3/26/2013

1

Matters of the Heart: Lipids, Angina, Acute Coronary

Syndrome, Congestive Heart Failure, Dysrhythmias(Is That All There Is?)

David M. Schneider, MDAssociate Clinical Professor of Family & Community Medicine, UCSFFull-Time Faculty Physician, Santa Rosa Family Medicine Residency

Review/Overview of Major Cardiology Topics

Review important info you’ve learned. Provide you with relevant diagnostic &

therapeutic info.Drop a few pearls. I will breeze over or skip some info that I

left in for your study. Focus on important issues.

Practice Board Question

1. What is the most common cause of death among women in the US?

A. Breast cancerB. Lung cancerC. Cardiovascular diseaseD. Gynecological cancersE. Influenza + pneumonia

Practice Board Question

1. What is the most common cause of death among women in the US?

A. Breast cancerB. Lung cancerC. Cardiovascular diseaseD. Gynecological cancersE. Influenza + pneumonia

3/26/2013

2

Practice Board Question

1. What is the most common cause of death among men in the US?

A. Breast cancerB. Lung cancerC. Cardiovascular diseaseD. Gynecological cancersE. Influenza + pneumonia

Practice Board Question

1. What is the most common cause of death among adults in the US?

A. Breast cancerB. Lung cancerC. Cardiovascular diseaseD. Gynecological cancersE. Influenza + pneumonia

Lipids

http://www.publicdomainpictures.net/view-image.php?image=11891&picture=hot-dog-and-chips

ATP III Basics Elevated LDL-C level is a major cause

of CAD. LDL-C is the primary target for lipid-

lowering therapy. Non-HDL-C is a secondary target for

lipid-lowering therapy. Therapeutic lifestyle change is an

“essential modality in clinical management,” at all degrees of risk.

3/26/2013

3

Dyslipidemia Screening

ATP III guidelines: all > age 20 every 5 years. USPSTF recommends screening:

All men > 35 (A). Men 20-35 (B) and women > 45 (A) at increased risk

for CHD (also women 20-45 @↑ risk—B). USPSTF: fasting or non-fasting TC and HDL-C.

LDL measurement requires fasting if calculating LDL (TC - HDL - TG/5)—most panels calculate.

Direct LDL does not require fasting but is expensive.

CAD Risk Factors Per NCEP ATP-III:

Age: male 45, female 55 or premature menopause w/o E replacement therapy

BP—HTN (>140/90 mmHg, or on med) Cigarette smoking (w/in 1 mo per ATP 3) Good cholesterol low—HDL <40 mg/dL Family Hx premature coronary heart disease:

definite MI or sudden death before 55 in male 1°relative, before 65 in female 1°relative

LDL is implicit—circular reasoning

ATP 3, 2002; http://www.uptodate.com/contents/atp-iii-guidelines-for-treatment-of-high-blood-cholesterol?source=search_result&search=atp+3&selectedTitle=1~71

© David M. Schneider

HDL-C: The Good Cholesterol

In both JNC-7 & NCEP ATP III, HDL-C>60 is a negative risk factor – removes 1 point.

LDL Goals

0 – 1 risk factors: LDL < 160 2 risk factors: <130, OPTION of <100CAD or CAD equivalent: <100, OPTION

of <70, esp for “very high risk pts”

Non-HDL goal = LDL goal + 30

KNOW THIS SLIDE

3/26/2013

4

Very High-Risk Patients

LDL-C goal ≤70 mg/dL Hx of MI CAD + other high risk conditions

– Diabetes– Metabolic syndrome– Continued ischemic pain despite optimal therapy

Multiple risk factors (esp DM) Severe/poorly controlled risk factors (esp

smoking)

CAD Equivalents (ATP III)

DM

Symptomatic carotid artery dz AAA Peripheral arterial dz

10-yr risk of 1st event >20% (Framingham). (probably CKD—not in ATP III yet)

Secondary Dyslipidemia

Per ATP III guidelines, assess for secondary dyslipidemia before initiation of lipid-lowering therapy Diabetes mellitus Hypothyroidism Obstructive liver disease Chronic renal failure Medications (thiazide diuretics,

antipsychotics)

Treatment of High LDL

STATINS!! Primary Prevention (less benefit):

– ↓ CAD, MI, sudden cardiac death (SCD).– May ↓ total mortality.

Secondary prevention (more benefit—bang-4-$):– ↓ CAD, MI, CV events.– Probably ↓ total mortality.– ↓ strokes.

NEJM 1995;333:1301-7; NEJM 2007;357:1477-86; JAMA 1998;279:1615-22; NEJM 2008;359:2195-2207; Lancet 2003;361:1149-58; ArchIM 1996;156:1158-72; Lancet 1994;344:1383-9; NEJM 1996;335:1001-9; Lancet

2002;360:7-22; Lancet 2003;361:1149–1158; NEJM 2004;350:1495–1504; Circulation 2000;102:1893–1900

3/26/2013

5

Statin-Related Side Effects

Statin Myopathy—2/3 occur w/in 6 mo. Myalgia (pain). Prox muscles. Myositis (elevated CK > 5-10 X ULN). <1%. Rhabdomyolysis (muscle necrosis, ↑↑↑ CK >

10X ULN, myoglobinuria [red-brown] +/- ARF).– Generally w/predisposing factors—drug

interactions, ?hypothyroidism.– No more statins!

>10X ULN D/C statin (& drink lots of H2O).

ArchIM 2005;165:2671-6; AmJMed 1991;91:25S-30S; ArchIM 1996;156:2085-92; BMJ. 2008;337:a2286; AmJCard 1991;68:1127-31; ArchIM 2003;163:688-92; JAMA 1990;264:71-5;

ArchIM 2003;163:553-64; AmJMed 2006;119:400-9; IntJCard 2007;119:374-6

Statin-Related Muscle Complaints

Lovastatin, simvastatin and atorvastatin are primarily metabolized by CYP 3A4. More interactions, more myotoxic.

Pravastatin, fluvastatin, pitavastatin and rosuvastatin – minimal 3A4 metabolism. Fewer interactions, less myotoxic.

Combination therapy: Ezetimibe NO ↑ risk of myopathy. Fenofibrate less risk of myopathy in combo

w/statins (vs gemfibrozil). Routine CK monitoring NOT recommended.

Common 3A4 Inhibitors

3 A’s: Amiodarone Antidepressants (fluoxetine, fluvoxamine, sertraline) Antifungals (azoles)

4 others: Macrolides (esp erythro + clarithro) Non-DHP CCB’s: diltiazem, verapamil Cyclosporine (transplant pts) PI’s – inhibit everything til proven otherwise

(+grapefruit juice > 1 quart/day!)

www.uptodate.com

© David M. Schneider

Prevention of Statin Myopathy

CoQ10 100 – 200 mg daily: No convincing evidence. Probably doesn’t hurt.

Vitamin D: No conclusive or convincing evidence. Probably doesn’t hurt (except high dose D in high

risk pts). Alternate day dosing.

Twice the dose every other day. Similar LDL results, no outcome data.

AmJHlthSysPharm 2004;61:515-9; AmJCard 2007;99:1409-12; AmJCard 2007 Nov;100:1400-3; AmJCard2012;110:526-9; JACC 2007;49:2231-7; Atherosclerosis 2007;195:e182-9; TranslRes 2009;153:11-9;

Atherosclerosis 2011;215:23-9; AmHtJ. 2002;144:674-7; J CVPharmacolTher 2003;8:123-6; AnnPharmacother. 2006;40:1917-23; AnnPharmacother. 2008;42:341-6; AmJCardio 2009;103:393-4

3/26/2013

6

More Statin Side Effects

Hepatic dysfunction: 0.4 – 3%. Consider D/C statin if ALT > 3X ULN.Diabetes risk (RR = 1.12):

High dose statins. Obesity, pre-DM @ risk. NNH = 498; however, NNT = 155. ? Peripheral neuropathy.

JHepatol 2012;56:374-80; Circ 2006;114:2788-97; EurJClinInvest 2000;30:980-7; Lancet 2002;360:7-22; BMJ. 2010;340:c2197; J AMA. 2011;305:2556-64; Lancet 2010;375:735-42; NEJM 2008;359:2195-207; Circ

2004;110(Suppl I):S834; Circ 2012; 126: e282-e284; Neurology 2002;58:1333-7; Lancet 2012;380:565-71

Liver Monitoring on Statins

2/28/12, FDA: No more routine liver monitoring in pts on statins. LFT’s “should be performed before starting statin

therapy and as clinically indicated thereafter.” Statin-induced hepatotoxicity (esp irreversible

liver damage) is “exceptionally rare,” & likely idiosyncratic (i.e., unpredictable).

Evidence does not show that periodic LFT monitoring detects or prevents get liver dz.

ArchIM 2003;163:688-92; JFamPrac 2001;50:927-8; http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm293623.htm

Fibrate Therapy Per ATP III, if triglycerides >500 mg/dL, initial

treatment should be with a fibrate to ↓ risk of pancreatitis. Fenofibrate ↓ CHD events, no effect on total mortality.

(FIELD trial). Fenofibrate has a lower risk of myopathy when

combined with statins; gemfibrozil is most appropriate if renal dysfunction is present.

Statins, niacin, or omega-3 fatty acids are all appropriate when TG’s are ↑, but <500 mg/dl.

Lancet 2005;366:1849-61; ATP 3—2002

Niacin in Patients with Low HDL Receiving Intensive Statin Therapy –

AIM-HIGHConclusion:

Among patients with atherosclerotic cardiovascular disease (2°prevention) and LDL cholesterol levels of less than 70 mg/dL, there was no incremental clinical benefit from the addition of niacin to statin therapy during a 36-month follow-up period, despite significant improvements in HDL cholesterol and triglyceride levels.

NEJM 2011;365:2255-67

3/26/2013

7

Omega-3 Fats and Sudden Death AHA guidelines suggest omega-3 supplements:

Preexisting disease High risk of disease High triglycerides GISSI found 850mg of EPA and DHA daily

decreased: Mortality Nonfatal MI Stroke Rate of sudden death

CAD: Angina, Acute Coronary Syndrome

http://www.publicdomainpictures.net/view-image.php?image=757&picture=breaking-heart

Angina: A Manifestation of CAD

Supply < demand (i.e., ↓ supply / ↑ demand). Retrosternal chest discomfort:

Squeezing, pressure-like, not necessarily pain. Also: heaviness, burning, choking. Back, neck, jaw, either/both arms.

Brought on by exertion, stress, cold temp, eating.

Relieved by rest, NTG (NOT a specific therapeutic challenge—esoph spasm, too).

http://www.uptodate.com/contents/pathophysiology-and-clinical-presentation-of-ischemic-chest-pain?source=search_result&selectedTitle=2~150#H1

DDx of Chest Pain

Cardiovascular Ischemic (<20-30%, but 2-4% of MI’s are

missed) Non-ischemic

– Aortic dissection*– Myocarditis– Pericarditis

NEJM 2000;342:1163-70

3/26/2013

8

Other Causes of CP

Pulmonary PE* Tension

pneumothorax* PNA Pleurisy/pleuritis Psych

Depression Anxiety d/o’s Somatoform d/o’s Delusional d/o’s

Musculoskeletal Cervical disc disease Costochondritis Fibromyalgia Herpes zoster (before

the rash) Neuropathic pain Rib fracture Sternoclavicular

arthritis

http://www.uptodate.com/contents/differential-diagnosis-of-chest-pain-in-adults?source=search_result&search=causes+of+chest+pain&selectedTitle=1~150

GI Causes of CP

Biliary Cholangitis Cholecystitis Choledocholithiasis Biliary colic

Peptic ulcer disease Nonperforating Perforating*

Esophageal Esophagitis Spasm Reflux Rupture*

Pancreatitis

Life-Threatening Causes of Chest Pain

Acute coronary syndrome* Aortic dissection* Pulmonary embolism* Tension pneumothorax* Esophageal rupture Perforated peptic ulcer

Life-Threatening Causes of Chest Pain

Dissection (aneurysm) Embolism (pulmonary)Acute coronary syndrome Tension PTXHole in GI tract

Esophageal rupture Perforated ulcer

© David M. Schneider

3/26/2013

9

65 y.o. Woman w/CP Wellens’ Syndrome—High Risk Deep T-wave inversions or biphasic T’s in

precordial leads. Changes classically occur during pain-free intervals.

Signifies severe LAD disease. Up to 75% will develop MI if untreated. Mean of 8.5 days from onset to MI – often AWMI.

Cardiac biomarkers normal or minimally ↑. 14-18% of pts presenting w/unstable angina.

AnnEmergMed 1999;33:347-51; AmJEmergMed 2002;20:638-43; AmHeartJ 1989;117(3):657-65; http://emedicine.medscape.com/article/1512230-overview; AmHeartJ 1989;117:657-65; AmHeartJ 1982;103:730-6

ASA in Primary Prevention

Much smaller benefit than in 2°prevention. Same risk of GI bleeding.USPSTF:

Men 45 to 79 when potential benefit (↓rate of MI) > risk of GI bleed.

Women 55 to 79 when potential benefit of ↓ in ischemic stroke > risk of GI bleed.

hemorrhage.all healthy M/W w/5-yr risk ≥3%.

http://www.uptodate.com/contents/benefits-and-risks-of-aspirin-in-secondary-and-primary-prevention-of-cardiovascular-disease?source=see_link#H611367213; AnnIM 2009;150:396-404 & 405-10; USPSTF

ASA Dosing in 1°Prevention

Largest trial used 75 – 325 mgOther trials have shown that low-dose (75

– 150 mg) is equivalent to medium-dose (160 – 325 mg) Acute events: wait a few minutes…

http://www.uptodate.com/contents/benefits-and-risks-of-aspirin-in-secondary-and-primary-prevention-of-cardiovascular-disease?source=see_link#H22; BMJ 2002;324(7329):71-86; AmJMed 2006;119:624-38

3/26/2013

10

Treatment of Stable Angina/CAD

Pharmacotherapy: Aspirin ß-blockers Ca++ channel blockers NitratesNon-pharmacologic therapy

Risk factor reductionNewer drug: ranolazine (Ranexa) – angina

resistant to other meds.

ASA—Now It’s 2°Prevention

ACCP: ASA indefinitely for all pts w/chronic stable angina, or clinical or lab evidence of CAD, or other CV dz. In pts w/occlusive CV event (nonfatal MI or

non-hemorrhagic stroke), ASA reduces risk of subsequent MI, stroke, vascular death.

http://www.uptodate.com/contents/benefits-and-risks-of-aspirin-in-secondary-and-primary-prevention-of-cardiovascular-disease?source=see_link#H19; AnnIM 2009;150:379-86; AmJMed 2008;121:43-9; BMJ

2002;324:71-86

ASA in DiabetesRecommended for all diabetics

w/evidence of cardiovascular dz (2°prevention)Recommended for 1°prevention in all

diabetics w/at least 1 risk factor Age >50 M/60 F y.o. —Albuminuria BP (HTN) —O-BEE-sity Cigarette smoker —Cholesterol ↑ FH CAD “ABC ABC Famil-ee” (© David M. Schneider)

http://www.uptodate.com/contents/overview-of-medical-care-in-adults-with-diabetes-mellitus?source=preview&anchor=H11&selectedTitle=1~150#H13; DiabCare 2010;33:1395-1402

ASA Issues

Enteric coating does not ↓ GI bleeding, may ↓ gastric erosions. ASA intolerance (~5%):

Clopidogrel (Plavix) is an alternative.– May have lower GI bleeding, but more non-

hemorrhagic SE’s (rash, diarrhea).– High cost, high NNT (i.e., low absolute benefit).

Non-ASA NSAID’s may ↑ CAD risk.

NEJM 2001;345:1809-17; JACC 2005;45:1295-1301; BMJ 2000;321:1183-7; ArchIM 2002;162:2197-2202

3/26/2013

11

Choice of ß-Blockers in Angina

All ß-blockers are equally effectiveCardioselective, longer-acting agents

generally preferred Metoprolol 25 mg twice daily (max 200 bid) –

may switch to metoprolol succinate (Toprol). Atenolol 25 mg daily (max 200 daily) – may

have higher mortality than other ß-Blockers.Resting bradycardia: use agent with

intrinsic sympathomimetic activity (ISA) Pindolol Acebutolol

http://www.uptodate.com/online/content/topic.do?topicKey=chd/10629#14

ß-Blocker Side Effects

BradycardiaHeart block BronchoconstrictionWorsening of PADCan precipitate or exacerbate CHF – esp

decompensated HF (6% w/carvedilol)

Calcium Channel Blockers

Reduce angina sx & increase exercise tolerance (no survival benefit).When to use CCB’s in angina:

ß-blockers contraindicated Side effects from ß-blockers Add to ß-blocker if ß-blocker monotherapy

ineffective (caution—drug interactions, negative inotropy/chronotropy)

Agent of choice for Prinzmetal’s angina

Variant (Prinzmetal’s) Angina

Spontaneous coronary artery spasm. Pts w/fewer risk factors, usu younger. Angina occurring at rest, pain may be severe. Usually normal exercise tolerance. Tends to occur in early morning. Transient ST elevation during episode. Arrhythmias may be a life-threatening

complication.

3/26/2013

12

Dx of Variant Angina

Standard exercise treadmill testing is useless (angina occurs @ rest).Dobutamine echo—sensitive, specific.Cardiac cath.

Ergonivine provokes vasospasm.

Note: may coexist with obstructive CAD.

Treatment of Variant Angina

CCB’s: nifedipine, verapamil, diltiazem.Nitrates: may be used in monotherapy, or

added to CCB. Avoid:

ß-blockers—esp nonselective. ASA—caution (inhibits prostacyclin). Triptans (provoke vasospasm)—also caution

w/obstructive CAD.

Non-Pharmacologic Therapy: Risk Factor Reduction

The usual: Treat HTN Treat hyperlipidemia (statins) Weight loss if indicated Glycemic control in diabetes Stop smoking Aerobic exercise – start low, go slow. Better

than stenting!– For NYHA Cl I – III angina in men not at high risk.

http://www.uptodate.com/contents/overview-of-the-care-of-patients-with-stable-ischemic-heart-disease?source=search_result&selectedTitle=1~150#24; Circulation. 2004;109(11):1371-8

PCI vs Optimal Medical Therapy of Stable Angina

COURAGE trial – 2007.NO difference in outcomes (all-cause

mortality, nonfatal MI, composite CV dz endpoint) in pts receiving optimal medical therapy vs those who received PCI (bare metal stent). Antianginal drug Anti-platelet drug Statins

NEJM 2007;356:1503-1516

3/26/2013

13

Pts in Whom Revascularization MAY Be Useful

Medical therapy does not provide sufficient relief. Intolerant of medical therapy. “High risk”:

L main dz. 3 vessel dz, esp w/low LVEF (<40%). 2 vessel dz w/high grade proximal LAD stenosis.

Circ 2011;124:2574-2609; http://www.uptodate.com/contents/medical-therapy-versus-revascularization-in-the-management-of-stable-angina-

pectoris?source=search_result&search=pci+in+stable+angina&selectedTitle=1~150

Stress Testing in Stable Angina

2007 ACC/AHA guidelines still recommend stress testing for most pts w/stable angina in order to: Evaluate efficacy of therapy Obtain prognostic info Identify “high risk” pts who might need PCI

http://www.uptodate.com/contents/stress-testing-to-determine-prognosis-and-management-of-patients-with-known-or-suspected-coronary-heart-disease?source=related_link

Angina in Women

Women are more likely than men to have atypical sx: Pain: more intense, sharp, burning Location: more often in neck, throat than men Provocative factors: more likely associated with

sleep, rest, mental stress NB: Women still get typical angina, too! Pearl: High index of suspicion for CAD in

women with risk factors or sx.

AmHtJ 2006;151(4):813-9; EurHtJ 2008;29(6):707-17; AmJCardiol 1994;74(3):226-31

Unrecognized MI in Women

MI is more likely to go undetected in women, esp young women (40% unrecognized 35 –39 yo vs 27% @ 75-79).

Women more likely than men to have pain in neck, jaw, back, & to have nausea w/CP.

Study of 515 women w/MI: Only 30% had prodromal CP. CP during MI in only 57%. Dyspnea in 58%.

EurHtJ 1998;19(7):1011-8; AnnIntMed 2001;134(11):1043-7; AmHtJ 1998;136(2):189-95; Circulation 2003;108:2619-23

3/26/2013

14

What is Acute Coronary Syndrome?

Insufficient blood flow to myocardium –most often results from CAD. Compromised blood flow to viable heart

muscle. Practically speaking: ACS means acute

MI or unstable angina.

http://www.americanheart.org/presenter.jhtml?identifier=3010002; http://www.nlm.nih.gov/medlineplus/magazine/issues/winter09/articles/winter09pg25-27.html

Unstable Angina Unstable angina:

Angina at rest (esp > 20 min) New onset angina limiting physical activity Increasing angina

– More frequent– Longer duration– Occurs with lower exertion

Angina that occurs early after infarction or revascularization is also considered by many to be unstable angina.

www.acc.org/qualityandscience/clinical/statements.htm; http://www.uptodate.com/contents/overview-of-the-acute-management-of-unstable-angina-and-non-st-elevation-myocardial-

infarction?source=search_result&selectedTitle=1~150; http://emedicine.medscape.com/article/159383-overview

Atypical MI Symptoms

Typical: Chest pain/angina N +/- V Indigestion Dyspnea Sweating Dizzy, lightheaded Fatigue Pain in:

– Either arm– Jaw– Neck– Back– Abdomen

Atypical: 1/3 had no CP. Atypical sx:

– Dyspnea alone– Weakness– N and/or V– Palpitations– Syncope– Cardiac arrest

More likely to be older, diabetic, women.

AFP 2005;72(1):119-26; http://www.uptodate.com/contents/management-of-suspected-acute-coronary-syndrome-in-the-emergency-department?source=search_result&selectedTitle=2~150; JAMA. 2000;283:3223-9; JACC 2007;50:e1-e157

UA vs MI

Unstable angina: NO elevation in cardiac enzymes +/- ischemic ECG changes—transientMI:

Elevated cardiac enzymes – rise & fall Evolving ECG changesCardiac enzymes may not rise for several

hours, so UA may be indistinguishable from non-ST elevation MI at presentation.

3/26/2013

15

Diagnosis of Acute MI

Rise & fall of cardiac biomarkers AND at least one of: Ischemic sx ECG changes Imaging evidence of new myocardial loss or

wall motion abnormality

Eur Heart J 2012 doi: 10.1093/eurheartj/ehs184 First published online: August 24, 2012; EurHeartJ2007;28:2525

ST Criteria for MI

ST Elevation (myocardial injury): ≥1 mm ST elevation in 2 contiguous leads. Persistent ST elevation may be LV aneurysm.

ST depression (myocardial ischemia): ≥1 mm of horizontal or downsloping ST depression

in 2 contiguous leads (“thumbs up is OK”). Q Waves (infarction): 1 box wide/1 box deep—2

contiguous leads. V2-V3 have different criteria—look at other leads.

JACC 2009;53:1003-11; EurHeartJ 2007;28:2525

Extensive Anterior + Lateral MI ECG Localization of MI: ST Elevations

V1 – V2: septal, anteroseptal V3 – V4: anterior, anteroseptal V4 – V6: lateral I, aVL, V5, V6: lateral II, III, aVF: inferior

Check V4R – V6R – RVMI (ACC/AHA)

ST depressions in V1-V2: consider posterior MI (check V7-V9)

3/26/2013

16

Reciprocal ECG Changes

ST depressions Anterior MI: II, III, aVF (inferior leads). Lateral MI: II, III, aVF (inferior) + V1-V2

(anterior). Inferior MI: V1-V3, I, aVL (anterior, +/-

lateral).

“Inferior partners with everything.”

Inferior MI, Reciprocal Depressions

Inferior MI R-Sided EKG

R Side

R

R

R

Inferior Wall MI w/Reciprocal Changes + Lat Ischemia

3/26/2013

17

Initial ECG in ACS

Initial ECG may be non-diagnostic in 45%, normal in 20% Early abnormalities include hyperacute T

waves If initial ECG is non-diagnostic in a pt in

whom there is high suspicion of MI (including continued sx), repeat ECG every 5 – 10 minutes (ACC/AHA).

JThrombThrombolysis 1998;6:63-74; AnnEmergMed 1998;31:3-11

Serial ECG’s

The key to electrocardiographic diagnosis of myocardial ischemia & infarction is serial ECG’s. Remember to order follow-up ECG’s. Even serial ECG’s are only 87% sensitive

for MI – use other criteria in addition to ECG.

JACC 1998;32(1):17-27

Diagnosis of Acute MI

Rise & fall of cardiac biomarkers AND at least one of: Ischemic sx ECG changes Imaging evidence of new myocardial loss or

wall motion abnormality

Eur Heart J 2012 doi: 10.1093/eurheartj/ehs184 First published online: August 24, 2012; EurHeartJ2007;28:2525

Cardiac Enzymes

Troponins most sensitive & specific. Normal serial troponin levels exclude MI, but do

not exclude unstable angina.CK-MB & myoglobin rise first. Low sensitivity until ≥4 – 6 hrs after sx onset. Enzymes may not rise for 12 hrs.

JACC 2000;3:959-69; EurHeartJ 2007;28:2525-38; Circulation 2004;110:e82-292; JACC 2007;50:e1-157

3/26/2013

18

Timing and Cardiac Enzymes

1st 6 hrs: CK-MB most sensitive CK-MB = myoglobin for specificity

Onset Peak Duration Myoglobin 1 – 4 hr 6 – 7 hr 24 hrCK-MB 3 – 12 hr 18 – 24 hr 36 – 48 hrTroponins 3 – 12 hr 18 – 24 hr 7 – 10 days

http://www.uptodate.com/contents/troponins-and-creatine-kinase-as-biomarkers-of-cardiac-injury?source=see_link

Other Cardiac Biomarkers

Myoglobin Earliest marker of MI. Sensitive but not specific. False positives due to skeletal muscle injury.

CK-MB Remains elevated for 36-48 hours following MI. Early peak (12-18 hours) suggests reperfusion.

CK-MB and myoglobin rise and fall more rapidly than troponin better for diagnosing reinfarction (Troponin still ↑).

Nonischemic Causes of Elevated Cardiac Enzymes

CHF Myocarditis Cardiac ischemia/injury without infarction Rapid atrial fib PE Proximal aortic dissection Chronic (or acute) renal insufficiency

Look for rise & fall – not just elevation.

Heart 2006;92:987–993; EurHtJ 2007;28:1598-1660

Steps in ACS Management

1-2-3 A-B-C.

3/26/2013

19

Steps in ACS Management

1. Emergency management.a) Monitor.b) MONA.

2. EKG.a) STEMI reperfuse.b) NSTEMI generally do not reperfuse.

3. ABC meds.

Acute Coronary Syndrome: Step 1

ABC’s (Airway, Breathing, Circulation) –now CAB in latest CPR ECGMonitor IV, labsMONA

Morphine Oxygen (Keep SpO2 ≥90%) NTG ASA

Step 1a: Initial Meds

Immediate ASA 162 – 325 mg chewed. CURRENT-OASIS 7 Trial:

– No difference in outcomes or bleeding using low dose (75-100 mg) or higher dose (300-325)

– There may be a change in the air…

Need rapid absorption—do NOT use EC. Do not use if anaphylactic reaction.

Chest 2008; 133:670S; NEJM 2010;363:930-43; www.acc.org/qualityandscience/clinical/statements.htm; J Am Coll Cardiol. 2008, 51: 210-2147

Initial Meds—Not ASA

Sublingual NTG 0.4 mg q 5 min X3Morphine 2 – 4 mg IV. Repeat prn.

Relieves pain, anxiety. Reduces sympathetic stimulation caused by

pain, anxiety

Chest 2008; 133:670S; www.acc.org/qualityandscience/clinical/statements.htm; J Am Coll Cardiol. 2008, 51: 210-2147

3/26/2013

20

Nitrate Precautions in ACS

Contraindicated if PDE-5 inhibitors within 24 hrs (hypotension): Sildenafil (Viagra™ and Revatio™) Vardenafil (Levitra™) Tadalafil (Cialis™, Adcirca™) – may need to wait

48 hrs. Extreme caution if inferior MI & possible R

ventricular involvement RVMI dependent on preload to maintain

cardiac output (RV not working well).– Give FLUIDS – ↑ neck veins are NOT due to fluid

overload in this situation!

http://www.uptodate.com/contents/nitrates-in-the-management-of-acute-coronary-syndrome?source=search_result&search=nitrates+and+tadalafil&selectedTitle=2~150

Step 2: Look at the ECG

ST elevation ST-elevation MI (STEMI) Prinzmetal’s angina (transient ST ↑)No ST elevation

ST depression – angina or NSTEMI T wave inversions – NSTEMI or increased risk

for acute MI – includes Wellens’ syndrome In setting of high suspicion of ACS, new

LBBB should be considered STEMI.

Step 3: ABC’s of MI Drugs

ASA B-blockersClopidogrel (esp if reperfusion)

© David M. Schneider

More Meds in STEMI

ß-blockers if not contraindicated. IV NTG if persistent pain, CHF, HTN

D/C NTG if BP too low—more important to give ß-blockers.

Replete K if below 4 (2X ↑ in VF if < 3.6).

www.acc.org/qualityandscience/clinical/statements.htm; JACC 2007;50(7):652-726

3/26/2013

21

ß-blocker Contraindications Active bronchospasm Severe bradycardia Heart block > 1°(if no pacemaker) Pulmonary edema Hypotension with or without shock Overt heart failure should be brought under

medical control 1st

Most pts w/MI d/t cocaine should not be treated with beta blockers (risk of coronary artery spasm, or severe HTN—Rx w/NTG/ASA and CCB; also BZD).

http://www.uptodate.com/contents/evaluation-and-management-of-the-cardiovascular-complications-of-cocaine-abuse?source=search_result&search=mi+in+cocaine&selectedTitle=1~150; http://www.uptodate.com/contents/beta-blockers-in-the-

management-of-acute-coronary-syndrome?source=search_result&search=beta+blocker+contraindications&selectedTitle=4~150

How & When to Give β-Blockers

Early β-blockade is preferred. IV β-blockers are recommended only for MI

pts w/o contraindications and with HTN @ presentation.

Otherwise, oral β-blockers within 24 hrs of presentation.

Pt w/early contraindications to β-blockers should be reassessed after 24 hrs for β-blocker appropriateness.

JACC 2007;50(7):652-726; Lancet 2005;366:1622-32

Meds in STEMI Already received ASA.Clopidogrel (added to ASA):

Benefits (↓ death, MI) in pts undergoing thrombolysis (no controlled studies of clopidogrel in PCI).

High dose clopidogrel (may overcome drug resistance)– 300 mg load if TL or no reperfusion → 75 mg/day– 300 – 600 load if PCI, then 150 mg daily X 6 more

days, then 75 mg daily.

Lancet 2010;376:1233-43; http://www.uptodate.com/contents/antiplatelet-agents-in-acute-st-elevation-myocardial-infarction; Lancet 2001;358:527-33; JAMA 2002;288:2411-20; NEJM 2010;362:1374-82; PRODIGY trial early

results http://www.theheart.org/article/1272023.do; JAMA 2007;297:159-68; JACC 2009;53:1399-1409; Circulation 2007;116:745-54; Circulation 2009;119:987-95; EurHtJ 2009;30:2714-21

Algorithmic Approach to STEMI

3/26/2013

22

STEMI Algorithm – 2

AFP 2009;79:1080-6

Management of STEMI

Job #1: Reperfusion If <12 hrs since onset of sx, PCI or

thrombolysis is indicated. PCI is preferred if it can be accomplished

within 90 minutes. If PCI not available or not within 90 min,

thrombolysis is an acceptable alternative.Do not wait for cardiac biomarkers. Just

do it!

http://www.uptodate.com/contents/overview-of-the-acute-management-of-st-elevation-myocardial-infarction?source=search_result&search=stemi&selectedTitle=1~150

ACS Therapy: PCI with Stent

Bare metal Bare metal = foreign body ↑ risk of in-stent

thrombosis – clopidogrel + ASA ↓ risk. 1 month post-stent if no MI, or 12 months if post-

MI. Epithelialization may progress to in-stent stenosis.

Drug-eluting Delay epithelialization, maintaining bare metal

longer; continue clopidogrel + ASA for 12 months.– Sirolimus (Cypher), Tacrolimus (Mahoroba), Paclitaxel

(Taxus).

http://content.onlinejacc.org/article.aspx?articleid=1147815; http://www.uptodate.com/contents/antiplatelet-therapy-after-coronary-artery-stenting?source=search_result&search=stent+in+mi&selectedTitle=1~150

ACS Therapy: Emergency CABG

Indications for early CABG > PCI: PCI failure or can’t be performed. Anatomy unsuitable for PCI (prior PCI, CABG). Persistent ischemia &/or hemodynamic

instability refractory to nonsurgical therapy. Surgery to be done for mechanical complication

of MI (rupture, mitral regurg, etc). Cardiogenic shock. Life-threatening ventric arrhythmias in presence

of L main stenosis ≥50% &/or 3-vessel CAD.

Circ 2011;124:2610-42

3/26/2013

23

Absolute Contraindications to Thrombolysis

H/O any intracranial hemorrhageH/O ischemic stroke w/in 3 months* Cerebral vascular malformation or 1°or

metastatic intracranial malignancy Sx/signs suggestive of aortic dissection Bleeding diathesis or active bleeding

(except menses**) Significant closed-head or facial trauma

w/in 3 monthshttp://www.uptodate.com/contents/fibrinolytic-therapy-in-acute-st-elevation-myocardial-infarction-

initiation-of-therapy?source=see_link&anchor=H69239847#H1

Relative Contraindications to TL

H/O chronic, severe, poorly controlled HTN, or uncontrolled HTN @ presentation (>180/110)H/O ischemic stroke >3 months previously Dementia Other intracranial disease Traumatic or prolonged (>10 min) CPR Major surgery w/in 3 weeks

Relative Contraindications – 2

Internal bleeding w/in 2-4 weeks or active peptic ulcer Noncompressible vascular punctures Pregnancy Current warfarin therapy (risk of bleeding

incr w/INR) For streptokinase or anistreplase - prior

exposure (more than five days previously) or allergic reaction to these drugs

Thrombolysis Summary

Contraindications: Bleed in brain or high risk of brain bleed. Meds or conditions that ↑ bleeding risk

anywhere.Use thrombolysis only if you have a

hospital or other institutional protocol or worksheet. Too hard to remember all contraindications &

requirements.

3/26/2013

24

Heparinoids in STEMI

Heparin (per ACC/AHA, evidence weak). PTT goal = 50 – 70 sec If pt will have a procedure (e.g., CABG)

which might require reversing the anticoagulant, use unfractionated heparin, as it is completely reversible w/protamine. If reperfusion, continue anticoagulation for at

least 48 hours.

http://www.uptodate.com/contents/antiplatelet-agents-in-acute-st-elevation-myocardial-infarction?source=search_result&search=gp+2b+3a+inhibitors+in+mi&selectedTitle=4~150

GP 2b/3a Inhibitors

GP IIb/IIIa inhibitors prior to PCI – only if heparin used. May add little to dual anti-plt therapy. Evidence changing rapidly. Consult cardiologist.

Thrombolysis—no evidence to support use. STEMI w/o reperfusion—no benefit. Higher bleeding risk w/renal insufficiency. Higher bleeding risk in women & elderly.

JAMA 2005;293(14):1759-65; Lancet 2001;357(9272):1905-14; JAMA 2002;288(17):2130-5; Lancet 2001;358(9282):605-13; AmHeartJ 2004;147(6):993-8; JACC 2003;42(8):1348-56

“PATCH” The Ailing Heart PCI (or thrombolysis w/protocol) ASA Thrombsis inhibitor (GPIIb/IIIa)?ClopidogrelHeparin(oids)

http://newopticalillusions.blogspot.com/2009/02/valentines-day-puppy-heart-illusion.html

More Meds in STEMI

Prior to D/C: ACEI, esp if abnormal LVEF or uncontrolled

risk factors.– ARB may be used if ACEI contraindicated or not

tolerated. Statin—high dose (atorvastatin 80 mg).

– ARMYDA-ACS (industry-sponsored) early atorvastatin (12 hr before PCI) improved 30-day outcomes.

– Caution: high-dose statins associated w/new DM—but benefit > risk.

JACC 2007;49(12):1272-8; JAMA 2011;305:2556-2564; JAMA 2001;285:1711-8

3/26/2013

25

Testing After STEMI

LVEF: ↓ EF → ↑ mortality. Echo—wait for recovery after reperfusion

(stunned myocardium) 14 days. Stress test (guide CV rehab, eval for

residual ischemia): If revascularization: few wks after D/C. No revascularization: pre-D/C, if no recurrent

angina or CHF. If reperfusion, wait.

Post-MI Survival

• ACE-inhibitors, ß-blockers, statins and ASA improve survival post MI.

• Nitrates, clopidogrel, calcium-channel blockers and digoxin may improve symptoms, but do not affect survival.

Non-ST Elevation ACS

ACS without ST elevation – unstable angina or NSTEMI UA: little/no rise in cardiac enzymes NSTEMI: enzymes rise—wait 4 – 12 hrsRisk stratification: TIMI risk score

High risk: may benefit from early PCI Thrombolysis is NOT useful in NSTEMI, and

may be harmful.

2007 Guideline—Summary of Who Benefits From Early Invasive Strategy Hemodynamic instability or cardiogenic

shock Severe LV dysfunction or heart failure Recurrent or persistent rest angina despite

intensive medical therapy New or worsening mitral regurgitation or

new ventricular septal defect Sustained ventricular arrhythmias Recent PCI (6 mo) Prior CABGEurHeartJ 2007;28:2525; Circ 1994;89(4):1545-56; JACC 1995;26(7):1643-50; JACC 2007;50:e1-157;

http://www.uptodate.com/contents/overview-of-the-acute-management-of-unstable-angina-and-non-st-elevation-myocardial-infarction?source=search_result&search=mana

3/26/2013

26

NSTEMI Management

Similar to STEMI except usually no reperfusion If reperfusion PCI, but not thrombolysis. ABC’s (stabilize) ASA ß-blockerOxygenMorphineNTG

NSTEMI Management: Differences vs STEMI

Enoxaparin instead of heparin (if no renal failure, and no CABG within 24 hr)

No reperfusion ⇒ pre-D/C stress test (as in STEMI)

Measure LVEF – echo (same) Statin (same) ?ACEI if EF <40%, DM, HTN (same, less

evidence) GP2b/3a inhib depends on troponin,

anticoagulant, other emerging factors.

http://www.uptodate.com/contents/antiplatelet-agents-in-acute-non-st-elevation-acute-coronary-syndromes?source=see_link

Summary of ACS Management

Everybody (unless contra) gets: ASA β-blocker Clopidogrel Morphine O2

NTG Statin Stress test:

– Pre-D/C if no reperf– Few weeks later if PCI

Low EF: ACEI Heparinoid:

Poss CABG: UFH STEMI + PCI: UFH STEMI + TL: enoxaparin STEMI w/o reperf: UFH

or enoxaparin NSTEMI:

– Invasive: UFH, bivalirudin– Non-invasive:

enoxaparin, fondiparinux

Congestive Heart Failure

http://www.publicdomainpictures.net/view-image.php?image=9967&picture=old-water-pump

3/26/2013

27

(Congestive) Heart Failure

Heart is unable to deliver blood at a rate sufficient to meet the body’s metabolic needs. >5 million Americans w/CHF.Nearly 1 million hospitalizations per year in

US.Readmission rate within 6 months is up to

50%.

http://uptodateonline.com/online/content/topic.do?topicKey=hrt_fail/18548#7

Mortality in CHF

Depends on: Age NYHA class Gender (women have better prognosis)

Diastolic HF has better prognosis Systolic HF: 15 – 19%/yr mortality Diastolic HF: 8 – 9%/yr Matched controls: 1 – 4%/yr

Causes of Death in CHF

Progressive pump failure

Arrhythmias/SCD

Risk Factors for CHF

Myocardial ischemia: #1 cause of systolic HF. Severe CAD. h/o MI. Evidence of hibernating myocardium. HTN (#1 cause of diastolic HF). LVH. African-Americans, Latinos, Native Americans

(probably related to HTN).

3/26/2013

28

Types of CHF

Systolic: ventricles don’t pump well Poor contractility (can’t pump) Low LVEF

Diastolic: ventricles don’t fill well Noncompliant (stiff) heart can’t relax Hypercontractility Nl – high LVEF

~ ½ = systolic, ~ ½ = diastolic (~50-50)

Types of Heart Failure

Harvard HealthSep 2008, http://www.health.harvard.edu/newsletters/Harvard_Womens_Health_Watch/2008/September/Heart_failure_in_women

Causes of Systolic CHF

Ischemic myocardial disease, CAD (angina) Alcoholic cardiomyopathy Diabetic cardiomyopathy Cocaine cardiomyopathy Drug-induced cardiomyopathy (eg, doxorubicin) Idiopathic cardiomyopathy Peripartum cardiomyopathy Myocarditis (antecedent viral illness) Preterminal valvular heart disease (murmur) Congenital heart disease with severe pulmonary

hypertension Meds (verapamil, ß-blockers, NSAID’s)

Causes of Diastolic CHF

Hypertension Severe aortic stenosis

Hypertrophic cardiomyopathy Restrictive cardiomyopathy

Ischemic myocardial disease, coronary artery disease

3/26/2013

29

http://www.uptodate.com/contents/evaluation-of-the-patient-with-suspected-heart-failure?source=search_result&selectedTitle=4~150#9

CHF Symptoms

History alone is sufficient to make dx. Fluid accumulation

SOB (exertional [DOE] usually occurs early) Edema RUQ discomfort (liver), ascites (esp w/R HF)Reduced cardiac output (nonspecific)

Fatigue Generalized weakness/malaise Anorexia

Severity of CHF

NYHA Class I - symptoms of HF only at activity

levels that would limit normal individuals Class II - symptoms of HF with ordinary

exertion Class III - symptoms of HF with less than

ordinary exertion Class IV - symptoms of HF at rest Therapeutic decisions still based on this

system

ACC/AHA Staging System

Stage A — High risk for HF, without structural heart disease or symptoms Stage B — Heart disease with

asymptomatic left ventricular dysfunction Stage C — Prior or current symptoms of

HF Stage D — Refractory end stage HF

Not as helpful in therapeutic decisions.

Diagnostic Modalities in CHF

CXR: cephalization of flow, cardiomegaly, Kerley (not curly) B lines, pulmonary edema, pleural effusion ECG: arrhythmia, AV block, evidence of

ischemic heart dz, LVH

3/26/2013

30

Circ 2009;119:1977-2016 ; J ACC 2007;50:187-204; http://www.uptodate.com/contents/evaluation-of-the-patient-with-suspected-heart-failure?source=search_result&selectedTitle=4~150#19

Echocardiography in CHF

Recommended for all new CHF pts (ACC/AHA) LVEF < 55% ⇒ systolic failure Diastolic dysfunction, abnormal filling, LVEF

>75% suggest diastolic failure.

Laboratory W/U of CHF

CBC (anemia exacerbates CHF) Lytes, BUN, Cr (follow diuretics, ACEI/ARB) LFT’s (hepatic congestion) Fasting glc or HbA1C (DM) Lipid profileUA If dilated cardiomyopathy of ? cause:

TSH (hyperthyroidism) (ACC says for all) Fe studies (% sat) – hemochromatosis

Circ 2009;119:1977-2016; http://www.uptodate.com/contents/evaluation-of-the-patient-with-suspected-heart-failure?source=search_result&selectedTitle=4~150#19

B-Natriuretic Peptide in CHF

BNP & nT-proBNP rise with worsening CHF. BNP or nT-proBNP added to clinical judgment

is better than either alone. Normal levels are sensitive for ruling out CHF

in pts with dyspnea. nT-proBNP < 300 ⇒ 98% negative predictive

value. BNP < 100 ⇒ 90% NPV; <50 ⇒ 97%.

↑ level ⇒ ↑ mortality in hospitalized pts & post-hospitalization (nTproBNP better).

3/26/2013

31

Limitations of BNP Measurement

Atrial fib raises BNP ⇒ reduced specificity in AF (must use higher cutoff).

Both are higher CKD, PE, lung disease(RHF), acute noncardiac illness (sepsis).

Both are lower in obese pts.

Treatment of CHF

Chronic systolic HF: Correct underlying causes (HTN, CAD,

valvular dz) Treat contributing/complicating conditions

(hypothyroid, DM) Reduce sodium intake D/C ETOH Healthy weight Exercise training reduces sx & hospitalization,

increases survival & QOL!

CircHeartFail 2010;3:659-67; JACC 2011;58:1780-91; JAMA 2009;301:1439-50; CochraneDatabase2010 Apr 14;(4):CD003331; EurJHeartFail 2010;12:706-15

Systolic Heart Failure Treatment

Low CO neurohumoral activation premature apoptosis of myocytes.

Preload reduction– Diuretics, nitrates

Afterload reduction– ACEI, ARB, hydralazine, nitrates

Sympathetic blockade– ß-blockers

Aldosterone-antagonist therapy– Spironolactone, eplerenone (Inspra)

http://www.uptodate.com/contents/pathophysiology-of-heart-failure-neurohumoral-adaptations?source=search_result&search=chf+neurohormonal+activation&selectedTitle=1~150

Pharmacotherapy of Systolic HF

Loop diuretics—sx relief only, no survival benefit.

ACEI in all pts (ARB if ACEI-intolerant). Improved survival (asymptomatic – severe). Check K & Cr 1-2 wk after dosage changes.

ß-blockers once stable on ACEI.Digoxin if continued sx, or for rate control

in A fib.

3/26/2013

32

Circ 2009;119:e391-e479; AnnIM 2001;134:550-60; J ACC1999;33:916-23; BMJ 1999;318:824-5

ß-Blockers in Systolic HF

Carvedilol, metoprolol XL, bisoprolol. Avoid agents with ISA (pindolol, acebutolol).Use in all systolic HF pts unless contraindic.Reduce all-cause mortality, hospitalization.

Best evidence in NYHA class II & III HF, probably class IV.

There is no absolute threshold ejection fraction. Sx may worsen for 4 – 10 weeks prior to

improving.

ß-blockers and Heart Failure

Contraindications to ß-blocker use include: Hemodynamic instability Heart block Bradycardia (>1°+ no pacemaker) Severe asthma (bronchospasm) ß-blockers may be initiated in pts w/mild

asthma or COPD—monitor. ß-blockers should be started when patient

is stable and euvolemic.

JACC 2004;43:1534-41

NEJM1997;336:525-33; JAMA 2003;289:871-8; J ACC 2005;46:497-504; Circ 2009;119:e391-e479

Role of Digoxin in CHF in 21st

Century LVEF <40%

Esp NYHA II – IV with persistent sx despite optimal therapy.

Maintain serum concentration 0.5 – 0.8. Serum concentration ≥ 1.2 is associated with

greater mortality, esp in women.May also be used in AFib pts for rate control.No survival benefitNo role in diastolic HF—no benefit (EF OK).

Aldosterone Antagonists

Spironolactone (cheap, old standby), eplerenone (Inspra™, fewer side effects but much more costly). Survival benefit in moderate-severe

systolic HF.Closely monitor Cr, calculated GFR, K.

Beware hyperkalemia – ACEI also raises K.

3/26/2013

33

Drugs w/Survival Benefit in CHF

ACEI generally use one ARB or the other Aldosterone antagonists β-blocker

A’s & B’s (Good grades help you live longer)

http://www.uptodate.com/contents/overview-of-the-therapy-of-heart-failure-due-to-systolic-dysfunction?source=see_link

African-Americans & Systolic HF

ACEI’s may be less effective in prolonging survival. ß-blockers may have reduced survival

benefit.May derive greater benefit than

Caucasians from hydralazine + nitrates, esp NYHA III - IV. May be reasonable in any pt who does not

respond to regimen—can be added.

http://circ.ahajournals.org/cgi/reprint/CIRCULATIONAHA.109.192064--2009

Ω-3 Fatty Acids

Ω-3 polyunsaturated fatty acids (PUFA’s) reduce all-cause mortality and combined endpoint of mortality + CV-related hospitalization.

Lancet 2008;372:1223-30

Drugs to Avoid or Use With Caution in CHF

NSAID’s

Thiazolidinediones (“glitazones”)

MetforminCilostazal (Pletal™) – for claudication: ↑

mortality in CHF pts. PDE-5 inhibitors (sildenafil, vardenafil,

tadalafil).

3/26/2013

34

Circ 2009;119:e391-e479; http://www.uptodate.com/contents/treatment-and-prognosis-of-diastolic-heart-failure#4

Treatment of Diastolic HF

Less evidence. ACC/AHA recommends only 4 modalities:

Control of systolic and diastolic HTN. Control of ventricular rate in pts w/atrial fib. Control of pulmonary congestion and

peripheral edema with diuretics. Coronary revascularization in pts with CAD in

whom ischemia is judged to impair diastolic function.

Preload & Diastolic HF Poorly compliant, hypercontractile LV is

very sensitive to preload reduction. Worsening cardiac output. Hypotension.Caution with:

Diuretics. ACEI (no survival benefit in these pts; may ↓

myocardial fibrosis, ↑ diastolic function). Nitrates (ß-blocker or CCB preferred in CAD). Sx of ventricular underfilling: weakness,

dizziness, near syncope, syncope.http://www.uptodate.com/contents/treatment-and-prognosis-of-diastolic-heart-failure#H1

Treatment of Acutely Decompensated CHF

Consider hospitalization—esp if sick.

2 g Na restriction.

Fluid restriction. 2L/day if Na < 130. Stricter if Na < 125 or worsening.

Oxygen

Circ 2009;119:e391-e479http://www.uptodate.com/contents/treatment-of-acute-decompensated-heart-failure-general-considerations?source=search_result&selectedTitle=4~150#1; J Card Fail 2010;16:e1-194

Pharmacotherapy of Acute Decompensated HF

Basically, systolic = diastolic. IV loop diuretics (expect & tolerate mild ↑Cr).Consider IV morphine, esp w/acute MI.Consider vasodilators:

For rapid sx improvement in admitted pts on diuretics—if no hypotension.

Rapid sx relief in pulm edema or severe HTN. Persistent severe HF despite aggressive tx.

3/26/2013

35

Vasodilators in CHF

IV NTG Hypotension HA IV nitroprusside

Cyanide accumulation Limit to 48 hrs ?IV nesiritide—↑ mortality Ensure adequate intravascular volume

J Card Fail 2010;16:e1-194

Continuation of Chronic HF Meds

ACEI/ARB: continue med during decompensation. Reduce in hypotension, hyperkalemia, ARF. ß-blockers:

Mild decomp: continue med (↑ mortality if not). Moderate-severe decomp: reduce or hold med

initially. If not on, start prior to D/C, but not in earliest

phase.

Circ 2009;119:e391-e479; AmJCardio 1997;79:794-8; JACC 2004;43:1534-41; AmHtJ 2007;153:82.e1-11

Differences in Management of Decompensated HF

Systolic: Reduce or hold ACEI, ß-blocker (usual

chronic systolic meds!!) if mod-severe decomp.

Diastolic: Control BP & tachycardia, so ACEI & ß-

blocker may be useful acutely. Do not use inotropes.

http://www.uptodate.com/contents/secondary-and-primary-prevention-of-sudden-cardiac-death-in-heart-failure-and-cardiomyopathy?source=see_link&anchor=H13#H1

So Who Gets an ICD in Chronic CHF?

Arrhythmia or severe. Survivors of SCD Symptomatic VTach Ischemic CM + LVEF ≤30% Nonischemic CM:

– NYHA II – III + LVEF ≤35%– NYHA III – IV + LVEF ≤35% + wide QRS (>120) –

use combo ICD + biventricular pacer

3/26/2013

36

Asymptomatic LV Dysfunction

Treatment with ACEI (enalapril) in pts w/LVEF ≤40% delays onset of overt CHF and prolongs life. Low EF defines LV dysfunction. However, CHF requires signs/symptoms. Therefore, this is not treatment of CHF.

Dysrhythmias

http://www.publicdomainpictures.net/view-image.php?image=13494&picture=drummer

Mobitz Type I Second-Degree AV Block (Wenckebach)

PRogressive PRolongation of PR interval until a P wave fails to conduct and a beat is “dropped.” AV node dz; can occur in athletes.If acute, likely d/t inferior ischemia (RCAAV node).No treatment, but consider underlying cause.

Mobitz Type IISecond-Degree AV Block

•Intermittently nonconducted P waves not preceded by PR prolongation and not followed by PR shortening.•Disease of the distal conduction system, below AV node: His-Purkinje system Usu wide QRS.•May progress to third-degree heart block, with no emerging escape rhythm.•Treatment: permanent pacemaker.

3/26/2013

37

Third-Degree AV BlockComplete Heart Block

•Regular rhythm with complete AV dissociation. Impulses generated by the SA node do not propagate to the ventricles. Two independent rhythms can be noted on the ECG.•Escape rhythm originates in the ventricles, wide-complex.•Treatment: permanent pacemaker.

Atrial Flutter

•Regular or regularly irregular narrow-complexrhythm that is typically rapid.•Vagal maneuver (arrow) slows AV conduction and makes the flutter waves more apparent (arrowheads).•Atrial rate is ~300. Conduction is expressed as atrial beats:ventricular beats (e.g., 3:1, 2:1).

Multifocal Atrial Tachycardia

• Irregular, narrow-complex rhythm with 3 or more P waves of variable morphology.

• Most common in patients with lung disease; can occur post-MI or with hypokalemia or hypomagnesemia.

• Rate may be reduced by using IV verapamil.• Differences from wandering atrial pacemaker (WAP):

significantly increased rate and almost invariable association of MAT with severe pulmonary disease.

Irregularly Irregular Rhythms

Look for P waves: P’s all same sinus arrhythmia

Different P’s WAP (MAT if fast)

No P Atrial fib

http://ekginterpretation.tripod.com/sinusMechanisms.html

3/26/2013

38

Atrial Fibrillation

• Irregularly irregular, narrow-complex rhythm that may be rapid. The atrial rate is >300 bpm.

• No discrete P waves or atrial flutter waves are noted.

Causes of Atrial Fibrillation

Pulmonary—COPD, PE IatrogenicRheumatic heart dz—MRAtherosclerosis—CAD, MI Thyroid—hyper Endocarditis Sinus node dz

+ETOH, HTN

Atrial Fibrillation Therapy

Steps in treatment:• Control rate• Select anticoagulation (ASA or warfarin)• Consider conversion to sinus rhythm

Medical/electrical

• If the ventricular rate exceeds 200 bpm, suspect a pre-excitation bypass tract—WPW.

NEJM 2010;362:1363-73

Rate Control in Atrial Fibrillation

• Lenient rate control (resting HR <110) ≅ strict rate control (<80 resting, <110 exercise).

• β-blockers: most effective HR control in AF, both at rest and during exercise.

• CCBs, esp diltiazem, ↓ rate (rest & exercise), but overall not as effective as β-blockers.

• Digoxin controls rate at rest; may not control rate with exercise – but no hypotension.

NEJM2002;347:1825-33; NEJM2010;362:1363-73; BrHtJ 1990;63:225-7

3/26/2013

39

Candidates for Rhythm Control in AF

Failure of rate control (incl persistent sx). Younger pts (esp who need high cardiac

performance). Early in natural hx of AF.

A Fib begets A Fib – longer you have it, longer you keep it.

More likely to stay in sinus rhythm:– No CHF or LV dysfunction.– No reversible underlying d/o (hyperthyroid, PE, etc).– LA <4.5 cm.

AnnIM 2003;139:1009-17; Europace 2008;10:21-7; http://www.uptodate.com/contents/rhythm-control-versus-rate-control-in-atrial-fibrillation?source=search_result&search=atrial+fibrillation+rhythm+control&selectedTitle=2~150

Atrial Fibrillation: CHADS2Congestive heart failure = 1 pointHypertension = 1 pointAge > 75 = 1 pointDiabetes = 1 pointPrior Stroke or TIA = 2 points

Score: 0 Low risk; ASA therapy 1 Moderate risk; ASA or warfarin therapy > 2 Moderate-high risk; warfarin therapy