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Clinical Conference

Clinical Conference. HPI. 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

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Clinical Conference

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  1. Clinical Conference

  2. HPI • 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.

  3. 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.

  4. Meds • 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

  5. Physical Exam • 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.

  6. 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

  7. EKG 11/06

  8. Old EKG 7/05

  9. ECHO 7/06

  10. 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.

  11. Stress Dipyridamole Gated SPECT Myocardial Perfusion Study • Ischemic changes in the apical and inferior walls w/ apical thinning • SSS 11 • EF 45%

  12. Cath

  13. 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…..

  14. 3 months later….. Presents to ER w/ c/p story and physical exam almost identical to that in Nov 06….however…..

  15. EKG

  16. EKG from 11/06

  17. 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…

  18. Pertinent Labs • 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

  19. Follow-up Labs • Troponin: 4.89 -> 6.36 • CKMB: 14.1 -> 13.5 • CK: 214 -> 250

  20. Cath

  21. Cath 3/07 • 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

  22. Now What??? Pt started on Reopro overnight and repeat cath the next morning….

  23. Cath 3/23/07 No significant change in thrombus burden…pt underwent thrombectomy and anticoagulation w/ heparin initiated post cath.

  24. 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.

  25. 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

  26. CAE Areas of involvement: Prox and mid RCA (68%): most common sites Prox LAD (60%) Prox LCx (50%) LM – rare, ~0.1%

  27. CAE Causes: Pahlavan PS et al, Clin Card, 2006

  28. 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

  29. CAE Epidemiology: Baman TS et al, AJC 2004

  30. 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

  31. CAE Management options: -aggressive risk factor modification -antiplatelet, anticoagulants -statins => may inhibit metalloproteinases -stenting e.g. covered stents -surgical excision, ligation, CABG

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