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Dusty Narducci, MD; Shivajirao Patil, MD; Matthew Zeitler, MD; Is an underlying cardiac Anne Mounsey, MD Department of Family Medicine & Orthopedics/ condition causing your patient’s , University of South Florida Health Carol and Frank Morsani ? Center for Advanced Healthcare, Tampa (Dr. Narducci); Department This review lists the questions to ask to obtain important of Family Medicine, East Carolina University, diagnostic clues and provides an algorithm for evaluating Greenville, NC (Dr. Patil); Department of Family palpitations when the initial Dx is not evident on EKG. Medicine, University of North Carolina, Chapel Hill (Drs. Zeitler and Mounsey)

Anne_mounsey@med. alpitations, the sensory perception of one’s heartbeat, PRACTICE unc.edu are reported in 16% of primary care patients, from RECOMMENDATIONS The authors reported no causes that are both cardiac (ie, ) and non- ❯ Order potential conflict of interest P 1 cardiac. Palpitations are usually benign; overall mortality is relevant to this article. for patients who have doi: 10.12788/jfp.0152 palpitations and risk approximately 1% annually. In fact, a retrospective study found factors for structural no difference in mortality and morbidity between patients with 2 . C palpitations and control patients without palpitations. How- ever, palpitations can reflect a life-threatening cardiac condi- ❯ Order stress testing for patients who have exertional tion, as we discuss in this article, making careful assessment 3 symptoms or multiple risk and targeted, sometimes urgent, intervention important. factors for coronary Here, we review the clinical work-up of palpitations, rec- disease. C ommended diagnostic testing, and the range of interventions for cardiac arrhythmias—ectopic beats, ventricular tachycar- ❯ Evaluate all patients who have associated dia (VT), and atrial (AF). with their palpitations for a cardiac cause. C Cardiac and noncardiac causes of palpitations Strength of recommendation (SOR) In a prospective cohort study of 190 consecutive patients A Good-quality patient-oriented evidence presenting with palpitations, the cause was cardiac in 43%, B Inconsistent or limited-quality psychiatric in 31%, and of a miscellaneous nature (including patient-oriented evidence medication, thyrotoxicosis, , , , am-  C Consensus, usual practice, opinion, disease-oriented phetamine, and ) in 10%; in 16%, the cause was evidence, case series undetermined.2 In this study, 77% of patients experienced a recurrence of palpitations after their first episode.2 Cardiac arrhythmias, a common cause of palpitations, are differentiated by site of origin—supraventricular and ventricu- lar. Noncardiac causes of palpitations, which we do not discuss here, include metabolic and psychiatric conditions, medica- tions, and substance use. (For a summary of the causes of pal- pitations, see TABLE 1.2-4) ❚ Common complaint: ectopic beats. Premature atrial contractions (PACs; also known as premature atrial beats, atri- al premature complexes, and atrial premature beats) and pre-

60 THE JOURNAL OF FAMILY PRACTICE | MARCH 2021 | VOL 70, NO 2 Palpitations are usually benign. But they can reflect a life-threatening cardiac condition, making careful assessment and targeted, sometimes urgent, intervention important.

mature ventricular contractions (PVCs; also and ischemic heart known as ventricular premature complexes disease. Therapy directed toward underlying and ventricular premature beats, and also of heart disease can reduce the frequency of a variety of possible causes) result in a feeling PVCs.7-9 of a skipped heartbeat or a flipping sensation in the chest. The burden of PACs is independently as- The diagnostic work-up sociated with mortality, cardiovascular hos- The most important goal of the evaluation pitalization, new-onset AF, and pacemaker of palpitations is to determine the presence, implantation. In a multivariate analysis, a or risk, of structural heart or coronary ar- PAC burden > 76 beats/d was an indepen- tery disease (CAD) by means of the history, dent predictor of mortality (hazard ratio , and electrocardiogra- [HR] = 1.4; 95% CI, 1.2-16); cardiovascular phy (EKG). Patients who have an increased hospitalization (HR = 1.3; 95% CI, 1.1-1.5); risk of structural heart disease need further new-onset AF (HR = 1.8; 95% CI, 1.4-2.2); evaluation with echocardiography; those and pacemaker implantation (HR = 2.8; at increased risk of CAD should have stress 95% CI, 1.9-4.2). Frequent PACs can lead to testing. cardiac remodeling, so more intense follow- Hemodynamically unstable patients up of patients with a high PAC burden might need admission; patients who have a history allow for early detection of AF or subclinical of syncope with palpitations usually should cardiac disease.5,6 be admitted for cardiac monitoring. Patients A burden of PVCs > 24% is associated who have had a single episode of palpitations with an increased risk of PVC-induced car- and have normal baseline results of labora- diomyopathy and . Polymorphic tory testing and a normal EKG, and no risk PVCs are more concerning than monomor- factors for structural heart disease or known phic PVCs because the former suggests the CAD, can usually be observed.3,4,10 Patients presence of more diffuse, rather than local- with an abnormal baseline EKG, recurrent ized, myocardial injury. The presence of palpitations (especially tachyarrhythmia), frequent (> 1000 beats/d) PVCs warrants or significant symptoms during palpitations evaluation and treatment for underlying (syncope, presyncope, dyspnea) need fur-

MDEDGE.COM/FAMILYMEDICINE VOL 70, NO 2 | MARCH 2021 | THE JOURNAL OF FAMILY PRACTICE 61 TABLE 1 What causes palpitations?2-4

Underlying condition or state Possible causes Bradyarrhythmia • Second- and third-degree • Severe sinus • Sinus pauses

Supraventricular arrhythmia • Accessory pathway (eg, • Atrioventricular nodal reentrant tachycardia Wolff-Parkinson-White syndrome) • Paroxysmal supraventricular tachycardia • • Premature atrial contractions • • • Ventricular arrhythmia • Premature ventricular contractions • and long-QT intervala •

High-output states • Anemia • Paget disease • Atrioventricular fistula • •

Medical and metabolic • • conditions • • • • Hypomagnesemia • • Medications • drugs • Vasodilators • Serotonin–norepinephrine reuptake • Withdrawal from beta-blockers inhibitors • Sympathomimetic agents Miscellaneous cardiac • Brugada syndrome conditions • Inappropriate tachycardia • Postural orthostatic tachycardia syndrome • Sinus tachycardia Psychosocial • • Depression • • Somatization Structural heart disease • Atrial myxoma • prolapse • • • Congenital heart disease • Stenotic or regurgitant • Dilated or hypertrophic obstructive Substance use • Alcohol • Marijuana • Caffeine intake (excessive) • • Illicit drugsb a Increases the risk of torsade de pointes. b , cocaine, Ecstasy (3,4 methylenedioxymethamphetamine [MDMA]).

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ther evaluation with ambulatory monitor- hypertrophic cardiomyopathy, congenital ing3,4,10 (FIGURE). coronary anomalies, and ion channelopa- thies, and can cause sudden cardiac death Take a thorough history; in athletes (estimated incidence, 1-3/100,000 ask these questions person–years12). ❚ Have the patient describe the palpita- ❚ Endeavor to identify underlying car- tions. The history should include the patient’s diac disease. A comprehensive history should detailed characterization of the palpitations also evaluate for risk factors and symptoms (sudden or gradual onset, rhythm, duration, (chest , dyspnea, diaphoresis, lighthead- frequency). Certain descriptions provide edness, syncope) of cardiac disease, such as possible diagnostic clues: CAD, valvular disease, cardiomyopathy, and • Palpitations lasting < 5 minutes are congenital heart disease, which increase the less likely to be of cardiac origin likelihood that the presenting complaint is a (likelihood ratio [LR] = 0.38; 95% CI, cardiac arrhythmia (LR = 2; 95% CI, 1.3-3.1).4 0.2-0.6).4 A history of syncope in a patient with palpi- • A patient who has a regular, rapid- tations should prompt evaluation for struc- pounding sensation in the neck has an tural heart disease, such as aortic or increased probability of atrioventricu- hypertrophic cardiomyopathy, in which out- lar (AV) nodal reentrant tachycardia flow-tract obstruction impairs (AVNRT) (LR = 177; 95% CI, 25-1251); and, subsequently, cerebral flow. Patients with absence of this sensation decreases ❚ Obtain additional key information. an abnormal the likelihood of AVNRT (LR = 0.07; Determine the following in taking the history: baseline EKG, 95% CI, 0.03-0.2).4 • Is there a family history of inherited recurrent • PACs and PVCs cause a sensation of a cardiac disorders or sudden cardiac palpitations, skipped heartbeat or a flipping sensa- death? or significant tion in the chest; they are not reported • What prescription and over-the-coun- symptoms as a sustained rapid heartbeat. ter medications is the patient taking? during • Patients with a supraventricular ar- How does the patient characterize palpitations rhythmia often report sudden onset his or her use/intake of recreational need evaluation and cessation of palpitations. drugs, nicotine, caffeine, and alcohol? with ambulatory • Patients with palpitations since child- • Does the patient have a history of monitoring. hood are more likely to have supraven- panic disorder, which lessens concern tricular tachycardia (SVT).4 about a cardiac cause (LR = 0.2; 95% CI, 0.07-1.01)?4 (Of note: A nonpsychiatric ❚ Elicit apparent precipitating and al- cause can coexist in such patients, and leviating factors. The history should include should be considered.) notation of situations that appear to the pa- tient to lead to palpitations (eg, context, posi- Physical examination clues, tional variation). Palpitations that affect sleep and the utility of vagal maneuvers (LR = 2.3; 95% CI, 1.3-3.9) and palpitations Although most patients in whom palpitations that occur at work (LR = 2.2; 95% CI, 1.3-5) in- are the presenting complaint are, in fact, crease the likelihood of a cardiac cause.4 Pal- during clinical assessment, pitations associated with sudden change in cardiovascular examination can assist in di- position, such as bending forward or squat- agnosing the arrhythmia or structural heart ting, are more likely due to AVNRT.11 disease: Ask about aggravating factors (eg, ex- • Resting bradycardia increases the ercise) and relieving factors (eg, rest, per- likelihood of a clinically significant ar- forming a ). Patients with rhythmia (LR = 3; 95% CI, 1.27-7.0).11 SVT are often able to have palpitations ter- • A murmur, such as a midsystolic click minated with a Valsalva maneuver, such as or holosystolic murmur, detected carotid sinus massage. Palpitations and syn- during the cardiac exam can indicate cope during exertion can be associated with ; a holosystolic

MDEDGE.COM/FAMILYMEDICINE VOL 70, NO 2 | MARCH 2021 | THE JOURNAL OF FAMILY PRACTICE 63 murmur, exacerbated upon perform- require patient activation; older manual sys- ing a Valsalva maneuver, suggests hy- tems require patient activation during symp- pertrophic cardiomyopathy. toms. • Visible neck pulsations detected dur- Two weeks of ambulatory EKG have ing assessment of the jugular venous proved sufficient for determining that there pressure, known as cannon atrial is a cardiac basis to palpitations. The diag- (cannon A) waves, reflect abnormal nostic yield of ambulatory EKG is highest contraction of the right against during Week 1 (1.04 diagnoses per patient), a closed during AV dis- compared to Week 3 (0.17 diagnoses per pa- sociation. have an LR tient).14 of 2.68 (95% CI, 1.25-5.78) for predict- Implantable loop recorders are placed ing AVNRT.4 subcutaneously to provide EKG monitoring for approximately 3 years. They are better ❚ Vagal nerve stimulation. In the rare suited for diagnosing infrequent palpitations. circumstance that a patient complaining of The diagnostic yield of an implantable loop palpitations is symptomatic during assess- recorder over the course of 1 year for the de- ment, several can be detected tection of an arrhythmia is 73%, compared with the use of vagal maneuvers. Interrup- to 21% for a 24-hour , electro- tion of the tachycardia during carotid mas- physiology studies, and 4 weeks of an external A comprehensive sage suggests a tachycardia involving the AV loop recorder.15 Implantable loop recorders history should junction (AVNRT), whereas only a temporary are often reserved for patients with palpita- also evaluate pause or reduction in frequency is more com- tions associated with unexplained recurrent for risk factors mon in atrial flutter, AF, and atrial tachycar- syncope.15 and symptoms dias. Carotid massage has no effect on the ❚ Lab work. A comprehensive metabolic of cardiac presentation of ventricular arrhythmias.10 panel, , lipid panel, disease (chest and panel should be ordered for all pain, dyspnea, Diagnostic testing and the role patients with palpitations. Possible addition- diaphoresis, of ambulatory monitoring al tests include a urine drug screen (when , ❚ . All patients with pal- recreational drug use is suspected); cardiac syncope). pitations should have a 12-lead EKG, which enzymes; N-terminal-pro hormone B-type may provide diagnostic clues (TABLE 210). natriuretic peptide (when there is evidence of ❚ Ambulatory monitoring. When the CAD or heart failure); and urinary catechol- EKG is nondiagnostic, ambulatory cardiac amines (when pheochromocytoma is sus- monitoring has an established role in the di- pected). agnosis of recurrent palpitations. In a small ❚ Other investigations. Echocardiogra- study of patients presenting with palpitations phy is indicated when structural heart dis- to a general practitioner, the deduction of ease is suspected (TABLE 12-4). Patients who those practitioners was wrong more than half have multiple risk factors for CAD or exer- the time when they predicted a ≤ 20% chance tional symptoms might warrant a stress test. of an arrhythmia based on the history, physi- cal exam, and EKG alone13—emphasizing the importance of ambulatory monitoring in pa- Management tients with recurrent palpitations. PACs and PVCs Which monitoring system is most suit- Typically, patients are counseled to mini- able depends on symptom frequency, mize potential adrenergic precipitants, such availability, cost, and patient competence. as smoking, alcohol, stress, and caffeine. Twenty-four- to 48-hour Holter monitoring However, limited studies have demonstrated can be used in cases of frequent (eg, daily) no significant arrhythmogenic potential of palpitations. An automatic external loop re- a modest dose of caffeine (200 mg), even in corder can be used for less frequent (eg, every patients with known life-threatening ventric- 30 days) symptoms. Most ambulatory EKG ular arrhythmias.16 Beta-blockers and non- is now automatic, and therefore does not dihydropyridine calcium channel blockers

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TABLE 2 Etiology of palpitations based on EKG findings10

EKG abnormality Associated diagnoses Ectopic beats Premature atrial contractions Premature ventricular contractions Irregularly irregular rhythm Atrial fibrillation

Prolonged QTc interval (> 460 msec [females]; > 440 msec Polymorphic ventricular tachycardia (eg, long QT syndrome) [males])

Pseudo-right and ST elevation in V1 and V2 Brugada syndrome Q waves, nonspecific ST segment and T-wave abnormalities Ischemic heart disease (left ) QRS voltage consistent with ventricular hypertrophy Hypertensive heart disease Hypertrophic cardiomyopathy as a substrate for ventricular arrhythmias "Slurred upstroke" of the QRS or delta wave with short PR Atrioventricular nodal reentrant tachycardia interval Wolff-Parkinson-White syndrome EKG, electrocardiography.

(CCBs) can reduce the severity of symptoms complex tachycardia (QRS > 120 ms) are related to premature ectopic beats and might generally more unstable and require more reduce their frequency, although response urgent therapy and cardiac consultation or is inconsistent. Use of these medications for referral. Hemodynamically stable patients PACs is largely based on expert opinion and with narrow-complex SVT (QRS < 120 ms) extrapolated from use in other supraventric- can be treated with IV , which has ular and ventricular arrhythmias. an 89.7% success rate.18,19 If adenosine is un- Implantable cardioverter defibrillator successful, is indicated. therapy is indicated in patients with nonsus- Stable patients with minimal symptoms tained VT due to prior myocardial infarction, and short episodes do not need treatment. left ventricular ≤ 40%, and ❚ Vagal maneuvers (eg, Valsalva maneu- inducible ventricular fibrillation or sustained ver; unilateral carotid massage after exclu- VT on electrophysiological study.7 sion of a carotid , with head tilted to the Patients with a high burden of ectopy side opposite the massage, and not for longer who do not respond to treatment with AV than 10 seconds; or applying an ice-cold wet nodal-blocking agents should be referred to towel to the face) have a success rate of about for other antiarrhythmic agents or 25% and are most effective when performed . Last, asymptomatic ectopy shortly after onset of arrhythmia. Vagal ma- does not need to be treated; there is no clear neuvers can be used in all patients while pre- evidence that suppression with pharmaco- paring to administer medications.20 therapy improves overall survival.15,17 Patients who need treatment can take the “pill-in-the-pocket” approach with single- Supraventricular tachycardia dose oral flecainide (3 mg/kg) or combined The priority when evaluating any tachycardia and propranolol. Flecainide has is to assess the patient’s stability. Unstable a 94% success rate; diltiazem–propranolol patients should be treated immediately, usu- has a lower success rate (61%) but a shorter ally with cardioversion, before an extensive time to conversion to .21 Patients diagnostic evaluation.18 Patients with wide- with sustained or recurrent episodes of SVT

MDEDGE.COM/FAMILYMEDICINE VOL 70, NO 2 | MARCH 2021 | THE JOURNAL OF FAMILY PRACTICE 65 FIGURE A plan for evaluating palpitations when the initial diagnosis is not evident on EKG

Assessment History, physical exam, EKG, appropriate lab testinga

Known structural heart disease or Known CAD or increased risk increased risk of structural heart of CAD disease

Low risk of structural High risk of structural Family history High risk of CADc Low risk of CAD heart disease heart diseaseb of sudden death

Single Recurrent Echocardiography and Stress test with or Single Multiple episode episodes ambulatory monitoring without ambulatory episode episodes monitoring

Observe Ambulatory Ambulatory monitoring Observe monitoring

CAD, ; EKG, electrocardiography. a Includes a comprehensive metabolic panel, complete blood count, lipid panel, and thyroid panel, plus other tests as indicated. (See the discussion in the text under, “Diagnostic testing and the role of ambulatory monitoring.”) b Risk factors for structural heart disease are , congenital heart disease, , cardiomegaly, known valvular disease, and a family history of cardiomyopathy or sudden death. c Risk factors for CAD are smoking, diabetes, hyperlipidemia, and .

should be referred to a cardiologist for chron- tion; however, there is no evidence that IV ic prophylactic drug therapy or radiofrequen- formulations of beta-blockers and CCBs are cy ablation. superior to oral formulations. Once the ven- tricular rate is controlled, patients can be Atrial fibrillation transitioned to an oral short-acting prepara- Hemodynamically unstable patients with AF tion of the selected agent, then converted to or atrial flutter, defined by the presence of an- an appropriate dosage of an extended-­release gina, decompensated heart failure, hypoten- preparation.22 sion, pulmonary edema, or evidence of organ Cardioversion can be performed in pa- hypoperfusion, should be electrically cardio- tients with AF < 48 hours. In patients with AF verted using synchronized direct current. > 48 hours, either 4 weeks of anticoagulation Hemodynamically stable patients with a can be given, followed by cardioversion, or rapid ventricular rate should be treated with transesophageal echocardiography should an IV or oral beta-blocker, CCB, or amioda- be performed to evaluate for atrial ; rone, or electrically cardioverted. IV medi- if atrial thrombus is absent, cardioversion can cations are typically preferred in the acute be performed.22 Transesophageal echocar- setting for ease and rapidity of administra- diography might be unnecessary in patients

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known to have been on sustained anticoagu- Catheter ablation is associated with a lower lation. AF recurrence rate (50%) than drug therapy ❚ Rate control is noninferior to rhythm (69%) at 3 years.28 control and does not decrease survival, func- ❚ Anticoagulation. Patients at high risk tional capacity, or quality of life. Rate-control of embolic based on their score on the medications include beta-blockers, nondihy- CHA2DS2-VASca risk stratification tool (ie, a dropyridine CCBs, amiodarone, and . score ≥ 2) should be anticoagulated.29,30 Op- In the AFFIRM (Atrial Fibrillation Fol- tions include a novel oral (dab- low-up Investigation of Rhythm Manage- igatran, rivaroxaban, apixaban, or edoxaban), ment) trial of 4060 patients, mortality was the preferred class of agents for nonvalvular the same with rhythm control (21.3%) and AF, and warfarin, with a target International rate control (23.8%) (HR = 1.15; 95% CI, Normalized Ratio of 2 to 3. Novel oral anti- 0.99-1.34), with no difference in the inci- coagulants have been compared to warfarin dence of cardiac death, arrhythmic death, or for prevention of stroke in AF and were found death due to stroke.23 In the RACE (RAte Con- more effective than warfarin, although at the trol versus Electrical cardioversion for per- expense of an increased risk of gastrointes- sistent atrial fibrillation) trial of 522 patients tinal bleeding.31 Percutaneous left atrial ap- with persistent AF, rate control was noninfe- pendage closure, using a device such as the rior to rhythm control (by cardioversion and Watchman implant, is a noninferior surgical drugs) for reducing morbidity and preventing method to prevent embolic stroke in patients When a patient cardiovascular death.24 One possible reason who are intolerant of, or have a contraindica- reporting a why the rhythm control strategy in the RACE tion to, anticoagulation.32 JFP history of trial did not show superiority is the low num- CORRESPONDENCE palpitations is ber of patients who achieved sustained sinus Anne Mounsey, MD, Department of Family Medicine, symptomatic rhythm.25 University of North Carolina, 590 Manning Drive, Chapel Hill, NC 27599; [email protected]. during The recommended ventricular rate has assessment, traditionally been 60 to 80 beats/min at rest several and < 110 beats/min during daily activities. tachycardias can However, a recent trial found fewer adverse References 1. Kroenke K, Arrington ME, Mangelsdorff AD. The prevalence of be detected with outcomes and no change in symptoms or the symptoms in medical outpatients and the adequacy of therapy. the use of vagal outcome of hospitalization in patients ran- Arch Intern Med. 1990;150:1685-1689. 2. Weber BE, Kapoor WN. Evaluation and outcomes of patients with maneuvers. domized to more lenient control (target rest- palpitations. Am J Med. 1996;100:138-148. ing , < 110 beats/min), although the 3. Giada F, Raviele A. Clinical approach to patients with palpita- tions. Card Electrophysiol Clin. 2018;10:387-396. mean of the actual lenient rate achieved was 4. Thavendiranathan P, Bagai A, Khoo C, et al. Does this patient 86 beats/minute.24 with palpitations have a cardiac arrhythmia? JAMA. 2009;302: 2135-2143. ❚ Rhythm control. Antiarrhythmic 5. Lin C-Y, Lin Y-J, Chen Y-Y, et al. Prognostic significance of prema- agents or procedural interventions can be ture atrial complexes burden in prediction of long-term outcome. J Am Heart Assoc. 2015;4:e002192. used in patients who fail or remain symptom- 6. Murakoshi N, Xu D, Sairenchi T, et al. Prognostic impact of su- atic despite rate control.26 Surgical measures praventricular premature complexes in community-based health checkups: the Ibaraki Prefectural Health Study. Eur Heart J. include AV node ablation with placement of 2015;36:170-178. a pacemaker; atrial pacing with an implant- 7. Ahn M-S. Current concepts of premature ventricular contrac- tions. J Lifestyle Med. 2013;3:26-33. able atrial defibrillator; the Maze procedure 8. Panizo JG, Barra S, Mellor G, et al. Premature ventricular com- (open-heart surgery) to interrupt reentrant plex-induced cardiomyopathy. Arrhythm Electrophysiol Rev. 2018;7:128-134. circuits in the left atrium; and percutaneous 9. Ng GA. Treating patients with ventricular ectopic beats. Heart. radiofrequency or cryotherapy ablation of 2006;92:1707-1712. 10 Raviele A, Giada F, Bergfeldt L, et al; European Heart Rhythm As- arrhythmogenic foci in and around the junc- sociation. Management of patients with palpitations: a position tion of the pulmonary and left atrium.27 paper from the European Heart Rhythm Association. Europace. 2011;13:920-934. There is no significant benefit to imme- 11. Chiou C-W, Chen S-A, Kung M-H, et al. Effects of continuous en- diate catheter ablation over standard medi- hanced on dual atrioventricular node and accessory cal therapy in adults with symptomatic AF in a Congestive heart failure, Hypertension, Age ≥ 75 years reducing the composite outcome of death, (doubled), Diabetes mellitus, Stroke (doubled), Vascu- stroke, serious bleeding, and . lar disease, Age 65–74 years, Sex category.

MDEDGE.COM/FAMILYMEDICINE VOL 70, NO 2 | MARCH 2021 | THE JOURNAL OF FAMILY PRACTICE 67 pathways. Circulation. 2003;107:2583-2588. fibrillation: Part I. Rate and rhythm control. Am Fam Physi- 12 Borjesson M, Pelliccia A. Incidence and aetiology of sudden cian. 2002;66:249-256. cardiac death in young athletes: an international perspective. Br 23. Wyse DG, Waldo AL, DiMarco JP, et al; Atrial Fibrillation Follow- J Sports Med. 2009;43:644-648. up Investigation of Rhythm Management (AFFIRM) Investigators. 13. Hoefman E, Boer KR, van Weert HCPM, et al. Predictive value of A comparison of rate control and rhythm control in patients with history taking and physical examination in diagnosing arrhyth- atrial fibrillation. N Engl J Med. 2002;347:1825-1833. mias in general practice. Fam Pract. 2007;24:636-641. 24. Van Gelder IC, Groenveld HF, Crijns HJGM, et al; RACE II Inves- 14 Zimetbaum PJ, Kim KY, Josephson ME, et al. Diagnostic yield and tigators. Lenient versus strict rate control in patients with atrial optimal duration of continuous-loop event monitoring for the di- fibrillation.N Engl J Med. 2010;362:1363-1373. agnosis of palpitations: a cost-effectiveness analysis. Ann Intern 25. Van Gelder IC, Hagens VE, Bosker HA, et al; Rate Control versus Med. 1998;128:890-895. Electrical Cardioversion for Persistent Atrial Fibrillation Study 15. Giada F, Gulizia M, Francese M, et al. Recurrent unexplained Group. A comparison of rate control and rhythm control in pa- palpitations (RUP) study: comparison of implantable loop re- tients with recurrent persistent atrial fibrillation. N Engl J Med. corder versus conventional diagnostic strategy. J Am Coll Cardiol. 2002;347:1834-1840. 2007;49:1951-1956. 26. Lafuente-Lafuente C, Valembois L, Bergmann J-F, et al. Antiar- 16.  Reiter MJ, Reiffel JA. Importance of beta blockade in the ther- rhythmics for maintaining sinus rhythm after cardioversion of apy of serious ventricular arrhythmias. Am J Cardiol. 1998;82: atrial fibrillation.Cochrane Database Syst Rev. 2015;(3):CD005049. 9I-19I. 27. Ramlawi B, Bedeir K. Surgical options in atrial fibrillation. J Tho- 17. Sheldon SH, Latchamsetty R, Morady F, et al. Catheter ablation rac Dis. 2015;7:204-213. in patients with pleomorphic, idiopathic, premature ventricular 28. Packer DL, Mark DB, Robb RA, et al; CABANA Investigators. Ef- complexes. Heart Rhythm. 2017;14:1623-1628. fect of catheter ablation vs antiarrhythmic drug therapy on mor- 18. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS tality, stroke, bleeding, and cardiac arrest among patients with guideline for the management of adult patients with supra- atrial fibrillation: the CABANA randomized clinical trial. JAMA. ventricular tachycardia: a report of the American College of 2019;321:1261-1274. Cardiology/American Heart Association Task Force on Clinical 29. Dooley P, Doolittle J, Knauss K, et al. Atrial fibrillation: effective Practice Guidelines and the Heart Rhythm Society. Circulation. strategies using the latest tools. J Fam Pract. 2017;66:16-26. 2016;133:e506-e574. 30. Aguilar MI, Hart R, Pearce LA. Oral versus anti- 19. Alabed S, Sabouni A, Providencia R, et al. Adenosine versus intra- platelet therapy for preventing stroke in patients with non-valvu- venous calcium channel antagonists for supraventricular tachy- lar atrial fibrillation and no history of stroke or transient ischemic cardia. Cochrane Database Syst Rev. 2017;10:CD005154. attacks. Cochrane Database Syst Rev. 2007;(3):CD006186. 20. Smith GD, Fry MM, Taylor D, et al. Effectiveness of the Val- 31. Ruff CT, Giugliano RP, Braunwald E, et al. Comparison of the ef- salva manoeuvre for reversion of supraventricular tachycardia. ficacy and safety of new oral anticoagulants with warfarin in pa- Cochrane Database Syst Rev. 2015;2015:CD009502. tients with atrial fibrillation: a meta-analysis of randomised trials. 21. Alboni P, Tomasi C, Menozzi C, et al. Efficacy and safety of out-of- Lancet. 2014;383:955-962. hospital self-administered single-dose oral drug treatment in the 32. Reddy VY, Sievert H, Halperin J, et al; PROTECT AF Steering Com- management of infrequent, well-tolerated paroxysmal supraven- mittee and Investigators. Percutaneous left atrial appendage clo- tricular tachycardia. J Am Coll Cardiol. 2001;37:548-553. sure vs warfarin for atrial fibrillation: a randomized clinical trial. 22. King DE, Dickerson LM, Sack JL. Acute management of atrial JAMA. 2014;312:1988-1998.

This supplement is jointly provided by Medical Education Resources and CMEology. The supplement is supported by an independent educational grant from Takeda Pharmaceuticals U.S.A., Inc. and Lundbeck. Setting the Stage for Major Depressive Disorder Recovery: Strategies for the Busy Care Provider CME/CE JOURNAL SUPPLEMENT Despite the availability of a variety of effective , the burden of inadequately treated major depressive disorder (MDD) in the United States remains deeply troubling. Primary care providers (PCPs) have a key role to play in alleviating the burden of inadequately treated MDD. In this article, we discuss practical strategies PCPs can use to ensure that their patients with MDD receive optimal treatment, focusing on patient-centered approaches that work in the real world.

This supplement can be found at MDedge Family Medicine www.mdedge.com/familymedicine

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