reliable method to measure WSS in vivo, computational fluid dynamics (CFD) techniques are increasingly used in these simulations to obtain patient-specific results. An accurate knowledge of the vulnerability of a particular aneurysm may have an impact on the decision to treat the aneurysm by endovascular techniques or through open surgery, or to postpone treatment.
Early studies made use of geometrical information derived from rotational 3D digital subtraction angiographic (DSA) image data of the aneurysm and the surrounding vasculature only. However, recent work has suggested that accurate patient-specific results can only be obtained if patient-specific physiological flow information as inflow boundary conditions are also considered in the simulations.
In a multi-modality approach, we have combined X-ray fluoroscopy, 3D DSA, time-of-flight magnetic resonance angiography, and phase contrast magnetic resonance imaging to enhance the quality of CFD simulations by incorporating patient-derived geometrical and physiological flow information. Recently, we have extended this approach to visualize and to quantify blood flow changes in the endovascular treatment of cerebral aneurysms using flow diverter techniques.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
The vertebral arteries arise as the first branch of the subclavian arteries. The course of the vertebral artery is then divided into 4 parts: V1, the part of the artery between its origin from the subclavian artery and where it enters the transverse process of the sixth cervical vertebra; V2, the boney part of the artery as it ascends through the transverse foramina of C6 to C1; V3, the extradural portion begins where it exits the transverse process of the atlas vertebra (C1) and winds anteriorly around the anterior aspect of the spinal cord; and V4, the intradural portion prior to joining the contra-lateral vertebral artery on the ventral aspect of the medulla oblongata.
There are numerous anatomical variations in the vertebral arteries:
Commonly one artery is much larger than the other (usually the left is larger)
Occasionally one artery is vestigial
The left vertebral may arise from the aortic arch, between the left common carotid artery and the left subclavian artery
The right vertebral artery may arise directly from the arch
Both vertebral arteries may arise from the arch
Origin of the vertebral artery may be double
Occasionally the vertebral artery is affected by fibromuscular dysplasia; however, the most common process involving the vertebral arteries is atherosclerosis. Typically plaque develops in the wall of the subclavian artery and involves the origin of the vertebral artery. Most of these stenoses are short and confined to the origin. Frequently, post stenotic dilation of the artery is evident. Because the vertebral arteries join to form the basilar artery in front of the brain stem, it is generally believed that both vessels need to be compromised to render the patient symptomatic. Furthermore, because the basilar artery has a variable communication with the anterior circulation via the posterior communicating arteries, even bilateral vertebral stenosis or occlusions may be tolerated, provided the circle of Willis and the anterior circulation are intact.
Most patients with vertebral arterial disease are asymptomatic. Those who are symptomatic present with a constellation of symptoms: dizziness, blurred vision, drop attacks, vertigo, and nystagmus. Diagnostic tests for vertebral artery disease include:
Ultrasound scanning, which may show absent flow in one or both vertebral arteries and flow velocity may be reduced secondary to orificial stenosis.
CT angiography and MR angiography, which may show stenosis at the origin of the vertebral artery, but this is inconsistent.
Contrast angiography, which is usually required for a definitive diagnosis.
Usually the vertebral artery is dilated beyond the stenosis. There are 3 surgical options for the treatment of orificial disease: 1) endarterectomy, 2) bypass, and 3) transposition into the carotid artery. Bypass using saphenous vein is also an option for the V3 segment, typically basing the bypass from the carotid artery. This presentation will discuss and demonstrate the technique and complications of these options.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest, and the following were reported: the author is a consultant for Boston Scientific Corporation, VNUS Medical Technologies, Inc., W.L. Gore & Associates, Inc., Abbott Laboratories, MAQUET, Siemens Healthcare, and Medtronic, Inc.; on the speakers bureau for Boston Scientific, W.L. Gore & Associates, Inc., and Medtronic, Inc.; is a shareholder in Hatch Medical, NorthPoint Domain, and Embrella Cardiovascular, Inc.; and receives research funding from Nycomed, Hansen Medical, W.L. Gore & Associates, Inc., Harvest Technologies, Boston Scientific, Lombard Medical Technologies, and Bolton Medical, Inc.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Neurosonology provides bedside assessment of blood flow in main cerebral arteries and visualization of structural intracranial abnormalities. In order to select the best treatment, one should differentiate whether the worsening of neurological status in days after the onset of subarachnoid hemorrhage (SAH) is caused by vasospasm, increased intracranial pressure, sepsis, electrolyte disturbance, or seizures. Different vascular imaging methods are able to detect vasospasm in 40-70% of SAH patients, but only 20-30% of them have clinically relevant consequences of vasospasm [i.e., delayed ischemic neurological deficit (DIND)]. Transcranial Doppler (TCD) detects the increase of blood flow velocity caused by narrowing of blood vessel diameter. In the case of the middle cerebral artery (MCA), mean velocities (MV) above 120 cm/s suggest vasospasm and when its diameter decreases from 3 mm to 1 mm the MV increases to over 200 cm/s, which correlates well with dind onset. Even small MV increases are detectable with TCD, and when they appear, measures to avoid DIND, such as hypervolemic, hemodilution and hypertensive (HHH) therapy, should be undertaken. When HHH therapy is initiated, increased volume of diluted blood increases MV and this increase should be differentiated from vasospasm. The ratio of MCA MV to internal carotid artery (ICA) MV (Lindegaard ratio) helps in confirming vasospasm (if ratio is >3) or hyperemia (if ratio is <3). Similar ratios are also established for posterior circulation vasospasm.
Invasive devices are the gold standard for monitoring intracranial pressure (ICP). As it is clearly an advantage not to perform invasive procedures before ICP starts increasing, TCD provides daily noninvasive bedside monitoring of patients in the neurological intensive care unit (NICU). Pulsatility index (PI) is a derived parameter that best correlates with the increase in ICP. Normal PI values are 0.7 ± 0.3. An indirect measure of ICP is the optic nerve sheath diameter (ONSD). This measurement requires linear ultrasound probes, which are standard equipment in the most NICUs today. Since the optic nerve sheath directly communicates with cerebrospinal fluid (CSF) cisterns, an increase in ICP broadens the onsd. Serial measurements beginning at arrival in the NICU are needed in order to follow the progression of ICP.
Imaging of intracerebral haemorrhage (ICH) patients by means of transcranial duplex ultrasound (TDUS) is a useful adjunct to computed tomography (CT) scanning. The major advantages of tdus in the NICU are its ability to be performed at the bedside and as often as needed; disadvantages are its low resolution and suboptimal bone windows. Serial examinations are mandatory since hematoma expansion is closely related to poor outcome and surgical treatment might be indicated in some cases. CT scanning is the gold standard and almost all admitted patients are scanned before they enter the NICU. It is recommended that the patients are scanned as soon as they arrive in the NICU. If the bone window appears to be adequate, further ultrasound images should be compared to the initial one.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
This presentation will focus on intracranial arterial anatomy. Using angiographic imaging modalities, as well as intraoperative pictures, we will walk the Circle of Willis and discuss its anatomy, embryology, and anatomical variants. The emphasis will be on those anatomic areas and variants with a propensity to develop aneurysms, or that impact decision-making in the treatment of cerebral aneurysms.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Isolated disease of the innominate artery is uncommon and most surgeons or interventionalists gain little experience in this area. The most common condition of the innominate artery requiring consideration of intervention is obstruction. Obstruction is most common from atherosclerosis, but is also seen in inflammatory conditions such as Takayasu’s arteritis. Aneurysmal disease is the next most common lesion, but usually is an extension of an arch aneurysm. Trauma affects the innominate artery with both penetrating and blunt injury. Deceleration injury most commonly causes transection at the aortic isthmus, but the take off of the innominate artery from the arch is the second most common site. Infection and trachea-innominate fistula from tracheostomy is a rare cause of injury, but the surgeon must understand its cause and repair.
There is general agreement that symptomatic obstructive disease should be treated. Symptoms may reference the right carotid or the right vertebral distributions as both are at risk from innominate artery disease. With little data to draw on there is less agreement concerning non-symptomatic obstructive disease. Commonly a stenosis of >75% has been used as an indication for intervention, but it is difficult to support this with data. In the unusual case that a coronary artery bypass is planned and the right internal mammary artery is to be used, then intervention is imperative. Intervention may be by open surgical bypass or an endovascular approach. Open approaches have used full sternotomy, partial upper right “J” mini sternotomy, and a right thoracotomy approach. Endovascular approaches have generally been from the femoral artery. Arch anatomy may make this difficult or impossible, and a brachial approach may be needed and the interventionalist must understand and be prepared for both approaches.
Aneurysmal disease is generally related to an extension of an arch or ascending aortic aneurysm. Repair can be achieved by standard open techniques as well as hybrid arch endograft techniques. Isolated innominate aneurysm is unusual and generally does not have adequate landing zones for endovascular repair.
Innominate artery penetrating trauma is generally repaired with an open approach because of the high association of other injuries needing repair. Innominate artery transection from blunt trauma occurs at its junction with the arch and cannot be sealed by endovascular approach without stent grafting the arch itself. This lesion is also generally repaired in an open fashion.
Short- and long-term outcomes have been reasonable in both approaches, although long-term patency of innominate occlusion repair is higher with open surgical procedures. No matter what approach is chosen, it is imperative that the clinician understand and screen for the high rate of significant coronary artery disease often associated with this disease.
Conflict of Interest Disclosure: The author has completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest, and the following was reported: the author is on the speakers bureau and receives research funding from Medtronic, Inc.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
In 2005, CPT codes were created for carotid artery stenting (CAS) with embolic protection (CPT code 37215) and without embolic protection (CPT code 37216). These bundled descriptors include ninety-day global services, all selective catheterization, pre- and post-stent angioplasty, and all radiology supervision and interpretation except at the great vessel origins. The CAS code is reported once, regardless of the number of stents implanted. However, diagnostic catheterization and imaging on the opposite side or within the vertebral arteries is separately reportable.
The Centers for Medicare and Medicaid Services (CMS) produced a 2005 CAS national coverage decision (NCD) that approves reimbursement only if a patient has: lateralizing transient ischemic attack or minor stroke (Rankin score <3), “high risk” for carotid endarterectomy, 70% or worse stenosis confirmed by angiography, and use of an embolic protection device. If CAS is planned but the embolic protection device cannot be advanced appropriately, the procedure, according to CMS guidelines, should be aborted and carotid endarterectomy (CEA) considered. Additionally, patients at high risk for CEA who have either symptomatic carotid artery stenosis between 50% and 70% or asymptomatic carotid artery stenosis >80% are acceptable for reimbursement in post- market clinical trials. Private insurers, for the most part, have followed CMS’s lead.
The CMS memo also includes 5 facility requirements with a 2-year re-accreditation process. To comply, each hospital must certify that it possesses an adequate imaging and equipment inventory, maintains appropriate consult support services, oversees a provider-credentialing venue, ensures a data-collection mechanism, and manages an internal analysis of outcomes at an interval less than every 6 months. The provider must also report his or her outcomes at least every 2 years, including any patient treated outside of the coverage criteria on a FDA-approved trial.
There have been multiple reconsiderations of this NCD for coverage of those individuals at high surgical risk from comorbidity or anatomic considerations. No expansion of coverage has occurred to date besides certification of flow-reversal as an appropriate embolic protection device.
CEA by either standard longitudinal arteriotomy or ever-sion technique is reported by CPT code 35301 (carotid, vertebral, or subclavian artery thromboendarterectomy by a neck incision). Insertion of a prosthetic (Dacron or polytetrafluoroethylene) patch is bundled, as is harvest of autogenous vein from a remote site for patch closure. Shunt insertion, whether elective or on-demand, does not have any additional reimbursement. When a patient has had prior carotid artery surgery, the add-on code 35390 may be reported in addition to 35301 to compensate the time and effort associated with a reoperative field.
In some circumstances, CEA is not possible or practical. Common carotid to ipsilateral internal carotid artery bypass with a vein is reported by CPT code 35501, while a crossover autogenous graft falls under CPT code 35509. Common carotid to ipsilateral carotid artery revascularization with a non-autogenous bypass is described through CPT code 35601. Crossover prosthetic carotid grafting has no specific stand-alone code at present and is therefore usually billed using CPT code 35261 (repair blood vessel with graft other than vein; neck).
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Atherosclerotic plaques develop over decades before they cause symptoms, which are typically due to plaque rupture with subsequent thrombosis causing arterial obstruction. In symptomatic cases, whether in the coronary or pre-cerebral circulation, invasive treatment has proven effective in preventing new ischemic episodes. In asymptomatic cases, invasive treatment is probably not effective in the majority of cases, at least as long as we consider degree of stenosis as our prime indicator.
Over the last decades medical treatment of risk factors for atherosclerosis has proven effective in symptomatic and asymptomatic cases. However, some patients still develop new ischemic symptoms despite “optimal” medical therapy. Therefore, new measures of plaque vulnerability as well as change of such plaque “features” over time are needed. With the current knowledge of the pathogenesis of atherosclerosis, stenosis is certainly not a reliable predictor, even though it has been an easy target to address clinically. Imaging to identify/monitor plaque features is developing quickly. Although the best image quality is obtained from magnetic resonance imaging, this method has serious drawbacks due to the resources needed for its use. The equipment is expensive, it requires special facilities to be used, and data acquisition and image reading, in particular, is time consuming. Alternatively, 3D ultrasound imaging may be performed quickly, although reading does require some time. However, since equipment is much less expensive and acquisition is fast, and because atherosclerosis is widespread in the community and may necessitate lifelong surveillance, ultrasound will most certainly be first-line technology for plaque identification and monitoring of treatment.
What kind of plaque modulation may be expected over time and/or from medical intervention? Certainly, slowing/halting of growth is feasible and has been shown to occur under some statin regimes. In addition, reduction of the necrotic lipid core may be an effect of statin treatment. New drugs/treatment principles are also emerging, with the possibility that anti-inflammatory treatment may offer new opportunities. This might result in both halting of plaque growth as well as change in morphology of the lesion!
This presentation will focus on emerging imaging opportunities, describe what can be expected of plaque modulation, and speculate on how monitoring will be meaningful and clinically applicable.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Thrombi that develop in left atrial appendage (LAA) are the primary source of cardioembolic strokes in atrial fibrillation (AF). Pharmacological strategies for stroke prevention in af are limited to anticoagulation, with a significant associated risk of hemorrhage, morbidity, and mortality. Alternative, non-pharmacological strategies to reduce stroke risk in AF by excluding the LAA from the circulation have been devised. Early efforts at open, surgical ligation of the LAA have not proven to prevent strokes in af due to inadequate standardization of the surgical technique, poor verification of LAA closure, and study design flaws. Recently, several percutaneous strategies to exclude the LAA have been proposed and show promise as effective tools for stroke prevention. These strategies will be discussed.
The Watchman device is a parachute-shaped nitinol device that is placed in the LAA neck via a trans-septal approach. After deployment, its surface endothelializes and the LAA ostium is sealed. In the PROTECT-AF study, the Watchman device proved to be non-inferior to warfarin oral anticoagulation in the prevention of strokes. It is currently undergoing study in a larger multicenter study in higher-risk patients. Several additional devices with different designs but a similar overall trans-septal deployment strategy are being proposed and studied in clinical trials. Potential problems of such trans-septally deployed devices stem from the fact that a foreign body is permanently implanted in the circulation, with risks of embolization, thrombosis, and perforation during implant.
To circumvent these issues, pericardial approaches have been proposed that attempt to ligate the LAA at its ostium by delivering a suture from the pericardial space. The Lariat device uses such an approach. Via a combined endovascularepicardial approach, using magnets to hold the LAA while a lasso-like suture is delivered over it, the LAA is ligated at its ostium, achieving a complete closure. Registry data supports the robustness of LAA closure, but stroke prevention and outcomes data are still lacking. Similar devices are likely to evolve in the future. The eventual role of LAA closure strategies, particularly in the face of new oral anticoagulants with improved safety profiles, is yet to be defined, but these strategies represent an appealing alternative to life-long drug therapy if procedural safety and stroke prevention outcomes support their promise.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Bypass surgery is an important intracranial revascularization option; however, this type of microsurgery is highly technically challenging. This study reviews the neurovascular experience of bypass surgery performed by 2 surgeons at our institution. Emphasis was placed on the development of this critical neurovascular skill in young neurosurgeons. A prospective neurosurgical database was maintained with clinical (presentation, management, and follow-up) data along with angiographic studies for a consecutive series of patients undergoing cerebrovascular bypass surgery by 2 neurosurgeons at a tertiary neurovascular center.
Over a 10-year period, 94 cerebrovascular bypass surgeries were performed. The overwhelming majority of cases were extracranial-intracranial (EC-IC) microanastomoses, with 5 cases of intracranial-intracranial (IC-IC) bypass. Twenty-three cases were performed as the main or adjunct treatment of complex, typically giant intracranial aneurysms. Fifteen bypasses used the superficial temporal artery as the donor vessel, and the remaining cases used either the saphenous vein or radial artery as the donor. Middle cerebral artery (MCA) branches were the recipient vessels in all but 4 cases, which used the posterior cerebral artery (PCA) branches as recipients. In the IC-IC bypass cases, 1 MCA-PCA bypass used a saphenous vein graft. The other 4 cases were performed by in situ technique or vessel re-implantation. All patients received 325 mg aspirin within 48 hours preoperatively and postoperatively for at least 3 months. Bypass patency was evaluated by postoperative cerebral angiograms and, more recently, with intraoperative catheter angiogram and/or indo-cyanine green video angiography. Technical success was achieved in 20 cases and graft patency was maintained in 10 of 13 cases with available late follow-up angiographic studies. Procedure-related complications with cerebral hemorrhage or ischemia occurred in 5 patients, resulting in 3 mortalities. All aneurysms were successfully excluded from cerebral circulation and no postoperative aneurysmal bleeding was noted. Among 15 patients with long-term follow-up, 12 had good performance status (Modified Rankin score less than 3).
The cerebrovascular bypass technique is an integral component of comprehensive neurovascular surgery today. The indications for bypass surgery may expand in the future. Technical proficiency can be obtained through laboratory practice and subspecialty training in high-volume neurovascular centers. In conclusion, good results can be achieved by young neurosurgeons.
Methodist Debakey Cardiovasc J. 2012 Jan-Mar;8(Suppl 1):S3–S19.
Increasing numbers of intracranial aneurysms are being treated with endovascular techniques. The safety and efficacy of interventional treatment may be more pronounced in deep vascular sites, like the anterior communicating complex (Acom) and basilar apex (BA), due to the technical challenges of open surgery. This study analyzes the neurovascular practice in the hybrid surgical management of deep intracranial aneurysms by a dual fellowship-trained neurosurgeon. A prospective neurosurgical database was maintained with clinical (presentation, management, and follow-up) data along with angiographic studies for a consecutive series of patients undergoing intracranial aneurysm treatment by a single surgeon at a tertiary neurovascular center.
Over 48 months, 82 Acom and 29 BA aneurysms were treated in 109 procedures. Acute subarachnoid hemorrhage (SAH) was present in 47 cases, for which 28 were treated endovascularly. In 62 unruptured cases, 26 were treated with clipping. Anterior communicating complex aneurysms were the most commonly treated intracranial aneurysms overall. All surgical approaches were based on pterional transsylvian technique. In 8 cases, modified orbitozygomatic extension was adopted to enhance surgical exposure. Direct clipping was applied in all cases, and temporary clipping for proximal control was applied in 29 cases. Complete aneurysm occlusion was documented in all cases by intraoperative catheter angiography and indocyanine green video angiography. One perioperative death from malignant cerebral edema occurred in a patient with Hunt & Hess grade 4 SAH from a ruptured Acom aneurysm. Four patients (all SAH) remained in poor neurological condition (Modified Rankin score greater than 3) 6 months after treatment. There was no post-operative rebleeding and no aneurysm retreatment was required.
In conclusion, microneurosurgery remains a safe and effective measure in the treatment of intracranial aneurysms, even for acom and BA regions. Clip ligation can achieve durable aneurysm occlusion with preservation of parent vasculature in well-selected patients. Ruptured wide-neck aneurysms, small dysplastic aneurysms, and aneurysm neck compromised by critical perforators are good indications for surgical clipping. Neurosurgeons with hybrid microsurgical and endovascular expertise in high-volume centers can provide comprehensive management options for challenging intracranial aneurysms and may achieve optimal patient outcomes.