CLINICAL CARDIOLOGY
Educational Objectives
| The goals of this program are to improve risk assessment for heart disease and improve overall cardiovascular
management. After hearing and assimilating this program, the clinician will be better able to:
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 | 1. Distinguish types of cardiac risk and risk-factor categories.
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| 2. Select patients for newer screening methods, such as C-reactive protein and 64-slice computed tomography
coronary angiography.
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| 3. Identify hair, skin, and eye signs associated with cardiac conditions.
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| 4. Evaluate irregular venous and carotid pulsations by palpation and physical examination.
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| 5. Palpate chest, abdomen, and extremities to identify cardiac abnormalities.
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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. Gibb spoke on April 25, 2008, in Urbana, IL, at Primary Care Cardiology 2008, presented by Carle Foundation
Hospital. Dr. Gazes was recorded in Charleston, SC, at Cardiology for the Primary Physician, presented May 28-31,
2008, by the Medical University of South Carolina. The Audio-Digest Foundation thanks the speakers and the sponsors
for their cooperation in the production of this program.
| RISK-FACTOR ASSESSMENT FOR HEART DISEASE —Matthew D. Gibb, MD, Assistant Professor, Department of Internal
Medicine, College of Medicine, University of Illinois at Urbana-Champaign, and Head of Cardiology Division, Carle
Clinic Association, Urbana, IL
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| Atheroma: symptomatically, presents in men >50 yr of age and women >60 yr of age; can produce obstructive plaque
and anginal symptoms; plaque rupture leads to thrombosis and acute occlusion of artery
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| End points for risk in cardiovascular disease (CVD): hard—total mortality; heart disease mortality; coronary
mortality; nonfatal myocardial infarction (MI); resuscitative cardiac arrest; stroke; used in clinical trials and population-
based studies; soft—revascularization (eg, angiography, stent placement, bypass surgery); occurrence of unstable angina
without death; days in hospital for cardiac events; progression of symptoms; time to first event; surrogate—used in research;
angiography; intracoronary ultrasonography (US); magnetic resonance imaging (MRI); quantitative calcium assessment
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| Types of risk: absolute—risk for event over prospective period of time; typically, absolute aggregate risk for MI, stroke, or
death over 10 yr; relative—incremental risk attributed to additive risk factors or reduction in risk due to therapy; based on
changes in absolute risk probability after introduction of various measures
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| Categories of risk factors: independent—causative; can contribute independently to development or progression of
disease; other—independent or causative probability not established, but seem to portray risk in, eg, population-based
studies or retrospective analyses of patients who had events; used in research to determine incremental values to further
refine absolute risk
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| Studies used for risk calculation: 1) Framingham Heart Study; ongoing population-based study; patients assessed every
2 yr; risk scores established for presence or absence of particular variables; used to assess probability, based on Framingham
population, of 10-yr aggregate risk for hard CV end point; as scores increase, probability of event increases; 2)
Prospective Cardiovascular Munster Heart Study (PROCAM) published in 1997; looked at 10856 men; 3) Systematic Coronary
Risk Estimation (SCORE); project published in 2003; analysis of morbidity and mortality databases of several European
countries; 4) Indiana Heart Project; ≈5-yr follow-up in 50,000 patients
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| Degrees of risk: low—<15% chance for MI or cardiac death over 10 yr; high—>20% probability of MI or cardiac death
over 10 yr; typically ≥3 major risk factors; patients often have established clinical evidence of vascular disease or one
high-level risk factor
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| Limitations: newer risk equations not built into calculators; metabolic syndrome, obesity parameters, insulin resistance,
and newer risk factors not factored into equations; population-based issues (eg, limited data on women and various ethnic
groups); sensitivity and specificity
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| C-reactive protein (CRP): acute phase reactant; elevated in inflammatory states; may be associated with low levels of
inflammation in certain types of vulnerable plaque; limitations—limited population data; weak indicator of total disease
burden; some associations variously weak or strong; recommendations—measure in intermediate-risk patients (ie, those
in whom 10-yr risk 10%-20%); use risk levels to triage patients into less or more aggressive strategies; population-based
screening not recommended; measurement should be done twice (2 wk apart) and results averaged; CRP level >10 mg/L
often indicates other inflammatory state (work-up required)
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| Lipoprotein A: clearly associated with risk; not affected by most lipid-lowering drugs; tends to be modified only by
high-dose niacin
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| Fibrinogen: not highly effective for assessing aggregate additional risk in asymptomatic patient
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| Homocysteine: highly correlated with risk for stroke, heart disease, and peripheral vascular disease; methylene tetrahydrofolate
reductase (MTHFR) mutation results in elevated levels; in 2006, studies showed no benefit of reduction of vascular
events when homocysteine lowered via folate or other B vitamins; low specificity for elevated level
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| Carotid B-mode US: measures intimal-medial thickness of carotid artery; degree of thickness correlates with risk for
CV events; easy; reliable; normal value, 0.36 to 0.90 mm (increases by 0.08 mm/yr in adults; thickness greater in men);
further refines risk in intermediate-risk patients; not expensive; lipid lowering with statin therapy may arrest progression
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| Coronary artery calcium scanning by computed tomography (CT): costs ≈$50; risk based on calcium scores
and distribution; study showed risk for cardiac event over several years of follow-up increases exponentially when coronary
artery calcium scores >200; adds value to Framingham risk score; high (≥98%) negative predictive value for future
cardiac events over 10 yr with negative calcium score (ie, zero); consider in intermediate-risk population; not recommended
for low-risk population
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| 64-slice CT coronary angiography (CTCA): high sensitivity and specificity for obstructive disease in proximal
two-thirds of major coronary arteries; negative result has high negative predictive value for cardiac event for ≤7 yr; patients
with negative calcium score and negative 64-slice CTCA unlikely to have MI or to die from heart disease in 7 to 10
yr; limitations—CTCA may be unreliable in patients with high calcium scores, due to interference with reading
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| Management approach: high risk—candidates for pharmacologic therapy; patients have ≥1 risk factors (eg, diabetes,
hypertension); intermediate risk—candidates for further risk stratification into higher or lower risk subset; higher-risk patients
may benefit from pharmacologic therapy or may be candidates for evaluation for ischemia; low risk—counsel
patients about diet; these individuals not candidates for pharmacologic therapy or further testing
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| Questions and answers: further evaluation of intermediate-risk patient—if asymptomatic, evaluate with one additional
measure (eg, CRP, carotid B-mode US); coronary artery calcium scanning by CT recommended; 64-slice CTCA can be
valuable but expensive; if symptomatic, order functional testing, eg, stress testing and imaging study; calcium score—
correlation between zero score and low risk in diabetic populations not as well known
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| BEDSIDE CARDIAC PEARLS —Peter C. Gazes, MD, Professor of Medicine, and Distinguished Professor of Cardiology,
Medical University of South Carolina, Charleston
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| Skin: silky—consider hyperthyroidism; dry and coarse—myxedema; scleroderma—50% show some pericarditis (20%
detected clinically); cardiomyopathy; cyanosis and clubbing—important in congenital heart disease and fibrosis; clubbing
without cyanosis may occur in patients with, eg, lung cancer and ulcerative colitis; in congenital heart disease, cyanosis
and clubbing in feet (but not hands) may be due to patent ductus arteriosus with pulmonary hypertension; rash and
nodules—erythema marginatum in children with low-flow murmurs and diffuse rash confined to trunk; nontender small
nodules at base of skull and around knuckles (resolve with steroids); pallor—elderly patients on aspirin who become
pale may have congestive heart failure (CHF), subclinical coronary disease, or mild hypertension (correcting anemia
helpful); absence of redness and lines on palms indicates hematocrit ≤20%; scars—palpate scars in patients with heart
failure (HF) to detect atrioventricular (AV) fistula; thrill and continuous murmur may be cause of HF; petechiae—in patients
with fever, consider endocarditis; livedo reticularis—fishnet appearance all over body; seen with collagen vascular
diseases; some patients >50 yr of age may have abdominal aneurysm and cholesterol emboli; splinter hemorrhages—
subungual in endocarditis; Osler’s nodes—painful tender nodes on tips of fingers in patients with endocarditis; Janeway
lesions—nontender erythema or ecchymosis on palms and soles; malar flush—sign of mitral disease; can be due to rheumatic
fever, pulmonary hypertension, or HF; xanthomas—rare; xanthelasmas; xanthoma tuberosum around tubercles; tendon
xanthomas (Achilles tendon should not be wider than index finger); patients have high cholesterol; if rash all over
body, patient has Frederickson’s type IV hyperlipidemia
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| Head: decreasing body and increasing hat size—Paget’s disease due to increased metabolic activity and vascularity of
bones; cardiomyopathy; hair—if brittle, consider myxedema; if fine and silky, consider hyperthyroidism
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| Eyes and ears: consider cataracts in diabetic patients with congenital heart disease, pulmonary stenosis, and patent ductus
arteriosis; iridodonesis (dancing iris; seen in Marfan syndrome); hypertelorism (eyes widely separated; consider pulmonary
stenosis, supravalvular aortic stenosis [patients have small chin with low ears], and calcium abnormality);
jaundice seen with aortic stenosis and valvular disease due to liver changes; blue sclera and valvular lesions due to osteogenesis
imperfecta (brittle bones); Argyll Robertson pupil (small pupil that reacts to accommodation effort, but not to
light; seen in patients with aortic insufficiency); arcus senilis (separation of iris pigment results in white rim where cornea
meets sclera; usually not visible in elderly patients); ears— low ears seen with supravalvular aortic stenosis; consider
pernicious anemia in patients with anemia and large ears
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| Voice and tongue: hoarseness due to, eg, enlarged pulmonary artery from congenital heart lesion or mitral disease, or
aortic aneurysm; macroglossia due to myxedema or amyloidosis
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| Neck: Kussmaul’s sign (inspiratory filling of neck veins in patients with CHF; consider right ventricular [RV] infarction
or constrictive pericarditis); venous pulsations—silhouette of deep jugular pulsations under sternocleidomastoid muscle
visible; look for a or v wave (generally, a wave); v wave most prominent in tricuspid insufficiency or atrial fibrillation; a
wave due to atrial contraction; c wave due to ventricular contraction and increase in tricuspid valve during systole “and
probably some artifact from carotid”; x descent; v wave due to built-up atrial pressure before opening of AV valve; y descent;
examination—speaker places patient in 45º position; observe neck veins and pulsations above clavicle; place vertical
ruler from Louis’ angle (at level of second intercostal space) and drop perpendicularly (with horizontal line) to level
of pulsation; pulsation normal if <3 cm above Louis’ angle; hepatojugular reflux—applying pressure to abdomen increases
pulsations (5 cm above Louis’ angle; early finding in CHF); prominent a wave may indicate obstruction in pulmonary
vasculature (pulmonary hypertension) or pulmonary valve or tricuspid valve; v wave prominent in tricuspid
insufficiency (pulsations may be at earlobe, causing head to rock from side to side [“no-no” sign]); cannon a wave—
flicker occurs when atrium contracts after AV valve closes (“blood goes back up neck”); flicker and slow heart rate occur
with third-degree AV block but not with sinus bradycardia
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| Carotid pulsations: aortic stenosis—parvus et tardus (ie, slow rising pulse) and harsh murmur “that sounds like a bulldog”;
since elderly patients may not have parvus et tardus, check degree of stenosis by length of murmur; pulsus
bisferiens—double-peak pulse; seen with wide-open aortic insufficiency, moderate aortic stenosis and insufficiency, and
idiopathic hypertrophic subaortic stenosis
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| Chest: pectus carinatum (“pigeon chest”; indentation in chest displaces heart forward, leading to low-flow murmurs);
straight back syndrome pushes heart forward, leading to low-flow murmurs; isolated dextrocardia—associated with congenital
heart diseases, often with absolute ventricular septum; patients with situs inversus may have Kartagener’s syndrome
(associated with sinusitis and bronchiectasis); palpate both sides of chest
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| Pulsations: sternoclavicular joints—in patients with chest pain and aortic insufficiency, consider dissecting aneurysm;
right aortic arch; aortic area—consider abnormality in aortic valve or ascending aorta; pulmonic area—consider pulmonary
hypertension, enlarged pulmonary artery from left or right shunt, or congenital heart disease; RV area—dynamic lift
with left or right shunt (eg, atrial or ventricular septal defect); most prominent with mitral insufficiency; sustained lift
with hypertrophy due to obstruction in pulmonary retreat; apical area—point of maximum impulse (PMI) usually left
ventricle (LV; PMI collapses medially; collapses laterally if RV); dynamic lift with aortic insufficiency; parvus et tardus
and sustained lift with concentric hypertrophy; ectopic area—consider ventricular aneurysm
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| Blood pressure (BP): auscultatory gap—may result in inaccurate systolic BP measurement; palpate pulse “until you
don’t feel it and that’s your systolic BP”; pulsus alternans—indicative of LV failure (eg, S3 gallop); best detected with
cuff when patient standing; pulsus paradoxus—in acute setting, consider cardiac tamponade; can occur with chronic
obstructive lung disease; best detected by cuff (no pulse sound with inspiration); Osler’s maneuver—in elderly patients
with wide pulse pressure, palpate radial pulse (“go proximal and press hard; obliterate it”); feel distally to determine
whether artery collapsed (if “knobby,” patient has sclerotic vessels); coarctation of aorta—consider in patients
with small legs and big arms; difference in systolic BP between arms ≥10 mm Hg—occurs in 25% of hypertensives, 1%
of normotensives
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| Abdomen: palpate liver (start above iliac crest); palpable spleen—consider endocarditis, severe HF, or tricuspid insufficiency;
pulsations—1) aortic pulsations pulsate anteriorly and laterally; 2) liver pulsates anteriorly and posteriorly; palpable
under twelfth rib (tricuspid insufficiency); palpate both sides of abdomen to detect abdominal aneurysm; 3) palpate
under xiphoid process towards chin; in patients with chronic obstructive lung disease, downward pulsation may indicate
RV enlargement and cor pulmonale
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| Extremities: check for polydactyly and congenital heart abnormality or Holt-Oram syndrome; consider hyperthyroidism
in patients with warm feet; pulsations—femoral arteries should feel equal; check popliteal artery, patella, and posterior
tibial artery; ≈8% of dorsalis pedis artery may not be palpable; Branham’s sign—palpable thrill over scar; in patients
with wide pulse pressure, obliteration by pressing proximally results in bradycardia; Adson’s maneuver—patients with
left chest pain may have cervical rib clamping down on artery; have patient stand with hand extended backward and neck
towards involved side; if rapid pulse obliterated with deep inspiration, consider scalenus anticus; ulcers—lateral ulcers
(eg, ulcers above malleoli in diabetic patients); venous ulcers have brownish discoloration; in patients with ulcers between
toes, consider AV fistula; edema—venous edema occurs with CHF (pitting lasts ≈1 min); may be due to tight
clothing or drugs (eg, nonsteroidal anti-inflammatory drugs [NSAIDs]); commonly caused by venous stasis; in CHF, left
leg may have more edema than right leg
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Suggested Reading
Adams JN et al: Aortic complications of Marfan's syndrome. Lancet 352:1722, 1998; Assmann G et al: Cardiovascular
risk assessment in the metabolic syndrome: results from the Prospective Cardiovascular Munster (PROCAM) Study.
Int J Obes (Lond) 32 Suppl 2:S11, 2008; Gaylord GM: Computed tomographic and magnetic resonance coronary angiography:
are you ready? Radiol Manage 24:16, 2002; Greenland P et al: Coronary artery calcium score combined
with Framingham score for risk prediction in asymptomatic individuals. JAMA 291:210, 2004; Erratum in: JAMA. 2004
Feb 4;291(5):563; Koenig W et al: C-reactive protein modulates risk prediction based on the Framingham Score: implications
for future risk assessment: results from a large cohort study in southern Germany. Circulation 109:1349, 2004;
Liao Y et al: How generalizable are coronary risk prediction models? Comparison of Framingham and two national cohorts.
Am Heart J 137:837, 1999; Lloyd-Jones DM et al: Framingham risk score and prediction of lifetime risk for coronary
heart disease. Am J Cardiol 94:20, 2004; Mowatt G et al: Systematic review of the clinical effectiveness and cost-
effectiveness of 64-slice or higher computed tomography angiography as an alternative to invasive coronary angiography in
the investigation of coronary artery disease. Health Technol Assess 12:1, 2008; Potter K: Homocysteine and cardiovascular
disease: should we treat? Clin Biochem Rev 29:27, 2008; Sasson Z et al: Are hepatic pulsations in dilated cardiomyopathy
with heart failure due to tricuspid regurgitation? Am J Cardiol 71:355, 1993; Sgambato A et al: Nodules with a
prominent vascular component. Arch Dermatol 144:702, 2008; Simon A et al: Intima-media thickness: a new tool for diagnosis
and treatment of cardiovascular risk. J Hypertens 20:159, 2002.
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