Clinical Conference

• 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.

HPI

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.

Other History

• 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

Meds

• 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:

– 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.

Physical Exam

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

Pertinent Labs

EKG 11/06

Old EKG 7/05

ECHO 7/06

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.

ECHO

Dipyridamole Gated SPECT Myocardial Perfusion Study

• Ischemic changes in the apical and inferior walls w/ apical thinning

• SSS 11

• EF 45%

Stress

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.

• PLAN: medical management– Started statin.– Up-titrated nitrates.– F/U as outpt…..

Cath

Presents to ER w/ c/p story and physical exam almost identical to that in Nov 06….however…..

3 months later…..

EKG

EKG from 11/06

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…

EXAM

• CK: 214

• CKMB: 14.1

• Trop: 4.89

• BNP: 316 (prior BNP was 112)

• Na: 146 / Cl: 106 / BUN: 17

• K: 4.1 / HCO3: 27 / Creat: 1.3

• 9.5>13.2<167

Pertinent Labs

• Troponin: 4.89 -> 6.36

• CKMB: 14.1 -> 13.5

• CK: 214 -> 250

Follow-up Labs

Cath

• 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

Cath 3/07

Pt started on Reopro overnight and repeat cath the next morning….

Now What???

No significant change in thrombus burden…pt underwent thrombectomy and anticoagulation w/ heparin initiated post cath.

Cath 3/23/07

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.

Coronary artery ectasia (CAE)

Types:

-Saccular

-Fusiform

CAE

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

Areas of involvement:

Prox and mid RCA (68%): most common sites

Prox LAD (60%)

Prox LCx (50%)

LM – rare, ~0.1%

CAE

Causes:

CAE

Pahlavan PS et al, Clin Card, 2006

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:

CAE

Baman TS et al, AJC 2004

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

CAE