Clinical Conference. 74 y/o female with hx of: –diastolic dysfunction –COPD –Lt ICA aneurysm...
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Transcript of Clinical Conference. 74 y/o female with hx of: –diastolic dysfunction –COPD –Lt ICA aneurysm...
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