|
 
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| REVIEW ARTICLE |
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| Year : 2015 | Volume
: 5
| Issue : 2 | Page : 99-105 |
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Craniofacial pain as manifestation of angina
AV Ratheesh, GP Sujatha, Ashok Lingappa
Department of Oral Medicine and Radiology, Bapuji Dental College and Hospital, Davangere, Karnataka, India
| Date of Web Publication | 10-Mar-2016 |
Correspondence Address:
Dr. A V Ratheesh
Department of Oral Medicine and Radiology, Bapuji Dental College and Hospital, Davangere, Karnataka - 577 004
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2231-6027.178499
The most common types of orofacial pain originate at the dental or periodontal region or in the musculoskeletal structures. However, sometimes a patient may present pain in these regions even though the source is located elsewhere in the body. One possible source of heterotopic pain is of cardiac origin, which pose a diagnostic challenge. In 6% of patients, craniofacial pain can be the first and the only symptom of cardiac ischemia. Misdiagnosis of these cases may lead to unnecessary dental treatment and a significant number of deaths due to atypical symptoms of coronary disease. Keywords: Angina, cardiac pain, orofacial pain
How to cite this article:
Ratheesh A V, Sujatha G P, Lingappa A. Craniofacial pain as manifestation of angina. Int J Oral Health Sci 2015;5:99-105 |
| Introduction | |  |
The concept of hritshoola - literally heart pain - was known to Sushruta (6th century BC).[1] The first detailed account of the angina pectoris was given by a medical person Dr. William Heberden (1710–1801) in the 18th century.[2] Angina pectoris refers to episodes of chest pain caused by myocardial ischemia secondary to coronary artery disease (CAD). CAD or ischemic heart disease (IHD) is a group of diseases that includes stable angina, unstable angina, myocardial infarction, and sudden coronary death.
| Epidemiology | | |
IHD is one of the most common, serious, chronic, and life-threatening disease. The prevalence of chronic angina is approximately 4–5%. The incidence of newly diagnosed angina within developed countries is approximately 46/100,000 population. Men constitute 70% of IHD patients. Males clinically manifest this condition at 50–65 years of age and females about 10 years later, following menopause. Women have more frequent angina, which will be associated with greater physical impairment and a poorer quality of life.[3] The WHO reports that the principal cause of death of people over 65 years is CAD, and as age increases, a substantial proportion of deaths due to IHD are among females. In 2013, IHD resulted in 8.14 million deaths (16.8%) globally, which was only 5.74 million deaths (12%) in 1990. In India, IHD accounted for around one-fourth of all deaths in 2008.[4]
| Pathophysiology | | |
Ischemia refers to a lack of oxygen due to inadequate perfusion of the myocardium, which causes an imbalance between oxygen supply and demand. The most common cause of myocardial ischemia is an obstructive atherosclerotic disease of epicardial coronary arteries.[5]
In heart, epicardial coronary arteries form the conductance vessels, which can constrict and relax. The intramyocardial vessels form resistance vessels, which exhibit changes in tone. Normal coronary circulation is dominated and controlled by the heart's requirements for oxygen. This need is met by the ability of the coronary vascular bed to vary its resistance. Normally, intramyocardial resistance vessels demonstrate an immense capacity for dilation. The coronary resistance vessels also adapt to physiologic alterations in blood pressure in order to maintain coronary blood flow at levels appropriate to myocardial needs.[6] Major risk factors of angina are given in [Table 1].
Angina results when there is an imbalance between the heart's oxygen demand and blood supply. This imbalance can result from an increase in demand for oxygen without a proportional increase in oxygenated blood supply. In atherosclerosis, the lumen of coronary arteries will be reduced, which limits the appropriate increase in perfusion when there is increased demand for blood flow. Epicardial coronary arteries are the major site of atherosclerotic disease. Segmental atherosclerotic narrowing of epicardial coronary arteries is caused most commonly by the formation of plaque, which is subject to fissureing, erosion, hemorrhage, and thrombosis. Any of these events can temporarily worsen the obstruction, reduce coronary blood flow, and cause myocardial ischemia.[7]
Coronary blood flow can also be limited by arterial spasm, arterial thrombi, and rarely, coronary emboli as well as by ostial narrowing due to luetic aortitis. Congenital abnormalities, such as the origin of the left anterior descending coronary artery from the pulmonary artery, which causes myocardial ischemia and infarction in infancy. In case of severe left ventricular hypertrophy due to aortic stenosis, myocardial ischemia can occur due to increased oxygen and limited coronary blood flow. Furthermore, an increase in oxygen demand due to left ventricular hypertrophy secondary to hypertension and a reduction in oxygen supply secondary to anemia can cause ischemia. In Prinzmetal's angina, there will be abnormal constriction of the conductance vessels leading to severe ischemia. Microvascular angina is a condition in which abnormal constriction or failure of normal dilation of the coronary resistance vessels occur and cause ischemia.
As a result of ischemia, myocardial tissue oxygen tension falls and may cause transient disturbances of the mechanical, biochemical, and electrical functions of the myocardium. Total or subtotal coronary occlusion lead to the development of severe ischemia, which is associated with almost instantaneous failure of normal muscle contraction and relaxation.
When ischemia is transient, it may be associated with angina pectoris; when it is prolonged, it can lead to myocardial necrosis and scarring with or without the clinical picture of acute myocardial infarction (AMI). Severity and duration of the imbalance between myocardial oxygen supply and demand determine whether the damage is reversible (<20 min for total occlusion in the absence of collaterals) or whether it is permanent, with subsequent myocardial necrosis (>20 min).[8]
| Classification | | |
American College of Physicians described angina as either “typical” or “atypical” on the basis of how many of the clinical features are consistent with exertional angina [Table 2].[9]
Angina pectoris is also graded into four classes according to the classification of Canadian Cardiovascular Society [Table 3].[10]
| Types of Angina | | |
- Stable angina, also known as effort angina, is characterized by central chest pain, discomfort, or breathlessness that is precipitated by exertion or other forms of stress promptly relieved by rest
- Unstable angina is also called “crescendo angina” or acute coronary syndrome. It is defined as angina pectoris that changes or worsens. It has, at least, one of the following three features: (a) It occurs at rest (or with minimal exertion), usually lasting 3–5 min. (b) It is severe and of new onset, (i.e., within the prior attack of 4–6 weeks). (c) It occurs with a crescendo pattern, (i.e., distinctly more severe, prolonged, or frequent than before)[11]
- Prinzmetal's angina is a variant form of angina in which patients will have normal coronary arteries or insignificant atherosclerosis. This is caused by spasms of the coronary artery. It is characterized by rest and nocturnal angina. It is more commonly seen in younger women
- Microvascular angina or angina syndrome X has clinical features of angina but normal coronary arteries on angiogram. It occurs as a result of spasm in the tiny blood vessels of the heart, arms, and legs. It is not characterized by arterial blockages; it is harder to recognize and diagnose
- Decubitus angina is characterized by angina when lying down. It is typically due to left ventricular dysfunction
- Silent ischemia is the absence of angina in the presence of documented ischemia which occur due to coronary artery or microvascular dysfunction.[8],[11]
| Clinical Features | | |
Patients with angina will be presenting with central chest pain, discomfort or breathlessness that is precipitated by exertion or other forms of stress and promptly relieved by rest. Some patients find the discomfort comes when they start walking which gradually disappear and that later it does not return despite greater effort (“warm-up angina”). This episodic clinical syndrome is due to transient myocardial ischemia. When the patient is asked to localize the sensation, he or she will typically press on the sternum, sometimes with a clenched fist, to indicate a squeezing, central, substernal discomfort (Levine's sign).[11]
Typically, angina last for 2–5 min. Pain can radiate to the left shoulder and to arms, especially to the ulnar surfaces of the forearm and hand. Pain can also arise in or radiate to the back, interscapular region, root of the neck, jaw, teeth, and epigastrium [Table 4]. Angina is rarely localized below the umbilicus or above the mandible. Occasionally associated dyspnea or shortness of breath, epigastric discomfort, or sweating. Patients may have repeated attacks of angina over a long period, or have a myocardial infarction soon after the first one or two attacks.[8]
| Angina Manifesting as Orofacial Pain | | |
Craniofacial pain can be the sole symptom of an AMI in 4% of patients.[12] This referred pain to craniofacial structures in angina can be due to the convergence of cardiac nociceptive inputs into the trigeminal system, and the upper cervical spine and central sensitization mechanisms are likely to be involved.[13] Upper cervical spine segments is a convergence area for trigeminal, visceral, and phrenic inputs.[14] It is seen that trigeminal subnucleus caudalis receives extensive convergence inputs from cutaneous, muscular, and visceral afferents.[15] There will be excitation of C1–C3 neurons which usually receive somatic inputs from the craniofacial structures by cardiac nociceptive afferent fibers. This may explain the referred pain to craniofacial structures during angina. Animal models indicate that vagal and sympathetic afferent fibers are involved in the transmission of nociceptive input from the heart to C1–C2 neurons. C1–C2 spinal neurons act as an integrating center.[16]
Experiments using electrical stimulation showed that spinothalamic tract neurons in C1–C2 related to somatic fields in the jaws and the neck were more reactive to vagal than to sympathetic system.[17]
From 1960 to 2015, twenty cases and two group studies [12],[18] have been reported of craniofacial pain caused by angina. Ten cases reported bilateral pain, and eight cases reported unilateral pain. Only left side was involved in five cases.[18],[19],[20],[21],[22],[23] One case reported the unique involvement of right side.[24] Pain in maxilla was seen in three cases.[19],[25],[26] The mandibular pain was reported in six cases.[21],[22],[24],[25],[27],[28] Tooth pain as the only symptom was present in two cases.[22],[29] Pain over zygoma and the temporal region was seen in three cases.[27],[30],[31] In two cases, pain of temporomandibular joint was present.[32],[33] Radiation of pain to the forehead was present in one case.[34] Two cases revealed teeth and jaw pain, but sites were not specified.[35],[36] Seven cases reported instances where jaw, tooth, or facial pain were the sole symptoms of cardiac insufficiency.[23],[27],[28],[29],[32],[33],[35] Eleven cases presented chest pain as another symptom of the cardiac ischemia.[12],[19],[20],[22],[24],[25],[26],[30],[31],[34],[36] Although jaw, tooth, or facial pain was the chief symptom of the other studies, they presented with additional pain symptoms including back, shoulder, clavicle, chest, arm, and neck pain.[12],[19],[20],[21],[22],[25],[31] Lack of changes in the electrocardiogram (ECG) and absence of chest pain may predispose for a missed diagnosis in these type of cases.
Kreiner et al.[12] in the study of 186 patients reported that the most frequently reported location of craniofacial pain was upper throat (81.7%), left mandible (45.1%), right mandible (40.8%) and left temporomandibular joint/ear region (18.3%). The ratio of bilateral referral pattern of pain in the craniofacial region versus. Unilateral was 6:1. The incidence of craniofacial pain was 6% in angina patients. Incidence is 6% in angina patients.
Danesh-Sani et al.[37] had done a prospective multicenter study of 248 patients with cardiac ischemia.About 85 patients (34.2%) reported craniofacial pain during a period of ischemia. About 72 patients (84.7%) experienced pain in the craniofacial region, chest, shoulders, and arms. About 13 patients (15.3%) reported pain in the craniofacial area with no other concomitant symptoms. Two patients (2.3%) reported toothache in the mandibular teeth on both sides. One hundred and twenty-nine patients (52%) experienced AMI in which sixty-two patients reported craniofacial pain as a symptom and two male patients (1.5%) experienced craniofacial pain as the only symptom.
| Diagnosis | | |
Most important for diagnosis is differentiating the quality of craniofacial pain from cardiac or dental origin. Referred cardiac pain will be presented as a tight and burning sensation while an odontogenic toothache will be throbbing and tingling. Referred cardiac pain will be aggravated or induced by exercise and improve at rest. Careful elicitation of pain history and meticulous patient assessment can be helpful in diagnostic decision making. If the facial pain aggravates when the patient gets more nervous/stressed, it point to the possibility of cardiac origin.[12]
The typical patient with angina will be a man of above 50 years and woman above 60 years of age. Proper history taking and thorough physical examination is important in diagnosis. Risk factors [Table 1] should be assessed along with the presence of valve disease (particularly aortic), left ventricular dysfunction (cardiomegaly, gallop rhythm) or other manifestations of arterial disease (carotid bruits, peripheral vascular disease) and conditions that may exacerbate angina (anemia, thyrotoxicosis).[8]
Basic investigations include resting and exercise ECG. Patients walk and/or run on a treadmill while blood pressure and electrocardiography readings are monitored. The patient should achieve at least 85% of the maximal heart rate as determined by age and gender. Coronary angiography is indicated when there is evidence of IHD. As the complexity of the clinical situation increases, the threshold for the performance of coronary angiography decreases and enhancement of the exercise stress test can be obtained through the use of radioisotopes. Patients unable to exercise can be evaluated by means of the administration of adenosine (initial dose of 6 mg intravenous [IV]) or dipyridamole (15 mg), which cause increased myocardial oxygen demand.[38]
Medical management of a patient with chronic stable angina involves identification and treatment of associated diseases that can precipitate or worsen angina, reduction in coronary risk factors, and application of general and nonpharmacologic methods, with particular attention toward adjustments in lifestyle, pharmacologic management, and revascularization by percutaneous catheter-based techniques or by coronary bypass surgery.[7]
Basically, management of IHD is directed at decreasing oxygen demand or improving myocardial blood flow and thus improving oxygen delivery. It can be medical therapy or surgical procedures, which include percutaneous transluminal coronary angioplasty (PTCA), and coronary artery bypass grafting (CABG). Medical therapy is indicated in cases of mild to moderate stable angina.[6]
Risk factors should be managed, especially hypertension and cigarette smoking. Beta-blockers are used to prevent increased heart rate and contractility. Calcium channel blockers (CCBs) are also effective in decreasing myocardial work and increasing blood flow through coronary artery vasodilatation, especially when angina is caused by vasospasm. Angiotensin-converting enzyme (ACE) inhibitors can be used as afterload-reducing medications. Nitrates are the basis for medical therapy directed at angina. Nitrates cause coronary and peripheral vasodilatation. As a result, there will be an increase in coronary blood flow and decrease in cardiac work. However, this therapy has significant side effects that limit patient tolerance. Prognostic therapies for angina include aspirin, glycoprotein IIb/IIIa receptor inhibitors (e.g., clopidogrel), and lipid-lowering drugs, which reduce mortality rates in patients with CADs.[39]
Coronary revascularization (PTCA or CABG) is reserved for patients with preserved ventricular function and severe stable or unstable angina. PTCA is used in cases of recurrent angina after CABG or angioplasty.[8]
| Dental Considerations | | |
Major concern while treating a dental patient with CAD is to prevent ischemia or infarction. These patients are at increased risk of demand related ischemia from increased heart rate or BP. Anxiety can increase heart rate and blood pressure and can provoke ischemia or angina. It is important to know if angina occurs at rest, and if there are precipitating factors such as exercise, climbing stairs or emotional stress. Frequency, duration, timing, severity of attacks, and response to medication should also be noted. Protocols to reduce anxiety should be considered according to the level of anticipated stress. Premedication with antianxiety drugs can be used. Conscious sedation with inhalational nitrous oxide/oxygen analgesia can be given (nitrous oxide <65%).
Preoperative glyceryl trinitrate (10 µg/min IV) and sometimes oral sedation (e.g., temazepam) are advised before invasive dental procedures. Dental care should be carried out with minimal anxiety along with monitoring of oxygen saturation, blood pressure, and pulse monitoring. Effective anesthesia is essential. Ready access to medical help, oxygen, and nitroglycerin are crucial.[40]
If a patient with a history of angina experiences chest pain in the dental surgery, the dental treatment should be immediately stopped. The patient should be positioned in upright sitting position. Administer glyceryl trinitrate 0.3–0.6 mg sublingually and oxygen inhalation. Vital signs should be monitored. Pain should be relieved in 2–3 min. If not, myocardial infarction is a possible cause, and medical help should be summoned.[41]
Pain that persists even after three doses of nitroglycerin which is given with 5 min interval for more than 15–20 min, or that is associated with nausea, vomiting, syncope or hypertension is highly suggestive of myocardial infarction. If pain persists, continue administering oxygen and 300 mg of chewable aspirin. Tricyclic antidepressants are best to be avoided as they can disturb cardiac rhythm. Sumatriptan, a neuroactive alkaloid used in the treatment of migraine, is contraindicated as it may cause coronary artery vasoconstriction. Conscious sedation and general anesthesia should be deferred for at least 3 months.[41]
Various cardiovascular drugs used can cause adverse effects in the oral cavity. Xerostomia is the most common adverse effect which is seen in 14.1% of patients.[42] Other adverse effects include lichen planus, aphthous ulcers, angioedema, dysgeusia, gingival enlargement, scalded mouth syndrome, cheilitis, glossitis, and pemphigus. An important class of cardiovascular drugs known to cause oral adverse effects includes ACE inhibitors, angiotensin II-AT1 receptor blockers, diuretics, CCBs, beta-adrenergic blockers and alpha-adrenergic blockers.[43],[44] In addition, antiarrhythmics such as phenytoin and amiodarone, and also potassium channel opener like nicorandil can cause oral adverse effects.[45],[46] Other drugs such as aliskiren (direct renin inhibitor) and clopidogrel (antiplatelet agent) have also been shown to cause oral adverse effects.[47],[48] These adverse effects have been linked to the polymorphism of cytochrome P450 system involved in the metabolism of these drugs.[49]
After angioplasty, elective dental care should be deferred for 6 months. Emergency dental care if needed should be given in a hospital setting. In patients with CABG, adrenaline/epinephrine-containing local anesthetic should not be used, because it may possibly precipitate arrhythmias. For the first couple of weeks after surgery, the patient may feel severe pain when reclining in the dental chair as a side effect of the surgery.[41] Dental care for high-risk patients should be ideally provided in the late morning or early afternoon.
For patients with vascular stents, prophylactic antibiotic coverage should be given if emergency dental treatment is required during the first 6 weeks postoperatively. American Heart Association recommends oral administration of amoxicillin 2 g preoperatively. Patients not able to take oral medication can be given 2 g ampicillin IM/IV. Clindamycin 600 mg can be given to those patients allergic to penicillins. Elective dental care should be deferred. Patients may require long-term anticoagulant medication, so the appropriate action is required to deal with any bleeding tendencies.[40]
| Conclusion | | |
Cardiac pain can present solely as tooth or jaw pain. In most cases, craniofacial pain of cardiac origin is usually accompanied by some of these other symptoms or by a suggestive history such as pain provoked by exercise. Health care and dental providers should be aware of the possibility of atypical presentations of cardiac ischemia when assessing patients with tooth, jaw, or facial pain should pay due considerations regarding better management of such cases.
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Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3], [Table 4]
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