ADVANCES IN CARDIOLOGY
| CORONARY ARTERY DISEASE —Carmelo J. Panetta, MD, Assistant Professor of Medicine, Division of Cardiology,
University of Minnesota Medical School, Minneapolis
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| Causes of acute coronary syndrome: complete or partial occlusion of vessel by thrombus or ruptured plaque; non-
ST segment elevation myocardial infarction (MI) with occluded side branch; dynamic obstruction (eg, vasospasm with
Prinzmetal’s angina); progressive narrowing of vessel (from, eg, atherosclerosis); chronic stable angina worsened by secondary
problems; arterial inflammation rare (can induce thrombus formation and embolization)
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| Diagnosis: rapid progression over time; often difficult for patients to define pain or discomfort; symptoms occur with exertion;
risk factors—tobacco use; high cholesterol; advanced age; diabetes; renal disease (glomerular filtration rate
[GFR] <60 mL/min); positive family history; hypertension; history of MI; patients with dyspnea on exertion (patient with
diabetes at risk for silent ischemia); American College of Cardiology (ACC) and American Heart Association (AHA)
recommend sending patients who call on telephone about chest pain to facility for evaluation by physician and electrocardiography
(ECG); confirming diagnosis and risk stratification—ECG; laboratory testing (eg, if negative, redraw in 6-
12 hr with troponin I or T, creatine phosphokinase-MB isoenzyme (CPK-MB), or myoglobin with CPK-MB or troponin);
coronary angiography and stress testing; higher troponin indicates higher mortality
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| Preventing thrombosis: heparin first-line therapy; low molecular weight heparin (LMWH; eg, enoxaparin) especially
if patient does not immediately undergo coronary angiography; unfractionated heparin reasonable if patient going to
catheterization laboratory within next 6 hr; aspirin; clopidogrel should be considered if patient not candidate for bypass
surgery or cannot tolerate aspirin; glycoprotein IIb/IIIa inhibitors—eg, abciximab; not recommended for patients undergoing
catheterization; shown to reduce clot progression and in smaller studies, clot regression; increases bleeding
rates with bypass surgery; in patients with varying IIb/IIIa inhibitors and LMWH or unfractionated heparin, minor bleeding
rate 5% to 13%, major bleeding rate (with bypass surgery) ≤11%; heparin-induced thrombocytopenia (HIT)—
sudden decrease in platelet count by >50% or count <100,000/µL; discontinue heparin and switch to argatroban or hirudin;
patients at risk for bleeding and thrombosis; contraindications for IIb/IIIa inhibitors include platelet count <100,000/
µL, recent surgery, recent stroke, or active bleeding; fondaparinux used off-label
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| Preventing sudden death: unless patient has heart failure, heart block, or severe asthma, make sure patient on β-
blocker; start with low dose (eg, 2.5 mg intravenously [IV]) and titrate up
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| Pain reduction and relief: nitroglycerin; morphine; calcium channel blocker and β-blocker in patients with unstable
angina; intra-aortic balloon pump—short-term use reasonable for patients with severe angina, hypotension, heart failure,
or not candidates for revascularization; invasive; increases risk for bleeding; O2 therapy for patients with chronic obstructive
pulmonary disease (COPD)
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| Treatment of inflamed plaque: statins; angiotensin-converting enzyme (ACE) inhibitors; cardiovascular diet, including
fish oil; exercise; control diabetes; tobacco smoking cessation; consider stopping estrogen replacement in recently
postmenopausal women; lower low-density lipoprotein (LDL); cocaine use—nitroglycerin and calcium antagonist first-
line therapy; β-blocker can be used in setting of hypertension or heart rate >100 beats per min (BPM); consider use of
coronary angiography or thrombolytics for persistent ST or T wave changes after use of nitroglycerin or calcium antagonists
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| Angina: consider other causes of chest pressure; history—pain or pressure with exertion (ask about stairs); can present
with specific exercises (rare); risk factors—diabetes; age >70 yr; history of coronary disease; male sex; postmenopausal
women; transient murmur; S3 ; hypotension; diaphoresis; pulmonary edema; rales; insulin-dependent diabetes (even at
young age); confirming diagnosis—ECG; echocardiography; baseline laboratory studies; stress imaging studies; computed
tomography (CT) angiography; coronary angiography
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| Stress ECG: specificity 90%, sensitivity 50%; best for patients with low probability of disease; problematic if patient on
digoxin, has left ventricular (LV) hypertrophy, or left or right bundle branch block; stress imaging studies reasonable if
chest pain continues for <20 min, markers negative, and ECG normal; types of stress imaging studies—exercise nuclear
imaging studies with thallium or technetium sestamibi; adenosine or dipyridamole nuclear studies acceptable, except
in setting of severe asthma; adenosine may have lower sensitivity and specificity in diabetic patients on dialysis;
exercise or dobutamine echocardiography; sensitivity of single photon emission computed tomography (SPECT) imaging
studies 82% to 98% (71%-94% with exercise echocardiography); exercise or dobutamine echocardiography and exercise
nuclear studies limited if patient unable to elevate heart rate
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| CT angiography: identifies presence (but not location) of blocked vessels; problems with older 16-slice CT—need
for reducing heart rate to <70 BPM, holding breath for 19 sec, and contrast load; greater radiation exposure than angiography;
not physiologic test for ischemia; new scanners in development; indications for cardiac catheterization—acute
coronary syndrome with positive troponin; new ECG or ST-T wave depression; chest pain consistent with angina at rest
or minimal activity; history of angioplasty within last 6 mo; history of coronary artery bypass grafting (CABG); ejection
fraction <40%; hemodynamic instability; hypotension; persistent arrhythmias; high-risk findings on stress imaging studies;
heart failure or worsening MR with angina
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| Coronary angiography: documents disease; helps visualize obstruction with contrast; intravascular ultrasonography
(IVUS) helpful for determining cross-sectional area of vessel lumen or percent of stenosis; fractional flow reserve physiologic
test determines significance of blocked vessel (>0.75 significant)
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| Management of lesions: determine number of vessels blocked and which vessels; medical management alone; coronary
artery bypass surgery; percutaneous coronary intervention (PCI); surgical laser transmyocardial revascularization (TMR);
enhanced external counterpulsation (reserved for patients who cannot be revascularized); spinal cord denervation; stem
cells or growth factors undergoing trial study; CABG vs medical therapy—CABG shown beneficial in patients with
mild to moderate symptoms due to coronary artery disease (CAD); CABG reduced mortality at 5 and 10 yr; 15% to 30%
of vein grafts shown to last ≥1 yr, 50% after 6 to 10 yr (rate can be reduced with tobacco smoking cessation, controlling
lipids, and antiplatelet therapy); be aware of limitations of older studies (eg, low-risk patients, few women); robotic
surgery—newer CABG method; minimally invasive; avoids sternal incision; no large scar; patients can drive sooner;
problems include bypass of 1 to 2 vessels, difficulty in patients with previous bypass, and internal mammary artery must
be intact
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| Percutaneous coronary intervention: performed same day as angiography; can be performed through radial artery;
progress with use of stents good; better tolerance of thienopyridines (eg, clopidogrel); PCI vs CABG—CABG better
than angioplasty for diabetic patients; risk for death from stenting equal to that of bypass surgery; problems with stenting
include formation of scar tissue inside stent and restenosis; PCI effective in patients with stable angina; use of drug-eluting
and Taxus stents does not prevent MI or death in patients with stable angina or lead to restenosis
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| HEART VALVE ABNORMALITIES —Gregory J. Dehmer, MD, Professor of Medicine, Texas A and M College of Medicine,
and Director, Cardiology Division, Scott and White Clinic, Temple, TX
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| Similarities between aortic stenosis (AS) and mitral stenosis (MS): few causes; acute stenotic diseases rare;
patient history and physical examination correlate with severity of disease; diagnostic testing excellent; echocardiography
clearly shows severity of disease; good correlation between LV function and disease severity; medical management
options limited, but usually straightforward; high likelihood of improvement after procedure (eg, surgery)
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| Similarities between aortic and mitral regurgitation (MR): many causes; acute regurgitant lesions occur; patient
history and physical examination not consistent with severity of disease; diagnostic testing good, but echocardiography
may not reflect degree of LV dysfunction; LV function can deteriorate while patient “looks perfectly good”;
many medical management options but not as clear; improvement not always guaranteed after procedure; “sneaky” diseases
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| Aortic outflow tract obstruction: supravalvular—usually presents in childhood; uncommon; subvalvular—eg,
hypertrophic cardiomyopathy in adults; valvular—1) congenital; seen in children; 2) bicuspid aortic valve or sclerotic
tricuspid aortic valve; usually develops during age 50 to 60 yr; murmur detected at age 30 to 40 yr with no hemodynamic
manifestations or symptoms; 3) age-related calcific degeneration; senile AS; affects ≈2% of individuals >65 yr of age,
but ≈29% of population have age-related thickening of valve leaflets with no real obstruction (aortic sclerosis without
stenosis); degenerative process with proliferative and inflammatory changes; occasionally associated with Paget’s disease
and end-stage renal disease; associated with risk factors for development of atherosclerosis; statins may be effective
treatment; rheumatic AS—isolated aortic rheumatic disease uncommon; mitral valve manifestations more common
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| Classic symptoms of AS: exertional angina; ≈50% of patients with AS may have coexistent coronary disease; exertional
syncope; dyspnea with exertion—severe forms can lead to heart failure; association of gastrointestinal (GI)
bleeding from angiodysplasia; once symptoms develop, average survival 2 to 5 yr; treatment not required during long latent
period (should be given once symptoms present)
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| Physical examination: carotid pulsation rises slowly and sustained; heart sounds—S1 usually normal; S2 usually single;
paradoxic splitting suggests association of left bundle branch block or severe LV dysfunction; S4 due to severe ventricular
hypertrophy; S3 with LV failure; murmur—correlates with severity of disease; begins in midsystole and
becomes longer and peaks later as AS progresses (indicates worsening of outflow obstruction); loudness alone not indicative
of severity
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| Echocardiography: transthoracic and transesophageal echocardiography (TEE) helpful; Doppler echocardiography for
mapping gradient across valve; aortic valve area must be reduced by ≈50% (ie, from ≈3.0 cm2 [normal] to <1.5 cm2 ) for
measurable gradient; goals—to diagnose and assess severity of suspected AS; to measure LV function; to reevaluate patients
with known AS and complaints of worsening symptoms; to reevaluate asymptomatic patients with known severe AS
(LV function may deteriorate before symptoms manifest; patients present with heart failure); echocardiography not indicated
for routine reevaluation of asymptomatic adult with known mild AS
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| Cardiac catheterization: not necessary if aortic valve disease alone suspected; for patients with symptomatic AS undergoing
coronary angiography; low-output, low-gradient AS—difficult to determine whether problem myocardial or
due to severely damaged ventricle; give inotropic drugs to stimulate ventricle to contract harder (if patient responds with
more flow across valve, valve replacement indicated; patients do well)
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| Changing paradigm for AS: current data show 70% of patients with severe AS develop symptoms or die in 3 to 5 yr;
recent studies show incidence of sudden death slightly higher than originally estimated; operative mortality reduced; improvements
in prosthetic valves (eg, longer lasting with better hemodynamic profile)
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| Key points in AS management: endocarditis prophylaxis; educate patients; activity restriction; exercise stress testing
in patients with mild AS often helpful; statins—mechanisms of age-related AS and atherosclerosis similar; data about
efficacy conflicting; valvuloplasty ineffective; indications for aortic valve replacement—symptomatic severe AS; severe
AS with need for coronary bypass surgery; moderate to severe AS in patients undergoing aortic surgery; percutaneous
replacement of aortic valve—valve mounted on stent and implanted percutaneously; may replace traditional aortic
valve replacement
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| Mitral stenosis: usually caused by rheumatic fever; clinical history—dyspnea with exertion; winter bronchitis; chest
pain; patients with severe obstruction occasionally have orthopnea; exercise testing (especially serial testing) helpful for
identifying deterioration in function; physical examination—S1 often accentuated, especially if valve somewhat pliable;
pulmonary hypertension; S2 may be accentuated; S3 rare, unless patient has MR; opening snap correlates with isovolumic
relaxation; aortic component of S2 and opening snap; typical murmur; echocardiography excellent for
determining severity of MS
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| Treatment of MS: prophylactic antibiotic therapy; treat anemia and infections aggressively and promptly; diuretics
helpful for improving symptoms; digoxin does not alter hemodynamics but may help control heart rate; agents that slow
heart rate (eg, β-blockers, rate-limiting calcium antagonists) often helpful and improve exercise capacity; new-onset
rapid atrial fibrillation poorly tolerated and may require emergency cardioversion; anticoagulation—indicated for patients
at high risk for embolization (ie, persistent or transient atrial fibrillation [especially in elderly]); maintain international
normalized ratio (INR) at 2 to 3; no firm evidence that anticoagulation therapy reduces incidence of pulmonary or
systemic emboli in patients with sinus rhythm; mitral valvuloplasty—excellent, but complications may occur; doubles
mitral valve area; improves other hemodynamic parameters; long-term results excellent (compares favorably to open and
closed mitral commissurotomy); mitral valve replacement—useful for severe cases; echocardiography criteria used to
determine whether balloon valvuloplasty can be done
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Educational Objectives
| The goal of this program is to educate the listener about coronary artery disease (CAD) and heart valve abnormalities. After
hearing and assimilating this program, the participant will be better able to:
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 | 1. Prevent thrombosis in patients with CAD.
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| 2. Evaluate patients with coronary disease using appropriate diagnostic tools.
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| 3. Compare aortic and mitral stenotic disease to regurgitant disease.
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| 4. Identify classic signs of aortic stenosis.
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| 5. Choose appropriate treatment for mitral stenosis.
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Discussed on This Program
Abciximab [ReoPro]
Argatroban
Aspirin (acetylsalicylic acid; ASA) [several trade names]
Clopidogrel bisulfate [Plavix]
Enoxaparin sodium [Lovenox]
Fondaparinux sodium [Arixtra]
Heparin sodium injection
Heparin sodium lock flush solution [Heparin Lock Flush, Hep-Lock, Hep-Lock U/P]
Hirudin (investigational)
Morphine sulfate (several trade names)
Nitroglycerin (several trade names)
Suggested Reading
Allison MA et al: Mitral and aortic annular calcification are highly associated with systemic calcified atherosclerosis.
Circulation 113:861, 2006; Coady E: Managing patients with non-ST-segment elevation acute coronary syndrome. Nurs
Stand 20:49, 2006; Bonow RO et al: ACC/AHA 2006 guidelines for the management of patients with valvular heart
disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
(writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): developed
in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography
and Interventions and the Society of Thoracic Surgeons. Circulation 114:e84, 2006; Cohn WE: Percutaneous
valve interventions: where we are and where we are headed. Am Heart Hosp J 4:186, 2006; Collard CD et al: Preoperative
statin therapy is associated with reduced cardiac mortality after coronary artery bypass graft surgery. J Thorac Cardiovasc
Surg 132:392, 2006; Davidson MJ et al: Percutaneous therapies for valvular heart disease. Cardiovasc Pathol
15:123, 2006; Elhendy A et al: Prognostic value of exercise stress technetium-99m-tetrofosmin myocardial perfusion
imaging in patients with normal baseline electrocardiograms. Am J Cardiol 98:585, 2006; Garcia-Orta R et al: Mitral
Valve Repair for Mitral Regurgitation. Rev Esp Cardiol 59:743, 2006; Gupta A et al: Coronary artery revascularization:
past, present, future: part II--newer technologies. Clin Cardiol 29:341, 2006; Holmes DR Jr: Antiplatelet therapy
after percutaneous coronary intervention. Cerebrovasc Dis 21 Suppl 1:25, 2006; Kongsaerepong V et al: Echocardiographic
predictors of successful versus unsuccessful mitral valve repair in ischemic mitral regurgitation. Am J Cardiol
98:504, 2006; Kounis NG et al: Coronary-artery stents. N Engl J Med 354:2076, 2006; Mehta RH et al: Challenges
in Predicting the Need for Coronary Artery Bypass Grafting at Presentation in Patients With Non-ST-Segment Elevation
Acute Coronary Syndromes. Am J Cardiol 98:624, 2006; Vats HS et al: Suspected clopidogrel resistance in a patient
with acute stent thrombosis. Nat Clin Pract Cardiovasc Med 3:226, 2006; Walther T et al: Minimally invasive surgery
for valve disease. Curr Probl Cardiol 31:399, 2006; Wasserman EJ et al: Atherothrombosis in acute coronary
syndromes: mechanisms, markers, and mediators of vulnerability. Mt Sinai J Med 73:431, 2006; Wu FY et al: Coronary
artery bypass grafting in patients with left ventricular dysfunction. J Chin Med Assoc 69:218, 2006.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. The following has been disclosed:
Dr. Panetta is a consultant for Acist Medical Systems, Inc. and Lumen Biomedical, Inc.
Dr. Panetta spoke on May 2, 2006, in Minneapolis, MN, at the 32nd Annual Family Medicine Review Update 2006,
presented by the University of Minnesota Medical School. Dr. Dehmer was recorded in Austin, TX, at the 22nd Annual
Family Medicine Review, presented April 5-8, 2006, by Scott and White and Texas A and M University System
Health Science Center College of Medicine, Temple, TX. The Audio-Digest Foundation thanks the speakers and the
sponsors for their cooperation in the production of this program.
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