cardiology-board-review-2008-1215092899624216-8

Todd C. Villines, MD

Cardiology ServiceWalter Reed Army Medical Center

Cardiology Board Review Part I

April 2008

http://www.wramc.amedd.army.mil/MainFrame.cfm

http://www.wramc.amedd.army.mil/index.htm

Outline – Part I

CAD Acute Coronary Syndromes (ACS) Chronic CAD

Valvular Heart Disease Congenital Heart Disease Physical Exam Pearls

A 55 yo male presents to your rural ER with 30 minutes of substernal chest pain, nausea and diaphoresis:

- Hx: HTN, tobacco abuse Rx: HCTZ, diltiazem SR

- P 96 BP 146/92 Apprehensive.

- RRR w/+S4. No murmur. Lungs – clear. Equal pulses.

- He is treated with ASA, heparin, IV beta-blocker.

a. clopidogrel 300 mg PO d. tPA

b. eptifibatide IV e. transfer to facility only 1.5 hrs

c. eptifibatide + ½ dose tPA away for primary angioplasty

Which of the following should be

done next ?:

Acute Coronary Syndromes

Revascularization

Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS)

Acute Coronary Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTEMI† STEMI

1.24 million Admissions per year

.33 million Admissions per year

Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69-171. *Primary and secondary diagnoses. †About 0.57 million

NSTEMI and 0.67 million UA.

ACS - Thrombolytics

Greatest benefit of thrombolytics in first 1-2 hours from symptom onset! (Golden Hour)

ABSOLUTE Contraindications

ThrombolyticsRelative Contraindications

ACS Things you must know…

Accelerated Idioventricular Rhythm (AIVR)

1.

2.

3.

4.

Rescue Angioplasty

If no reperfusion

in 60-90 mins.

(20-40% will not

reperfuse)

If hemodynamically stable: no treatment!

(CK washout)

Primary PCI Absolute

contraindication to thrombolytics

STEMI Guidelines: Door to balloon: <90

minutes Highest risk

patients benefit the most Treatment of choice

in cardiogenic shock

Late presentation Rescue angioplasty

Primary PCI

Primary PCI

STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 min of first medical contact as a systems goal.

STEMI patients presenting to a hospital without PCI capability, and who cannot be transferred to a PCI center and undergo PCI within 90 min of first medical contact, should be treated with fibrinolytic therapy within 30 min of hospital presentation as a systems goal, unless fibrinolytic therapy is contraindicated.

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII


Facilitated PCI

Meta-analysis: Facilitated PCI vs

Primary PCI

1.03(0.15-7.13)

3.07(0.18-52.0)

1.43(1.01-2.02)

1.03

(0.49-2.17)

Mortality Reinfarction Major Bleeding

Fac. PCIBetter

PPCIBetter

Fac. PCIBetter

PPCIBetter

Fac. PCIBetter

PPCIBetter

Keeley E, et al. Lancet 2006;367:579.

0.1 1 10 0.1 1 10 0.1 1 10

1.38 (1.01-1.87)

1.71 (1.16 - 2.51)

1.51 (1.10 - 2.08 )

Lytic alone N=2953

IIb/IIIa alone N=1148

Lytic +IIb/IIIaN=399

All (N=4500)

1.40 (0.49-3.98)

1.81

(1.19-2.77)

A planned reperfusion strategy using full-dose fibrinolytic therapy followed by immediate PCI is not recommended and may be harmful.

Facilitated PCI using regimens other than full-dose fibrinolytic therapy might be considered as a reperfusion strategy when all of the following are present:a. Patients are at high risk,b. PCI is not immediately available within 90 minutes, andc. Bleeding risk is low (younger age, absence of poorly controlled hypertension, normal body weight).

Facilitated PCI



Rescue and Late PCI

Wijeysundera HC, et al. J Am Coll Cardiol. 2007;49:422-430.

Meta-analysis: Rescue PCI vs Conservative Tx

Outcome Rescue PCI Conservative Treatment

RR (95% CI) P

Mortality, %(n)

7.3(454)

10.4(457)

0.69(0.46–1.05)

.09

HF, % (n)

12.7(424)

17.8(427)

0.73(0.54–1.00)

.05

Reinfarction,% (n)

6.1(346)

10.7(354)

0.58(0.35–0.97)

.04

Stroke, % (n)

3.4(297)

0.7(295)

4.98(1.10–22.48)

.04

Minor bleeding,% (n)

16.6(313)

3.6(307)

4.58(2.46–8.55)

<.001

In 3 trials, enrolling 700 patients that reported the composite end point of all-cause mortality, reinfarction, and HF, rescue PCI was associated with a significant RR reduction of 28% (RR 0.72; 95% CI, 0.59-0.88; P=.001)

A strategy of coronary angiography with intent to

perform PCI (or emergency CABG) isrecommended in patients who have receivedfibrinolytic therapy and have:

a. Cardiogenic shock in patients < 75 years who are suitable candidates for revascularization

b. Severe congestive heart failure and/or pulmonary edema (Killip class III)

c. Hemodynamically compromising ventricular arrhythmias.




Rescue PCI

Rescue PCI

A strategy of coronary angiography with intent to

perform PCI (or emergency CABG) isreasonable in patients ≥ 75 years who

havereceived fibrinolytic therapy, and are incardiogenic shock, provided they are

suitablecandidates for revascularization.


Rescue PCI

A strategy of coronary angiography with intent to perform rescue PCI is reasonable for patients in whom fibrinolytic therapy has failed (ST-segment elevation < 50% resolved after 90 min following initiation of fibrinolytic therapy in the lead showing the worst initial elevation) and a moderate or large area of myocardium at risk [anterior MI, inferior MI with right ventricular involvement or precordial ST-segment depression].


Rescue PCI

A strategy of coronary angiography with intent to perform PCI in the absence of any of the above Class I or IIa indications might be reasonable in moderate- or high-risk patients, but its benefits and risks are not well established. The benefits of rescue PCI are greater the earlier it is initiated after the onset of ischemic discomfort.


Rescue PCI

A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is not recommended in patients who have received fibrinolytic therapy if further invasive management is contraindicated or the patient or designee do not wish further invasive care.


Analgesia

Morphine remains Class I for STEMI although may increase adverse events in UA/NSTEMI

NSAID medications increase mortality, reinfarction, and heart failure in proportion to degree of COX-2 selectivity Discontinue on admission for STEMI Do not initiate during acute phase of

management

Patients routinely taking nonsteroidal anti-

inflammatory drugs (NSAIDs) (except for

aspirin), both non-selective as well as COX-2

selective agents, prior to STEMI should have

those agents discontinued at the time of

presentation with STEMI because of the

increased risks of mortality, reinfarction,

hypertension, heart failure, and myocardial

rupture associated with their use.


Analgesia

NSAIDs (except for aspirin), both

nonselective as well as COX-2 selective

agents, should not be

administered during hospitalization for

STEMI

because of the increased risks of mortality,

reinfarction, hypertension, heart failure,

and

myocardial rupture associated with their

use.


Analgesia

Beta-Blockers

TREATMENT: Metoprolol 15 mg iv over 15 mins, then 200 mg oral daily vs matching placebo

INCLUSION: Suspected acute MI (ST change or LBBB) within 24 h of symptom onset

EXCLUSION: Shock, systolic BP <100 mmHg, heart rate <50/min or II/III AV block

1 OUTCOMES: Death & death, re-MI or VF/arrest up to 4 weeks in hospital (or prior discharge)

Mean treatment and follow-up: 16 days

COMMIT: Study design

Effects of Metoprolol

Lancet. 2005;366:1622.

Death13%

P=0.0006

ReMI22%

P=0.0002

VF15%

P=0.002

Totality of Evidence (N = 52,411)COMMIT (N = 45,852)

Increased early risk of

shock

Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms

Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease).

It is reasonable to administer an IV beta blocker at the time of presentation to STEMI patients who are hypertensive and who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease).

Beta-Blockers



IV beta blockers should not be administered to STEMI patients who have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease).

Beta-Blockers


Anticoagulants

Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (Level of Evidence: C) and preferably for the duration of the index hospitalization, up to 8 days (regimens other than unfractionated heparin [UFH] are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparin-induced thrombocytopenia with prolonged UFH treatment). (Level of Evidence: A)

Anticoagulant regimens with established efficacy include:♥ UFH (LOE: C)♥ Enoxaparin (LOE:A)♥ Fondaparinux (LOE:B)



Anticoagulants

For patients undergoing PCI after havingreceived an anticoagulant regimen, the

followingdosing recommendations should be

followed:

a. For prior treatment with UFH: administer additional boluses of UFH as needed to support the procedure taking into account whether GP IIb/IIIa receptor antagonists have been administered. (Level of Evidence: C) Bivalirudin may also be used in patients treated previously with UFH. (Level of Evidence: C)


Recommendation continues on the next slide.

Anticoagulants

b. For prior treatment with enoxaparin: if the last SC dose was administered within the prior 8 hours, no additional enoxaparin should be given; if the last SC dose was administered at least 8 to 12 hours earlier, an IV dose of 0.3 mg/kg of enoxaparin should be given.

c. For prior treatment with fondaparinux: administer additional intravenous treatment with an anticoagulant possessing anti-IIa activity taking into account whether GP IIb/IIIa receptor antagonists have been administered.



Anticoagulants

Because of the risk of catheter thrombosis,fondaparinux should not be used as the soleanticoagulant to support PCI. An additionalanticoagulant with anti-IIa activity should beadministered.


ExTRACT-TIMI 25: Primary End Point (ITT) Death or Nonfatal MI

0

3

6

9

12

15

0 5 10 15 20 25 30

Pri

mary

En

d P

oin

t (%

) Enoxaparin

UFH

Relative Risk0.83 (95% CI, 0.77 to

0.90)P<.001

Days after Randomization

9.9%

12.0%

Lost to follow-up = 3

17% RRR

Adapted with permission from Antman EM, et al. N Engl J Med. 2006;354:1477-1488.

CLARITY-TIMI 28 Primary Endpoint:Occluded Artery (or D/MI thru Angio/HD)

PlaceboClopidogrelLD 300 mgMD 75 mg

P=0.00000036P=0.00000036

Odds Ratio 0.64(95% CI 0.53-0.76)

Odds Ratio 0.64(95% CI 0.53-0.76)

Clopidogrelbetter

Placebobetter

n=1752 n=1739

Sabatine N Eng J Med 2005;352:1179.

STEMI, Age 18-75

15.0

21.7

0

5

10

15

20

25

Occ

lud

ed A

rter

y o

r D

eath

/MI

(%)

1.00.4 0.6 0.8 1.2 1.6

36%Odds

Reduction

36%Odds

Reduction

De

ad

(%

)

Days Since Randomization (up to 28 days)

Placebo + ASA: 1,846 deaths (8.1%)

Clopidogrel + ASA:1,728 deaths (7.5%)

0.6% ARD7% RRR P = 0.03

N = 45,852 No Age limit ; 26% > 70 y

Lytic Rx 50%

No LD given

COMMIT: Effect of CLOPIDOGREL on Death In Hospital

Chen ZM, et al. Lancet. 2005;366:1607.

Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy.

Treatment with clopidogrel should continue for at least 14 days.

Thienopyridines



In patients < 75 years who receive fibrinolytic therapy or who do not receive reperfusion therapy, it is reasonable to administer an oral clopidogrel loading dose of 300 mg. (No data are available to guide decision making regarding an oral loading dose in patients ≥ 75 years of age.)

Long-term maintenance therapy (e.g., 1 year) with clopidogrel (75 mg per day orally) can be useful in STEMI patients regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy.


Thienopyridines


It is reasonable for patients with STEMI who do not undergo reperfusion therapy to be treated with anticoagulant therapy (non-UFH regimen) for the duration of the index hospitalization, up to 8 days.

Convenient strategies that can be used include those with LMWH (Level of Evidence: C) or fondaparinux (Level of Evidence: B) using the same dosing regimens as for patients who receive fibrinolytic therapy.

Anticoagulants




Coronary arteriography may be considered as part of an invasive strategy for risk assessment after fibrinolytic therapy (Level of Evidence: B) or for patients not undergoing primary reperfusion. (Level of Evidence: C)

Invasive Evaluation



Secondary Prevention

Ask, advise, assess, and assist patients to stop smoking – I (B)

Clopidogrel 75 mg daily: PCI – I (B) no PCI – IIa (C)

Statin goal: LDL-C < 100 mg/dL – I (A) consider LDL-C < 70 mg/dL – IIa (A)

Daily physical activity 30 min 7 d/wk, minimum 5 d/wk – I (B)

Annual influenza immunization – I (B)

• A fasting lipid profile should be assessed in all patients and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event. For hospitalized patients, initiation of lipid-lowering medication is indicated as recommended below before discharge according to the following schedule:

• LDL-C should be < 100 mg/dL.• Further reduction to < 70 mg /dL is reasonable.

(Class IIa; LOE: A) • If baseline LDL-C is ≥ 100 mg/dL, LDL-lowering

drug rx should be initiated.• If on-treatment LDL-C is ≥ 100 mg/dL

intensify LDL-lowering drug rx (may require LDL-lowering combination is recommended.

• If baseline LDL-C is 70 to 100 mg/dL, it is reasonable to treat to LDL-C < 70 mg/dL. (Class IIa; LOE: B)

Lipid management:2007 goal:LDL-C << than 100 mg/dL (if TG ≥ 200 mg/dL, non–HDL-C < 130 mg/dL

Goals Class I Recommendations

Secondary Prevention and Long Term Management

NEW

NEW

If TG are ≥ 150 mg per dL or HDL-C < 40 mg per dL, weight management, physical activity, and smoking cessation should be emphasized.

If TGs are 200 to 499 mg per dL, non–HDL-C target should be less than 130 mg per dL.

If TGs are 200 to 499 mg/dL, non–HDL-C target is < 130 mg/dL. (Class I; LOE: B); further reduction of non–HDL-C to < 100 mg dL is reasonable. (Class IIa; LOE: B)

Therapeutic options to reduce non–HDL-C include:•More intense LDL-C-lowering rx is indicated•Niacin (after LDL-C-lowering rx) can be beneficial (Class IIa; LOE B)•Fibrate therapy (after LDL-C-lowering rx) can be beneficial (Class IIa; LOE B)

If TG are ≥ 500 mg/dL, therapeutic options indicatedand useful to prevent pancreatitis are fibrate or niacinbefore LDL-lowering rx; and treat LDL-C to goal after TG-lowering rx. Achieving non–HDL-C < 130 mg/dL is recommended.

Lipid management:(TG 200 mg/dL or greater)Primary goal:Non–HDL-C < 130 mg/dL



NEW

• For all patients, it is recommended that risk be assessed with a physical activity history and/or an exercise test to guide prescription.

• For all patients, encouraging 30 to 60 min of moderate-intensity aerobic activity, such as brisk walking, on most, preferably all, days of the week, supplemented by an increase in daily lifestyle activities (e.g., walking breaks at work, gardening, household work).

• Advising medical supervised programs (cardiac rehabilitation) for high-risk patients (e.g., recent acute coronary syndrome or revascularization, HF) is recommended.

• Encouraging resistance training 2 d per week may be reasonable (Class IIb; LOE: C)

Physical activity:2007 Goal:30 min 7 d per wk; minimum 5 d per wk



NEW


For all post-PCI STEMI stented patients without aspirin resistance, allergy, or increased risk of bleeding, aspirin 162 to 325 mg daily should be given for at least 1 month after bare-metal stent implantation, 3 months after sirolimus-eluting stent implantation, and 6 months after paclitaxel-eluting stent implantation, after which long-term aspirin use should be continued indefinitely at a dose of 75 to 162 mg daily.

Antiplatelet agents/ anticoagulants: Aspirin


CHANGED TEXT

http://www.health-first.org/hospitals_services/heart_institute/heart_assoc/images/anticoag.gif

Goals Recommendations

In patients where the physician is concerned about the risk of bleeding lower-dose 75 to 162 mg of aspirin is reasonable during the initial period after stent implantation. (Class IIa; LOE: C)

Antiplatelet agents/ anticoagulants: Aspirin


NEW REC


Goals Class I RecommendationsFor all post-PCI patients who receive a drug-elutingstent (DES), clopidogrel 75 mg daily should begiven for at least 12 months if patients are not athigh risk of bleeding.

For post-PCI patients receiving a bare metal stent(BMS), clopidogrel should be given for a minimumof 1 month and ideally up to 12 months (unless thepatient is at increased risk of bleeding; then itshould be given for a minimum of 2 weeks).

Antiplatelet agents/ anticoagulants: Clopidogrel


CHANGED TEXT


Goals Recommendations

For all STEMI patients not undergoing stenting(medical therapy alone or PTCA without stenting), treatment with clopidogrel should continue for at least 14 d. (Class I; LOE: B)

Long-term maintenance therapy (e.g., 1 year) with clopidogrel (75 mg per day orally) is reasonable in STEMI patients regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. (Class IIa; LOE: C)

Antiplatelet agents/ anticoagulants: Clopidogrel


NEW RECS


Goals Class I RecommendationsManaging warfarin to INR = 2.0 to 3.0 for paroxysmal or chronic atrial fibrillation or flutter is recommended, and in post-STEMI patients when clinically indicated (e.g., atrial fibrillation, left ventricular thrombus).

Use of warfarin in conjunction with aspirin and/orclopidogrel is associated with increased risk ofbleeding and should be monitored closely.

In patients requiring warfarin, clopidogrel, andaspirin therapy, an INR of 2 to 2.5 is recommended with low dose aspirin (75 to 81 mg) and a 75 mg dose of clopidogrel.

Antiplatelet agents/ anticoagulants: Warfarin


NEW REC

NEW REC

CHANGED TEXT

• Acetaminophen, ASA, tramadol, narcotic analgesics (short term)

• COX-2 Selective NSAIDs

• Nonacetylated salicylates

• Non COX-2 selective NSAIDs

• NSAIDs with some COX-2 activity

Stepped Care Approach To Pharmacologic Therapy for Musculoskeletal Symptoms with Known Cardiovascular Disease or Risk Factors for

Ischemic Heart Disease

Select patients at low riskof thrombotic events

Prescribe lowest doserequired to control symptoms

Add ASA 81 mg and PPI to patients at increased risk of thrombotic events *

• Regular monitoring for sustained hypertension or worsening of prior blood pressure control), edema, worsening renal function, or gastrointestinal bleeding.

• If these events occur, consider reduction of the dose or discontinuation of the offending drug, a different drug, or alternative therapeutic modalities, as dictated by clinical circumstances.

* Addition of ASA may not be sufficient protection against thrombotic eventsAntman EM, et al. J Am Coll Cardiol 2008. Published ahead of print on December 10, 2007. Available at http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001.

http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001


ACE inhibitors should be started and continued indefinitely in all patients recovering from STEMI with LVEF ≤ 40% and for those with hypertension, diabetes, or chronic kidney disease, unless contraindicated.

ACE inhibitors should be started and continued indefinitely in patients recovering from STEMI who are not lower risk (lower risk defined as those with normal LVEF in whom cardiovascular risk factors are well controlled and revascularization has been performed), unless contraindicated.

Among lower risk patients recovering from STEMI (i.e., those with normal LVEF in whom cardiovascular risk factors are well controlled and revascularization has been performed) use of ACE inhibitors is reasonable. (Class IIa; LOE: B)

Renin-Angiotensin-Aldosterone System Blockers: ACE Inhibitors


NEW REC

CHANGED TEXT

NEW REC

Goals Class I RecommendationsUse of ARBs is recommended in patients who are intolerant of ACE inhibitors and have HF or have had a STEMI with LVEF ≤ 40%.

It is beneficial to use ARB therapy in other patients who are ACE-inhibitor intolerant and have hypertension.

Considering use in combination with ACE inhibitorsin systolic dysfunction HF may be reasonable.

Renin-Angiotensin-Aldosterone System Blockers: ARBs


NEW REC

NEW REC

CHANGED TEXT


Use of aldosterone blockade in post-STEMI patients without significant renal dysfunction or hyperkalemia is recommended in patients who are already receiving therapeutic doses of an ACE inhibitor and beta blocker, have an LVEF of ≤ 40% and have either diabetes or HF.

Renin-Angiotensin-Aldosterone System Blockers: Aldosterone Blockade


CHANGED TEXT


It is beneficial to start and continue beta- blocker therapy indefinitely in all patients who have had MI, acute coronary syndrome, or left ventricular dysfunction with or without HF symptoms, unlesscontraindicated.

Beta- Blockers


CHANGED TEXT

A 55 yo male presents to your rural ER with 1-hour of sub-sternal chest pain, nausea and diaphoresis:

- BP 110/68 Following SL NTG, BP falls to 90/50

A. Suspected Diagnosis?:

As you give tPA + heparin, which of the following are most appropriate next tx?:

a. Additional IV metoprolol d. IV fluid bolus

b. Start nitroglycerin drip e. Place a PA catheter

c. Dopamine drip

A 55 yo male presents to your rural ER with 1-hour of sub-sternal chest pain, nausea and diaphoresis:

- You give the patient tPA, IV fluids and his blood pressure increases and his symptoms and ECG changes are resolving.

- You notice that his heart rate significantly drops to 40 bpm.

- The BP remains stable and the patient has no symptoms.

a. Place a transvenous pacemaker d. Observation. Give

b. Atropine 0.5 mg IV atropine if develops sx’s or

c. Atropine 1.0 mg IV hemodynamic change.

Mobitz I, 2nd-degree AVB (Wenckebach)

Transvenous Pacing & MI Location

Inferior MI Sinus bradycardia

(Bezold-Jarish) common

Block at AV node• Stable escape rhythm• AV block is usually

transient & well-tolerated

TV Pace: Mobitz II or higher &: Symptoms that are

unresponsive to atropine

Anterior MI Block usually below

AV node

TV Pace: New bifasicular

block Mobitz II or worse

regardless of symptoms

Outline

Arrhythmias & ECGs

A 68 yo male presents to your ER after 60 minutes of substernal chest pain, nausea and diaphoresis:

- Hx: HTN, DM, HLD, Distant MI

- P 96 BP 146/92 RRR w/+S4. No murmur. Lungs – clear.

- ECG: 1mm ST-depression infero-laterally that resolves slowly with B-blocker, nitroglycerine & morphine.

- He rules in for MI: peak MB 30, trop-T 2.4.

After stabilization on medical therapy, you recommend which of the following

tests to risk stratify this patient?:a. Exercise stress test d. Myocardial Perfusion Imaging

b. Stress Echo e. None of the above

c. Cardiac Catheterization

Post MI Risk Stratification

What is the overall best predictor of survival post-MI?:

LV Ejection Fraction (EF)

Non-STEMI / UA Risk Stratification is key!

Immediate High Risk• Cardiogenic shock / severe CHF /

ischemic MR w/hemodynamic change

• Recurrent angina despite maximal medical therapy

• Unstable ventricular arrhythmias

Urgent Cath

*Don’t give thrombolytics

in NSTEMI!

High Risk• (+) enzymes

• Dynamic ECG changes

• Clinical CHF

• Depressed LV EF

• GIIb/IIIa

• Early invasive

- Cath during initial

Hospitalization

Intermediate Risk• Diabetics, PVD, Age >65

• Prior MI (hx or q-waves on ECG)

• Aspirin use

• Rest angina, < 20 minutes

• No dynamic ST changes

• Baseline pathologic q-waves

• Negative enzymes

Low Risk• None of above

• Minimal risk factors

• Minimal or atypical symptoms

In General:• Best medical

therapy

• In general: Non-invasive risk stratification

• Cath for:

• High-risk non-invasive testing results

• Pre-existing lifestyle-limiting angina

Non-STEMI / UA Risk Stratification is key!

MI: Initial Medical Therapy

*Clopidogrel: post-stenting

- Bare-metal stent: at least 4 weeks and no surgery for 6 weeks

- Drug-eluting stent (sirolomus, paclitaxel): plavix for 3 months (sirolomus/Cypher) to 6 months (paclitaxel/Taxus) MINIMUM

- Often given for 1 year (CURE Trial) unless contraindication

*162-325mg

Heparin: *60 U/kg bolus then

12U/Kg/Hr in patients given

lytics or IIb/IIIA

MI: Initial Medical Therapy

*Warfarin x 3-6 months: LV thrombus, large anterior MI with akinetic anterior wall.

-Don’t give warfarin to a patient simply with a depressed EF without Afib or embolism or thrombus (controversial)

*

Post-MI Complications

Acute pulmonary edema, hypotension, new decrescendo systolic murmur at apex

PA Catheter (wedged):

Papillary Muscle Rupture

Treatment: Afterload reduction

• Nitrates• IABP

Emergent surgical repair


Papillary Muscle Rupture

Inferior MI’s (PDA) Due to single blood

supply to postero-medial papillary muscle


LV Free Wall Rupture:

Large, STEMI, 1st MI, Anterior MI (LAD) Less common with early reperfusion but may

occur earlier (classically ~7d) Treatment: emergent surgery,

pericardiocentesis, supportive measures

Acute hypotension, JVD, muffled heart sounds

Equalization of diastolic pressures on PA catheter


Ventricular Septal Rupture (Acute VSD):

Location less important: Anterior = Inferior Treatment

• Unstable patient = urgent surgery• Afterload reduction, IABP, supportive measures

Hypotension, JVD, holosystolic murmur with a thrill

PA catheter: “step up” in oxygen saturation from RA to RV

SCD Prevention Post-MIPrimary Prevention

Referral for AICD if (MADIT I): Non-sustained VT > 48 hours after

MI EF <35% Inducible, non-supressable VT on

EP study Best benefit: lower EF (<26%), wide

QRS, CHF Wait > 1 month post-MI & 3mos.

post CABG MADIT II: Prior MI + EF 30%

No EP study

1 ° SCD PreventionNon-ischemic Cardiomyopathy

All-cause mortality at 5 yearsAmiodarone vs placebo

HR 1.06, p=0.529ICD vs placebo

HR 0.77, p=0.007

28.9%

34.1%35.8%

0%

5%

10%

15%

20%

25%

30%

35%

40%

ICD Amiodarone Placebo

28.9%

34.1%35.8%

0%

5%

10%

15%

20%

25%

30%

35%

40%

ICD Amiodarone Placebo

% M

ort

alit

y

SCD-HeFT ½ non-ischemic EF ≤ 35% Amio = Placebo

Chronic CAD The ‘Big 4’:

Aspirin B-blocker (especially post-MI & depressed EF)

• Non-dihyrdropyridine CCB (diltiazem) if B-blocker intolerant

Statin Ace-I (HOPE & EUROPA trials –vs- PEACE trial)

Nitrates (know dosing, tolerance) Recent change: 1 spray, if not gone 911 / ER

Non-dihydropyridine CCB (e.g,. amlodipine) – may use with B-blocker

No estrogen for CAD: primary prevention (WHI) or secondary prevention (HERS)

Chronic CAD

Know methods to reduce risk (Board Favorites!): Smoking cessation Diet Weight loss Exercise Lipid management

Lipid Management

xx*CAD Equivalents:

- ASPVD - Diabetes - Multiple risk factors (Framingham > 20%)

• 2004 ATP III Modifications:

• In high risk patients: LDL-C goal < 70 is a therapeutic option based on recent clinical trial data (Heart Protection Study, PROVE-IT)

• High risk: may start statin if LDL-C 100-129 simultaneously with lifestyle changes.

• High risk: If baseline LDL is <100, can start statin

• If high risk & high TGs or low HDL-C: use fibrate or niacin to get non-HDL-C to 30mg/dl higher than LDL goal and to raise HDL

• Moderately high risk (2+ risk factors, 10-20% risk): LDL<100 optional goal

Lipid Management LDL goal – get there 1st!

HDL and TG’s are secondary targets Once LDL to goal:

“Non-HDL chol.” goal: 30 higher than LDL goal• (LDL+VLDL+TG’s) – incorporates all atherogenic particles

Low HDL (<40 men, <50 women) Exercise, smoking cessation Niacin (most potent), fibrates

Notes on Revascularization 2 Goals

Symptom relief (angina): PCI or CABG Improved survival: CABG

PCI: better than medications for relief of angina & ischemia from obstructive CAD

Stenting Complications: Early (1st month)

• Acute thrombosis: 24 hours (not subtle - MI)• Sub-acute thrombosis: usually < 4 weeks (not subtle - MI) • With DES (drug-eluting stents), can occur later until fully

endothelialized Late: in-stent restenosis: 1-6 months (angina)

• Reduced by DES• Brachytherapy – FDA approved treatment for symptomatic

restenosis (not for prevention!) – no longer done due to DES!!

Indications for CABG

Left Main > 50% Left main equivalent:

>70% proximal LAD & proximal Left Circumflex 3 vessel obstructive CAD, especially if:

Depressed EF Diabetics

2 vessel CAD with proximal LAD disease & Depressed EF <OR> Treated diabetics

“Don’t stent the left main”

Stress TestingExercise ECG

Sens & Spec = ~ 70%… Bayesian approach to using for diagnosis:

High pre-test probability: negative test won’t change management

Low pre-test probability: false + > true + Best: intermediate pre-test probability

Go directly to imaging (for diagnosis): LBBB, paced rhythm – use pharm stress Uninterpretable ECG: ST-dep >1mm (e.g. LVH) Inability to exercise Prior revascularization (to localize)

Stress TestingExercise ECG

Contraindications: AS Others (common

sense) Reasons to stop High-risk findings

Low-functional capacity

Drop in Systolic BP during exercise

Marked ST-changes Prolonged ST-changes

>2 mm

Stress TestingPerfusion Imaging & Stress Echo

More expensive Increased sensitivity & specificity Bayesian approach

Low-pre-test probability + positive stress ECG Localizes ischemia

Patients with prior revascularization Poor prognosis:

Multiple defects, Large defects, increased lung uptake, transient ischemic dilation of LV cavity

Normal study – has good prognosis Adenosine / Persantine: avoid if COPD,

asthma

Endocarditis Prophylaxis Due to limited data re: efficacy of ID

prophylaxis, AHA guidelines revised 2007 Major change: only give IE prophylaxis to

those at HIGHEST RISK: Prosthetic heart valves (mechanical and bio) Prior history of IE 6 months post-repair of congenital defect (whether

by surgery or catheter) Repaired congenital defect with residual defect Complex cyanotic congenital heart disease Valvulopathy in a transplanted heart

Endocarditis Prophylaxis

No prophylaxis:1. Bicuspid AoV

2. Acquired valvular heart disease

3. Prior surgical valve repair

4. Isolated SECUNDUM ASD

5. Surgically repaired ASD, VSD or PDA

6. Pacemakers, defibrillators

7. History of rheumatic disease without valvular dysfunction

8. Deliver or C-section

Endocarditis Prophylaxis

Changes: limited procedures need prophylaxis: Dental procedures

GI, GU, Resp and skin:• Only if doing procedure involving active infected tissue

with ‘bugs’ known to cause IE: must be on abx at time of procedures

Endocarditis ProphylaxisNo Post-treatment

Situation Agent

Regimen: single dose 30 to 60 min before procedure

Adults Children

Oral Amoxicillin 2 g 50 mg/kg

Unable to take oral medication

Ampicillin 2 g IM or IV 50 mg/kg IM or IV

OR

Cefazolin or ceftriaxone 1 g IM or IV 50 mg/kg IM or IV

Allergic to penicillins or ampicillin - oral

Cephalexin* 2 g 50 mg/kg

OR

Clindamycin 600 mg 20 mg/kg

OR

Azithromycin or clarithromycin

500 mg 15 mg/kg

Allergic to penicillins or ampicillin and unable to take oral medication

Cefazolin or ceftriaxone 1 g IM or IV 50 mg/kg IM or IV

OR

Clindamycin 600 mg IM or IV 20 mg/kg IM or IV

Aortic Stenosis History: angina, syncope, CHF (classic triad) Exam:

Crescendo-decrescendo murmur Best at RUSB; may be heard at apex (Gallavardin’s) Radiates to carotids Increases with squatting Delayed & diminished carotid upstroke +S4 & sustained PMI Soft or delayed A2; loss of physiologic splitting Increased severity if:

• Later peaking murmur• Soft or absent S2• Loss of physiologic splitting (single S2)• Diminished carotid upstroke

Aortic Stenosis Prevalence increases with age

(“senile, calcific AS”) Young patient with ejection

click = bicuspid Ao valve ~1 in 200 people 30-40% with coarctation have a

bicuspid Ao Valve Increased risk for aortic

dissection or ascending aneurysm

ECG: LVH, LAE; LBBB in some

Echo: accurate Measures velocity Gradient = 4v2

Aortic Valve Area: <1 cm2 severe

Aortic Stenosis Bleeding tendency:

Increased colonic angiodysplasia Acquired vonWillebrand disease

Cath: not needed to “confirm” echo data Usually done to eval for obstructive CAD in

patients referred for aortic valve replacement Treatment

No medical treatment Beware of vasodilators or diuretics (decrease

preload) Symptoms = surgery! No role for balloon valvuloplasty

Aortic Stenosis

Surgical Therapy (cont.) Symptoms = surgery! Prostheses:

• Mechanical – more durable; requires anticoagulation

• Bioprosthetic: less durable; short-term coumadin only

• Infective endocarditis risk is the same in both types of valves

50 yo M c/o progressive DOE and fatigue. BP 160/58. Pulse is bisferens.

- CV exam: systolic thrill at the apex & over the bounding carotid arteries. + systolic ejection sound. +S3, soft S1 and a decrescendo diastolic murmur at the base that is high-pitched, early peaking and last throughout diastole.

- Also: 3rd and 4th interspaces at LLSB you hear a presystolic rumble.

- An echocardiogram confirms your clinical impression

You recommend which of the following?:a. MV replacement and AV replacement with a mechanical

prosthesis

b. MVR and AVR with a bioprosthesis in the aortic position.

c. AVR with a mechanical prosthesis.

d. Vasodilator therapy and observation for six months.

e. Diuretic therapy and observation for six months.

Aortic InsufficiencyChronic

History – well-tolerated until severe CHF symptoms when severe

Exam: Wide pulse pressure accounts for myriad of

peripheral pulsating organs• Water-hammer pulses, etc…

Auscultation• Early diastolic, decrescendo murmur• Blowing (“cooing dove”, “wind blowing through

leaves”), high-pitched• Pt. sitting up, leaning forward• Afterload sensitive – increases with handgrip• Austin-Flint (diastolic): mimic MS due to AR jet

Aortic InsufficiencyChronic

Etiologies:

Treatment: Surgery if: symptoms, EF<50% or increasing LV cavity size on serial echocardiograms

Mechanical AVR if <65 yo Bioprosthetic AVR if > 65 yo or can’t take coumadin

Aortic InsufficiencyAcute!

Medical emergency Hx: severe symptoms

Cardiogenic shock, syncope Exam – classic exam signs not usually

present Softer, shorter diastolic murmur (may not even

be audible) Etiologies: endocarditis, aortic dissection,

trauma, mechanical valve dysfunction Treatment: emergent surgery

Mitral Stenosis

Etiology: Rheumatic Fever History: disease often latent

Dyspnea – often misdiagnosed as asthma in young pt. Hemoptysis, hoarseness New-onset atrial fibrillation (esp. during pregnancy)

• Don’t tolerate tachycardia well due to transmitral pressure

Exam: Loud S1 Opening snap in early diastole (after S2) Diastolic rumble Loud P2 if pulmonary hypertension

Mitral Stenosis

ECG: LAE, RAE RVH (RAD) - No LVH

Treatment Medical: lasix, ? B-blockers, limit activity Correct: if mod-severe MS + symptoms or pulmonary

hypertension Balloon valvuloplasty if possible based on valve

characteristics (unlike in AS) Open commissurotomy, surgical repair or

replacement

55 yo M with a 5 year hx of a “murmur”. No symptoms but he admits to doing little activity. He no longer walks to

the office and does not have to walk stairs to the 3rd floor “because there is an elevator”.

- Exam: Normal carotids. Clear lungs. PMI is diffuse in the 5th intercostal space, midclavicular line.

- Grade III/VI holo-systolic murmur heard best at the apex.

- Echo: floppy mitral valve with severe posterior leaflet prolapse, severe MR. Mildly dilated LV with EF 45-50%

You recommend which of the following?:

a. Close observation and repeat TTE with clinical change.

b. Start ramipril and repeat TTE in 4 months.

c. Refer to surgery for mitral valve replacement.

d. Refer to surgery for mitral valve repair.

e. Start long-actin nifedipine and repeat TTE in 1 year.

Mitral RegurgitationChronic

History: reflect poor cardiac output & elevated LA pressures Dyspnea / CHF

Multiple Etiologies Exam:

HSM murmur best at apex; may radiate to axilla Increases: afterload (sustained handgrip) or

Increased venous return (leg elevation) Decreases with standing, valsalva, inspiration Hyperdynamic apical impulse Soft S1 Little respiratory variation Wide splitting of S2 (early closure of A2)

Mitral RegurgitationChronic

Medical Treatment Afterload reduction Diuresis

Surgical: repair (rather than valve replacement) if feasible! Timing – controversial; want to perform

BEFORE LV dysfunction occurs In general – severe MR &:

• Symptoms• EF <55-60%• Dilating LV size on TTE• Afib • Pulmonary HTN

Mitral RegurgitationMitral Valve Prolapse

Most common valvular cause of MR & need for MVR

Exam: Mid-systolic click followed by murmur (“click-

murmur syndrome”) Maneuvers that decrease Preload (valsalva,

standing) move clicks closer to S1 and murmur starts earlier

Ejection sound of AS or PS – does not move

Mitral RegurgitationMitral Valve Prolapse

Spectrum of disease Concern – “floppy” redundant MV leaflets

with MR and myxomatous changes Mild increase risk for embolic stroke No anticoagulation prophylaxis

SBE prophylaxis if: MR OR myxomatous leaflets on echo

Mitral RegurgitationAcute MR

Also: Ischemic Ruptured chord in

severe MVP Large V-waves on PA

catheter Decrescendo systolic

murmur at apex

Most common cause: endocarditis

R-sided Murmurs in Brief

TR Usually secondary: RV dilation or pulmonary

hypertension • PE, numerous causes of pulmonary HTN, RV disease

Murmur (when heard): HSM LLSB – increases w/inspiration

Prominent V-waves, pulsatile liver Endocarditis in drug users TS + TR, flushing, diarrhea = carcinoid syndrome Tx – underlying cause, ring if fixing mitral valve

PS – congenital; ejection click Noonan’s syndrome: low-set ears + PS Tx – balloon valvuloplasty

Congenital Heart Disease

Atrial Septal Defect (ASD)A 30 yo female is found to have cardiomegaly on a CXR obtained as part of routine physical examination. She

is active, can walk indefinitely without symptoms.

- Cardiac exam: grade II/VI SEM at the 2nd intercostal space, LUSB. 2nd heart sound is widely split and does not very with respiration.

- CXR: cardiomegaly with full pulmonary vascular markings.

- Echo: enlarged RV and paradoxical septal motion.

DIAGNOSIS ?

Atrial Septal Defect (ASD) Exam (cc: “SOB”)

SEM LUSB Fixed splitting of S2 RV volume overload

Secundum: 70% IRBBB or RBBB, right axis NO SBE prophylaxis if isolated

Primum: IRBBB or RBBB, left axis Associated MV or TV disorders

Treatment: closure for Qp/Qs >1.5:1 or symptoms, in general

Surgical or percutaneous Amplatzer device – FDA approved 2001

1. Secundum

2. Primum

3. Sinus venosus

4. Coronary Sinus

4

2

Patent Foramen Ovale PFO

Common: 20-30% of all patients Usually not patent if LA pressure > RA

pressure & not “stretched” Consider PFO or ASD if cryptogenic stroke in

a young patient• Especially with atrial septal aneurysm

Consider eval for clotting disorder Long-term warfarin (over ASA) for clinical

event Closure if recurrent event on anticoagulation

(FDA guidelines) or large shunt

Ventricular Septal Defect

Most close in childhood spontaneously or surgically

+ Endocarditis prophylaxis Exam

• Loud murmur w/thrill (gr. 3-6), pan-systolic• Afterload dependent – increases with sustained

handgrip (like MR)• Large – pulmonary HTN (loud P2), RV heave

Treatment – closure if large

Congenital Heart DiseaseOthers

Patent Ductus Arteriosus (PDA)

Preferential clubbing of toes (but not fingers) if R to left shunt

Tx: surgical ligation or other form of closure

Continuous “machine-gun murmur

Heard in infraclavicular fossa

Congenital Heart DiseaseOthers

Coarctation of the Aorta

CXR• Loss of aortic knob• Rib notching due to collateral

recruitment Increased circle-of-Willis berry

aneurysms (CVA) Bicuspid AoV – 40-60% Turner’s Syndrome

Ejection click & SEM at LLSB Delayed femoral pulses Hypertension in arms

Physical Exam Pearls…

Physiologic Splitting S2: splits with inspiration Persistently Split S2

Delayed closure of Pulmonic Valve Normal respiratory variation RBBB, PE, Pulmonic Stenosis, PVC from LV

Paradoxically Split S2 Splits during EXPIRATION Delayed closure of Aortic valve LBBB, Severe AS, RV pacemaker, PVC from RV

Fixed Splitting of S2: fixed A2-P2 = ASD Bisferens pulses: significant AI; HCM; AV

fistula

Todd C. Villines, MD

Cardiology ServiceWalter Reed Army Medical Center

Cardiology Board Review Part II2008

http://www.wramc.amedd.army.mil/MainFrame.cfm

http://www.wramc.amedd.army.mil/index.htm

Outline – Part I

CAD Acute Coronary Syndromes (ACS) Chronic CAD

Valvular Heart Disease Congenital Heart Disease Physical Exam Pearls

Outline – Part II

CHF / Cardiomyopathies Arrhythmias & ECGs Pericardial Disease Peripheral Vascular Disease Preoperative Evaluation Miscellaneous Test Taking Strategies

CHF – Systolic Dysfunction Most common:

Ischemic Hypertensive Dilated CM

Evaluation Cause usually evident

in history Extensive workup

usually not needed or revealing

Echo Ischemic evaluation Thyroid studies for all Consider iron studies

Chronic Treatment Systolic CHF

ACE-I – all patients B-blockers: metoprolol sustained release,

carvedilol and bisoprolol Benefit in all classes – class I-IV if used

appropriately Start when patient is clinically stable and

euvolemic “Start slow & go slow”

Spironolactone (RALES): class III & IV – on other standard therapies

Chronic Treatment Systolic CHF

Digoxin – sxs despite Ace-I, BB, diuretic & possibly spironolactone No reduced mortality Reduces symptoms & hospitalizations Careful in renal dysfunction

Warfarin – for afib, mechanical valve, embolic event (not just if depressed EF)

Can use amlodipine for BP – no effect on mortality No diltiazem or verapamil

Non-pharmacologic interventions

Systolic DysfunctionTherapy Overview

xx

Cardiac Resynchronization Therapy (CRT)“Biventricular Pacing”

Current Indications NYHA class III or IV heart failure LVEF ≤ 35% In NSR (not studied in afib) Evidence of ventricular dyssynchrony

• Currently: based on QRS width

• QRS > 120 msec– Most evidence in LBBB, but RBBB included

• FUTURE: echo evidence of dysynchrony better than ECG

Most also candidates for ICD

CRT: CARE HF Trial

NYHA III or IV LVEF ≤ 35% In NSR QRS > 120 msec Bi-V –vs- Meds alone

Improved Symptoms CV Death CV Hospitalization Total Mortality

Chronic Treatment Primary Diastolic CHF

Clinical syndrome of CHF with LVEF > 50% Causes – many: HTN, ischemia or infarct,

infiltrative diseases Amyloid on echo: “sparkling”, thick myocardium

Treatment – no consensus Treat HTN aggressively Lasix for symptoms Good rate control – esp. with a-fib Ace-I, BB No digoxin Address ischemia – if a factor

• Revascularization, nitrates, b-blockers

CHF Exacerbation Acute Treatment

You know this stuff! Identify precipitating factors

• Ischemia, diet, arrhythmia, anemia, infection, thyroid, etc…

• Know drugs to avoid & that can exacerbate systolic CHF:

– Metformin, NSAIDS, Thiazoladinediones & ALL antiarrhythmic medications except Amiodarone

Standard therapies – common sense• Diuresis, afterload, nitrates, oxygen• Vasopressors & inotropes - if needed

Sudden Death in the YoungThings to Think about

Hypertrophic Cardiomyopathy Anomalous coronary artery Inherited Long-QT syndrome

Sudden death with startling Brugada Syndrome RV Dysplasia Premature CAD Coronary Dissection Drug-induced (esp. cocaine) Idiopathic / Familial PE

Hypertrophic Cardiomyopathy

History Often no symptoms 15-25% prior syncope – with exertion 20-30% chest pain Dyspnea, palpitations, fatigue

Physical Exam** (know this) Murmur: crescendo-decrescendo at LLSB Increased murmur with decreased LV cavity size

(decreased venous return) • with standing, valsalva or nitro

No radiation to neck and brisk carotid upstroke (unlike AS)

Also: MR, S4, prominent PMI

Hypertrophic Cardiomyopathy ECG

LVH, LAD pseudoinfarct pattern (prominent septal q waves infero-

laterally) Echo

Concentric form Asymmetric form– commonly involving the septum (HOCM)

No competitive sports Tx:

B-blocker or CCB (control rate for filling) Surgical myectomy OR non-surgical ethanol septal ablation

if significant outflow gradient: ~5% of patients currently.

Atrial Fibrillation

Atrial Fibrillation Evaluation

ALL: thyroid studies, Echo & CXR Look for underlying cause of new onset or

accelerated rate in chronic afib patient Acute Management

Unstable = urgent cardioversion Stable

• Control Rate: BB, CCB 1st line– Digoxin – slower onset and not good for high adrenergic tone

• Anticoagulation – if able & indicated– Risk factors for CVA: CHF, increasing age, hx of HTN, diabetes,

hx of CVA/TIA, structural heart dz (LAE, significant valvular disease)

Atrial Fibrillation New onset: known < 48 hours

Consider cardioversion • Anticoagulation (Lovenox, UFH)• Chemical: ibutilide best acutely

– risk of torsades with severe LV dysfunction

• Electrical - synchronized• Coumadin for 3-4 weeks after (“atrial stunning”)

> 48 hours or unknown: 2 choices Warfarin x 3-4 weeks then cardioversion TEE to r/o thrombus & cardioversion Coumadin for 3-4 weeks

Atrial FibrillationAnticoagulation

Aspirin Lone = <65 yo, no structural heart disease, & no

HTN Contraindication to warfarin (intracranial bleed or

neoplasm, serious falls risk) All others get warfarin… ACTIVE-W: ASA + Plavix inferior to coumadin

Anticoagulation 3-4 weeks prior to elective cardioversion 3-4 week after cardioversion…at least

• In general, need long-term if indicated INR 2-3 for chronic & paroxysmal

• Similar risk for stroke!

Atrial FibrillationAntiarrhythmic Therapy

Average efficacy of antiarrhythmics: 50-60% Rate control – vs- Rhythm control:

AFFIRM – no difference in QOL, stroke risk Increased strokes in rhythm control arm when

stopped warfarin because of recurrent afib

So…either option is fine if no symptoms but BOTH take warfarin if indicated (see prior slide)

Use of Antiarrhythmics:• Don’t tolerate a-fib hemodynamically (CHF patient,

restrictive cardiomyopathy, etc…)

• Symptoms of afib (palpitations) despite rate control


Amiodarone Best efficacy at maintaining NSR Least pro-arrhythmic Drug of choice if CAD or depressed EF Know: interacts with warfarin & digoxin (increases

potency of both) Know: side-effects

• Thyroid – baseline, at 3 months, then every 6 months• Pulmonary – baseline PFTs and CXR; CXR q 6 months.

PFTs with any symptoms or CXR change.• Liver – baseline LFTs and every 6 months• Corneal – baseline optho exam, then for symptoms

Atrial Flutter

Treated similarly to atrial fibrillation (anticoagulation, rate control)

More difficult to rate control than fib Often coexists with atrial fibrillation Can be terminated with overdrive pacing Consider curative ablation if difficult to manage

Narrow complex & rate ~150: think flutter ?

http://www.emedu.org/ecg/images/ans/2afl_2a.jpg

Multifocal Atrial Tachycardia

Pulmonary disease Theophylline Use Low K+ & Mg+

Treatment: underlying cause + :

Rate control – no digoxin No cardioversion if stable

Re-entrant tachycardias: AVNRT, AVRT Therapy:

Acute & Stable: 1. Vagal maneuver. 2. Adenosine 6-12 mg IVP3. AV Nodal agents

Chronic – BB; most can be ablated if recurrent or frequent

PSVT

Symptoms or A-fib: referral for ablation A-fib that is usually wide-complex and irregular Associated with Ebstein’s anomaly

Downward displacement of TV valve

Wolf-Parkinson-White 22 yo with a history of frequent palpitations

A-fib in WPW: “Wide complex, irregular” Tx: IV Procainamide…NOT dilt, verapamil, b-blocker or digoxin!

Wolf-Parkinson-White 22 yo with “rapid heart beat” goes to ER. BP is stable.

Treatment?

Wide-Complex Tachycardia

Wide-complex tachycardia VT –vs - SVT with aberrancy

Wide-Complex Tachycardia

Assume VT History - older age, heart disease, CAD

AV-dissociation = VT Capture or Fusion beats = VT QRS duration: wider more likely VT RBBB with LAD – likely VT


PVC’s Never treat asymptomatic PVCs Risk of ventricular ectopy is related to underlying

structural heart disease

Know ACLS 2000 Guidelines re: WCT VF or pulseless VT

• Shock x 3, epi or vasopressin, then Amio (not lidocaine)

Stable, monomorphic VT• Procainamide• If depressed EF Amio

A 35 yo male presents to the emergency room complaining of chest pain for the past 24 hours.

- Pain is worse when lying flat and worse with deep inspiration.

- No JVD. BP 136/76 Normal heart sounds except for a friction rub.

Acute Pericarditis: 1. Diffuse ST-elevation & 2. PR-depression

*may evolve to T-wave inversions (later)

Dx - at least 2:

1. Chest pain

2. ECG changes

3. Rub

Acute Pericarditis

MANY Causes: Viral / Idiopathic – most

common Search for underlying

cause - guided by the history Don’t “pan-lab”! Consider HIV / ppd Usually not 1st

presentation of systemic disease

Echo all to rule-out large effusion

MB & Troponin + in up to 25% of

patients

Chest Pain suggestive of Pericarditis

ECG Diagnostic ?

Age < 40 & no other suspected systemic illness or traumatic

ANY: JVD, Pulsus Paradoxus, +Cardiac Enzymes, Poor Pain

Control in ER, No social support

Admit / Reconsider

If YES to ANY =Admit + Echo

Consider:

1. MI2. Aortic Dissection 3. PE 4. Pneumothorax

5. Esophageal Rupture 6. Pancreatitis

Suspect Pericarditis ?YES

ECHO

NO

Large or Moderate Effusion

Small Effusion

-NSAIDS & F/U

NO

One Approach

(MKSAP)

Who to Admit ?

Admit:

- suspect serious underlying cause

(e.g. - uremic) or on

immunosuppressive

Acute Pericarditis

Refractory symptoms: further diagnostic work-up Suspect Tb if persistent symptoms after 2

weeks and risk factors Treatment

NSAIDS Also, may use colchicine up front Steroids – ONLY if refractory and an

underlying cause has not been found• 7-10 day tapering course

Despite treatment, the patient returns complaining of problems “catching his wind”.

- P 105 BP 90/60 PA Cath: RA 18mmHg PA 32/18 PCWP 19

- Physical Exam signs ?

- ECG Findings ?

- Echo Findings ?

- Treatment ?

- Etiologies ?

Pericardial Effusion

Pericardiocentesis Indications Tamponade Hemopericardium Suspected bacterial or tuberculous

pericarditis• Pericardial window biopsy best to dx Tb

Rapid reaccumulation post-drainage

55 yo F with hx of Breast CA treated with surgery & XRT 12 years ago complains of DOE x 1 yr.

- CXR: Recurrent R effusion. TTE – no effusion.

- BP 110/60 P 110. JVP 12 & increases with inspiration.

Which of the following is the next most appropriate test??:

a. Liver scan d. Spiral CT of lungs

b. Bilateral mammogram e. Transesophageal Echo (TEE)

c. MRI of heart

Dx: Constrictive Pericarditis Clinically: Suggestive history + signs of RV failure, DOE Exam:

Kussmaul (increased JVD with inspiration) – with prominent x & y descent of venous waves

Diastolic Knock (audible S3) RV overload signs

Constrictive Pericarditis

Etiologies: XRT, post-surgery, post-pericarditis -

Tb, cocci (long-list) CXR: pericardial calcification on

lateral Best: CT or MRI - pericardial

thickening (>4-5mm) Echo in all to assess hemodynamics

TTE: insensitive to pericardial thickness PA Cath: equalization of pressures Treatment:

Pericardiectomy if severe symptoms & can tolerate the procedure

pp

68 yo M found to have mid-line pulsatile mass.

Hx: HTN, CABG Rx: ASA, ramipril, atenolol, HCTZ

Careful ROS – no symptoms (no abd pain, back pain, etc)

P 78 BP 132/84 Ultrasound: 5.5 cm AAA below renals

Which is most appropriate at this time?

a. Increase B-blocker to pulse of 60 d. Increase ACE-I

b. Repeat u/s in 1 year e. Refer for surgical repair

c. Tell patient to limit physical activity

Dx: AAA Surgery

Abdominal: >4.5-5.0 cm or expanding (.5cm/6 mos or 1cm/yr) Thoracic AA & no sx’s: >6cm or compressing local structures

If no indication for surgery, serial u/s surveillance

Carotid Disease

Know when to refer to surgery! AHA guidelines:

Symptomatic Patients• TIA or CVA past 6 mos + >70% stenosis of

ipsilateral carotid• Acceptable: Sx’s + 50-69% stenosis

Asymptomatic Patients• Stenosis 60% + surgical risk <3% + life-

expectancy > 5 years

Reminder: PVD = CAD for lipid management, risk-factor reduction

Aortic Dissection Hx: “ripping” CP radiating to back

HTN, Marfan’s**, crack cocaine use, bicuspid aortic valve

Exam: HTN, AI murmur, muffled heart sounds if extends to pericardium

CXR – widened mediastinum Dx: TEE, CT or MRI

Aortic Dissection - Treatment IV B-blocker (labetolol) first! – reduce sheer stress Nitroprusside if needed (SBP>100 after labetolol) &

only with b-blocker first! If ascending aorta involved (type A) = surgery Non-ascending aorta = medical therapy Beware – can involve coronary ostia (MI) Variant – Aortic intramural hematoma – treat the

same as dissection (no heparin / anti-coagulants)Classification

Peripheral Arterial Disease

Atherosclerosis of arteries to legs ABI < 0.90 – good screening tool

Best if do before & after exercise Claudication: pain relieved with rest Pseudo-claudication with spinal stenosis: pain

relieved with SITTING (not standing still)

Vascular surgeries – high-risk surgeries; account for 70% of operative mortality Preop guidelines – know these!

Buerger disease (thromboangiitis obliterans) – medium/small artery necrosis ONLY if smokes

77 yo male pre-op aorto-bifemoral bypass for severe PVD.

Hx: DM II, tobacco use. No hx of MI or heart problems.

Able to walk 1 city block slowly – limited by claudication.

ECG – inferior MI – age-undetermined.

What do you recommend to the surgeons?

a. Proceed to surgery – no further preop evaluation

b. Preop Catheterization & Revascularization if needed

c. Preoperative dipyridamole-thallium myocardial scintigraphy

d. Cancellation of surgery - surgical risk too high

Pre-Operative EvaluationA Must Know!

Risk Stratify the Patient

Risk Stratify the Surgery

Miscellaneous

Strep bovis endocarditis Order a colonoscopy

Cannon a-waves A-V dissociation

• Complete heart block, RV Pacing (not a-v sequential)

Reasons for endomyocardial biopsy Transplant rejection (rarely adriamycin

toxicity) Rarely done Low-yield in sarcoid; ETOH CM – use hx

Test Taking Strategies

Rest prior to the test – they are long days Time is not an issue with this test (unlike the in-

service exams) If you don’t know, trust your training experience

& judgment “Is this how we would treat this patient at Walter

Reed?” “Is this how we do things here?”

You know this stuff & come from a premier program!

Test Taking Strategies

Rely on your knowledge Don’t watch for patterns (“last 2 answers were C so

this one can’t be C”) Steady pace & don’t panic if you don’t know a

question My personal method:

Before reading the question, I quickly scan the answers to see what type of question is it

• Don’t actually read the answers or think about them yet.• e.g. - Are they asking for medicines or treatments ?,

diagnoses ?, best test to order ?, etc… This helps me pick up on what is important as I read

the often long clinical scenarios

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