Noninvasive Evaluation Of

Pretest Likelihood of CAD



s1 of 3 sx


2 of 3 sx


3 of 3 sx








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40 49







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60 69







ix: (1) substernal cheit pain. (2) provoked by exertion, (3( relieved by rest or

NTG (N£JM H7i)0O:1JSO)

Exercise tolerance test ("stress test") (NE>m 2001:3441840)

• Indications: dx CAD, evaluate Pts w/ known CAD & A in clinical status, risk stratify Pts s/p

ACS. evaluate exercise tolerance, localize ischemia (radionuclide imaging required)

• Contraindications:

Absolute: AMI w/in 48 h. high-risk UA. acute PE. severe AS. uncontrolled CHF, uncontrolled arrhythmias, myopericarditis. acute aortic dissection Relative: LM CAD. mod valvular stenosis, severe HTN. HCMP. high-degree AVB. severe electrolyte abnl, inability to exercise

• Exercise: standard Bruce (Se 60%; Sp 75%; Se • 50% for 1VD. >85% for 3VD or LM).

modified Bruce (begins w/o treadmill incline), submax (if <3 wks post-MI).or sx-limited hold antianginal mcds if trying to dx CAD; give if assessing if Pi ischemic on meds

• Pharmacologic: if unable to exer. or low exer. tol. (Se & Sp exercise; better if LBBB)

coronary vasodilators (will reveal CAD. but will not tell you if Pt ischemic): dipyridamole or adenosine (may precipitate bradycardia and bronchospasm) chronotropes/inotropes ( physiologic): dobutamine (may precipitate tachyarrhythmias)

• Imaging: used for Pts w/ uninterpretable baseline ECG. after indeterminate ECG test, pharmacologic tests, or localization of ischemia)

uninterpretable ECG: paced. LBBB. resting ST; 1 mm. dig.. LVH ( Se. i Sp). WPW SPECT (thallium-201 or ""Tc-sestamibi) or PET (rubidium-82; usually wI pharm test):

I Se ( 85%) and Sp (-75%): can ECG-gate to assess LV systolic fxn; tt cost echocardiography:' Se (-85%) and Sp ( 75%); operator-dependent; t cost Test results

• HR (must achieve :t85% of max predicted HR (220-age) for exercise test to be dx).

BP response, peak double product (HR > BP). HR recovery (HR^ HRi mlMr; nl >12)

• Max exercise capacity achieved (METS or mins)

• Occurrence of symptoms (at what level of exertion and similarity to presenting sx)

• ECG changes: downsbping or horizontal ST i predictive of CAD (but distribution of ST 1

do not localize ischemic territory); ST T highly predictive

• Duke treadmill score exercise mins - (5 x max ST dev) (4 x angm3 index) [0 none. 1

nonlimiting, 2 limiting]; score -5 <1% 1-y mort; 10 to -4 2 3%; - 11 — >5%

• Imaging: radionuclide defects or echocardiography wall motion abnormalities reversible defect ischemia; fixed defect infarct false ? : breast -• ant "defect" and diaphragm — inf "defect" false 0 may be seen if balanced ischemia High-risk test results (PPV 50% for LM or 3VD.. consider coronary angiography)

• ECG: ST i ¿2 mm or -1 mm in stage 1 or in -5 leads or -5 min in recovery; ST t;VT

• Physiologic: i BP. exercise < 4 METS. angina during exercise. Duke score • 11; EF <35%

• Radionuclide: -1 Ig or -2 mod. reversible defects, transient cavity dilation. T lung uptake

Myocardial viability

• Goal: identify hibernating myocardium that could regain fxn after revascularization

• Options: MRI (Se -95%. Sp 70%). PET (Se 90%. Sp 75%). dobutamine stress echo (Se 70%. Sp 85%): rest-redistribution thallium (Se 90%. Sp 55%)

Coronary calcium score <jama 2004:291210)

• Quantitative evaluation of extent of calcium and thus estimate of plaque burden

• Not able to assess % narrowing. ? risk stratification if intermed. Framingham risk score CT & MR coronary angiography (nqm 2001:345 1863; jama 2006:296.403; jacc 2006:48 1475)

• Assess for significant stenoses: Se & Sp 85% (for 64-slice CT)

• Up to 30% of segments nonevaluable (wI 16-slice CT. fewer w/ newer generation CT)

and calcium generates artifact

• Image quality best at slower & regular HR (give [5-blockers if possible, goal HR 55-60)


Indications for coronary angiography in stable CAD or asymptomatic Pts

• CCS class lll-IV angina despite medical Rx or angina + systolic dysfxn

• High-risk stress test findings (see prior topic)

• Uncertain dx after noninvasive testing (& compelling need to determine dx). occupational I

need for definitive dx (eg, pilot), or inability to undergo noninvasive testing

• Systolic dysfxn with unexplained cause

• Survivor of SCD, polymorphic VT, sustained monomorphicVT

• Suspected spasm or nonatherosclerotic cause of ischemia (eg. anomalous coronary)

Pre-cath checklist

• Document peripheral arterial exam (femoral. DP. PT pulses; femoral bruits)

• ✓ CBC. PT. & Cr; give IVF bicarb, acetylcysteine, see "CIARF"); blood bank sample

• ASA 325 mg; consider clopidogrel pretreatment (300-600 mg s2-6 h before PCI)

Coronary revascularization in stable CAD tjacc 2006;47:ei;;ACC 2004;44o2 13)

• CABG J mortality c/w med Rx (albeit before statins & ACEI/ARB) in Pts w/ 3VD. left main.

or 2VD wI critical prox LAD. and espec. if I EF (but viable myocardium)

• PCI 1 angina c/w med Rx; does not i D/MI (COURAGE, nejm 2007:356:1503)

• PCI comparable to CABG in Pts w/o 3VD. w/o DM. and nl EF

• In general, for stable CAD w/o critical anatomy and w/o I EF. initial focus should be on optimal medical therapy

• If revasc deemed necessary. PCI preferred if limited # of discrete lesions, nl EF. no DM.

poor operative candidate; CABG preferred if extensive or diffuse disease, i EF. DM. or concomitant valvular heart disease

• Balloon angioplasty: effective, but c/b dissection and by elastic recoil & neointimal hyperplasia restenosis; now reserved for small lesions. ? some SVG lesions

• Bare metal stents (BMS): I elastic recoil — 33-50% i restenosis & repeat revasc (to

10% by 12 mos) c/w balloon angioplasty, requires ASA lifelong & clopidogrel xa4 wks

• Drug-eluting stents (DES) (nejm 2006:354.483); i neointimal hyperplasia -75% ;

restenosis. 50% I clinical need for repeat revasc (to <5% by 12 mos). & no A death/Ml over 1 y c/w BMS; requires ASA lifelong & clopidogrel x y (Ore 2007:115:813)

Post-PCI complications

• Postprocedure / vascular access site, distal pulses. ECG. CBC. Cr, CK-MB

• Bleeding hematoma /overt bleeding: manual compression, reverse/stop anticoag retroperitoneal bleed: may present with i Hct • back pain; T HR & I BP late;

Dx: abd/pelvic CT (I ); Rx: reverse/stop anticoag. IVF/PRBC as required if bleeding uncontrolled, consult performing interventionalist or surgery

• Vascular damage pseudoaneurysm: triad of pain, expansile mass, systolic bruit; Dx: U/S; Rx: manual compression. U/S-directed compression or thrombin injection, or surgical repair AV fistula: continuous bruit; Dx: U/S; Rx: surgical repair

1 perfusion to LE (embolization, dissection, thrombus): loss of distal pulse; Dx: angio; Rx: percutaneous or surgical repair

• Other local: nerve injury, infection

• Ml: >3x ULN of CK-MB occurs in 5-10%; Qw Ml in <1%

• Renal failure: contrast-induced manifests w/in 24 h, peaks 3-5 d (see "CIARF")

• Cholesterol emboli syndrome (typically in middle-aged & elderly and w/Ao atheroma)

renal failure: late and progressive, cos in urine mesenteric ischemia, abd pain. LGIB, pancreatitis intact distal pulses but livedo pattern and toe necrosis Hollenhorst plaques in retinal arteries

• Stent thrombosis: p/w acute chest pain & STE; requires urgent return to cat/i lab.

Acute thrombosis often due to mechanical complication (underexpansion of stent or unrecognized dissection) or d/c of antiplt Rx (JAMA 2005:293:2126). Risk oi \ate stent thrombosis may be higher with DES than BMS <jacc 2006.48:2584).

• In-stent restenosis: mos after PCI. gradual return of typical anginal sx (10% p/w ACS)

Due to combination of elastic recoil (i w/ stenting vs. balloon angioplasty) and neointimal hyperplasia (i w/ DES vs. BMS) and not recurrent atherosclerosis.

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