Carotid calcifications on panoramic radiography identify an asymptomatic male patient at risk for stroke A case report Laurie C. Carter, DDS, MA, PhD, a Kelly Tsimidis, DDS, b and Jude Fabiano, DDS, c Buffalo, N.Y. STATEUNIVERSITYOF NEW YORK AT BUFFALOSCHOOL OF DENTALMEDICINE Although stroke may be preventable, a major challenge is to find effective methods of detection of stroke-prone patients. Most noncardiogenic strokes occur as a result of atherosclerosis involving the proximal internal carotid artery, calcifications of which can be detected on dental panoramic radiography. This report describes the case of an asymptomatic patient whose dental radiographic findings led to carotid endarterectomy. Calcifications were viewed bilaterally in the soft tissues of the neck in the area of the carotid bifurcation on a screening panoramic radiograph of an asymptomatic 75-year-old man. Subsequent duplex Doppler ultrasound revealed extensive atherosclerotic changes bilaterally with critical stenosis (90%+) in the right internal carotid artery. Carotid digital subtraction angiography revealed a 95%+ stenosis at the origin of the right internal carotid artery. The patient underwent right carotid endarterectomy involving the internal, external, and common carotid arteries. Twelve months later the patient was alive and well. Dental panoramic radiography represents a useful imaging modality for detection of some asymptomatic stroke-prone patients. Identification of calcifications in the area of a patient's carotid vasculature should prompt expeditious referral to a physician for a cerebrovascular and cardiovascular work-up as part of an active stroke prevention strategy. (Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 1998585:119-22)
There is no doubt that carotid calcifications can be detected in the extracranial carotid vasculature on dental panoramic radiography.t However, although calcification of the coronary arteries is a well-established marker for significant cardiovascular disease, the relation of carotid calcification to clinical cerebrovascular events is as yet undefined. 2 Fortunately, calcified extracranial carotid arteries are amenable to further noninvasive investigation by duplex Doppler and Bmode ultrasound imaging. What follows is the case history of an asymptomatic individual who initially appeared at the dental clinic with carotid calcifications, as revealed on dental radiography.
CASE REPORT A 75-year-old man came to the clinics of the School of Dental Medicine for fabrication of complete dentures. A screening panoramic radiograph on January 5, 1996, revealed the presence of multiple punctate and irregular heterogeneous radiopacities. They were arranged in a verticolinear This project was supported in part by a grant from the National Institutefor Dental Research (5T35 DE07106-15). aAssociateProfessor and Director, Oral and MaxillofacialDiagnostic Imaging Clinic. bFormerly senior dental student; currentlygeneral practice resident, Strong Memorial Hospital, Rochester, N.Y. cClinicalAssistant Professor, Oral Diagnostic Sciences, and private practice, Amherst, New York. Received for publication Apr. 14, 1997; accepted for publication May 28, 1997. Copyright Š 1998 by Mosby, Inc. 1079-2104/98/$5.00 + 0 7/16185782
fashion bilaterally in the soft tissues of the neck, inferior to the angle of the mandible, and adjacent to the hyoid bone and the C3 and C4 vertebral bodies (Fig. 1). The radiographic impression was consistent with calcification of the carotid vasculature bilaterally in the area of the bifurcation and the internal carotid artery (ICA). Physical examination was negative for neck bruits, and the patient denied any history of overt transient ischemic attacks (TIAs). He did, however, suffer from lightheadedness on standing and from vertigo, for which he took meclizine (12.5 mg/day). Risk factors for cerebrovascular disease included a history of smoking, a myocardial infarction after a 1-month history of unstable angina (in February of 1993), and a subsequent quadruple coronary bypass and marginal endarterectomy. At the time of the bypass, it was noted that the patient's coronary vessels were highly calcified. On March 13, 1996, the patient was referred to his internist for cerebrovascular assessment. On March 29, 1996, sonographic examination of the bilateral carotid vasculature was performed by means of the duplex scanner with imaging and Doppler evaluation, including color Doppler. Extensive atherosclerotic changes containing calcium were observed at the right carotid bifurcation. Peak velocities were 430 cm/sec in the right proximal ICA and 276 crrdsec in the right external carotid artery (ECA). On the left side, the atherosclerotic changes were somewhat less pronounced. Peak velocities were 188 cm/sec in the left proximal ICA and 133 cm/sec in the proximal ECA. Carotid sonography identified carotid stenosis bilaterally with a critical stenosis (90%+) in the right ICA (Fig. 2). Stenosis was determined to be 90% in the right ECA, 70% in the left ICA, and 55% in the left ECA. On April 19, 1996, carotid digital subtraction angiography revealed a stenosis greater than 95% at the origin of the right ICA for a 2.5-cm 119
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B Fig. 1. A, Screening panoramic radiograph of 75-year-old man reveals multiple punctate and irregular heterogeneous radiopacities (arrows) bilaterally in soft tissues of neck, inferior to angle of the mandible, adjacent to hyoid bone and C3C4. B, Schematic representation of panoramic radiograph indicates location of calcifications in solid black. Fig. 3. Digital subtraction angiography revealed stenosis greater than 95% at torigin of right internal carotid artery (arrowhead).
On April 23, 1996, the patient underwent right carotid endarterectomy involving the ICA, the common carotid artery, and the ECA. In the right ICA, nearly complete occlusion with very irregular and thrombotic plaque was noted by the vascular surgeon. As of November 1997, the patient was ambulatory, fully functional, and pleased with the outcome.
Fig. 2. Duplex Doppler ultrasound revealed critical stenosis (90%+) in right proximal internal carotid artery with peak velocity of 430 cm/sec. This represents more than five-fold increase in normal velocity of blood flow of 65-80 cm/sec in this portion of the vessel, indicating stenosis of more than 90%.
segment (Fig. 3), as well as a high-grade stenosis at the origin of the right ECA. The left ICA showed a 60% to 65% stenosis and marked tortuosity just beyond its origin. The left ECA appeared widely patent. Blood chemistry revealed elevated total cholesterol (248 mmol/L) and elevated triglycerides (178 retool/L).
DISCUSSION Stroke represents the third leading cause of death in the United States and imposes enormous physical, emotional, and financial burdens on its victims and on society at large. Approximately 550,000 Americans suffer cerebrovascular accidents annually; of this number, approximately 400,000 survive with varying degrees of debilitation. 3 Taylor et al. 3 calculated the aggregate lifetime cost associated with first ischemic strokes occurring in 1990 to have been $29 billion. Reduction in morbidity and mortality via early identification of stroke-prone patients would prove to be of powerful humanitarian and economic significance. Calcification is a morphologic complication in the evolution of atheromatous plaquel In a histologic study, Fisher et al. 4 reported a strong quantitative parallel
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between calcification in the carotid siphon or carotid sinus and advanced atherosclerosis in the sinus itself. Culebras and associates 5 investigated 40 patients with unilateral symptoms of hemispheric ischemia with contrast-enhanced computed tomography of the neck. Linear-regression analysis of the data revealed that calcification was associated more frequently with severe luminal stenosis (> 75% reduction) than with any other tabulated morphologic complication of the plaque. 5 Culebras et al.5 concluded that calcification in carotid atheromas should be "acknowledged and tallied as an independent variable in studies correlating carotid plaque with the risk of occurrence of hemispheric symptoms since the natural history of this complication of atheroma formation remains largely unknown." Doris et al. 2 found a statistically significant association between the degree of calcification revealed on plain radiography and carotid atherosclerotic disease as demonstrated by digital subtraction angiography (p = 0.0001). They concluded that evidence of carotid artery calcification on plain radiographs served as a marker for significant extracranial carotid disease. 2 Friedlander and Lande 6 first described the presence of calcifications in the area of the carotid vasculature on the dental panoramic radiographs of 2% of 1000 male veterans attending a dental outpatient clinic. Friedlander and colleagues 7 viewed carotid calcifications on the dental panoramic radiographs of 37% of 19 Caucasian men admitted to a Veterans Affairs Medical Center hospital for treatment of recen[ strokes. The preponderance of risk factors such as prior TIAs and cerebrovascular accidents in the aforementioned population skewed the group in favor of the evolution of a future stroke. In the first reported series s,9 of carotid artery calcifications observed on panoramic radiographs in an ambulatory general dental outpatient clinic population, 3.6% of 1175 patients with a mean age of 40.1 years displayed carotid calcifications. Only one patient experienced TIAs. In a continuation study, 143 (5.2%) of 2752 newly accepted dental clinic patients were noted to have punctate or verticolinear calcifications in the distribution of the carotid bulb (inferior to the mandibular angle and adjacent to the hyoid bone and C3-C4) or in the proximal internal carotid artery (posterior to the ramus and adjacent to C2-C3). 1° Although interviews with the 143 calcification-bearing patients revealed a high incidence of recognized risk factors for atherosclerosis, only 3 of these patients (2.1%) expressed a history of visual, sensory, and/or motor TIAs. Dental panoramic radiography represents a useful imaging modality for the identification of some asymptomatic patients at heightened risk for stroke. Identification of calcifications in a patient's carotid vas-
culature should prompt expeditious referral to the patient's physician for a cerebrovascular and cardiovascular work-up as part of an active stroke prevention protocol. Indeed, evaluation of films already obtained in the course of routine dental treatment might prove to have significant public health utility in the identification of stroke-prone patients. Such identification could lead to aggressive lifestyle modifications, pharmacologic therapies, or, as in the case of the patient described in this report, surgical interventions that would increase the length and quality of life for these individuals. Recent clinical trials have advocated carotid endarterectomy to establish revascularization of stenotic lesions with over 60% luminal reduction in both symptomatic and asymptomatic patients.11,la There is a paucity of data on the frequency and distribution of qualitatively defined carotid atheromas in patients not referred for study on the basis of cardiovascular or cerebrovascular disease symptoms. Data on the prevalence of qualitative lesions in community-based populations not selected by disease may be of utility in clinical and public health policy decision-making. These studies indicate the need for large-scale outcome assessments correlating the detection of carotid calcifications on dental radiographs in free-living asymptomatic patients with specific evidence of cerebrovascular disease, as well as with event data such as ultimate incidence and death rate from cerebrovascular accident or myocardial infarction with or without interventional therapy . 13 The authors thank William B. Cline, MD, for his assistance with the evaluation and management of the patient discussed in this report. REFERENCES
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Reprint requests: Laurie C. Carter, DDS, PhD Associate Professor and Director Oral and Maxillofacial Diagnostic Imaging Clinic 355 Squire Hall School of Dental Medicine State University of New York at Buffalo Buffalo, New York 14214-3008