Clinical Conference
HPI
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74 y/o female with hx of:
– diastolic dysfunction
– COPD
– Lt ICA aneurysm
– presents to the ER 3 MONTHS AGO with chest pain
– CHEST PAIN:
• Left sided
• started at rest
• 7/10
• throbbing, intermittent and non-radiating
• No alleviating or exacerbating factors
• Some shortness of breath which was relieved with her home O2.
• No associated palpitations, diaphoresis, nausea.
Other History
PMH:
• Diastolic dysfunction
• Left ICA Aneurysm
• COPD
• HTN
• Glaucoma
• s/p abd hysterectomy ~2000
Social Hx:
• quit tobacco many years ago
• denied EtOH and drugs
FH:
• Denies family history of DM, HTN, CAD.
Meds
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Asa 325mg Po Qday
Digoxin 125mg Po Qod
Isosorbide Dinitrate 40mg Tid
Lisinopril 40mg Po Qday
Metoprolol 200mg Po Qday
Simvastatin 20mg Po Qday
Hydralazine 100mg Po Tid
Lansoprazole 30mg Po Qday
Lasix 20mg Po Bid
Physical Exam
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Vitals: T: 36.6, BP:156/104, HR: 75, RR: 18, SaO2: 96% on 2L
Gen: alert and oriented X3, no acute distress
Heent: op clear, poor dentition, eomi, right eyelid slightly edematous
Cardiovascular:
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Non-displaced non-sustained PMI ; no thrills or heave
Nl carotid upstroke and volume; no bruits
RR, No S3 or S4
II/VI holosytolic murmur at LLSB; no friction rub.
JVP 7; no HJR
Warm LE, no edema.
Nl radial, femoral, DP and PT pulses.
• Pulm: clear bilaterally without crackles
• Abd: soft, non-tender, normoactive bowel sounds, no ascites; no
organomegaly.
Pertinent Labs
Na: 139
K: 3.9
BUN:20
Creat: 0.9
CK: 125
CKMb: 1.3
Trop: <0.05
Lipids:
TC 169
Trig 110
HDL 41
LDL 106
EKG 11/06
Old EKG 7/05
ECHO 7/06
ECHO
TWO-DIMENSIONAL STUDY
• Global left ventricular function is normal.
• Left ventricular wall thickness is moderately increased.
• The aortic valve is mildly sclerotic but opens well.
DOPPLER EVALUATION
• Mild tricuspid regurgitation.
• The pulmonary artery systolic pressure is 31mmHg.
• Left ventricular inflow pattern reflects diastolic dysfunction. Pulmonary vein flow is
normal.
CONCLUSION
• Normal left ventricular size and systolic function (function has very significantly
improved from study of 7/5/05).
• Diastolic dysfunction.
Stress
Dipyridamole Gated SPECT Myocardial Perfusion Study
• Ischemic changes in the apical and inferior walls w/ apical thinning
• SSS 11
• EF 45%
Cath
Cath
LHC 11/06:
• LEFT MAIN: Angiographically normal.
• LEFT ANTERIOR DESCENDING: Mild diffuse disease; 30% mid.
• LEFT CIRCUMFLEX CORONARY ARTERY: Mild diffuse disease; segments
appears slightly diffusely aneurysmal.
• RIGHT CORONARY ARTERY: Slow flow through right coronary artery; is
dominant, tortuous right coronary artery; diffusely aneurysmal.
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PLAN: medical management
– Started statin.
– Up-titrated nitrates.
– F/U as outpt…..
3 months later…..
Presents to ER w/ c/p story and physical exam almost identical to that in Nov
06….however…..
EKG
EKG from 11/06
EXAM
Unchanged from previous, specifically:
no rales
no s3, no change in the prior murmur
no le edema
carotid exam w/ continued nl upstroke and volume.
C/P resolved w/ IV BB and nitrates…
Pertinent Labs
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CK: 214
CKMB: 14.1
Trop: 4.89
BNP: 316 (prior BNP was 112)
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Na: 146 / Cl: 106 / BUN: 17
K: 4.1 / HCO3: 27 / Creat: 1.3
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9.5>13.2<167
Follow-up Labs
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Troponin: 4.89 -> 6.36
CKMB: 14.1 -> 13.5
CK:
214 -> 250
Cath
Cath 3/07
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diffusely ectatic/aneurysmal coronaries
TIMI2 flow in the left system
TIMI1 flow in the right system
saddle proximal LAD/DIAG filling defect with extension of the defect into the
DIAG1
mid LCX - 50%
ostial RCA - 50%
severely depressed LVEF globally, diffuse moderate-severe HK with
somewhat worse anterolateral wall, EF 30-35%, trivial MR, no LV-AO gradient
at time of pullback
Now What???
Pt started on Reopro overnight and repeat cath the next morning….
Cath 3/23/07
No significant change in thrombus burden…pt underwent thrombectomy and
anticoagulation w/ heparin initiated post cath.
Coronary artery ectasia (CAE)
Also known as aneurysmal CAD
Definition: localized or diffuse nonobstructive lesions of the
epicardial coronary arteries that exceed the diameter or
the normal adjacent segments of the largest coronary
vessel
Per CASS registry: dilatation is > or = to 1.5 times the
adjacent normal coronary artery.
CAE
Types:
-Saccular
-Fusiform
Classifications: (Markis et al, AJC 1976)
Type I: diffuse ectasia with aneurysmal lesions in two vessels
Type II: diffuse ectasia in one vessel and discrete ectasia in another
Type III: diffuse ectasia in one vessel
Type IV: discrete ectasia in one vessel
CAE
Areas of involvement:
Prox and mid RCA (68%): most common sites
Prox LAD (60%)
Prox LCx (50%)
LM – rare, ~0.1%
CAE
Causes:
Pahlavan PS et al, Clin Card, 2006
CAE
Pathogenesis
-poorly understood
-possible factors that are involved in vessel wall weakening:
-systemic hypertension
-inflammatory stimuli e.g. tobacco
-hyperhomocysteinemia
-genetic factors, assoc with HLA genes
-increased inflammatory response in the vessel wall
-activation of matrix metalloproteinases, may degrade
structural proteins of connective tissue
CAE
Epidemiology:
Baman TS et al, AJC 2004
CAE
Presentation:
-typically present with exertional angina
-usually do not present with AMI, sudden
death
-can be complicated by thrombus formation,
distal embolization, shunt formation,
rupture
-assoc with microvascular dysfunction
CAE
Management options:
-aggressive risk factor modification
-antiplatelet, anticoagulants
-statins => may inhibit metalloproteinases
-stenting e.g. covered stents
-surgical excision, ligation, CABG