Cardiovascular Disease Part 2 Jeffrey Zimmet MD, PhD Associate - - PDF document

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Cardiovascular Disease Part 2 Jeffrey Zimmet MD, PhD Associate - - PDF document

UCSF, Department of Medicine, CME UCSF Internal Medicine Board Certification and Recertification Review Cardiovascular Disease Part 2 Jeffrey Zimmet MD, PhD Associate Professor of Medicine University of California San Francisco July 2015


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UCSF, Department of Medicine, CME 1

UCSF Internal Medicine Board Certification and Recertification Review

Cardiovascular Disease – Part 2

Jeffrey Zimmet MD, PhD Associate Professor of Medicine University of California San Francisco July 2015

Disclosures

l None

UCSF, Department of Medicine, CME 2

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3

From ABIM blueprint for Internal Med Board Exams

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CASE 1: 45 y.o. male, with no PMH, presents with chest pain x 8 hours

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Case 1: What is the next step?

1) Start aspirin and heparin therapy 2) Start aspirin, low dose heparin and

lytic therapy

3) Perform cardiac catheterization 4) Perform echocardiogram 5) Not sure

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Acute Pericarditis

l Characterized by pleuritic, positional chest

pain, a rub, possibly a pericardial effusion, EKG with diffuse ST-elevation and PR- depression, and PR-elevation in aVR

l Cardiac enzymes can be elevated l Usually responds to oral NSAIDs l Colchicine recommended as adjunctive

therapy.

l Thrombolytics may result in life-threatening

hemorrhagic tamponade

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Question 2: Thrombolytic therapy is strictly contraindicated in all of the following except:

1) Presence of AV-malformations in the

brain

2) Any prior history of embolic stroke 3) Recent GI bleed within 1 month 4) Patient with metastatic disease to the

brain

5) All of the above

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Absolute Contraindications

  • Any prior intracranial hemorrhage
  • Known structural cerebral vascular lesion

(e.g., arteriovenous malformation)

  • Known malignant intracranial neoplasm

(primary or metastatic)

  • Ischemic stroke within 3 months EXCEPT

acute ischemic stroke within 3 hours

  • Suspected aortic dissection
  • Active bleeding (excluding menses)
  • Significant closed-head trauma or facial

trauma within 3 months

ACC/AHA Guidelines 2004

Contraindications and Caution with Lytic Therapy

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  • History of chronic, severe, poorly controlled

hypertension

  • Severe uncontrolled hypertension on presentation

(SBP > 180 mm Hg or DBP > 110 mm Hg)

  • History of prior ischemic stroke greater than 3

months, dementia, or known intracranial pathology not covered in contraindications

  • Traumatic or prolonged (> 10 minutes) CPR or major

surgery (< 3 weeks)

  • Recent (< 2 to 4 weeks) internal bleeding
  • Noncompressible vascular punctures
  • For streptokinase/anistreplase: prior exposure (> 5

days ago) or prior allergic reaction to these agents

  • Pregnancy
  • Active peptic ulcer
  • Current use of anticoagulants: the higher the INR,

the higher the risk of bleeding

Relative Contraindications To Lytics

ACC/AHA Guidelines 2004

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Case 3: 57 year old diabetic with dyslipidemia

l A 57-year-old woman with adult-onset

diabetes mellitus has the following lipid profile:

Total serum cholesterol of 178 mg/dL LDL cholesterol level of 98 mg/dL HDL cholesterol of 35 mg/dL Triglyceride level of 492 mg/dL

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Case 3

l Has been compliant with a low-fat, low-

cholesterol, diabetic diet.

l Glycohemoglobin A1C = 6.6% on oral

therapy.

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Case 3: Which of the following is the recommended initial drug therapy for this patient?

  • 1. A fibrate
  • 2. Niacin
  • 3. A statin
  • 4. Ezetimide
  • 5. A bile acid resin
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Major Risk Factors for CV Disease

l 4 major modifiable traditional CV risk factors:

l Smoking l Diabetes Mellitus l Hypertension l Hyperlipidemia

l 80-90% patients with CAD have ≥1 CAD RF;

>95% with a fatal CAD event had ≥1 CAD RF.

JAMA, August 20, 2003, vol 290, pp.891-97, 898-904.

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Hyperlipidemia in Diabetics

l Diabetes mellitus is a coronary artery disease

equivalent, and risk factor targets for patients with diabetes are the same as those in patients with established coronary disease.

l This is irrespective of age or other risk factors.

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Log-Linear Relationship Between LDL-C Levels and Relative Risk for CHD

3.7 2.9 2.2 1.7 1.3 1.0 40 70 100 130 160 190 Relative Risk for Coronary Heart Disease (Log Scale) LDL-Cholesterol (mg/dL)

Grundy, S. et al., Circulation 2004;110:227-39.

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Risk Category LDL-C Goal Initiate TLC Consider Drug Therapy High risk: CHD or CHD risk equivalents (10-year risk >20%) <100 mg/dL (optional goal: <70 mg/dL) ≥100 mg/dL >100 mg/dL (<100 mg/dL: consider drug

  • ptions)

Moderately high risk: 2+ risk factors (10-year risk 10% to 20%) <130 mg/dL ≥130 mg/dL >130 mg/dL (100-129 mg/dL: consider drug

  • ptions)

Moderate risk: 2+ risk factors (10 year risk <10%) <130 mg/dL ≥130 mg/dL >160 mg/dL Lower risk: 0-1 risk factor <160 mg/dL ≥160 mg/dL >190 mg/dL (160-189 mg/dL: LDL-lowering drug optional)

ATP III LDL-C Goals

Grundy, S. et al., Circulation 2004;110:227-39.

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2013 ACC/AHA Guidelines on the Assessment

  • f Atherosclerotic Cardiovascular Risk

l New Pooled Cohort Equations for

atherosclerotic cardiovascular disease (ASCVD) risk assessment

l Statin therapy recommended in 4 groups,

with de-emphasis of other drug classes (e.g. fibrates, niacin, ezetimibe)

l No LDL-C or non-HDL-C treatment targets

2013 ACC/AHA Guidelines :No Cholesterol Treatment Target Goals

l Appropriate intensity of statin therapy is

recommended to reduce the risk of ASCVD by lowering LDL-C and non- HDL-C

l “Treat to target” and “lower is best”

strategies are no longer advocated

l More clinical trials are needed

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Pooled Cohort Equations for Risk Assessment

l Equations predict 10-year risk of stroke &

myocardial infarction

l Former guidelines focused only on heart

attacks

l Highlights the large burden of disability from

nonfatal events

l Separate equations for nonwhite

populations

l Importance of race/ethnicity in risk of ASCVD

Statin Therapy Recommended in Four Groups

  • 1. Individuals with known ASCVD
  • 2. Individuals with LDL-C ≥190 mg/dL
  • 3. Individuals 40 to 75 years of age with

diabetes and LDL-C 70-189 mg/dL

  • 4. Individuals 40 to 75 years of age with

estimated 10-year ASCVD risk ≥7.5% and LDL-C 70-189 mg/dL

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Treatment Threshold: 7.5%

l Lowered from former threshold of 20% risk of MI

  • ver 10 years or > 10% with multiple risk factors

l Based on NHANES data:

l Men

l 50% of all African-American men and 30% of white

men in 50s

l Almost all men in 70s

l Women

l 70% African-American women and 60% white women

in 60s

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Treatment Options

l Statins: Preferred agent;modest effects on TG,

HDL.

l Fibrates ↓TG 20-50%, ↑HDL 10-20%.

l VA-HIT Study: Gemfibrozil reduced MI/ cardiac

death.

l ACCORD study (added to statin) negative

l Niacin: ↓TG 20-50%, ↑HDL 20-35%.

l Negative AIM HIGH study

l Omega-3 fatty acids: ↓TG 20-30%, ↑HDL 1-3%. l Ezetimibe is an intestinal brush border

cholesterol absorption inhibitor. Lacking

  • utcomes data.
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Case 4: 72 y.o. woman with NSTEMI

l A 72-year-old woman comes to the

emergency department with several episodes

  • f substernal chest pressure over the past 24
  • hours. She has had four episodes of chest

pressure occurring at rest and lasting 20-40 minutes.

l History of hypertension, diabetes, and current

smoking.

l Medications include aspirin 325 mg daily;

hydrochlorothiazide 25 mg daily; and glyburide 5 mg twice daily.

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Case (cont’d)

l Vital signs: pulse is 80/min and regular,

blood pressure is 145/75 mmHg. Chest with basilar crackles and cardiac examination reveals a + S4.

l ECG shows 2-mm ST-segment

depression in leads V3-V6.

l Serum troponin I is elevated at 3.7 ng/

mL.

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Case 4

  • 1. Schedule an exercise stress test within 48 hours.
  • 2. Begin intravenous heparin.
  • 3. Begin intravenous heparin and eptifibatide, and

schedule an exercise stress test within 48 hours.

  • 4. Begin intravenous heparin and eptifibatide, and

schedule coronary angiography within 48 hours. Therapy with aspirin, sublingual nitroglycerin, and a β–blocker is begun. The patient is admitted to the coronary care unit. Which of the following should you do next?

Spectrum of Acute Coronary Syndromes

Stable Angina Unstable Angina Non-Q wave MI Q wave MI ST Elevation MI Non ST Elevation ACS

ECG - ST↑ CK-MB Troponin I or T CRP ECG - ST↓

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TIMI Risk Score For UA/NSTEMI 7 Independent Predictors

1.

Age > 65 years

2.

> 3 CAD risk factors (high cholesterol, family history, hypertension, diabetes, smoking)

3.

Prior coronary artery disease (stenosis > 50 %)

4.

ST-segment deviation on the ECG

5.

> 2 anginal events < 24 hours

6.

ASA in last 7 days

7.

Elevated cardiac biomarkers (troponin or CK-MB)

Antman et al, JAMA 2000; 284 : 835-842.

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TIMI Risk Score For UA/NSTEMI UFH Group TIMI 11B (N= 1957)

4.7 8.3 13.2 19.9 26.2 40.9 10 20 30 40 50 0-1 2 3 4 5 6-7

D/MI/Urg Revasc (%) Number of Risk Factors % Pts: 4.3 17.3 32.0 29.3 13.0 3.4

χ2 trend P <0.001

Antman et al, JAMA 2000; 284 : 835-842.

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EARLY INVASIVE STRATEGY

Class I Indications

Any of the high-risk indicators (Level of Evidence: A) a) Recurrent angina at rest/low level activity despite Rx b) Elevated Troponin c) New ST-segment depression d) Rec. angina/ischemia with CHF symptoms e) Positive stress test f) EF <0.40 g) ↓ BP h) Sustained VT i) PCI <6 months, prior CABG

UA/NSTEMI 2002

14.5 24.2 16.9 14.3

5 10 15 20 25 30

TnT - TnT +

(%)

CONSERVATIVE INVASIVE

TACTICS: Troponin T: at 6 months

TnT cut point = 0.01 ng/ml (54% of Pts TnT +)

Death, MI, Rehosp ACS at 6 Months OR=0.52 *p<0.001

Interaction P<0.001

p=NS

*

N=414 N=396 N=463 N=495

Cannon, AHA, Nov 15, 2000, New Orleans, LA.

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11.8 20.3 12.8 16.1 19.5 30.6

5 10 15 20 25 30 35 Low 0-2

  • Intermed. 3-4

High 5-7 Death/MI/ACS Rehosp (%)

TIMI Risk Score

CONS

TACTICS: TIMI UA Risk Score at 6 months

% of Pts: 25% 60% 15%

INV

OR=0.75 CI (0.57, 1.00)

de Winter RJ et al. N Engl J Med 2005; 353:1095-1104.

ICTUS: Major results at one year

End point Early invasive strategy (%) Selective invasive strategy (%) p Death/MI/ rehospitalization for angina 22.7 21.2 NS Death 2.5 2.5 NS MI 15.0 10.0 0.005 Rehospitalization for angina 7.4 10.9 0.04

Invasive versus Conservative Treatment in Unstable Coronary Syndromes

“optimal medical therapy: Aspirin, enoxaparin, clopidogrel, atorvastatin”

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Relative-Risk of all cause Mortality: A meta-analysis of contemporary trials

(FRISC-II, ICTUS, ISAR-COOL, VINO, RITA-3, TIMI-18, TRUCS)

Bavry AA et. al. JACC 2006;48:1319-25

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Case 4 Evaluation

l TIMI Risk Score 6/7 = high-risk. l Early coronary angiography is preferred

strategy.

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Cardiac Catheterization

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Case 5: 75 year old woman with NSTEMI

l A 75-year-old woman with no past medical

history presents to the ED 4 hours after the

  • nset of stuttering, severe substernal chest

pain with radiation to the left arm and jaw.

l After two sublingual nitroglycerin tablets, the

patient is free of chest pain.

l Electrocardiography reveals 2-mm ST-

segment depression in leads II, III, and aVF.

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Case 5 (cont’d)

l The initial troponin I level is elevated at

8 ng/mL.

l The patient has no clear-cut medical

contraindications to anticoagulation. The patient is treated with aspirin, intravenous β-blocker, and intravenous nitroglycerin.

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Case 5: In addition to the medications that have been started, which of the following would be the most optimal management strategy at this time?

  • 1. Unfractionated heparin
  • 2. Enoxaparin
  • 3. Clopidogrel
  • 4. Clopidogrel, unfractionated heparin
  • 5. Clopidogrel, enoxaparin, diltiazem
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Therapies in NSTEMI

l LMWH versus UFH? l Dual anti-platelet therapy – when and for

how long to treat?

l Bivalirudin?

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LMWH versus UFH in ACS

l Advantages of LMWH:

l More predictable absorption (low degree of

protein binding)

l More predictable anticoagulant effect (no

need to monitor PTTs)

l Higher activity against factor Xa l Fewer adverse effects, including

thrombocytopenia

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8.6 7.1 0.82 (0.69-0.97) 18 0.02 6.5 5.2 0.79 (0.65-0.96) 21 0.02 5.3 4.1 0.77(0.62-0.95) 23 0.02 1.8 1.4 0.80 (0.55-1.16) 20 0.24 B B B B 0.5 1 2 Day 2 8 14 43 UFH (%) ENOX (%) OR (95 CI) Favors ENOX Favors UFH % P O.R.

TIMI 11B/ESSENCE Meta-analysis: Enoxaparin vs. Unfractionated heparin

Heterogeneity: All P=NS

Death or MI

Antman, Circulation 1999;100:1602-8.

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SYNERGY

Superior Yield of the New Strategy of Enoxaparin, Revascularization and Glycoprotein IIb/IIIa Inhibitors

Primary end point Enoxaparin Heparin Hazard ratio 95% CI Death/MI (%) 14 14.5 0.96 0.86-1.06

The SYNERGY Trial Investigators. JAMA 2004; 292:45-54.

  • 10 000 high-risk ACS patients, median age = 68, 34% women
  • Randomized to enoxaparin or UFH
  • >90% of patients went to the cath lab early (median of 21 hrs)
  • 57% received a IIb/IIIa blocker
  • 66% received clopidogrel
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SYNERGY - Bleeding Events

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Antman et al, JAMA 2000; 284 : 835-842.

Enoxaparin UFH P-value (n = 4993) (n = 4985) GUSTO severe 2.9 2.4 0.106 TIMI major - clinical: 9.1 7.6 0.008 CABG-related 6.8 5.9 0.081 Non-CABG-related 2.4 1.8 0.025 H/H drop - algorithm 15.2 12.5 0.001 Any RBC transfusion 17.0 16.0 0.155 ICH < 0.1 < 0.1 NS

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Therapies in NSTEMI

l LMWH versus UFH? l Dual anti-platelet therapy – when and for

how long to treat?

l Angiomax?

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Primary ¡End ¡Point ¡-­‑ ¡MI/Stroke/CV ¡ Death ¡

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Clopidogrel + ASA*

3 6 9

Placebo + ASA*

Months of Follow-Up

11.4% 9.3%

20% RRR P < 0.001 N = 12,562 12

* In combination with standard therapy The CURE Trial Investigators. N Engl J Med. 2001;345:494-502.

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Fox et al. Circulation. 2004;110:1202-1208.

Medical Rx Group

Placebo Clopidogrel RR: 0.80 (0.69-0.92)

0.20 4 0.15 0.10 0.05 0.0 100 200 300

Clopidogrel

0.20 4 0.15 0.10 0.05 0.0 100 200 300

PCI Group

Placebo RR: 0.72 (0.57-0.90)

0.20 4 0.15 0.10 0.05 0.0 100 200 300

CABG Group

Placebo Clopidogrel RR: 0.89 (0.71-1.11)

CURE: ¡Benefit ¡by ¡RevascularizaDon ¡

CVD/MI/Stroke CVD/MI/Stroke CVD/MI/Stroke

Placebo + ASA* N = 6303 Clopidogrel + ASA* N = 6259

CURE ¡-­‑ ¡Bleeding ¡Results ¡

  • Major ¡bleeding

¡2.7% ¡3.7%** ¡ ¡ Life-­‑threatening ¡bleeding ¡1.8% ¡2.2% ¡† ¡ ¡ ¡ Non-­‑life-­‑threatening ¡bleeding ¡0.9% ¡1.5% ¡‡ ¡ ¡ ¡

  • Minor ¡bleeding

¡2.4% ¡5.1% ¡§ ¡ End Point

* In combination with standard therapy ** P = 0.001; † P = NS; ‡ P = 0.002; § P < 0.001. The CURE Trial Investigators. N Engl J Med. 2001;345:494-502.

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Therapies in NSTEMI

l LMWH versus UFH? l Plavix therapy – when and for how long to

treat?

l Bivalirudin?

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Moderate- high risk ACS

ACUITY Study Design

Angiography within 72h

Aspirin in all Clopidogrel dosing and timing per local practice

UFH or Enoxaparin + GP IIb/IIIa Bivalirudin + GP IIb/IIIa Bivalirudin Alone

R*

*Stratified by pre-angiography thienopyridine use or administration

Moderate-high risk unstable angina or NSTEMI undergoing an invasive strategy (N = 13,800)

ACUITY Design. Stone GW et al. AHJ 2004;148:764–75

Medical management PCI CABG

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Ischemic Composite Endpoint

5 10 15 5 10 15 20 25 30 35

Cumulative Events (%) Days from Randomization

Estimate

P

(log rank)

7.3% UFH/Enoxaparin + IIb/IIIa (N=4603) Bivalirudin + IIb/IIIa (N=4604)

0.37

7.7% Bivalirudin alone (N=4612)

0.30

7.8%

UFH/Enoxaparin + GPI vs. Bivalirudin + GPI vs. Bivalirudin Alone

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Major Bleeding Endpoint

5 10 15 5 10 15 20 25 30 35

Cumulative Events (%) Days from Randomization

Estimate

P

(log rank)

5.7% UFH/Enoxaparin + IIb/IIIa (N=4603) Bivalirudin + IIb/IIIa (N=4604)

0.41

5.3% Bivalirudin alone (N=4612)

<0.0001

3.0%

UFH/Enoxaparin + GPI vs. Bivalirudin + GPI vs. Bivalirudin Alone

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Medical Therapy for UA/ NSTEMI

l Antianginal therapy: β-blockers, nitrates. l Antiplatelet therapy: aspirin, clopidogrel, plus GP IIb/IIIa

receptor inhibitors for high-risk patients.

l Newer anti-platelet agents: prasugrel, ticagrelor. Equal to

  • r better than clopidogrel, but more bleeding.

l Antithrombotic therapy: UFH, LMWH, Direct Thrombin

Inhibitors, Factor Xa inhibitor (Fondaparinux).

l Secondary prevention: lifestyle modifications, ACEI,

statins, glycemic control.

UCSF, Department of Medicine, CME 54

Case 6: 63 y.o. woman with STEMI

l A 63-year-old non-English-speaking woman

comes to the emergency department because

  • f severe, steady precordial discomfort that

began 10 hours ago. She thought that the chest pain may have been indigestion, but she had no relief with an antacid.

l She has a history of hypertension. She is

taking no medications.

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Case 6 (cont’d)

l Her heart rate is 92/min, and her blood

pressure is 150/90 mmHg. Her lungs are clear to auscultation and cardiac examination reveals an S4.

l Her electrocardiogram shows 3-mm ST-

segment elevation in leads II, III, and aVF.

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Case 6 continued

l She is given a chewable aspirin, morphine 4

mg intravenously, metoprolol 5 mg intravenously, and nitroglycerin 20 µg/min intravenously with a decrease in her chest pain intensity from severe to moderate.

l A hospital in the next county (1.5 hours away

by ambulance) recently established a program that provides 24-hour angioplasty services.

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Case 7: Which of the following should be considered in the decision of whether to refer this patient for treatment?:

  • 1. Thrombolysis has a better outcome than

angioplasty (with or without stenting) in this patient.

  • 2. Thrombolysis and angioplasty (with or without

stenting) are equivalent in outcome for this patient.

  • 3. Angioplasty (with or without stenting) has a

better outcome than thrombolysis in this patient.

  • 4. Neither thrombolysis nor angioplasty (with or

without stenting) should be performed in this patient.

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Glagov’s Model of Vascular Remodeling

Glagov S et. al. NEJM 1987

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Angiography Cannot Account for Coronary Remodeling

3.1 mm 3.1 mm IVUS IVUS

Adopted from Kinlay, S.

Angiogram

Plaque Rupture

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TIMI Risk Score for STEMI

Age 65-74 ≥ 75 DM/HTN or angina Weight < 67 kg Time to rx > 4 hrs Anterior STE or LBBB HR >100 SBP < 100

Historical Exam Presentation

Killip II-IV 2 points 3 points 1 point 3 points 2 points 1 point 1 point 1 point 2 points Risk Score = Total (0 -14)

Morrow DA, Circulation 2000; 102: 2031

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“The longer you wait, the worse the outcome”

Antman E. et al. 2004, ACC/AHA Practice Guidelines

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STEMI Reperfusion Therapy

Efficacy of thrombolysis falls off significantly >6 hours after onset of

  • symptoms. PCI preferred for late

presentation AMI patients.

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Coronary Flow Rates with Lytics

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Coronary Flow Rates with PCI

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Reperfusion

The medical system goal is to facilitate rapid recognition and treatment of patients with STEMI such that door-to- needle (or medical contact–to-needle) time for initiation

  • f fibrinolytic therapy can be achieved within 30

minutes or that door-to-balloon (or medical contact–to- balloon) time for PCI can be kept within 90 minutes.

ACC/AHA Guidelines 2004

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Fibrinolytic Therapy

Advantages

l Widely available l Rapid, simple

therapy

l Cardiologist not

required Limitations

l 1-2% intracranial

bleeding

l ~50% with slow/no flow l Rescue PCI at ↑ risk,

delayed

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Primary PCI

Limitations

l Access l Delay in restoring flow

if transferred

l Expense, logistics

Advantages

l Highly successful

(~>95%)

l Early risk stratification l Earlier discharge l Fewer intracranial

bleeds

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Primary PTCA vs. Thrombolytic Therapy

For every 1000 pts treated, PTCA compared with lytic therapy:

20 lives saved 43 re-MI prevented 13 ICH prevented Meta-analysis of 23 trials suggests that primary PTCA is preferred over lytic therapy

Keely et al. Lancet 2003

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SLIDE 36

UCSF, Department of Medicine, CME 36

UCSF, Department of Medicine, CME 71

Cases when PCI preferred to Fibrinolysis

l Contraindications to fibrinolysis:

l PCI shown to have high success rate l Lower one-year mortality compared to

historical controls

l Late presentation (>6 hours) l CABG patients l Cardiogenic shock

UCSF, Department of Medicine, CME 72

Prior to PCI – totally occluded RCA

slide-37
SLIDE 37

UCSF, Department of Medicine, CME 37

UCSF, Department of Medicine, CME 73

After PCI – RCA s/p stenting

Recommendations for Triage and Transfer for PCI (for STEMI)

I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III

NEW Recommendation

Each community should develop a STEMI system of care following the standards developed for Mission Lifeline including:

  • Ongoing multidisciplinary team

meetings with EMS, non-PCI-capable hospitals (STEMI Referral Centers), & PCI-capable hospitals (STEMI Receiving Centers)

UCSF, Department of Medicine, CME

slide-38
SLIDE 38

UCSF, Department of Medicine, CME 38

Recommendations for Triage and Transfer for PCI (for STEMI) (cont.)

NEW Recommendation

I I I IIa IIa IIa IIa IIa IIa IIb IIb IIb IIb IIb IIb III III III III III III I I I IIa IIa IIa IIa IIa IIa IIb IIb IIb IIb IIb IIb III III III III III III I I I IIa IIa IIa IIa IIa IIa IIb IIb IIb IIb IIb IIb III III III III III III IIa IIa IIa IIa IIa IIa IIb IIb IIb IIb IIb IIb III III III III III III

It is reasonable to transfer high risk patients who receive fibrinolytic therapy as primary reperfusion therapy at a non- PCI capable facility to a PCI-capable facility as soon as possible where either PCI can be performed when needed or as a pharmacoinvasive strategy.

UCSF, Department of Medicine, CME UCSF, Department of Medicine, CME 76

Case 8: 52 y.o. man with angina

A 52 year-old man with type-2 diabetes mellitus, atrial fibrillation, hyperlipidemia, and hypertension presents to your office with a new symptom of exercise-induced chest

  • tightness. He describes a squeezing

substernal sensation with radiation down his left arm. The discomfort comes on reliably with 1-2 blocks of brisk walking and is relieved with rest.

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SLIDE 39

UCSF, Department of Medicine, CME 39

UCSF, Department of Medicine, CME 77

Case 8 (cont’d)

l Medications: metoprolol 50mg bid,

amlodipine 10mg qd, ASA 81mg qd, Warfarin and fluvastatin 20mg qhs.

l His resting blood pressure and pulse

are 110/70 mmHg and he is in atrial fibrillation with a pulse of 90 bpm.

UCSF, Department of Medicine, CME 78

Case 8: The next most appropriate step is to obtain:

  • 1. Highly reactive CRP level to assist with

risk stratification

  • 2. Electron beam CT to determine degree
  • f coronary calcification
  • 3. Multislice Coronary CT scan
  • 4. Invasive coronary angiography
  • 5. No further diagnostic testing
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SLIDE 40

UCSF, Department of Medicine, CME 40

UCSF, Department of Medicine, CME 79

Framingham Risk Score

l Prognostic value for primary prevention

population.

l Includes the following variables:

l Sex l Age l Total cholesterol l HDL l Smoking (current) l Systolic blood pressure l Diabetes

UCSF, Department of Medicine, CME 80

C-Reactive Protein

l C-reactive protein adds prognostic information

to that conveyed by the Framingham risk score (Nurses Health Study).

l Whether CRP is just a marker of inflammation,

  • r a causal agent increasing the risk of MI

awaits further investigation.

l CRP most useful in providing further risk

assessment in healthy men and women with an intermediate risk score.

Ridker P, et al. NEJM. 2002; 347: 1557-65.

slide-41
SLIDE 41

UCSF, Department of Medicine, CME 41

UCSF, Department of Medicine, CME 81

Case 8 Answer Critique

l

CRP: Patient should be on maximal RF modification regardless of CRP level.

l

EBCT: Unhelpful in patient with classic angina.

l

MultiSlice Coronary CT scan: less reliable when:

Ø Irregular HR (such as A-fib) Ø Tachycardia Ø Elevated Calcium score Ø Possibly prior stents (especially when

the vessel is small)

UCSF, Department of Medicine, CME 82

Case 9: 56 y.o. man with heart failure post-MI

l A 56 year-old man is seen days following an acute

ST-segment elevation myocardial infarction. At that time, he had atypical symptoms of epigastric pain and presented to the hospital 12 hours after onset of pain with dyspnea.

l In the ER, he was found to have ST-segment

elevations in leads V1-V4 with elevated jugular venous pressure, hypoxia, and rales in both lung fields.

l Following successful coronary stenting of the left

anterior descending coronary artery occlusion, he was left with a significant anterior wall motion abnormality.

slide-42
SLIDE 42

UCSF, Department of Medicine, CME 42

UCSF, Department of Medicine, CME 83

Case 9 continued

l He is currently on ASA, metoprolol,

clopidogrel, an ACE inhibitor and a statin.

l An echocardiogram showed a persistent

anterior wall motion abnormality with an

  • verall left ventricular ejection fraction of

35%.

UCSF, Department of Medicine, CME 84

Case 9 continued

Vital signs are BP 132/70 mmHg, HR 70 bpm, RR 18/minute, and O2 saturation 94% on room air. Physical exam reveals mildly elevated jugular venous filling pressure, a third heart sound, basilar crackles, with no peripheral edema.

slide-43
SLIDE 43

UCSF, Department of Medicine, CME 43

UCSF, Department of Medicine, CME 85

Case 9: The most important medicine to add to his heart failure regimen would be:

  • 1. Low dose digoxin
  • 2. Nitrates
  • 3. Eplerenone
  • 4. Hydralazine
  • 5. Angiotensin receptor blocker

UCSF, Department of Medicine, CME 86

EPHESUS TRIAL --- STEMI, EF <40% and CHF

Eplerenone 25 mg, up-titrated to 50 mg daily

slide-44
SLIDE 44

UCSF, Department of Medicine, CME 44

UCSF, Department of Medicine, CME 87

Case 10: 64 y.o. man with new Heart Failure CC: A 64 year-old man is hospitalized because of dyspnea and leg edema. He has a longstanding history of essential hypertension that is treated with a thiazide diuretic and amlodipine.

UCSF, Department of Medicine, CME 88

Case 10 continued

l PE: HR 110, BP 180/98, RR 20,

afebrile JVP 10 cm, basilar rales, S3, S4, no murmur, 2+ pitting edema

l ECG: sinus tachycardia with LBBB l CXR: large heart, mild pulmonary

edema

l Labs: normal

slide-45
SLIDE 45

UCSF, Department of Medicine, CME 45

UCSF, Department of Medicine, CME 89

Case 10 continued

l Echocardiography shows left ventricular

ejection fraction of 25%. He has mild mitral and tricuspid regurgitation with an estimated pulmonary artery systolic pressure of 40 mmHg.

l He receives furosemide, three boluses of 60

mg intravenously over a 24-hour period and improves rapidly with diuresis of 2,400 mL.

UCSF, Department of Medicine, CME 90

Case 10: All of the following statements are true except:

  • 1. Ischemic work-up should be undertaken
  • 2. Beta-blocker therapy should be initiated

irrespective of whether coronary artery disease is diagnosed

  • 3. Ace-inhibitor therapy will decrease mortality
  • 4. Digoxin will improve symptoms and decrease

mortality

  • 5. Implantable defibrillator should be

considered if the ejection fraction remains <35% despite medical therapy

slide-46
SLIDE 46

UCSF, Department of Medicine, CME 46

UCSF, Department of Medicine, CME 91

AHA/ACC Heart Failure Guidelines: Stages of Heart Failure

l A: Patients at high risk of developing

heart failure because conditions associated with heart failure are present, but with no overt structural/functional abnormalities of the heart and no heart failure symptoms or signs

l Examples: Hypertension, diabetes mellitus,

coronary heart disease, cardiotoxin exposure, family history of DCM, past rheumatic fever, hemochromatosis

UCSF, Department of Medicine, CME 92

AHA/ACC Heart Failure Guidelines: Stages of Heart Failure

l B: Patients with overt heart disease that

is strongly associated with developing heart failure but who have never shown signs or symptoms of heart failure

l Examples: Ventricular hypertrophy, cardiac

chamber dilation, asymptomatic valve disease, prior MI or angina

slide-47
SLIDE 47

UCSF, Department of Medicine, CME 47

UCSF, Department of Medicine, CME 93

AHA/ACC Heart Failure Guidelines: Stages of Heart Failure

l C: Patients with prior or current symptoms of

heart failure associated with structural heart disease

l Examples: Dyspnea, fatigue, fluid retention or other

signs and symptoms due to cardiac dysfunction

l D: Patients with advanced structural heart

disease and marked symptoms of heart failure at rest despite maximal treatment and require specialized interventions

l Examples: Frequent CHF hospitalizations, hospital

bound on inotropes, heart transplant candidate, hospice patient

UCSF, Department of Medicine, CME 94

When evaluating a patient with heart failure, keep a wide differential in mind:

slide-48
SLIDE 48

UCSF, Department of Medicine, CME 48

UCSF, Department of Medicine, CME 95

Medical Management of HF (1)

l β -blockers: indicated in patients with LV

systolic dysfunction irrespective of CAD

l ACEIs: indicated in patients with LV

systolic dysfunction without a contraindication

l ARBs: for patients intolerant to ACEIs

  • Cough with ACEIs in 5-10% of white patients
  • f European descent; up to 50% of Chinese

patients; non-productive; usually appears within first months of therapy; disappears within 1-2 weeks of discontinuation of therapy; re-appears within days of re-challenge.

UCSF, Department of Medicine, CME 96

Medical Management of HF (2)

l Nitrates/hydralazine: for patients

intolerant to ACEIs/ARBs (i.e., renal insufficiency); or, in addition to optimal therapy in African-American patients (A- HeFT Trial).

l Digoxin: decreases HF symptoms and

reduces rehospitalization.

l Diuretics:

l Loop diuretics: for symptoms of congestion l Thiazide diuretics: for concomitant hypertension l Aldactone: beneficial in patients with severe class III-IV

HF (Rales trial) and in patients with AMI and LV dysfunction (EPHESUS trial)

slide-49
SLIDE 49

UCSF, Department of Medicine, CME 49

UCSF, Department of Medicine, CME 97

Sudden Cardiac Death in Heart Failure (SCD-HEFT) Trial

Bardy GH et al, NEJM 2005

Benefit of ICD in both ischemic and non-ischemic cardiomyopathy

UCSF, Department of Medicine, CME 98

Case 11: 43 year old man with severe chest pain

l Sudden onset of severe, crushing,

retrosternal chest pain.

l His initial ECG showed sinus tachycardia with

anterior lead ST-segment elevation.

l Five hours after the onset of pain, he received

thrombolytic therapy in the emergency department with only transient relief.

l He now has progressive dyspnea and is

unable to lie flat.

slide-50
SLIDE 50

UCSF, Department of Medicine, CME 50

UCSF, Department of Medicine, CME 99

Case 11 cont’d

l Physical examination: pulse 150/min with

  • ccasional irregularity, respirations labored at

28/min, and blood pressure is 90/60 mm Hg.

l He appears diaphoretic, ashen, and

apprehensive.

l Jugular venous pressure cannot be

estimated, carotid pulsation is thready, and the lungs have crackles bilaterally.

l Cardiac examination reveals a soft first heart

sound, a soft, widely split second heart sound, and a third heart sound, but no murmur.

UCSF, Department of Medicine, CME 100

Case 11 ECG: 1 hour after lytics

slide-51
SLIDE 51

UCSF, Department of Medicine, CME 51

UCSF, Department of Medicine, CME 101

Case 11: This patient is most

likely experiencing which of the following complications?

l 1) Pericarditis. l 2) Ventricular septal rupture. l 3) Free wall rupture. l 4) Cardiogenic shock. l 5) Ventricular tachycardia.

UCSF, Department of Medicine, CME 102

Cardiogenic Shock

l 5-15% STEMI cases. l When AMI involves >40% of

myocardium.

l In-hospital mortality 50%.

slide-52
SLIDE 52

UCSF, Department of Medicine, CME 52

UCSF, Department of Medicine, CME 103

Management

l Intubation if necessary. l Pressors.

l Dopamine l Dobutamine l Levophed

l Primary PCI. l Consider IABP (neg result of IABP SHOCK

II trial)

l Avoid early beta blockade.

UCSF, Department of Medicine, CME 104

Case 12: 38 year-old woman with chest pain

l To the ED with severe retrosternal CP. l She reports that this is the fourth such

episode in the last week, the previous episodes having terminated spontaneously.

l She has no risk factors for coronary

artery disease but does have a history

  • f migraine headaches.
slide-53
SLIDE 53

UCSF, Department of Medicine, CME 53

UCSF, Department of Medicine, CME 105

Case 12 cont’d

l Physical examination: pulse of 110/min, blood

pressure of 140/90 mm Hg.

l ECG shows 2-mm ST-segment elevation in

leads V1-V3, with reciprocal depression in leads II, III, AVF.

l The pain resolves within minutes of

sublingual nitrate administration and a repeat electrocardiogram shows complete resolution

  • f the ST-segment changes.

UCSF, Department of Medicine, CME 106

Case 12: Which of the following is the most likely pathogenesis?

l 1) Pericarditis. l 2) Coronary artery dissection. l 3) Coronary thrombosis. l 4) Coronary vasospasm. l 5) Esophageal spasm.

slide-54
SLIDE 54

UCSF, Department of Medicine, CME 54

UCSF, Department of Medicine, CME 107

Prinzmetal’s Angina

l Younger women. l Associated with vasospastic disease

(i.e., migraine HA).

l Diagnosis:

l History of nitrate-responsive CP, no CAD. l ECG during pain showing STE l Holter study l Ergonovine provocation in cath lab

(controversial!)

UCSF, Department of Medicine, CME 108

Spontaneous Coronary Dissection

l Rare condition, sometimes associated

with pregnancy

l High morbidity l PCI preferred for persistently-occluded

artery (conservative strategy if possible)

l Long-term aspirin, beta-blockers.

slide-55
SLIDE 55

UCSF, Department of Medicine, CME 55

UCSF, Department of Medicine, CME 109

Case 13: 44 year-old man presents for the first time to your clinic for routine visit

l Has no complaints. l No prior medical history. l No medications. l PE: Chest CTA, RRR, physiologic split

S2, no murmur.

l Since it is the first visit, a routine EKG is

performed.

UCSF, Department of Medicine, CME 110

Case 13: ECG

slide-56
SLIDE 56

UCSF, Department of Medicine, CME 56

UCSF, Department of Medicine, CME 111

Case 13: Which of the following is the

most appropriate next step?

l 1) Chest X-ray. l 2) Exercise stress electrocardiography. l 3) Dipyridamole radionuclide imaging. l 4) Electron beam CT. l 5) Repeat the EKG.

UCSF, Department of Medicine, CME 112

Incorrect Lead Placement

Remember to check for axis:

  • QRS axis
  • P-wave axis
slide-57
SLIDE 57

UCSF, Department of Medicine, CME 57

UCSF, Department of Medicine, CME 113

EKG – correct precordial lead placement

UCSF, Department of Medicine, CME 114

Case 14: 65 year-old woman to ED with severe CP

l CP began suddenly 2 hours ago while

lifting boxes. She is not short of breath, but she is nauseated. The pain has not been relieved by oxygen or nitroglycerin.

l PMHx: poorly controlled hypertension,

chronic renal insufficiency, and current smoking.

slide-58
SLIDE 58

UCSF, Department of Medicine, CME 58

UCSF, Department of Medicine, CME 115

Case 14 cont’d

l PE: blood pressure 100/52 mm Hg in

both arms, pulse 120/min and regular. Remainder of her physical examination unremarkable.

l ECG: sinus tachycardia, left ventricular

hypertrophy, and no ST segment changes.

UCSF, Department of Medicine, CME 116

CXR

slide-59
SLIDE 59

UCSF, Department of Medicine, CME 59

UCSF, Department of Medicine, CME 117

Case 14: Which of the following diagnostic tests should be done next?

l A) Transthoracic echocardiogram. l B) Emergent coronary angiogram. l C) Transesophageal echocardiogram. l D) Gastrograffin esophageal swallow.

UCSF, Department of Medicine, CME 118

Thoracic Aortic Dissection

l Risk Factors: hypertension, atherosclerosis,

Marfan’s, connective tissue disease .

l History: severe, sudden, abrupt onset; tearing

quality with radiation to the back.

l PE: AI, unequal peripheral pulses

uncommon.

l ECG: LVH. l CXR: widened mediastinum (PPV 50%).

slide-60
SLIDE 60

UCSF, Department of Medicine, CME 60

UCSF, Department of Medicine, CME 119

Aortic Dissection Diagnosis

l Rapid diagnosis critical. l TEE, contrast CT, aortography, or MRI.

UCSF, Department of Medicine, CME 120

Case 15: 55 year-old man with CAD, ESRD, HTN with CP

l CP at rest, no improvement with NTG. l PE: anxious and diaphoretic. HR 80/min

and regular, BP 85/55 mm Hg, and falls by 12 mm Hg during inspiration. CVP

  • 12. Remainder unremarkable.
slide-61
SLIDE 61

UCSF, Department of Medicine, CME 61

UCSF, Department of Medicine, CME 121

Case 15: ECG

UCSF, Department of Medicine, CME 122

Case 15 cont’d

l RA

12 mm Hg

l RV

16/10 mm Hg

l PA

16/12 mm Hg

l PCW 8 mm Hg l CI

1.6 L/min/m2.

slide-62
SLIDE 62

UCSF, Department of Medicine, CME 62

UCSF, Department of Medicine, CME 123

Case 15: What is the most likely diagnosis?

l 1) Pulmonary embolism. l 2) Acute pericarditis. l 3) Fluid overload. l 4) Right ventricular infarction. l 5) Pericardial tamponade.

UCSF, Department of Medicine, CME 124

RV Infarction

l RCA occlusion, proximal to RV marginal

branches.

l Triad of hypotension, elevated CVP,

clear lung fields.

l Pulsus paradoxus may be present. l ECG: STE in V4R.

slide-63
SLIDE 63

UCSF, Department of Medicine, CME 63

UCSF, Department of Medicine, CME 125

Tamponade

l Same triad of hypotension, elevated

CVP, clear lungs.

l No STE on ECG (or diffuse if

pericarditis).

l Echocardiography to differentiate MI

versus pericarditis with tamponade.

UCSF, Department of Medicine, CME 126

Case 16: 70 year-old man with 90 minutes of CP

slide-64
SLIDE 64

UCSF, Department of Medicine, CME 64

UCSF, Department of Medicine, CME 127

Case 16: In addition to aspirin, which of the

following is the best management strategy?

l 1) Percutaneous coronary intervention. l 2) Nitrates, β-blocker, and angiotensin-converting

enzyme inhibitor.

l 3) Thrombolytic therapy and intravenous heparin. l 4) Half-dose thrombolytic therapy, glycoprotein

IIB/IIIa receptor inhibitor, and heparin.

UCSF, Department of Medicine, CME 128

Posterior MI

l LCx or distal branch off RCA occlusion. l Prominent R waves V1-3. l Horizontal ST-depression V1-3. l Posterior leads often helpful.

slide-65
SLIDE 65

UCSF, Department of Medicine, CME 65

UCSF, Department of Medicine, CME 129

Occluded LCx/OM

UCSF, Department of Medicine, CME 130

s/p PCI

slide-66
SLIDE 66

UCSF, Department of Medicine, CME 66

UCSF, Department of Medicine, CME 131

Post-PCI ECG

UCSF, Department of Medicine, CME 132

Should Gp IIb/IIIa inhibitors be given in addition to lytic therapy?

slide-67
SLIDE 67

UCSF, Department of Medicine, CME 67

UCSF, Department of Medicine, CME 133

Primary Endpoint: 30 Day Mortality

Days

% Mortality 5.9% 5.6% p = 0.43 for superiority

  • Std. Reteplase (n = 8260)

Abciximab + ↓ Dose Reteplase (n = 8328)

GUSTO V AMI

Non-Inferiority RR 0.95 (95% CI, 0.84-1.08)

Lancet 2001; 357:1905-14

UCSF, Department of Medicine, CME 134

0.5 1.1 0.4 1.2 0.3 1.5 0.4 2.1

1 2 3 % of Patients

  • Std. Dose Reteplase (n = 8260)

Abciximab + ↓ Dose Reteplase (n = 8328)

p = 0.66 < 70 yrs > 75 yrs > 70 yrs < 75 yrs

ICH by Age Group

* Significant treatment interaction for the age 75 dichotomy; p = 0.033

p = 0.53 p = 0.27* p = 0.069*

12/1088 24/1149 28/7179 37/7172 25/2030 31/2135 21/6193 24/6230

Lancet 2001; 357:1905-14 Prespecified Age 70 Analysis / Post-Hoc Age 75 Analysis

GUSTO V AMI

slide-68
SLIDE 68

UCSF, Department of Medicine, CME 68

UCSF, Department of Medicine, CME 135

Case 17: 46 y.o. female collapses in the ER (BP 180/88)

UCSF, Department of Medicine, CME 136

Case 17: What is the next best therapeutic test:

1) Cardiac echocardiography to rule out

tamponade

2) Chest CT to rule out dissection 3) Head CT to rule out hemorrhage 4) Cardiac catheterization/PCI 5) None of the above

slide-69
SLIDE 69

UCSF, Department of Medicine, CME 69

UCSF, Department of Medicine, CME 137

Case 18: 18 y.o. male presents to the clinic for routine examination

l He has no prior medical history and

takes no medications

l He is very active in sports and wants a

medical clearance letter from you to participate in varsity college basketball

l PE – normal l EKG – shown …..

UCSF, Department of Medicine, CME 138

Case 18 continued – EKG

slide-70
SLIDE 70

UCSF, Department of Medicine, CME 70

UCSF, Department of Medicine, CME 139

Case 18: Which of the following increases the risk of sudden death in this patient?

1) Prior history of syncope 2) Family history of sudden death 3) Frequent runs of non-sustained VT 4) LV wall thickness of >30 mm 5) All of the above

UCSF, Department of Medicine, CME 140

Risk Factors for sudden death in Hypertroprophic Cardiomyopathy per ACC/ESC Guidelines

Major Cardiac arrest (VF) Spontaneous sustained VT Family history of premature sudden death Unexplained syncope LV thickness ≥ 30 mm Abnormal exercise BP Non-sustained VT (Holter) Possible in Individual Patients Atrial fibrillation Myocardial ischemia LV outflow obstruction High-risk mutation Intense (competitive) physical exertion

slide-71
SLIDE 71

UCSF, Department of Medicine, CME 71

UCSF, Department of Medicine, CME 141

Case 19: 51 y.o. male with syncope while waiting for the bus

l Otherwise healthy l No PMH l No medications l No family history of sudden death l PE normal l EKG …..

UCSF, Department of Medicine, CME 142

Case 19: EKG

slide-72
SLIDE 72

UCSF, Department of Medicine, CME 72

UCSF, Department of Medicine, CME 143

Case 19: Which one of the following is the best next test:

1) Activate the cath lab if within 90

minutes

2) Lytic therapy if cath lab can not be

activated within 90 minutes

3) Call the Electrophysiology service 4) Leave me alone, I am getting tired! 5) None of the above

UCSF, Department of Medicine, CME 144

Brugada Syndrome

l Estimated 3-9% of out-of-hospital causes of VF

arrest

l Heritable disorder of the sodium channel

(SCN5A) and makes patients susceptible to polymorphic VT and sudden death

l No structural heart disease l EKG with ST elevation in precordial leads (V1

and V2) – these changes can be dynamic and associated with RBBB

l Patients with Brugada Syndrome who present

with syncope have a 2-year risk of sudden cardiac death of 30% à ICD is therefore recommended.

slide-73
SLIDE 73

UCSF, Department of Medicine, CME 73

UCSF, Department of Medicine, CME 145

Case 20: For which of the following should antibiotic prophylaxis be recommended?

  • A. Mitral valve prolapse with no murmur
  • B. Mitral valve prolapse with a murmur
  • C. Prior history of endocarditis
  • D. Bicuspid Aortic valve
  • E. All of the above

UCSF, Department of Medicine, CME 146

New(ish) AHA Recommendations …..

l

artificial heart valves

l

a history of infective endocarditis

l

certain specific, serious congenital (present from birth) heart conditions, including:

Ø

unrepaired or incompletely repaired cyanotic congenital heart disease, including those with palliative shunts and conduits

Ø

a completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first six months after the procedure

Ø

any repaired congenital heart defect with residual defect at the site or adjacent to the site

  • f a prosthetic patch or a prosthetic device

l

a cardiac transplant that develops a problem in a heart valve.

slide-74
SLIDE 74

UCSF, Department of Medicine, CME 74

UCSF, Department of Medicine, CME 147

Case 21: After placement of a drug eluting stent in the right coronary artery, when should the patient have elective surgery?

  • A. 6 weeks
  • B. 3 months
  • C. 6 months
  • D. 12 months
  • E. None of the above

UCSF, Department of Medicine, CME 148

What to do with Patients Awaiting Surgery after PCI?

l Is there an optimal delay after coronary

stenting prior to non-cardiac surgery?

l Analysis of the Mayo Clinic PCI and

Surgical databases (1990-2000)

l 207 patients identified who underwent

surgery after a successful PCI with Bare Metal Stent

l How did they do?

Wilson SH et al JACC 2003;42:234-40

slide-75
SLIDE 75

UCSF, Department of Medicine, CME 75

UCSF, Department of Medicine, CME 149

Wilson SH et al JACC 2003;42:234-40

Complications of non-cardiac surgery after coronary PCI

It is suggested that post PCI with a BMS, surgery be delayed by 6 weeks What to do with DES????

UCSF, Department of Medicine, CME 150

Case 22: Which of the following are contraindications to the placement

  • f an intra-aortic balloon pump?
  • A. Severe PVD
  • B. Aortic dissection
  • C. Aortic aneurysm
  • D. Severe aortic valve regurgitation
  • E. All the above
slide-76
SLIDE 76

UCSF, Department of Medicine, CME 76

UCSF, Department of Medicine, CME 151

IABP Pumping

DEFLATES INFLATES

Courtesy of Duy Nguyen, UCSF

UCSF, Department of Medicine, CME 152

Indications for IABP placement

l Cardiogenic shock l Acute MI l Dilated cardiomyopathy with poor cardiac output l Mechanical complications of MI l Papillary muscle rupture → MR l Ventricular Septal Defect (VSD) l Valvular Heart Disease l Mitral regurgitation (especially acute MR) l Aortic Stenosis complicated by hypotension or

coronary insufficiency / Refractory myocardial ischemia

l Facilitated revascularization for high-risk cases

slide-77
SLIDE 77

UCSF, Department of Medicine, CME 77

UCSF, Department of Medicine, CME 153

Case 23: Patient with leg pain with ambulation sees you in clinic. Ankle-brachial index is ordered and it is 1.4. This reflects that:

  • A. ABI > 1.0 is normal
  • B. No more vascular testing is required

as the pain is most likely non- vascular given high ABI

  • C. ABI of > 1.2 is not predictive of risk
  • f future events
  • D. A and B are correct
  • E. None of the above are correct

ABI =

  • Cornerstone of PAD Diagnosis
  • Ankle and brachial systolic pressures taken using a

hand-held Doppler device

  • Supine position
  • After 5+ minutes of rest

The ¡Ankle-­‑Brachial ¡Index ¡

Ankle ¡systolic ¡pressure ¡ Brachial ¡systolic ¡pressure ¡

Normal ABI 0.90-1.30 PAD ABI <0.90 Severe PAD ABI <0.40 Non-compressible ABI >1.30

slide-78
SLIDE 78

UCSF, Department of Medicine, CME 78

Performance ¡of ¡the ¡ABI ¡Test ¡

TEST SENSITIVITY SPECIFICITY ABI 95-97% 99-100% PULSE EXAM (DP) PULSE EXAM (PT) 50% 71% 73% 91%

Ouriel K, et al. Surgery. 1982 Jun;91(6):686-93. Criqui Circ 1985;71:516

Pulse ¡Volume ¡Recordings ¡

Upper thigh Lower thigh Calf Ankle Upper thigh Lower thigh Calf Ankle

Pulse Volume Recordings

Iliac/common femoral SFA/popliteal Below knee

slide-79
SLIDE 79

UCSF, Department of Medicine, CME 79

LimitaDons ¡of ¡the ¡ABI ¡

  • Appropriately ¡trained ¡staff ¡to ¡perform ¡it ¡
  • ABI ¡correlates ¡poorly ¡with ¡symptoms ¡and ¡funcDonal ¡

limitaDons ¡

  • Decreased ¡sensiDvity ¡for ¡mild ¡disease ¡or ¡inflow ¡disease ¡

– Exercise ¡ABI ¡criDcal ¡for ¡paDents ¡with ¡ suspected ¡PAD ¡and ¡normal ¡resDng ¡ABI ¡

  • Falsely ¡elevated ¡ABI ¡for ¡pa2ents ¡with ¡“medial ¡

calcinosis” ¡ ¡or ¡calcified ¡vessels ¡

– Diabetes ¡mellitus ¡ – Renal ¡failure ¡ – Hyperparathyroidism ¡

¡ Do ¡Non-­‑Compressible ¡Vessels ¡Have ¡any ¡Meaning ¡for ¡a ¡ DiabeDc? ¡ ¡ ¡Yes! ¡

§ Non-­‑compressible ¡vessels ¡(high ¡ABI) ¡ independent ¡predictor ¡of ¡adverse ¡outcome ¡ § Significant ¡PAD ¡is ¡generally ¡present ¡though ¡ ABI ¡number ¡is ¡not ¡interpretable ¡ § Do ¡not ¡consider ¡an ¡ABI ¡> ¡1.3 ¡“normal” ¡

slide-80
SLIDE 80

UCSF, Department of Medicine, CME 80

Toe-­‑Brachial ¡Index ¡

n RaDo ¡of ¡toe ¡pressure ¡to ¡brachial ¡ pressure ¡ n Room ¡must ¡be ¡warm ¡to ¡avoid ¡ vasoconstricDon ¡ ¡ n Great ¡toe ¡pressure ¡measured ¡ using ¡small ¡digit ¡cuff ¡and ¡a ¡flow ¡ sensor ¡ – Doppler ¡ – Strain ¡gauge ¡ – Photoplethysmography ¡ n Digital ¡vessels ¡almost ¡always ¡ compressible ¡ n Normal ¡TBI ¡> ¡0.7 ¡

Bonham PA. Nursing. 2003;33:54.

ABI ¡and ¡CV ¡Risk ¡ ¡

Resnick, et al. Circulation. 2004; 109(6) 733.

A l l C a u s e M

  • r

t a l i t y ABI

N=4393 American Indians Strong Heart Study

Optimal ABI?

slide-81
SLIDE 81

UCSF, Department of Medicine, CME 81

ABI ¡Increases ¡CV ¡Risk ¡PredicDon ¡Beyond ¡the ¡ Framingham ¡Score ¡

  • ABI ¡CollaboraDon. ¡JAMA ¡(2008) ¡
  • Meta-­‑analysis ¡of ¡16 ¡cohort ¡studies ¡involving ¡480,325 ¡person-­‑

years ¡of ¡data ¡ – e.g., ¡ARIC, ¡Edinburgh, ¡Framingham ¡offspring, ¡Strong ¡Heart, ¡ San ¡Diego, ¡Ronerdam ¡

  • Lowest ¡risk ¡of ¡death ¡in ¡ABI ¡1.11 ¡– ¡1.4 ¡range ¡
  • For ¡each ¡Framingham ¡risk ¡category, ¡low ¡ABI ¡(<.91) ¡doubles ¡CV ¡

event ¡and ¡death ¡rate ¡

  • ABI ¡adds ¡addiDve ¡informaDon ¡to ¡Framingham ¡risk ¡score ¡

– Risk ¡reclassificaDon ¡or ¡modificaDon ¡of ¡treatment ¡

  • 19% ¡of ¡men ¡
  • 36% ¡of ¡women

¡ ¡ ABI Collaboration. JAMA. 2008;300:197.