EPIDEMIOLOGY

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AF is the most common sustained cardiac dysrhythmia, and it affects nearly 2.5 million Americans.⁵ In the general population, the prevalence is 0.4 percent, but it increases with age such that 3.8 percent of people 60 years of age and 9.0 percent of those older than 80 years have the disorder. Men are at higher risk of experiencing AF (5.8 percent) than are women (2.8 percent) in the group aged 65 to 69 years, but in the group aged 70 to 79 years the risk is essentially the same (men, 5.9 percent, and women, 5.8 percent).⁶ The disorder also commonly is seen in people who had myocardial infarction, coronary artery disease, congestive heart failure, valvular heart disease, cardiomyopathy, hypertension, diabetes, obesity and thyrotoxicosis.⁷

AF increases the risk of stroke four- to fivefold and is responsible for approximately 15 percent of all ischemic strokes and almost 25 percent of strokes occurring in people 80 years or older.⁸ It also increases by threefold the risk of congestive heart failure.⁹ People with AF and a concurrent second cardiovascular disease (for example, hypertension, coronary artery disease) have about a twofold increase in mortality, but it remains unclear if the increase is secondary to AF and the associated rapid ventricular rate or the underlying cardiovascular disease.¹⁰ During the next 40 years, the number of Americans diagnosed with AF is expected to rise to almost 16 million given the expected aging of the population and the concomitant increase in chronic illnesses associated with its development.^11–13

	CARDIAC PHYSIOLOGY

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The SA node, a small mass of tissue with the characteristics of both muscle and nerve that is situated in the right atrial wall, generates (depolarizes) nerve impulses that initiate each heartbeat. The fibers of the SA node fuse with the surrounding atrial muscle fibers so that the action potential generated in the nodal tissue spreads rapidly, evenly and uniformly throughout both atria and produces atrial contractions (that is, the atrial component of systole). This electrical wave front does not immediately pass into the ventricles because they are insulated from the atria by fibrous heart valves. Interspersed among the atrial muscle fibers, however, are several internodal fiber bundles that conduct the impulse to the atrioventricular (AV) node, which is located in the lower part of the interatrial septum. In the AV node, there is a short delay in the transmission of the impulse to the ventricles, which permits the atria to complete their contractions (consistent with the P wave on the electrocardiogram [ECG]) and empty their blood into the ventricles that already are partially filled with blood that had passively drained from the large veins (vena cava on the right side and the pulmonary veins [PVs] on the left side) into the atria during diastole. Once the impulse leaves the AV node, it descends in the interventricular septum via the bundle of His and terminates in the Purkinje fibers of the ventricle walls, causing them to contract (that is, the ventricular component of systole), as noted on the ECG by the presence of the QRS complex.

	CARDIAC PATHOPHYSIOLOGY

TOP ABSTRACT EPIDEMIOLOGY CARDIAC PHYSIOLOGY CARDIAC PATHOPHYSIOLOGY DIAGNOSIS MEDICAL MANAGEMENT DENTAL CONSIDERATIONS MEDICATION INTERACTIONS WITH... CONCLUSION References

 
The pathophysiology of AF is highly diverse and spans the spectrum from a dysrhythmia developing in response to structural and functional remodeling as a consequence of a pre-existing illness such as hypertension, congestive heart failure, lung disorder and thyroid disease, to a primary electrical disturbance. For example, hypertension commonly is accompanied by increased atrial stiffness and compensatory changes in the left ventricle, including hypertrophy and diastolic dysfunction. The resultant increase in left ventricular diastolic pressure is transmitted to the left atrium and pulmonary vasculature causing structural and functional changes. These changes include atrial dilatation, atrial fibrosis and atrial myocyte degeneration. Such changes result in altered atrial electrophysiology, resulting in multiple chaotic electrical discharges that form wavelets instead of the classic P wave and originate from atrial components other than the SA node.^14–16 These abnormal discharges are rapid (350–600 impulses per minute) and irregular, and they spread throughout the atria in a random pattern that depolarizes only small islets of myocardium and result in only localized minicontractions. Thus, the atrial chambers quiver rather than synchronously contract as a whole.

The atrial blood that should have been propelled into the already partially filled ventricles contributing to cardiac output remains in both atria. The loss of this additional contribution to ventricular filling (termed "atrial kick") results is as much as a 20 to 30 percent loss of cardiac output.¹⁷ Furthermore, the residual atrial blood hinders blood from leaving the lungs and traveling to the left atrium. This results in excess fluid in the lungs (pulmonary edema) and leads to shortness of breath. The residual atrial blood also hinders the return of blood from the systemic circulation to the right atrium and results in fluid accumulation (edema) in the ankles and abdominal organs. The presence of both pulmonary and ankle edema often is categorized as congestive heart failure. The residual atrial blood (most specifically, that in the left atrial appendage, a small cul-de-sac in the atrial chamber) is relatively stagnant and prone to form thrombi. These thrombi can embolize into the systemic circulation, in which they may occlude any number of vessels, including, most disastrously, a cerebral artery, causing an ischemic stroke.¹⁸

The rapid irregular electrical discharges from atrial sites other than the SA node then pass through the AV node at random, causing the ventricles to contract irregularly and usually rapidly (greater than 130 beats per minute). The increased effort from rapid ventricular contractions requires that the heart muscle be supplied with additional oxygenated blood. However, because of the rapidity of ventricular contractions, there is inadequate time for them to fill with blood completely. Suboptimal emptying of the atria compounds this problem. Consequently, less blood is pumped into the systemic circulation with each contraction, and this blood is less than optimally oxygenated because its flow was impaired when it passed through the lungs initially. The increased heart rate also compromises flow into the coronary arteries that supply the heart muscle during diastole. When the oxygen demand of the cardiac muscle exceeds the ability of the coronary arteries to supply the heart with oxygen-rich blood, the patient develops angina.

Other groups of patients with AF are those with ectopic foci located in the narrow band of tissue that surrounds the openings of the four PVs in which they enter the left atrium. The juxtaposition of two types of tissue—that is, PV endothelium and atrial endocardium with differing electrical properties—likely predisposes patients to the development of AF.^19,20 AF also may occur in people younger than 60 years with no clinical or echocardiographic evidence of cardiopulmonary disease and is referred to as "lone AF." Some researchers believe this is brought about during stress and fatigue or with excessive use of coffee, alcohol and cigarettes. In addition, there are numerous people with the disorder who remain asymptomatic (termed "silent AF") and do not receive a diagnosis until they have a stroke.

	DIAGNOSIS

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The initial evaluation of a patient who may be experiencing the first AF episode begins by taking a detailed history and conducting a physical examination. The history focuses on the symptoms associated with AF. The first step during the examination is palpation of the pulse for any irregularity (with or without an accompanying tachycardia). Consistent with AF is an irregularly irregular pulse. In patients 60 years and older, this finding has a sensitivity of 94 percent but a specificity of 72 percent and requires further diagnostic testing.²¹ Further physical examination focuses on signs of atherosclerosis and heart failure, including arterial bruits and jugular venous distension, and a detailed heart examination. A standard 12-lead ECG is performed to evaluate the patient’s heart rhythm and is a key step in the diagnosis of AF. The blood is tested for thyroid, renal and hepatic function, and a chest radiograph is obtained to evaluate the lung parenchyma and pulmonary vasculature.

The paroxysmal form of AF, lasting just minutes or hours with the heart rate spontaneously returning to normal between episodes, is difficult to diagnose. The ECG performed at the initial visit to the physician’s office may not show the problem. In these cases, the patient is asked to wear an ambulatory ECG monitoring device, which records the heart’s rhythm over a prolonged period.

The persistent form of AF, which lasts until it is treated, is diagnosed more easily. Physicians can recognize the abnormal beats by taking the patient’s pulse and can hear the rapid and irregular heartbeats using a stethoscope. Because of the varying stroke volumes resulting from varying periods of diastolic filling, not all ventricular beats recognized by auscultating the heart with a stethoscope produce a palpable peripheral pulse. Confirmation of the diagnosis is obtained with a standard ECG. The chaotic electrical activity produces irregular "fibrillatory waves" (rapid oscillations), which replace the recognizable P waves of atrial depolarization. These deflections vary in size, shape and timing, and they are accompanied by the irregular occurrence of normal-appearing QRS complexes of ventricular depolarization with a rate that usually ranges between 100 and 160 beats per minute. In elderly patients, the ventricular rate often is slower.

	MEDICAL MANAGEMENT

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Medical experts have determined that administering medications that slow the ventricular rate in combination with other drugs to prevent thrombus formation is associated with fewer drug-related adverse events. There also is no loss in survival advantage when these medications are compared with those that restore and maintain sinus rhythm in patients older than 60 years who have the persistent form of the disease.^22–24 These medications slow the ventricular rate by retarding the conduction of electrical impulses through the AV node. Beta-blockers (atenolol, carvedilol, metoprolol, propranolol) and calcium channel blockers (diltiazem, verapamil) are the medications prescribed most frequently because they control the patient’s heart rate during both rest and activity. Few patients are prescribed digoxin, which is effective in slowing the heart rate only when the patient is not physically active. A combination of agents may be used for rate control. Slowing the rate of ventricular contractions enhances cardiac output, as more time is available for atrial contraction and ventricular filling. This often results in relief from symptoms of dizziness, weakness and shortness of breath.

The determination of stroke risk caused by cardiogenic thombi often is guided by the CHADS2 score, which is an acronym for an index that gives 1 point each for Congestive heart failure, Hypertension, Age 75 years or older and Diabetes mellitus, as well as two points for a prior Stroke or transient ischemic attack. Patients with a score of zero are treated with aspirin (81–325 milligrams), owing to the low stroke rate. Those with a score of 1 are prescribed either aspirin or the anticoagulant warfarin sodium (Coumadin, DuPont Pharmaceuticals, Wilmington, Del.) depending on the patients’ preferences, bleeding risk and access to good international normalized ratio (INR) monitoring. Warfarin inhibits the biologically active forms of the vitamin K–dependent factors II (prothrombin), VII, IX and X, as well as the regulatory factors protein C, protein S and protein Z. It is recommended that patients with a score 2 or higher receive warfarin therapy owing to the high stroke risk.²⁵

Warfarin decreases the risk of ischemic stroke by 68 percent, but it is associated with an increased risk of hemorrhagic stroke and extracranial bleeding in such sites as the gastrointestinal tract.^26,27 The dosage level is titrated so that it takes the blood approximately two and one-half times (range, two to three times) the normal amount of time to clot, which equates to a "prothrombin time" expressed as an INR of 2.5.²⁸ A number of risk factors for bleeding while receiving anticoagulation therapy have been identified, such as an INR greater than 3, adverse drug interactions (see below), poorly controlled hypertension, liver disease, chronic renal failure and being 65 years and older, as well as psychosocial risk factors associated with nonadherence (such as substance abuse including excessive use of alcohol and psychiatric illness).²⁹ Patients who are unable or unwilling to monitor their INR levels sometimes are prescribed antiplatelet medications such as aspirin, clopidogrel or both, but these therapies are less effective than warfarin in preventing embolic strokes.³⁰

The process of resetting the heart to sinus rhythm, known as cardioversion, often is used to reduce symptoms such as exercise intolerance and may improve left ventricular function (ejection fraction).³¹ Cardioversion can be accomplished by administering antidysrhythmic medications or delivering an electrical shock to the heart. Most antidysrhythmic medications (amiodarone, sotalol, dofetilide, flecainide, propafenone) approved by the U.S. Food and Drug Administration convert AF to sinus rhythm by blocking the channels in the walls of cells through which ions travel (sodium, potassium and calcium channels and beta-adrenergic channels), thereby slowing the electrical conduction velocity and delaying repolarization. Restoration of sinus rhythm also controls and regularizes the ventricular rate.³² These medications are effective in 50 to 60 percent of patients, but because they often fail, anticoagulant agents usually are prescribed continuously to reduce the stroke risk. These medications also have numerous adverse systemic side effects.³³ Of specific concern to dentists is that amiodarone interacts with warfarin, thereby increasing the anticoagulation effect.³⁴ Sotalol may cause or exacerbate lung disease, thus compromising the safety of inhalation anesthesia.

Cardioversion also can be performed by transmitting a low voltage (nontissue-destroying amounts) of electrical current to the heart through paddles applied to the external surface of the chest wall. The electric shock, synchronized to the R wave on the patient’s ECG, stops the abnormal electrical activity of the heart briefly, permitting the SA node to resume its role as the primary pacemaker. This process is successful in more than 95 percent of patients, but in approximately 75 percent of these people, AF returns in 12 to 24 months. Anticoagulant agents also usually are prescribed for these patients because rhythm therapy may fail without warning.

AF ablation can be accomplished by destroying the tissues (arrhythmogenic foci) that cause aberrant electrical discharges known as "hot spots." These sites, which are identified during the electrophysiological mapping process, are destroyed by radio frequency energy (or cryoenergy, lasers, microwaves or ultrasound) delivered by catheters threaded up toward the heart from the blood vessels in the groin. The catheter is inserted percutaneously into the femoral vein and then advanced into the inferior vena cava and then into the right atrium. From here, left atrium access is accomplished by means of an interarterial septal puncture.³⁵ Hot spots frequently are located in the narrow band of tissue (a sleeve of myocardium) that surrounds the openings of the four PVs where they enter the left atrium.³⁶ Encircling and isolating these sites with catheter-produced scars prevents transmission of these PV foci to the rest of the heart and corrects AF in 80 percent of patients. During cardiac surgery, a maze procedure can be performed in which a series of mazelike incisions or radio frequency burns are made in the atria in an attempt to eliminate AF. Other patients’ cardiac situations require that radio frequency energy be applied to the AV node to destroy small components of tissue. This prevents the atria from sending too many electrical impulses to the ventricles and impairing ventricular function. However, a permanent pacemaker then must be implanted under the skin, usually below the clavicle. Electrodes from the pacemaker’s generator are threaded through veins, which return to the heart. Small electrical impulses are sent along these leads to the heart to establish ventricular sinus rhythm. This procedure almost always improves the patient’s quality of life, but because the atria continue to fibrillate, anticoagulant medications still are required.

	DENTAL CONSIDERATIONS

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Most patients with AF can be treated safely in the dental office when specific precautions are taken (Table 1). Consultation with the patient’s physician to discuss the safest venue for providing dental treatment often is appropriate, especially for people who have advanced comorbid diseases that are treated with multiple drug regimens. Patients requiring general anesthesia are treated best in a hospital or fully equipped ambulatory surgical care center.

The dental literature presents conflicting infor mation as to the potential danger posed by ultrasonic scalers and electrosurgical units, as they may produce electromagnetic interference, which can impair pacemaker function. In 1998, Miller and colleagues³⁷ conducted an in vitro test and found that ultrasonic scalers and electrosurgical units did interfere with pacemaker function. Furthermore, in a 2000 position paper, the American Academy of Periodontology advised that practitioners avoid using magnetostrictive ultrasonic scalers (but not piezoelectric scalers) owing to the potential deleterious effects that they may have on pacemaker function.³⁸ In 2005, however, Patel and colleagues³⁹ conducted an in vivo test and found that ultrasonic scalers and electronic pulp testers did not adversely affect pacemaker function. Similarly, in 2007, Brand and colleagues⁴⁰ found that ultrasonic tooth scalers and electrosurgical units did not impair pacemaker function. Further confounding this issue are articles in the medical literature that suggest that patients with pacemakers are at risk from electrosurgical units, be they monopolar units in which the electric current spreads out and penetrates the patient’s entire body or bipolar units in which electric current flows only to the spot between the tips of the instrument.^41–43 In view of the conflicting information in the scientific literature, the various types of implantable pacemakers, the many types of ultrasonic scalers and electrosurgical units on the market and the various venues in which dentists practice (that is, dental office operatories, ambulatory surgical clinics and main operating rooms of hospitals), it would be prudent for dentists to use hand instruments for scaling and root planing and a scalpel for incising tissue when treating patients with permanent implantable pacemakers.

Minor dental procedures—such as administering infiltration local anesthetic, placing restorations, fabricating fixed and removable prosthetic appliances and supragingival scaling and polishing—usually do not require that dentists consider the patient’s INR, but prudent dentists will consult with the physician responsible for the patient’s warfarin therapy before performing more invasive procedures. The discussion between practitioners should include the patient’s recent INR values, access to the patient’s INR value on the day of surgery,⁴⁴ plans to optimize blood pressure control to minimize intraoperative bleeding, and an assurance that the patient is not also receiving antiplatelet agents (such as aspirin, clopidogrel or both).⁴⁵ Although it is common for physicians to concur with or support the American Heart Association (AHA) guidelines that permit interruption of anticoagulation therapy for up to one week for surgical procedures that carry a risk of bleeding,⁴⁶ dentists should make physicians aware of the American Dental Association Council on Scientific Affairs (ADA CSA) guidelines that recognize that, while the AHA guidelines may be germane for patients undergoing general surgery, orthopedic surgery and so forth, they are not applicable for patients undergoing dentoalveolar surgery.⁴⁷ Furthermore, dentists should note that the ADA CSA, the British Dental Association and the Haemostasis and Thrombosis Task Force of the British Committee for Standards in Haematology⁴⁸ have reviewed the scientific literature^49–55 and have concluded that warfarin therapy should not be discontinued for patients undergoing routine dentoalveolar surgery if their INR is 4 or less. This is because the difficulty in predicting the drop in the INR value in any given patient and because the risk of a patient’s experiencing a thromboembolism (which may be lethal) clearly outweighs the risk of a patient’s experiencing excessive postoperative oral bleeding. These conclusions should be reassuring to physicians, because this level of anticoagulation therapy is in excess of the 2.0 to 3.0 range (2.5 target) typically prescribed for patients with AF and, thus, provides an even greater margin of safety.⁵⁶ Most of these studies, however, evaluated patients having up to five simple tooth extractions (with most patients having between one and three extractions) and there are no studies to date involving significant numbers of patients having more extensive surgeries such as six or more extractions, removal of impacted teeth, alveolectomies or tori removal.⁵⁷

In a literature review, Scully and Wolff ⁵⁸ identified certain procedures or precautions that may limit intraoperative and postoperative hemorrhaging in patients who are receiving warfarin therapy when undergoing oral surgery. They found that administration of local anesthetic agents containing vasoconstrictors helps maintain a dry surgical field and that intraligamentary and intrapapillary injections are preferred to regional blocks if the patient’s INR is greater than 3.0 because of an anecdotal risk of bleeding into the floor of the mouth and fascial planes of the neck, which can lead to obstruction of the airway.

To minimize the risk and extent of postoperative bleeding, the number of teeth extracted at one sitting should be limited, and, when required, teeth should be sectioned to limit the need for ostectomies.⁵⁹ When ostectomies are required, subperiosteal-tension–free flaps should be developed and minimal bone should be removed to preserve the elements of the socket’s bony walls to enhance clot stabilization. All granulation tissue should be curetted from the surgical site, resorbable gelatin or oxidized cellulose materials should be placed in the socket, the bony wound should be compressed, soft tissues should be apposed closely and tight multiple interrupted sutures should be placed. Patients should be asked to bite on saline-soaked gauze compresses for 30 minutes after surgery. Some clinicians augment the above procedures by also having patients rinse their mouths with an antifibrinolytic agent such as epsilon-aminocaproic acid (or tranexamic acid), four times per day for two minutes.^60,61

The AHA’s guidelines may be applicable when dentists are planning more complex and invasive maxillofacial surgical procedures, such as an extraoral open reduction of facial fractures that is associated with extensive bleeding in patients without a history of stroke, transient ischemic attack, systemic embolisms or a mechanical heart valve.⁶² Patients’ warfarin therapy should be managed in cooperation with the patients’ physicians, and patients’ INRs must be evaluated on the day of surgery. Older people are slower to normalize an elevated INR and may experience warfarin-related bleeding at lower INRs than do younger people.^63–65 In some instances, physicians may prescribe "bridging anticoagulation" of subcutaneous low-molecular-weight heparin (LMWH) to shorten the time that the patient is unprotected from thromboembolisms.^66–68 Typically, the last preoperative dose of LMWH is administered 24 hours before surgery. The first postoperative dose is given no earlier than 24 hours after surgery, commonly on the second postoperative day when hemostasis has been secured.⁶⁹ Warfarin therapy may be reinstituted on the evening of surgery if hemostasis has been assured; if not, then it is started 24 hours postoperatively.

	MEDICATION INTERACTIONS WITH WARFARIN

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Medications prescribed with warfarin that may alter the risk of experiencing hemorrhage, irrespective of whether they directly alter the INR value, are shown in Table 2. These interactions are relatively rare, but they are unpredictable and may vary depending on dosage, duration, intermittent versus long-term use and other factors.^70–72 Concomitant adjustments in warfarin dosage may need to be made by patients’ physicians to maintain the desired degree of anticoagulation therapy and to minimize the risk of bleeding.

Acetaminophen should be avoided because a study has shown that taking four regular strength (325 mg) tablets of acetaminophen per day for longer than one week significantly increases the risk of markedly elevating the INR value.⁷⁶ This occurs because one of acetaminophen’s metabolites inhibits a key enzyme in the vitamin K cycle required for the liver’s production of coagulation factors.⁷⁷

Certain medications, when taken over a number of days with warfarin, may increase the patient’s INR value and risk of hemorrhage unless the warfarin dosage is adjusted.⁷⁸ This occurs because warfarin prevents the metabolism of vitamin K to its active form, which is needed in the liver’s synthesis of specific clotting factors. This effect is amplified by certain antibiotics (tetracyline, ampicillin and amoxicillin plus clavulanic acid), which further decrease available vitamin K because they destroy some of the normal intestinal bacteria that produce it.^79–82 The patient’s INR and risk of hemorrhage also may be increased by medications such as metronidazole and the macrolides (erythromycin, azithromycin, clarithromycin) because they inhibit the normal metabolism of warfarin.^83,84 Similarly, azole anti-fungal agents such as ketoconazole, fluconazole and itraconazole may increase the patient’s INR by inhibiting the metabolism of warfarin.^56,85 However, a single dose of an antibiotic such as amoxicillin, ampicillin, azithromycin or clarithromycin is unlikely to have any signifi cant effect on the patient’s INR.⁸⁶ If a full antibiotic course is indicated, the narrow-spectrum penicillin V (or clindamycin for those allergic to penicillin) is the preferred medication.⁸⁷

Other medications that may interact adversely with the therapeutic agents used to treat AF and render them less effec tive include dicloxacillin, nafcillin, phenobarbital and chloral hydrate, which can induce enzyme systems to rapidly metabolize warfarin.⁸⁸ NSAIDs prescribed for more than three weeks can impair the effec tiveness of β-blockers to limit the heart rate, and erythromycin and tetracycline can induce digitalis toxicity.^89,90

	CONCLUSION

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As the population in the developed world ages, an increasing number of patients with AF will be treated with invasive dental interventions. Dentists must be familiar with the pathophysiology of AF and the medical treatment options. Some of these therapeutic regimens can affect dental treatment with regard to the surgical risk of hemorrhage and the need for consultation with the patient’s physician when prescribing medications that may alter the effects of anticoagulant agents.