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Matters of the Heart: 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
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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
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
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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
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
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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
Cause of CP
History Exam Lab/X-Ray EKG
Dissecting Aneurysm
•Sudden onset, tearing pain•Chest, back
•↓ pulseUE/carotid (15%)•SBP L/R ∆ •AR mur (32%)
•90% abnl; 75% widened mediastinum
•NSSTT chg—30%•Ischemia 15%
Pulmonary Embolism
•SOB•Pleuritic/no CP•Unilat LE edema
•Tachypnea•Tachycardia
•Usu WNL•Hampton’s hump (infarct)
•Sinus Tach•RV strain•S1Q3T3 ~10%
Acute Coronary Syndrome
•Ischemic CP•SOB, palp, sweat, N/V (infer)
•Often WNL•Signs of HF, hemo instability
•Troponins ↑•CXR usu WNL, may show HF
•ST ↑, new Q, new LBBB, etc
Tension PTX
•Sudden onset SOB•Pleuritic CP
•↓ Breathsounds•Subcu emphy-sema (rare)
•PTX •WNL
Esophageal rupture
•May follow N/V, EGD•SOB
•Hamman’scrunch
•Mediastinal air, pleural effusion
•WNL
http://www.uptodate.com/contents/evaluation-of-chest-pain-in-the-emergency-department?detectedLanguage=en&source=search_result&search=diagnosis+of+chest+pain&selectedTitle=2~150&provider=noProvider#H1;
JAMA. 2000;283(7):897-903
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
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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—32% ↓) > risk of GI bleed. (Grade A)
Women 55 to 79 when potential benefit of ↓ in ischemic stroke > risk of GI bleed. (Grade A)
ACCP 2014: All healthy adults >50.– [FDA 2014: No ASA in 1°prevention—NOT on exam]
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;
Chest 2012;141(2_suppl):7S-47S; http://www.fda.gov/drugs/resourcesforyou/consumers/ucm390574.htm
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
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
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ASA in DiabetesRecommended for all diabetics
w/evidence of cardiovascular dz (2°prevention)Recommended for 1°prevention in all
diabetics w/↑ CV risk 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 2014;37(Suppl1):S5-13
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
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)
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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. ETT is useless (occurs @ rest).
– Dobutamine echo—sensitive, specific.
Transient ST elevation during episode. Arrhythmias—life-threatening complication. Treatment: CCB +/- nitrate.
Avoid ß-blockers, triptans.
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
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Pts in Whom Revascularization MAY Be Useful
Medical therapy does not provide sufficient relief of sx. 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
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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.
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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
Licensed for reuse, CC 3.0http://commons.wikimedia.org/wiki/File:Thumbs-up-icon.png by me user debivort 12.06; ECG Learning Center, authored by Frank G Yanowitz, MD, at http://ecg.utah.edu/lesson/10
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)
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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
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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, but add little to
dx of MI (except $). 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
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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.
**Steps in ACS Management**
1. Emergency management.a) Monitor.b) MONA.
2. EKG.a) STEMI reperfuse.b) NSTEMI generally do not reperfuse.
3. (ABC)2 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
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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
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.
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Step 3: ABC’s of MI Drugs
ASA + AnticoagulantB-BlockersClot inhibitor (non-ASA antithrombotic) +
Cholesterol (statin)
© David M. Schneider
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
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
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
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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
Antithrombotics in STEMI
In addition to ASA. Loading dose. If PCI:
Clopidogrel (Plavix) 600 mg. Prasugrel (Effient) 60 mg (NOT if H/O CVA or
TIA). Ticagrelor (Brilinta) 180 mg (preferred). If thrombolysis:
Clopidogrel 300 mg if age ≤ 75; 75 mg if > 75.
Circulation 2013;127:529-55
More Meds in STEMI
Prior to D/C: 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.
ACEI, esp if abnormal LVEF or uncontrolled risk factors.– ARB may be used if ACEI contraindicated or not
tolerated.
JACC 2007;49(12):1272-8; JAMA 2011;305:2556-2564; JAMA 2001;285:1711-8
Algorithmic Approach to STEMI
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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 p-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
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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.
“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
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.
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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 CABG
EurHeartJ 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
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
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**Summary of ACS Management**
Everybody (unless contra) gets: ASA β-blocker Clopidogrel/Ticagrelor Morphine O2
NTG Statin Stress test/echo:
– 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
And REPERFUSION!! (when appropriate
Congestive Heart Failure
http://www.publicdomainpictures.net/view-image.php?image=9967&picture=old-water-pump
(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
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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).
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
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New Terminology
Heart failure w/reduced ejection fraction (HFrEF) = systolic dysfunction (EF ≤40).Heart failure w/preserved ejection fraction
(HFpEF) = diastolic dysfunction (EF ≥50).HFpEF, borderline: EF 41-49.
JACC 2013;62(16):1495-539
Causes of Systolic CHF (HFrEF)
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 (HFpEF)
Hypertension Severe aortic stenosis
Hypertrophic cardiomyopathy Restrictive cardiomyopathy
Ischemic myocardial disease, coronary artery disease
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
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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.
JACC 2013;62(16):1495-539
Diagnostic Modalities in CHF
CXR: cephalization of flow, cardiomegaly, Kerley (not curly) B lines, pulmonary edema, pleural effusion—all HF pts should get CXR.
ECG: arrhythmia, AV block, evidence of ischemic heart dz, LVH—all HF pts should get ECG.
JACC 2013;62(16):1495-539
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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; JACC 2013;62(16):1495-539
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).
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.
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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.
JACC 2013;62(16):1495-539 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.
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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;43:1534-41JACC 2013;62(16):1495-539; NEJM1997;336:525-33; JAMA 2003;289:871-8; JACC 2005;46:497-504; Circ
2009;119:e391-e479
Role of Digoxin in CHF in 21st
Century LVEF <40% (HFrEF/systolic):
Persistent sx despite optimal therapy. ↓ hospitalization. Maintain serum concentration 0.5 – 0.8. Concentration ≥ 1.2 ↑ mortality (esp 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.
Drugs w/Survival Benefit in CHF
ACEI use one or the ARB other—NOT both 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
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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
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).
JACC 2013;62(16):1495-539
Treatment of Diastolic HF
Less evidence. ACC/AHA recommends only 4 modalities:
Control of systolic and diastolic HTN.–Β-blocker, ACEI, or ARB reasonable.
Control of pulmonary congestion and peripheral edema with diuretics.
Control of ventricular rate in pts w/atrial fib. 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
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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 VTE prophylaxis.Continue medical therapy & increase loop
diuretics.JACC 2013;62(16):1495-539; Circ 2009;119:e391-e479
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
JACC 2013;62(16):1495-539; http://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.
Vasodilators in CHF
IV NTG Hypotension HA IV nitroprusside
Cyanide accumulation Limit to 48 hrs ?IV nesiritide—may improve sx acutely, ↑
mortality w/prolonged use. Ensure adequate intravascular volume.
J Card Fail 2010;16:e1-194; JACC 2013;62(16):1495-539
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Device Therapy in HF
ICD: prevent death d/t arrhythmia.Cardiac resynchronization therapy (CRT):
Ventricular dyssynchrony = disrupted relationship between normal atrial contraction & normal ventricular contraction.
May occur w/severe HF with or w/o BBB. Return poorly functioning ventricles, w/ or w/o
block, to better function.
Device Therapy in HF
ICD SCD survivor (unless
definite transient cause, unlikely to recur).
Symptomatic VT. Post-MI:
≥40 days p-MI, expected to live ≥1 yr:
– EF ≤35%, NYHA 2-3.– EF ≤30%, NYHA 1.
CRT (pacemaker): EF ≤35%:
– QRS ≥150, NYHA 2-4.– QRS 120-149 + LBBB +
NYHA 2-4.– QRS 120-149 + non-
LBBB + NYHA 3-4.
A bunch of other maybe’s.
JACC 2013;62(16):1495-539
JACC 2013;62(16):1495-539
How the @#$! To Remember?
Arrhythmia or severe systolic failure. Survivors of SCD. Symptomatic VTach. Consider in all pts w/LVEF ≤35%.
– If post-MI, wait ≥40 days.
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.
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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.
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.
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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).•Management similar to Atrial fib.
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
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.
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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
Newer Anticoagulants
No lab monitoring.No antidotes/reversal agents. Limited studies. Insufficient time for post-marketing SE’s.No head-to-head studies among new
agents. Still many drug interactions – metabolized
by CYP 3A4 &/or P-gp (P-glycoprotein efflux transporters).
CochraneDatabaseSystRev 2013;8:CD008980; Lancet Online Epub doi:10.1016/S0140-6736(13)62343-0
Newer Anticoagulants
Compared to warfarin: = or lower ischemic stroke. = or lower major bleeding. More GI bleeding. Avoid:
GFR <30 (<25 apixaban). Prosthetic heart valve. Mitral stenosis, or other valve lesion that
might require replacement.
CochraneDatabaseSystRev 2013;8:CD008980; Lancet Online Epub doi:10.1016/S0140-6736(13)62343-0
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Newer Anticoagulants
Dabigatran (bid drug—NNT = 172): ↓ hemorrhagic stroke. ↑ MI by 27% (NS) — NNH 370. 41%↑ GI bleeding (NNH~30-45).Rivaroxaban (once daily—NNT = 200-333):
Noninferior. ↓ intracranial hemorrhage & fatal bleeding. Apixaban (bid—NNT = 333):
↓ all-cause mortality
CochraneDatabaseSystRev 2013;8:CD008980; Lancet Online Epub doi:10.1016/S0140-6736(13)62343-0; Circ 2012;125:669-76; ArchIM 2012;172:397-402; JAMA Int Med 150-151; NEJM 2011;365:883-91; NEJM 2011;365:981-92
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
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
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Extra Material
Licensed for reuse, CC3.0, http://en.wikipedia.org/wiki/File:Polydactyly_01_Lhand_AP.jpg, from en:User:Drgnu23 via en:user:Grendelkhan, en:user: Raul654, and en:user:Solipsist
CAD: Angina, Acute Coronary Syndrome
http://www.publicdomainpictures.net/view-image.php?image=757&picture=breaking-heart
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.
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.
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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.
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 is out. Earliest marker of MI. Sensitive but not specific. False positives due to skeletal muscle injury.
CK-MB adds little to dx or prognosis. Remains elevated for 36-48 hours following MI. Early peak (12-18 hours) suggests reperfusion.
Although CK-MB rises and falls more rapidly, troponin still preferred, incl dx of reinfarction.
GP 2b/3a Inhibitors
Falling out of favor. 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
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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
Congestive Heart Failure
http://www.publicdomainpictures.net/view-image.php?image=9967&picture=old-water-pump
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Ω-3 Fatty Acids
Ω-3 polyunsaturated fatty acids (PUFA’s) reduce all-cause mortality and combined endpoint of mortality + CV-related hospitalization.
Controversy.
Lancet 2008;372:1223-30
Differences in Management of Decompensated HF
Diastolic: May be less risk of ACEI & ß-blockers in short
term. Control BP & tachycardia, so ACEI & ß-
blocker may be useful acutely. Do not use inotropes.
