ISSUES OF THE HEART
Educational Objectives
| The goal of this program is to improve the management of common heart conditions. After hearing and assimilating
this program, the clinician will be better able to:
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 | 1. Predict risk for stroke and need for anticoagulation therapy in patients with atrial fibrillation (AF).
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| 2. Discuss the management of AF with rate control or rhythm control.
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| 3. Manage patients with heart failure based on the American College of Cardiology and American Heart Association
staging criteria.
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| 4. Review data about angioplasty in patients with stable angina.
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| 5. Identify patients who may benefit from angioplasty, based on findings of the Clinical Outcomes Utilizing Revascularization
and Aggressive druG Evaluation (COURAGE) trial.
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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 following has been disclosed: Dr. Bush is on the Speakers’ Bureau for Bristol-
Myers Squibb, Sanofi-Aventis, and Toshiba. Dr. Bush has received research funding from Toshiba. Drs. Marine and Jaski and the
planning committee reported nothing to disclose.
Acknowledgements
Drs. Marine and Bush spoke in Baltimore, MD, at the 35th Annual Current Topics in Geriatrics, presented January 17-
19, 2008, by the Johns Hopkins University School of Medicine. Dr. Jaski was recorded in San Diego, CA, on August
3, 2007, at the San Diego Academy of Family Physicians’ 50th Annual Postgraduate Symposium Family Medicine Update
2007. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production
of this program.
| ATRIAL FIBRILLATION —Joseph E. Marine, MD, Assistant Professor of Medicine, Johns Hopkins University School of
Medicine, and Director of Electrophysiology, Johns Hopkins Bayview Medical Center, Baltimore, MD
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| Risk factors: 2- to 6-fold increased risk for stroke with atrial fibrillation (AF), 1.5- to 2.0-fold increased risk for mortality;
advanced age; prevention—good control of hypertension and diabetes; general cardiac risk factor reduction
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| Electrocardiographic (ECG) findings that mimic AF: atrial flutter—masked by frequent premature ventricular
contractions (PVCs; rhythm irregular); sawtooth pattern in inferior leads; focal atrial tachycardia (may be irregular); sinus
rhythm with frequent atrial premature contractions (APCs); tremor artifacts
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| Mechanisms: multiple wavelet hypothesis (chaotic atrial activation produces chaotic pattern on ECG); changes in atrial
substrates (eg, atrial enlargement, atrial fibrosis); vagal intervention can lower refractory period; triggers—reentrant supraventricular
tachycardia; atrial flutter; atrial premature beats and focal atrial arrhythmias originating from pulmonary
veins most common
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| Anticoagulation and stroke prediction: based on consensus document published by American College of Cardiology
(ACC) and American Heart Association (AHA); CHADS2 scoring based on congestive heart failure (CHF; including left
ventricular dysfunction [LVD] or other major structural heart disease; 1 point), hypertension (1 point), age >75 yr (1 point),
diabetes (1 point), and previous transient ischemic attack (TIA) or stroke (2 points); patients with AF and no risk factors can
be treated with aspirin (81-325 mg/day); patients with high-risk factor (eg, mitral stenosis) or ≥1 moderate risk factor (ie,
CHAD score ≥2) should be treated with warfarin (be concerned about hemorrhage)
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| Stroke prevention: ximelagatran—oral direct thrombin inhibitor; fixed dosing with no monitoring; showed same reduction
in thromboembolism as adjusted-dose warfarin; not approved by Food and Drug Administration (FDA), due to
6% incidence of abnormal liver function tests (LFTs) and 2 cases of fatal liver failure; other agents in development; 90%
of thromboemboli in AF originate from left atrial appendage, leading to thrombus formation (left atrial appendage occluders
in clinical trials)
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| Rate control vs rhythm control: rate control—many patients with AF minimally symptomatic; avoids toxicity of antiarrhythmic
drugs; rhythm control—addresses risk for tachymyopathy; hemodynamic benefits; Atrial Fibrillation Follow-up
Investigation of Rhythm Management (AFFIRM) trial—patients (mean age 70 yr) with mildly symptomatic AF
and ≥1 stroke risk factor; cumulative mortality over 5 yr equal for both arms, with slight trend in favor of rate control;
≈60% of patients in rhythm control arm achieved and maintained normal sinus rhythm at last follow-up, compared to
35% in rate control arm; stroke risk not reduced by rhythm control (may be due to discontinuation of warfarin in patients
who achieved rhythm control); conclusions—reinforcement of anticoagulation for stroke prevention based on risk factors,
not on patient’s rhythm at presentation; no objective benefit of rhythm control over rate control in AF
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| Agents for rate control: small study of 12 male veterans with chronic AF saw poor rate control with digoxin alone;
best rate control seen with digoxin and atenolol (atenolol alone nearly as effective); diltiazem alone and diltiazem with
digoxin “somewhere in the middle”; speaker starts with β-blocker (if contraindicated, use diltiazem or verapamil);
digoxin—used as second-line agent (useful in patients with heart failure [HF] and low ejection fraction [EF]) or as second
agent when single agent inadequate; poor choice for paroxysmal AF; does not prevent recurrences of paroxysmal
AF; poorly controls rate when patients in AF; check LV function (LVF) periodically; use Holter monitoring and exercise
stress testing; “ablate and pace”—particularly useful for refractory elderly patients; implantation of single-chamber
pacemaker for patients with permanent AF, dual-chamber for paroxysmal AF; biventricular pacemakers for patients with
baseline CHF and poor LVF; useful if medical rate control unsuccessful and patients not candidates for rhythm control
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| Rhythm control: for patients unable to tolerate rate control strategy or who do not want to commit to permanent AF; antiarrhythmic
drug first-line therapy; class Ia agents—eg, quinidine, procainamide; obsolete; high side effect profile; low efficacy;
class Ic agents—eg, flecainide, propafenone; well tolerated in patients with structurally normal hearts; paresthesias and
chest pain occasional side effects; can cause atrioventricular (AV) block in patients with preexisting conduction system disease;
contraindicated in patients with history of coronary disease or significant structural heart disease; class III agents—eg,
sotalol, dofetilide; torsades de pointes in 1% to 3% of patients; initiate in hospital with 2- to 3-day loading protocol;
amiodarone—combined effects; can cause bradycardia, AV block, and torsades de pointes (rare); monitor for pulmonary side
effects (eg, fibrosis, bronchiolitis obliterans); hypothyroidism occurs in 5% to 10% of patients; hyperthyroidism less common
but more severe problem (discontinue drug immediately and refer to endocrinologist); nausea; increased LFTs (less common);
cirrhosis (rare); neurologic side effects (eg, ataxia, tremor, neuropathy) occur in ≤40% of elderly patients; corneal deposits
common; optic neuropathy rare; can cause increased photosensitivity (recommend sunblock) and blue-gray discoloration of
skin (discontinue drug); drug interactions include increased levels of warfarin, digoxin, and statin; effective agent for rhythm
control in AF
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| Algorithm for maintenance of sinus rhythm: in patients with structurally normal heart or hypertension with minimal
left ventricular hypertrophy (LVH), start with flecainide or propafenone (if ineffective, use sotalol and amiodarone); in
patients with hypertension and substantial LVH, use amiodarone; in patients with coronary disease, use class III agent, with
amiodarone as second-line therapy; treat patients with frank CHF and LVD with amiodarone; follow-up in patients on
amiodarone—baseline history, physical examination, ECG, LFTs, thyroid function tests, pulmonary function tests, and
chest x-ray; reduce warfarin and digoxin dose; weekly international normalized ratio (INR) until patient on stable doses of
amiodarone and warfarin; after 6 mo, repeat history and physical examination, ECG, LFTs, and thyroid function tests; perform
chest x-ray and eye examination annually; caution patients about pulmonary toxicity (immediate notification required
if patient develops progressive unexplained dyspnea or dry cough)
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| Ablation: surgical maze procedure—atrium divided into electrically separate pieces so wavelets unable to maintain themselves;
80% to 95% of patients maintain long-term sinus rhythm; catheter ablation—less invasive; initial attempts marked
by poor success and high complication rates; French study—found 95% of triggers of AF originate from pulmonary veins;
ablating focus in pulmonary vein led to short-term success of stopping paroxysmal AF; current technique—imaging study
(ie, computed tomography [CT] or magnetic resonance imaging [MRI]) used as model; multiple small ablation lesions
made around ostium of pulmonary veins to electrically isolate musculature; takes 3 to 6 hr; success rate, 50% to 75% (better
for paroxysmal than for long-standing AF); total complication rate, ≈7%; ablation reserved for selected patients with significant
symptoms, patients who failed antiarrhythmic drug therapy, and patients with fairly good risk profiles for comorbidities
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| Summary of AF management: baseline work-up—ECG; chest x-ray; echocardiography; thyroid function tests; determine
whether patient candidate for anticoagulation; rate control strategy for all patients; cardioversion for most patients at
initial presentation of sustained AF; recurrences—if symptoms minimal or patients asymptomatic, long-term rate control
and anticoagulation strategies reasonable; if symptoms significant, initiate antiarrhythmic drug and repeat cardioversion
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| HEART FAILURE —Brian E. Jaski, MD, Associate Clinical Professor, Department of Medicine, University of California,
San Diego, School of Medicine; Director, Advanced Heart Failure and Cardiac Transplant Program, and Medical Director,
Clinical Cardiology, Sharp Memorial Hospital, San Diego
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| Heart failure: shortness of breath, fatigue, dizziness, low energy, somnolence, edema, enlarged neck veins, congestion
on x-ray in dyspneic patients, and B-type natriuretic peptide (BNP) >100 pg/mL; neurohormonal activation progresses to
myocardial toxicity and injury; adverse remodeling and progressive worsening of LVF can be reversed (to some degree)
with neurohormonal blockers; risk factors—coronary artery disease (CAD); hypertension; angina; myocardial infarction
(MI); LVD; associated with sudden death; diabetes; tobacco smoking; dyslipidemia
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| ACC and AHA staging of HF: stage A—risk factors for structural heart disease, but no impairment; stage B—previous
MI and LVD, but no clinical syndrome of CHF; may have decreased EF; requires more aggressive therapy; stage C—previous
or current symptoms associated with HF and LVD; stage D—refractory symptoms; includes patients considered for aggressive
therapy (eg, heart transplantation) or hospice care; unidirectional progression of HF; New York Heart Association
(NYHA) classification (class I [asymptomatic] to class IV [symptoms at rest]) important, but can change as symptoms change
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| Management: stage A—treatment and prevention of cardiovascular disease; treat hypertension; mandate tobacco cessation;
treat lipid disorders; encourage exercise; discourage illicit drug and excess alcohol use; control metabolic syndrome;
normotensive patients with manifest vascular disease (eg, history of carotid endarterectomy) should be on angiotensin-
converting enzyme (ACE) inhibitor or angiotensin-receptor blocker (ARB; avoid hypotension and other side effects); aspirin
in vascular disease; stage B—perform same measures as in stage A, plus prevention and reversal of cardiac remodeling;
ACE inhibitors or ARBs in patients with history of MI or LVD; use echocardiography to detect decreased LVF in
patients with no history of MI; β-blockers for patients with history of MI and EF <40%; asymptomatic patients with EF
≤35% at risk for sudden death (consider referral for implantable cardioverter-defibrillator [ICD]); stage C—same recommendations
as for stages A and B; restrict salt intake; treat symptoms with diuretics; consider neurohormonal blockade;
selective use of digoxin; aldosterone blockade for patients with NYHA class III and IV symptoms; hydralazine; nitrates;
consider resynchronization therapy in patients with wide (≥120 msec) QRS complex; stage D—consider heart transplantation;
LV assist device; investigational therapy (eg, gene therapy, stem cell therapy); prepare patients with comorbidities
(eg, elderly patients) and family for entry into hospice care
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| REVASCULARIZATION SURGERY VS MEDICAL THERAPY FOR CARDIAC PATIENTS —David E. Bush, MD, Associate
Professor of Medicine, Johns Hopkins University School of Medicine, and Director, Cardiac Catheterization Laboratory,
Johns Hopkins Bayview Medical Center, Baltimore, MD
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| Revascularization: 1970s to 1980s—study showed certain patients (particularly patients with left main CAD or advanced
CAD and impaired LVF) who underwent surgical revascularization did better than patients who received medical
therapy; in patients with acute coronary syndrome (eg, unstable angina, non-ST elevation MI), studies showed that watching
and waiting associated with better outcomes than immediate catheterization; 1990s—large number of trials showed
patients with acute coronary syndrome (ie, troponin leak or ECG changes) had better results with catheterization than
with watching and waiting; more aggressive medical therapy showed better incidence of cumulative events, compared to
waiting with prolonged antithrombotic treatment; patients with acute coronary syndrome do better with revascularization
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| Risk factors: diabetes; poor LVF; troponin leaks; patients who do better with revascularization include patients with left main
CAD, 3-vessel disease with poor LVF, and acute coronary syndrome
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| Stable angina: no thrombus involvement, just narrowed artery; unable to predict location of MI with angiography; meta-
analysis showed percutaneous coronary intervention (PCI) no better than medical management; Asymptomatic Cardiac Ischemia
Pilot (ACIP) study and Swiss Interventional Study on Silent Ischemia Type II (SWISSI II) found lipid targets “not
what one would hope for,” compared to current standards; risk factors additive (“need more comprehensive approach”);
angioplasty—improves exercise capacity; reduces symptoms; unclear whether angioplasty prolongs survival or decreases
risk for morbid events, compared to optimal medical therapy
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| Clinical Outcomes Utilizing Revascularization and Aggressive druG Evaluation (COURAGE) trial:
looked at best available medical therapy with and without angioplasty in patients with angina; median follow-up 4.5 yr;
catheterization performed to exclude patients with left main CAD, 3-vessel disease with poor LVF, poor LVF, and patients
not candidates for angioplasty; primary outcomes, all-cause mortality or MI; results—angioplasty with stent placement
conferred no survival benefit; no subgroups (eg, patients with previous MI or diabetes and degree of angina) in
which point estimate favored coronary intervention for preventing death or MI; angina—significant improvement seen in
both groups; angioplasty group improved more quickly, but improvement equivalent after 2 yr; >10% of patients in medically
treated arm received coronary intervention; 10% who started in coronary intervention group required another coronary
intervention or coronary artery bypass; safe to identify and treat patients without significant proximal left anterior
descending (LAD) CAD or left main CAD first (“and see how they do; most do just fine on medicine”); angina improves
with aggressive medical therapy as well as coronary intervention
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| Cardiac CT: CT angiography able to predict need for revascularization as effectively as traditional coronary angiography;
may have difficulty identifying small vessels; accurate in identifying larger vessels; may be helpful for determining whether
some patients with significant angina (eg, elderly with contraindications) need more aggressive therapy (reasonable to perform
CT first and if patient has high-risk anatomy, perform revascularization procedure as indicated); in other patients, initiate
aggressive medical therapy; 20% to 30% may be refractory to medical therapy (perform revascularization procedure;
two-thirds of patients given aggressive medical therapy without catheterization “might do just fine”); exclude high-risk patients
and manage others with medical therapy; when high-risk patients with stable angina excluded, early revascularization
does not confer survival benefit (those refractory to medical therapy have option for revascularization if symptoms not controlled)
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Suggested Reading
Epstein AE et al: Mortality following ventricular arrhythmia suppression by encainide, flecainide, and moricizine after
myocardial infarction. The original design concept of the Cardiac Arrhythmia Suppression Trial (CAST). JAMA 270:2451,
1993; Erne P et al: Effects of percutaneous coronary interventions in silent ischemia after myocardial infarction: the
SWISSI II randomized controlled trial. JAMA 297:1985, 2007; European Heart Rhythm Association; Heart
Rhythm Society et al: ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation--executive
summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines
for the Management of Patients With Atrial Fibrillation). J Am Coll Cardiol 48:854, 2006; Fang MC et al: National
trends in antiarrhythmic and antithrombotic medication use in atrial fibrillation. Arch Intern Med 164:55, 2004; Farshi R et
al: Ventricular rate control in chronic atrial fibrillation during daily activity and programmed exercise: a crossover open-label
study of five drug regimens. J Am Coll Cardiol 33:304, 1999; Gage BF et al: Validation of clinical classification schemes
for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 285:2864, 2001; Gibbons RJ: Based
upon the results of the COURAGE clinical trial, what is the best treatment for stable angina? MedGenMed 9:49, 2007;
Howard PA et al: Drug therapy recommendations from the 2005 ACC/AHA guidelines for treatment of chronic heart
failure. Ann Pharmacother 40:1607, 2006; Marine JE: Catheter ablation therapy for supraventricular arrhythmias. JAMA
298:2768, 2007; McMurray J et al: Practical recommendations for the use of ACE inhibitors, beta-blockers, aldosterone
antagonists and angiotensin receptor blockers in heart failure: putting guidelines into practice. Eur J Heart Fail 7:710, 2005;
Moe GW: B-type natriuretic peptide in heart failure. Curr Opin Cardiol 21:208, 2006; Olsson SB et al: Stroke prevention
with the oral direct thrombin inhibitor ximelagatran compared with warfarin in patients with non-valvular atrial fibrillation
(SPORTIF III): randomised controlled trial. Lancet 362:1691, 2003; Pepine CJ et al: Factors influencing clinical
outcomes after revascularization in the asymptomatic cardiac ischemia pilot (ACIP). ACIP Study Group. J Card Surg 14:1,
1999; Pundziute G et al: Prognostic value of multislice computed tomography coronary angiography in patients with
known or suspected coronary artery disease. J Am Coll Cardiol 49:62, 2007; Shaw LJ et al: Optimal medical therapy with
or without percutaneous coronary intervention to reduce ischemic burden: results from the Clinical Outcomes Utilizing Revascularization
and Aggressive Drug Evaluation (COURAGE) trial nuclear substudy. Circulation 117:1283, 2008.
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