Spontaneous Carotid Artery Research Articles

Advances in Emerging Therapies 2010

In 2010, there were significant advancements in stroke prevention, whereas there were fewer studies that unearthed new ground on treatment of acute stroke and rehabilitation. We first discuss important pivotal studies in stroke prevention followed by acute treatment and rehabilitation. ### Prevention #### Homocysteine, Folic Acid, and B Vitamins Approximately 90% of all strokes are attributable to vascular risk factors.1 Homocysteine has also been identified as another risk factor for stroke. VITAmins TO Prevent Stroke (VITATOPS) aimed to assess whether daily administration of folic acid, vitamin B6, and vitamin B12 in patients with recent stroke or transient ischemic attack lowers homocysteine and reduces major vascular events. The data overall and pooled analysis of individual patient data showed that B vitamins have no or at most a marginal positive effect on reducing vascular events.2 #### Blood Pressure There is a correlation between blood pressure levels and risk of stroke. Data from Rothwell and colleagues now show that not only blood pressure levels, but also blood pressure variability account for stroke risk. A meta-analysis of antihypertensive drug trials found that calcium channel blockers and nonloop diuretic drugs were more effective than other antihypertensive agents to reduce blood pressure variability.3 Drug-class effects on interindividual variation in blood pressure can explain differences in effects of antihypertensive drugs on risk of stroke independently of their effects on mean systolic blood pressure. This means that the ideal antihypertensive agent should lower both blood pressure levels and variation in blood pressure to reduce stroke risk; however, we currently do not have such agents in our pharmacopeia for stroke prevention. #### Antithrombotic Drugs and Cerebrovascular Diseases New data have emerged on some age old questions about carotid dissection and intracranial stenosis. The use of aspirin or anticoagulation in spontaneous carotid artery dissection is a matter of debate with little data to guide decision-making. Data within a nonrandomized study suggest that the frequency …

Spontaneous internal carotid artery dissection in dystrophic bullous epidermolysis - association or determinant factor?

Pathogenesis of spontaneous carotid artery dissection (sCAD) is still a domain of research. Classical inherited connective tissue disease, primary or systemic arteriopathies and ultrastructural alterations of the arterial wall were reported in sCAD. We report a case of sCAD in a middle-aged woman with dystrophic epidermolysis bullosa, an inherited blistering disease due to a deficiency of type VII collagen at the basement membrane zone (BMZ).

Listening to the diagnosis: a physician’s account of spontaneous carotid artery dissection

A healthy 52-year-old male (J.L.A.) experienced a right pulsatile tinnitus (PT). It was synchronous with cardiac systole, was noticed initially at night, and became objectively audible. Valsalva’s maneuver markedly diminished its intensity. There were no previous trauma, otalgia, hypoacusis, fever, nasal congestion, cough, headache or any neurological symptom. Arterial pressure, ECG, chest X-ray, neuro-otological examination, otoscopy, audiometric testing, tympanometry and cerebral magnetic resonance (MR) imaging were unrevealing. A cerebral magnetic resonance angiography (MRA) raised the suspicion of a possible dissection of an extracranial right internal carotid artery (ICA) near the skull base. Subsequently, a cervical CT angiography (CTA) and a cervical MR angiography (MRA) yielded the diagnosis of right steno-occlusive (less than 50% luminal stenosis) ICA dissection, extending from 1 cm above the carotid bulb to the cranial base, ending just proximal to the petrous carotid canal. The dissection was associated with a medium-sized saccular pseudoaneurysm located near the skull base—C1-C2 level. Digital subtraction angiography (DSA) confirmed the diagnosis and showed bilateral fibromuscular dysplasia of carotid arteries as the cause of the dissection (Fig. 1). No intravascular intervention (i.e., stenting) was considered necessary due to the high location of the pseudoaneurysm and the lack of neurological symptoms. Treatment with intravenous heparin was followed by aspirin. Tinnitus gradually disappeared in 4 days. At follow-up, CT demonstrated resolution of the luminal stenosis and thrombosis of the false lumen, although the pseudoaneurysm remained unchanged.

Dynamic Internal Carotid Artery Dissection Demonstrated by Carotid Duplex Ultrasound

Background Carotid artery dissection is an important cause of stroke in young adults. Because warning signs usually precede stroke, the timely diagnosis of carotid dissection can have a significant clinical impact. We present a case of spontaneous carotid artery dissection with dynamic findings on duplex ultrasound examination. Case Report A 47-year-old man presented with acute neurologic symptoms. Carotid duplex ultrasound demonstrated a high resistive waveform in the right internal carotid artery (RICA) with absent end-diastolic flow (peak-systolic velocity [PSV] = 49 cm/sec, end-diastolic velocity = 0 cm/sec), a narrowing of the lumen in the distal RICA with low velocity flow (PSV = 10 cm/sec), and eventual loss of flow. The right common carotid artery demonstrated a high resistive waveform. The use of magnetic resonance angiography confirmed the presence of distal RICA dissection. The patient was treated with antiplatelet therapy and had marked clinical improvement within 48 hours. A duplex ultrasound study performed 24 hours after the first study demonstrated dramatic restoration of the diastolic flow in the RICA (PSV = 97 cm/sec, EDV = 44 cm/sec) with normalization of the Doppler waveforms. Repeat magnetic resonance angiography demonstrated near complete resolution of the RICA dissection, correlating with the ultrasound findings. Conclusion Our case demonstrates the potentially dynamic nature of carotid artery dissection and the utility of duplex ultrasound as an invaluable tool in the early diagnosis and management of this disorder. In addition, the case demonstrates the importance of carotid Doppler waveform clues as indirect evidence of more distal cerebrovascular disease that warrants further investigation.

Acquired infantile Horner syndrome and spontaneous internal carotid artery dissection: A case report and review of literature

Horner syndrome, a triad of ptosis, anisocoria, and anhidrosis, results from interruption in the oculosympathetic pathway. It is classically described as either congenital or acquired to depict its underlying pathophysiology and requisite work-up. We report a case of a 10-month-old infant presenting with an acute onset of left Horner syndrome secondary to a spontaneous extracranial internal carotid artery dissection. To the best of our knowledge, this is the first case report in the literature of acute onset of acquired infantile Horner syndrome in association with spontaneous carotid artery dissection confirmed with magnetic resonance angiogram.

Bilateral internal carotid artery occlusions in a pediatric patient with refractory acute myeloid leukemia

Thromboembolism is a well-known complication of cancer including acute myeloid leukemia (AML) especially in patients with high myeloblast counts. However, spontaneous vaso-occlusion in the main arteries is very rare especially in patients with low blast counts and no pre existing vasculopathy. We report the case of a 3-year-old male with refractory AML who developed spontaneous bilateral internal carotid artery occlusion with diffuse cerebral infarcts. Strokes are rarely secondary to spontaneous carotid artery thrombosis and few cases have been reported in the literature.

Horner's syndrome—not to be sneezed at

Although no robust evidence is available for the routine use of anticoagulants, imaging studies suggest that most complications are due to thromboembolic events rather than insuffi cient fl ow. A retrospective analysis of 298 patients, found a 2-6% risk of subsequent ischaemic stroke with antiplatelet or anticoagulant therapy, with no signifi cant diff erence between the two. 5 Sneezing is an unusual but recognised cause of spontaneous carotid artery dissection; Horner’s syndrome may be the sole presenting feature, therefore a high index of suspicion is required.

Local Symptoms and Recanalization in Spontaneous Carotid Artery Dissection

To the Editor: We congratulate Nedeltchev and coworkers for their meritorious report1 on recanalization of spontaneous internal carotid artery dissection. The strengths of this work are a fairly large patient population compared with most previous reports and the repeated ultrasound examinations of the vasculature at 1, 3, 6, and 12 months. Recanalization always occurred within 6 months, but not later. We, having similar experience, currently repeat vascular imaging only at 6 months. Nedeltchev et al discuss that they did not detect any beneficial effect of complete recanalization and refer to 2 articles that do not directly support their view; of these, one is a small study on 60 cervical artery dissection patients treated with anticoagulants2 and the second3 is a review in Spanish …

Spontaneous bilateral carotid artery dissection in a woman presenting with isolated headache

Spontaneous bilateral carotid artery dissection in a woman presenting with isolated headache

Aspirin or Anticoagulation to Prevent Stroke in Carotid Dissection

Spontaneous extracranial internal carotid artery dissection is an uncommon cause of acute ischemic stroke. Treatment is aimed at prevention of

High-resolution MR imaging of periarterial edema associated with biological inflammation in spontaneous carotid dissection

It has been suggested that spontaneous cervical carotid artery dissection (sCAD) may result from arterial inflammation. Periarterial edema (PAE), occasionally described in the vicinity of the mural hematoma in patients with sCAD, may support this hypothesis. Using cervical high-resolution magnetic resonance imaging, three readers, blinded to the mechanism of carotid artery dissection, searched for PAE, defined as periarterial T2-hyperintensity and T1-hypointensity, in 29 consecutive CAD patients categorized as spontaneous CAD (sCAD, n = 18) or traumatic CAD (tCAD, n = 11; i.e., major head or neck trauma within 2 weeks before the clinical onset). The relationships between PAE, inflammatory biological markers, history of infection and CAD mechanism were explored. Multiple CADs (n = 8) were found only in sCAD patients. Compared with tCAD, patients with sCAD were more likely to have a recent history of infection (OR = 12.5 [(95%)CI = 1.3-119], p = 0.03), PAE (83% vs. 27%; OR = 13.3 [(95%)CI = 2.2-82.0], p = 0.005) and to have elevated CRP (OR = 6.1 [(95%)CI = 1.2-32.1], p = 0.0002) or ESR (OR = 8.8 [(95%)CI = 1.5-50.1], p = 0.002) values. Interobserver agreement was 0.84 or higher for PAE identification. sCAD was associated with PAE and biological inflammation. Our results support the hypothesis of an underlying arterial inflammation in sCAD.

Recanalization of Spontaneous Carotid Artery Dissection

In a cohort of 249 patients with 268 spontaneous carotid artery dissections, these authors asked how often, when, and to what extent the arterial lumen

An unusual clinical presentation of ischemic stroke due to carotid dissection: The wrist drop

We report a patient with sudden onset of right wrist drop mimicking radial nerve palsy, found to be due to a borderzone infarct due to spontaneous carotid artery dissection (CAD).

Extracranial Carotid and Vertebral Artery Dissection: A Review

Dissection of the extracranial carotid and vertebral arteries is increasingly recognized as a cause of transient ischemic attacks and stroke. The annual incidence of spontaneous carotid artery dissection is 2.5 to 3 per 100,000, while the annual incidence of spontaneous vertebral artery dissection is 1 to 1.5 per 100,000. Traumatic dissection occurs in approximately 1% of all patients with blunt injury mechanisms, and is frequently initially unrecognized. Overall, dissections are estimated to account for only 2% of all ischemic strokes, but they are an important factor in the young, and account for approximately 20% of strokes in patients less than 45 years of age. Arterial dissection can cause ischemic stroke either by thromboemboli forming at the site of injury or as a result of hemodynamic insufficiency due to severe stenosis or occlusion. Available evidence strongly favors embolism as the most common cause. Both anticoagulation and antiplatelet agents have been advocated as treatment methods, but there is limited evidence on which to base these recommendations. A Cochrane review on the topic of antithrombotic drugs for carotid dissection did not identify any randomized trials, and did not find that anticoagulants were superior to antiplatelet agents for the primary outcomes of death and disability. Healing of arterial dissections occurs within three to six months, with resolution of stenosis seen in 90%, and recanalization of occlusions in as many as 50%. Dissecting aneurysms resolve on follow-up imaging in 5-40%,decrease in size in 15-30%, and remain unchanged in 50-65%. Resolution is more common in vertebral dissections than in carotid dissections. Aneurysm enlargement occurs rarely. The uncommon patient presenting with acute hemodynamic insufficiency should be managed with measures to increase cerebral blood flow, and in this setting emergency stent placement to restore cerebral perfusion may be considered, provided that irreversible infarction has not already occurred.

Spontaneous Bilateral Carotid Artery Dissection: Diagnosis and Follow-up with MDCT

Carotid artery dissection is usually unilateral. Rarely bilateral forms can be seen. Recent studies have shown the efficacy of computed tomography angiography (CTA) in the diagnosis of carotid dissection. Herein we report a case with bilateral carotid artery dissection diagnosis and follow-up which was carried out using mainly CTA.

Neck Hematoma Caused by Spontaneous Common Carotid Artery Rupture

We present a case of an 83-year-old male without previous history who presented with a cervical hematoma, initially misdiagnosed as a neck phlegmona. In the course of the diagnostic workup, the hematoma enlarged, thereby causing respiratory distress because of upper airway compromise. The endotracheal intubation was lifesaving. Later, contrast enhanced computed tomography revealed hematoma in the region of the left common carotid artery. Emergency surgery evacuated the hematoma and repaired a slit-like defect of the left common carotid 2 cm before bifurcation. The patient was discharged on the seventh postoperative day in good condition. We discuss four aspects of the case, namely, the rarity of the condition and the variety of causes, the diagnostic and treatment strategy, the uncertain reasons for spontaneous ruptures of the carotid, and the operative techniques for hematoma evacuation and definitive hemostasis. The optimal strategy for cases of cervical hematoma is the following: intubation, diagnosis, and surgery.

Symptomatic spontaneous intracranial carotid artery dissection treated with a self-expanding intracranial nitinol stent: a case report

Background Although extracranial carotid dissection with stroke is common, intracranial dissection with stroke is rare. Stenting has been used to treat extracranial carotid dissections. Intracranially, however, it is only recently that stents have become a feasible option for this disease. We present a case of a spontaneous intracranial CAD with progressive symptoms despite medical management treated with a self-expanding intracranial micronitinol stent. Case Description A 47-year-old, right-handed woman presented to the emergency department after noticing left-sided face and arm weakness and numbness, along with slurred speech. The patient was started on aspirin 325 mg/d orally and lovenox 40 mg/d subcutaneously. On hospital day 2, the patient was noted to have repeated episodes of weakness and numbness on the left side and MRI evidence of a new stroke. A diagnostic cerebral angiogram from a selective right internal carotid injection revealed a flow-limiting stenosis secondary to a dissection of the supraclinoid internal carotid artery with severe flow limitation to the hemisphere. Endovascular management was decided on, and a Neuroform stent measuring 4.5 × 20 mm (Boston Scientific Corporation, Natick, Mass) was deployed across the dissection with significant improvement of flow to that hemisphere on the poststent angiogram. Conclusions This case illustrates the successful off-label use of a self-expanding intracranial nitinol stent to treat a symptomatic intracranial internal CAD in the setting of failure of traditional medical management. This is a promising application of novel endovascular technology.

Risk stratification after myocardial infarction: a new method of determining the neural component of the baroreflex is potentially more discriminative in distinguishing patients at high and low risk for arrhythmias

We hypothesize that the neural component (NC) of the baroreflex sensitivity (BRS) is a better risk stratifier for ventricular tachycardia/fibrillation (VT/VF) than conventional BRS itself, because it is both independent of vessel wall stiffness and can be measured non-invasively. NC was determined by correlating spontaneous carotid artery diameter variations with R-R interval variations using spectral analyses. In consecutive outpatient populations with chronic coronary artery disease the ability of the NC to distinguish post-myocardial infarction (MI) patients at risk for VT/VF (post-MI(HIGH RISK)) from post-MI less prone to arrhythmias (post-MI(LOW RISK)) was compared with the pressure-derived BRS(phenyl) and BRS(spectral) method. Ninety-six patients, i.e. 28 post-MI(LOW RISK), 28 post-MI(HIGH RISK) [a LVEF(left ventricular ejection fraction) <30% and/or history of VT/VF] and 40 healthy controls were enrolled. With NC, rather than with BRS methods, median values for post-MI(HIGH RISK) were smaller than for post-MI(LOW RISK) patients (NC, P = 0.03; BRS(spectral), P = 0.35; BRS(phenyl), P = 0.63). Variability of R-R interval (LF = 0.04-0.15 Hz) was significantly larger in the control group than in the post-MI(HIGH RISK) and post-MI(LOW RISK) group (P < 0.01 and P < 0.01). To separate post-MI(HIGH RISK) from post-MI(LOW RISK) patients, a linear combination of age and the logarithm of the NC measurement was constructed as a risk index. By optimizing the intercept of this line, an optimal sensitivity and specificity pair was determined. The sum of optimal specificity and sensitivity was higher for NC (155) than for BRS(spectral) (133) and BRS(phenyl) method (132). With all methods, values for post-MI patients were significantly smaller than for controls. NC may be superior to conventional BRS measures in identifying post-MI patients at high risk for VT/VF.

Spontaneous carotid artery dissection: a rare cause of cerebrovascular accident

We present the case of a young woman who developed a cerebrovascular accident due to a spontaneous internal carotid artery dissection. We stress the importance of clinical clues to diagnosis: ipsilateral facial pain and a partial Horner’s syndrome are the most frequent clinical manifestations. Compared to patients with atherosclerotic cerebrovascular disease, these patient are younger and typically do not have the classical cardiovascular risk factors. The diagnosis should be confirmed with duplex ultrasound and magnetic resonance imaging or computed tomographic angiography.In many cases, optimal therapy consists of ‘watchful waiting’ and prompt initiation of oral anticoagulants (during 3 to 6 months) and aspirin or clopidogrel in case of late presentation without ischaemic symptoms. Endovascular or surgical treatment is rarely needed.The overall prognosis is more benign compared to atherosclerotic cerebrovascular disease, although a somewhat elevated risk for recurrent dissection is observed.

Spontaneous bilateral carotid and vertebral artery dissections associated with multiple disparate intracranial aneurysms, subarachnoid hemorrhage and spontaneous resolution: Case report and literature review

Spontaneous bilateral carotid and vertebral artery dissections (CADs and VADs) are rare. A 29-year-old female presented with a collapse, 4 weeks after a sudden onset of severe neck and shoulder pain. CT scan revealed diffuse subarachnoid hemorrhage (SAH) and early hydrocephalus. Angiography revealed bilateral CADs and VADs, along with multiple fusiform and saccular aneurysms. Systemic vessels – including the renal arteries – were normal, and no risk factors or underlying vasculopathy were apparent. The presumed source of SAH (a posterior cerebral artery aneurysm) was successfully clipped. Each dissection, by contrast, was managed conservatively with heparin prophylaxis; and spontaneous CAD and VAD resolution occurred within 6 months. We present a unique case of four-vessel dissection associated with multiple disparate saccular and fusiform aneurysms. We suspect that underlying vasculopathy – perhaps novel – may become apparent with time.