CARDIAC UPDATE: PART I
Educational Objectives
| The goals of this program are to improve the management of atrial fibrillation (AF) and review the cardiac effects of some
commonly prescribed drugs. After hearing and assimilating this program, the clinician will be better able to:
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 | 1. Describe the advantages and disadvantages of cardioversion in the emergency department.
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| 2. Prescribe the appropriate rate control agent in a patient with AF.
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| 3. Discuss the need for anticoagulation after cardioversion.
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| 4. Identify drugs that have adverse effects to the heart.
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| 5. Describe the cardiovascular benefits of estrogen and testosterone.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning
committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest.
Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a
proprietary business or commercial interest. For this program, the faculty and planning committee reported nothing to disclose.
Acknowledgements
Dr. Casaletto was recorded at Emergency Medicine 2008—Moving Forward, held March 31 to April 2, 2008, in
Scottsdale, AZ, and sponsored by the Mayo Clinic Scottsdale College of Medicine, Mayo School of Continuing Medical
Education, in cooperation with Maricopa Integrated Health Systems, and endorsed by the Arizona College of
Emergency Physicians. Dr. Paauw was recorded at the 2007 Washington Chapter Scientific Meeting, held November
1-3, 2007, in Seattle, WA, and sponsored by the Washington Chapter of American College of Physicians. The Audio-
Digest Foundation thanks Drs. Casaletto and Paauw and the sponsors for their cooperation in the production of this
program.
| ACUTE MANAGEMENT OF ATRIAL FIBRILLATION —Jennifer J. Casaletto, MD, Assistant Professor of Clinical
Emergency Medicine, University of Arizona College of Medicine, and Associate Residency Program Director, Maricopa
Medical Center, Phoenix, AZ
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| General facts: definition—chaotic depolarization of atrium; recently shown that most of impulses that start atrial fibrillation
(AF) come from pulmonary arteries (where ablation performed); exposes atrioventricular (AV) node to 300 to 600
impulses/min, resulting in rapid ventricular response (RVR); decreased diastolic time results in decreased coronary perfusion
and decreased cardiac output (CO); detrimental in majority of older patients with coronary artery disease (CAD); 3
types—acute, paroxysmal, and chronic; acute—either new onset (<48 hr) or patient already has AF, but current episode
lasted only ≈48 hr; paroxysmal—patient in AF from seconds to hours or majority of year in AF; always ends spontaneously;
chronic—always in AF; most AF narrow-complex (impulse passes down AV node, resulting in narrow QRS complex);
differs in underlying bundle branch block (BBB), Ashman phenomenon, and Wolff-Parkinson-White syndrome
(WPW); Ashman phenomenon—related to R-R intervals; with shorter R-R interval, bundle branches have no time to repolarize;
right bundle branch takes longer to repolarize than left (right bundle pattern seen); WPW—results in wide complex
with AF, with rates >220/min; wide complex with delta wave not most common form; 10% to 40% of patients
develop AF; 90% of AV re-entrant tachycardias orthodromic (conducted down through AV node back to atria through accessory
pathway; narrow complex with no delta wave); antidromic pattern—more commonly seen and recognized;
passes down through accessory pathway and back through AV node; has tendency for wide complex and delta wave;
thought that when AV tachycardia degenerates into AF, conduction often starts down accessory pathway (resulting in
wide complex and rates ≈250/min); faster the occurrence, the more likely to degenerate into defibrillation (most likely
how sudden death occurs in WPW)
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| Etiology: includes congestive heart failure (CHF), hypertension (HTN), valvular disease, and idiopathic; meta-analysis—
obesity added (relative risk 1.49 [50 times more likely in morbidly or severely obese]); risk for AF accelerated by obesity
and correlates with body mass index (BMI)
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| Cardioversion in emergency department (ED): indicated in patient with rapid AF and severe cardiopulmonary or
hemodynamic instability; American College of Cardiology (ACC) and American Heart Association (AHA) state that if
AF acute (new onset or <48 hr) and safety profile of patient excellent for ED cardioversion, perform; in symptomatic AF,
cardioversion in ED not recommended (risk for embolism and risk from conscious sedation outweigh benefits);
diltiazem—studies looked at safety in AF patients with CHF; good hemodynamic profile; successful in cardioverting
chemically and controlling rate; patients usually difficult to cardiovert chemically or electrically (due to large dysfunctional
left ventricles); also more likely to harbor clot and emboli during cardioversion than average patient in ED, even
those in acute AF; in these patients, control rate first with diltiazem, then transesophageal echocardiography (TEE)-
guided cardioversion
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| When anticoagulation contraindicated: cardioversion not necessarily recommended; Atrial Fibrillation Follow-up
Investigation of Rhythm Management (AFFIRM) trial and RAte Control Versus Electrical Cardioversion for Persistent AF
(RACE) trial looked at long-term rhythm control vs rate control; need for anticoagulants or rate of stroke without anticoagulants
same (≈5% annually); contraindications for anticoagulation—those with acute traumatic episode and at risk for
bleeding (in-hospital cardioversion indicated); those at risk for fall (hospitalization better option)
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| Arguments for ED cardioversion: safety, ability to discharge from ED, high patient satisfaction, and reduced need for
anticoagulation; study of inpatients—showed 30% first-drug success rate for conversion; 60% overall success rate (using
1-4 drugs); 13% had complications, of which >60% bradyarrhythmias that required treatment; ≈250 electrical cardioversions;
1 in 10 patients had complications; previous myocardial infarction (MI) only risk factor identified for complications
after chemical or electrical cardioversion; study of ED patients—289 patients with acute-onset AF; performed chemical
and electrical cardioversions; majority of chemical cardioversions with ibutilide or amiodarone (success rate ≈50%); 30%
of patients electrically cardioverted, with ≈90% success rate; complication rate <50% of that seen with inpatients (possibly
due to different patient choice; unstable patients who required immediate electrical cardioversion not included); 95% of
complications minor; 97% discharged, with 10% recidivism rate in first week; study—found shorter length of stay in hospital
with electrical cardioversion in ED and at lower cost than patients on rate control; no complications at 4 wk; 100% patient
satisfaction; anticoagulation (study)—14% of patients with first-time AF for <48 hr had 10% risk for clot on TEE;
despite normal TEE, 6% of patients on AF <48 hr embolized; clot may form immediately after electrical cardioversion, so
patient still requires anticoagulation
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| Arguments against ED cardioversion: 66% of patients spontaneously cardiovert in first 24 hr; 0% to 7% risk for
embolization immediately after cardioversion of acute AF (actual rate 1.5%-1.6%, based on meta-analysis); may not get
back atrial kick for 3 days to 4 wk (depending on length of time patient in AF); medications for chemical cardioversion
decrease blood pressure (BP) and may cause arrhythmia; sedation risks highest in those who require cardioversion in ED
(ie, those with borderline BP or multiple medical problems where RVR places them at higher risk); possible increased
cost (current studies show ED cardioversion may save money)
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| Rate control vs rhythm control: AFFIRM and RACE trials and 3 shorter trials compared attempted rhythm control
with rate control; both had 4.5% to 5% risk for cerebrovascular accident (CVA) annually without anticoagulation; reduction
in all-cause mortality and hospitalizations seen with rate control
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| How to perform cardioversion: nearly 90% success rate in acute AF with electrical cardioversion (≈50% with chemical
cardioversion); anterior-posterior pad placement better than apex-base; size of pads does not matter; smallest possible diameter
of chest; keep electricity closest to heart (at expiration); synchronize; how much—with monophasic defibrillators, 2005 AHA
guidelines recommend starting at 100 joules (J); only 40% of patients convert at 100 J but nearly 80% convert with 200 J; with
monophasic defibrillators, start at 200 J to minimize shock to heart, with second shock, if necessary, at 360 J; caveats—for patient
on digoxin at therapeutic levels, start at 10 to 20 J and increase in increments of 10 to 20 J; for patient with known or suspected
digoxin toxicity, electrical cardioversion contraindicated (more likely to go into malignant ventricular rhythm, eg,
intractable ventricular fibrillation); study—compared monophasic and biphasic defibrillators at 150 J; biphasic found more effective;
with biphasic defibrillator, start at 150 J (200 J for monophasic); sedation—all agents have disadvantages; speaker favors
etomidate because of its stable hemodynamic profile
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| Rate control agents: verapamil—calcium channel and AV nodal blocker; compared to diltiazem, more negative inotrope;
causes more hypotension; not safe in CHF; dose 5-mg increments up to 20-mg bolus initially, then 5 to 24 mg/hr; decreases
hemodynamic stability in CHF and AF; not recommended for use with other AV nodal blockers, eg, metoprolol;
contraindicated in WPW; diltiazem—number one agent for patients with AF with RVR; calcium channel and AV nodal
blocker; less negative inotrope than verapamil; in mild to moderate CHF, safe and has stable hemodynamic profile; bolus
of 5- to 10-mg increments up to 50 mg initially, then 5 to 20 mg/hr; use with caution in hypotension and in patients on β-
blockers; contraindicated in AV nodal blockade and WPW; several meta-analyses suggest that calcium pretreatment (given
before verapamil) reduces hypotension, but one study (double-blind, placebo-controlled) found that calcium pretreatment
made no difference in mean systolic pressure; esmolol—expensive; difficult to mix and titrate; more hypotension and CHF
than diltiazem; if not contraindicated, diltiazem better choice; use with caution in chronic obstructive pulmonary disease
(COPD) and asthma; also caution in CHF and hypotension; hemodynamic profile less favorable than that of diltiazem;
suitable in patients whose AF with RVR caused by thyrotoxicosis or acute MI ( β-blocker then more favorable than calcium
channel blocker); metoprolol—cheaper and easier to use than esmolol; use with caution in COPD, asthma, and bradycardia
(more difficult to “shut off” than esmolol); contraindicated in CHF, low BP, and long-term calcium channel blocker use;
same advantages as esmolol; diltiazem recommended for most patients; β-blocker appropriate for patient with AF and
RVR caused by thyrotoxicosis or ischemia; digoxin—mean time to control rate ≈3 hr, compared to 5 to 7 min with diltiazem;
electrocardioversion risky in presence of digoxin toxicity; speaker finds no role for digoxin as acute rate control
agent; amiodarone—controls rate through β-blocking effect (slows down conduction through AV node); negative inotrope;
less effective for rate control than magnesium; less effective than diltiazem in head-to-head trials; dose 150 mg or
300 mg initially over 10 min, then 1 mg/min infusion; side effects include hypotension and torsades de pointes; AHA 2005
guidelines say number one choice in WPW, although recent case data show otherwise; given orally, highly effective in controlling
rates in patients with accessory pathway (desethyl metabolites stop conduction through ventricular tissue); given
intravenously, preferentially blocks AV node; 3 case studies looking at patients with accessory pathway who degenerated
into ventricular fibrillation when given amiodarone; several small studies show more stable hemodynamic profile and better
rate control with amiodarone in critically ill patients (more research needed); no longer choice for WPW;
procainamide—blocks sodium channel influx and potassium channel efflux, thereby prolonging refractory period of all
heart tissue; quick onset (40-60 min); dose 30 mg/min, with maximum dose of 17 mg/kg; concern about hypotension; may
be drug of choice in AF; ibutilide—faster and more effective in patients with narrow-complex AF and causes less hypotension;
concern with prolonged QT interval and torsades de pointes; patients most likely to present with accessory pathway
younger and less likely at risk for ventricular arrhythmias; safer than amiodarone (neither preferentially blocks AV node);
magnesium—prolongs atrial and AV nodal refractory period; rate and rhythm control effects equivalent to those of amiodarone,
digoxin, and verapamil; dose varies (initial bolus 2-7 g, with infusion time of 1-24 hr); same caution as when given
to obstetric patient and in renal failure, respiratory failure, and hypotension with rapid infusion; has advantage when combined
with standard rate reduction therapy; summary—diltiazem recommended, unless ischemia and thyrotoxicosis
present, then use esmolol or metoprolol; if WPW or accessory pathway present, procainamide or ibutilide; consider adding
magnesium
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| Anticoagulation: first myth—that no clot forms in first 2 to 3 days; study showed left atrial clot found in 14% of patients
believed (based on symptoms) in AF for <48 hr; suggests that even in these patients, may need TEE before cardioversion;
second myth—that no thrombus on TEE equals no risk for embolism with cardioversion; study found 6% risk
for embolism even after negative TEE (not all acute AF patients); 40% showed increased echo contrast immediately after
cardioversion (swirling of blood that predisposes to clot); suggests need for anticoagulation after cardioversion; AHA
recommendations—necessary to give heparin in pericardioversion period even if TEE negative; give warfarin for 4 wk
after cardioversion, with target international normalized ratio (INR) of 2:3; long term, aspirin given for low-risk patients
and warfarin for high-risk patients or those with chronic or paroxysmal AF; high-risk factors—age >70 yr, hypertension,
diabetes, or known CAD; British study compared aspirin to warfarin in patients >85 yr of age and showed warfarin group
had no increased incidence of major hemorrhage and 50% risk for CVA
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| DRUGS THAT CAN HAVE ADVERSE EFFECTS ON THE HEART: PART I —Douglas S. Paauw, MD, Professor of
Medicine, University of Washington School of Medicine, Seattle
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| Drugs for migraine: ergotamine and methysergide (discontinued)—6 to 20 yr of use may result in heart murmur, eg, mitral
regurgitation; pathophysiology similar to that of carcinoid syndrome; triptans—injectable sumatriptan causes major
side effects, including chest pain and MI (most patients had underlying CAD); some case reports of similar side effects
with oral triptans; large study found that triptan use did not increase risk for stroke, MI, or cardiovascular death; safe, but
more care needed with older patients or those with significant cardiovascular risk
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| Fenfluramine and phentermine (“fen-phen”): major study in 1997 of 24 women (mean age 44 yr) who presented
with cardiovascular symptoms or new murmurs average of 12 mo after starting fen-phen; echocardiography showed unusual
valve morphology and regurgitation (lesions similar to those from ergotamine and methysergide); histopathology
same as in carcinoid- and ergotamine-induced valve disease
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| Dopamine agonists: study—looked at valvular heart disease with certain dopamine agonists; 31 cases of newly diagnosed
valve regurgitation (6 on pergolide, 6 on cabergoline, and 19 not on any dopamine agonist in past year); pergolide
(Permax) taken off market in March 2007
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| Estrogen: study—looked at coronary artery calcifications in postmenopausal women on estrogen; after hysterectomy,
women received conjugated estrogens or placebo; Agatston calcium score 83 for those receiving estrogen and 123 for
those on placebo; risk for extensive calcification (score >300) 40% less in those receiving estrogen
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| Testosterone: meta-analysis—found prostate events statistically significant at rate of 112/1000 patient-years (double
risk of placebo group), but no one prostate event dominant; hematocrit (HCT) increased in testosterone group, with HCT
>50% most frequent testosterone-related adverse event (6.5%); no significant change in incidence of cardiovascular
events, sleep apnea, or death; study—compared testosterone to placebo in 10 men with angina and hypogonadism; time
to 1-mm ST depression on treadmill testing improved by average of 74 sec; total cholesterol and mood improved on testosterone;
conclusions—safe to replace testosterone in hypogonadal elderly patients; possible cardiac benefit in certain
situations; important to follow HCT in patients on testosterone
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| Statins and antioxidants: study—160 participants with coronary disease and low high-density lipoproteins (HDL)
and normal low-density lipoproteins (LDL) randomly assigned to simvastatin, niacin, and antioxidants or placebo; end
points evidence of change in coronary stenosis and occurrence of first cardiovascular event; protective increase in HDL
with simvastatin attenuated by use of antioxidants; best combination simvastatin and niacin without antioxidants
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Suggested Reading
Camm AJ et al: Rate control in the medical management of atrial fibrillation. Heart 93:35, 2007; Davison S et al: New
markers for cardiovascular disease risk in women: impact of endogenous estrogen status and exogenous postmenopausal hormone
therapy. J Clin Endocrinol Metab 88:2470, 2003; Gjesdal K et al: Digitalis: a dangerous drug in atrial fibrillation?
An analysis of the SPORTIF III and V data. Heart 94:191, 2008; Hagens VE et al: Effect of rate or rhythm control on quality
of life in persistent atrial fibrillation. Results from the Rate Control Versus Electrical Cardioversion (RACE) Study. J Am
Coll Cardiol 43:241, 2004; Kim SS et al: Electrical and pharmacologic cardioversion for atrial fibrillation. Med Clin North
Am 92:101, 2008; Kirwan LD et al: Acute and chronic effects of hormone replacement therapy on the cardiovascular system
in healthy postmenopausal women. J Clin Endocrinol Metab 89:1618, 2004; Malkin CJ et al: Effect of testosterone
therapy on QT dispersion in men with heart failure. Am J Cardiol 92:1241, 2003; Onalan O et al: Meta-analysis of magnesium
therapy for the acute management of rapid atrial fibrillation. Am J Cardiol 99:1726, 2007; Ozaydin M et al: Effect of
atorvastatin on the recurrence rates of atrial fibrillation after electrical cardioversion. Am J Cardiol 97:1490, 2006; Padanilam
BJ et al: Atrial fibrillation: goals of therapy and management strategies to achieve the goals. Med Clin North Am
92:217, 2008; Snow V et al: Management of newly detected atrial fibrillation: a clinical practice guideline from the American
Academy of Family Physicians and the American College of Physicians. Ann Intern Med 139:1009, 2003; Tousoulis D
et al: Statins and antioxidant vitamins: should co-administration be avoided? J Am Coll Cardiol 47:1237; author reply 1237,
2006; Waldo AL: A perspective on antiarrhythmic drug therapy to treat atrial fibrillation: there remains an unmet need. Am
Heart J 151:771, 2006; Waller EA et al: Valvular heart disease in patients taking pergolide. Mayo Clin Proc 80:1016,
2005; Watson T et al: Cardioversion for atrial fibrillation: does inflammation matter? Am J Cardiol 99:1617, 2007.
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