Troponin-T: 0-0.2ng/ml binds to Tropomyosin onset in _3-4 hours_ \ \ \ USED MOST OFTEN\ \ return to normal after 10-14 days Troponin-I: 0-0.1ng/mL Inhibits actomyosin ATPase levels return to normal after 4-7 days Troponin-C binds to calcium to initiate contraction can't differentiate between cardiac and smooth muscle troponin-C

Type I: caused by atherothrombotic coronary artery Type II: mismatch of O2 supply/demand Type III: MI with unexpected death before drawing biomarkers Type IV: 4a: associated with PCI complications from procedure 4b: PCI related due to stent/scaffold thrombosis Type V: MI associated with CABG

CAD & ACS Flashcards by Gillian Collom

Define Ischemic Heart Disease

narrowing of 1 or more of the coronary arteries

-this impedes coronary blood flow → deprives the tissues of oxygen supply → increases the oxygen demand

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what is the leading cause of death for both men & women in the US?

Heart Disease

Middle aged men > women

post-menopausal women → increased incidence 2-3x

50% manifest as chronic stable angina

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What is under the umbrella of Ischemic Heart Disease

IHD:
- Chronic Stable Angina
- Acute Coronary Syndromes (ACS)
  - Unstable angina
  - Non-STEMI
  - STEMI

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Cardiac Conditions that are associated with Angina

Most common = atherosclerotic plaques
Vasospasm
- less common → no atherosclerotic disease = Prinzmetal’s angina (beta-blockers worsen this)
Aortic Dissection
Aortic Stenosis
Pericarditis
Severe Uncontrolled HTN

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Non-Cardiac Conditions Associated with Angina

anxiety
anemia
carbon monoxide poisoning
PUD, GERD
PE, pneumothorax, pulmonary HTN, thryotoxicosis

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Symptoms of Chronic Stable Angina

predictable
associated with exercise or emotional stress
last a short amount of time (≤ 5 min)
disappears with rest or use of nitro

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Symptoms of Unstable Angina

occurs even at rest
change in usual pattern of angina
unexpected
more severe and lasts longer than stable angina (~30min)
may not disappear with rest or use of angina medication
might signal a heart attack
no biomarkers (i.e. troponin is not elevated)
Abnormal EKG but no ST elevation

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Types of Troponin

Troponin-T: 0-0.2ng/ml
- binds to Tropomyosin
- onset in 3-4 hours ***USED MOST OFTEN**
- return to normal after 10-14 days
Troponin-I: 0-0.1ng/mL
- Inhibits actomyosin ATPase
- levels return to normal after 4-7 days
Troponin-C
- binds to calcium to initiate contraction
- can’t differentiate between cardiac and smooth muscle troponin-C

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Types of STEMIs

Type I:
- caused by atherothrombotic coronary artery
Type II:
- mismatch of O2 supply/demand
Type III:
- MI with unexpected death before drawing biomarkers
Type IV:
- 4a: associated with PCI complications from procedure
- 4b: PCI related due to stent/scaffold thrombosis
Type V:
- MI associated with CABG

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Primary Prevention vs Secondary Prevention

Primary Prevention:
- before the person has the disease
Secondary Prevention:
- managing the disease, preventing an event from happening AGAIN
BAAAS:
- Beta-blocker
- Anti-platelet therapy
- ACE-I or ARB
- Statin

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General Meds/Factors to prevent ACS and death

Control modifiable risks
- dyslipidemia
- HTN
- DM
antiplatelet agents
ace-i/ARBs
Statins

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Meds to Prevent Recurrent Ischemic Symptoms

Beta-blockers
CCB
-long-acting nitrates
Ranolazine

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Meds to Relieve acute symptoms

Short Acting Nitrates

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Antiplatelet Classes

ASA and P2Y12 inhibitors

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ASA

aspirin (NSAID)

inhibits cyclooxygenase (COX enzyme) → reduces thromboxane synthesis → inhibits the activation of platelets

Not for adults <50 or >70
81-162 mg Qday

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P2Y12 Inhibitors

inhibit platelet activation and aggregation!!

Clopidogrel
- prodrug (activated by 2C19) + irreversible inhibition
- DDI with PPI (espec omeprazole)
- Qday
Prasugrel
- highest Potency
- prodrug (unaffected by 2c19) + irreversible inhibition
- Qday
Ticagrelor
- not a prodrug
- REVERSIBLE inhibition
- dosing BID not Qday (so less popular)
SEs:
- cough, HTN, dizziness, HA, bleeding, edema, bradycardia, dyspnea

Nitrates MOA, DDI & SEs

MOA:
- nitrates → nitric oxide → activates guanylate cyclase in smooth muscle → increased cGMP → release of Ca2+ from muscle cells → smooth muscle relaxation
- primarily cause VENODILATION which reduces preload
  - but higher doses can cause arterial dilation which reduces afterload and BP
    - dilating the coronary arteries = increase oxygen supply
DDI: CONTRAINDICATED:
- PDE5 inhibitors → ***severe hypotension, syncope or MI****
  - sildenafil/tadalafil
- lidocaine → increased risk of methemoglobinemia
- dihydroergotamine (DHE = migraine med) → decrease nitrate efficacy, increase DHE level → vasoconstriction → angina
- EtoH → severe hypotension
SEs:
- Severe hypotension
- methemoglobinemia
  - (heme can no longer carry o2 because it has be oxidized by NO)
- HA
- dizziness
- Can develop tachyphylaxis so must allow up to 14 hours of nitro free intervals Qday

Short Acting and Long Acting Nitrates

Short-Acting Nitrates:
- Topical:
  - nitro-bid – 2% ointment
    - need 10-12h nitrate free interval Qday
  - nitro-dur – transdermal
- Sublingual spray:
  - nitrolingual → 1-2 sprays q5min PRN
  - Nitromist
- Sublingual Tab:
  - nitrostat = 0.4mg SL q5min prn
Long Acting:
- isosorbide mononitrate
  - dosing 1-2x/day
- isosorbide dinitrate
  - dosing 1-3x/day

Use of Beta-Blockers in CAD & ACS and what to avoid

Why:
- reduce the HR → decrease myocardial oxygen demand
- slow HR → prolong diastole → increased coronary blood flow
- stabilize the membrane to prevent arrhythmias
- decrease risk of reinfarction → improves survival
  - metoprolol, propranolol, carvedilol
Avoid:
- the ISA + Agents (carteolol, acebutolol) because they have intrinsic sympathomimetic activity → produces a lesser reduction of oxygen demand
- non-selective agents for asthmatic patients
- avoid beta-blockers in treating prinzmetal angina → can WORSEN SXS

CCB and preventing recurrent ischemic symptoms: MOA, Efficacy, & ContraIndications

MOA:
- decrease wall tension (afterload)
- decrease contractility → decreased myocardial demand for oxygen
- non-dihydropyridine slow SA & AV node conduction → further decreases the oxygen demand
  - more effect as antianginal than dihydropyridine
- dilate coronary arteries (all CCBs) → increase oxygen supply and relieve spasm
Efficacy:
- same as beta blockers
- good alternative if BB is contraindicated
- Dihydropyridines + CCB = relieve sx better than either one alone
  - CI: do not give non-dihydropyridine + BB → SEVERE bradycardia
Contraindication for IHD:
- pre-existing conduction disease without pacemaker (non-dihydropyridines)
- concurrent use with negative inotropic agent (beta blockers)
- short acting dihydropyridine (ie nifedipine, nicardipine)
  - high risk for hypotension

CCB and preventing recurrent ischemic symptoms: MOA, Efficacy, & ContraIndications

MOA:
- decrease wall tension (afterload)
- decrease contractility → decreased myocardial demand for oxygen
- non-dihydropyridine slow SA & AV node conduction → further decreases the oxygen demand
  - more effect as antianginal than dihydropyridine
- dilate coronary arteries (all CCBs) → increase oxygen supply and relieve spasm
Efficacy:
- same as beta blockers
- good alternative if BB is contraindicated
- Dihydropyridines + BB = relieve sx better than either one alone
  - CI: do not give non-dihydropyridine + BB → SEVERE bradycardia
Contraindication for IHD:
- pre-existing conduction disease without pacemaker (non-dihydropyridines)
- concurrent use with negative inotropic agent (beta blockers)
- short acting dihydropyridine (ie nifedipine, nicardipine)
  - high risk for hypotension

Non-dihydropyridines

Diltiazem & Verapamil

slow SA & AV node conduction → further decrease oxygen demand
best for antianginal use
- better than dihydropyridines
decrease contractility → decreased oxygen demand
dilate the coronary arteries
good alternative if beta blockers are contraindicated
contraindications:
- - beta blockers → risk of SEVERE bradycardia
- preexisting conduction disease without a pacemaker
- - short acting dihydropyridines (ie nifedipine, nicardipine)
    - high risk of Hypotension

Ranolazine (Ranexa)

Approved as first line for CHRONIC STABLE ANGINA but normally reserved for refractory angina

Minimal effects on HR & BP
MOA:
- inhibits sodium channel opening during phase 0 → prevents influx of sodium into the ICF
SEs:
- QT prolongation, syncope, bradycardia
- hypotension, tinnitus, blurred vision, vertigo
Contraindications:
- liver cirrhosis
- tx with CYP3A4 inhibitors (ketoconazole, clarithromycin, nelfinavir)
- tx with CYP 3a4 inducers

Summary for Stable IHD

Treatment Algorithm for Stable Angina

Tx of Prinzmetal Angina

**AVOID BETA-BLOCKERS** * For Sx relief: Nitroglycerin IR * if HTN = CCB effective as monotherapy +/- Long acting nitrates * if hypotension → LA nitrates

Unfractionated Heparin (UFH): MOA, indications, & contraindications

longer sugar chain so **inhibits Factor Xa + Thrombin (IIa)** * _Indications_: * STEMI: pts undergoing PCI and pts txed with fibrinolytics * NSTEMI: in combo with antiplatelet therapy for conservative or invasive approach PCI * _Contraindications_: * active bleeding, hx of heparin-induced thrombocytopenia, severe bleeding risk, recent stroke

Low-Molecular Weight Heparin: MOA, indications, contraindications

**Enoxa**_parin_**** Shorter sugar chain so only **inhibits factor Xa** NOT thrombin (IIa) * _indications_: * STEMI:in pts receiving fibrinolytics * NSTEMI: in combo with aspirin for conservative or invasive approach * _Contraindications_: * active bleeding * hx of heparin-induced thrombocytopenia, severe bleeding risk * recent stroke * if CrCl \< 15mL/min * avoid if CABG surgery planned

Bivalirudin (Angiomax)

**Direct thrombin inhibitor** → binds 2 of 3 sties on Thrombin used when pt has heparin-induced thrombocytopenia * _indications_: * NSTEMI: for invasive strategy * PCI in STEMI * _Contraindications_: * active bleeding, severe bleeding risk

Initial Tx in STEMI & NSTEMI

oxygen (if O2 sat \<90%), SL NTG, aspirin, morphine sulfate, IV NTG

After initial tx: STEMI ≤ 12 hours

* Reperfusion Therapy: * Option 1: * higher-dose statin before primary **PCI** * then clopidogrel, prasugrel or ticagrelor (P2Y12 inhibitors → inhibit activation and aggregation of platelets * then Bivalirudin (thrombin inhibitor) alone or UFH + GP IIb/IIIa receptor blocker * then Beta-blocker, ACE-i/ARB, eplerenone (spironolactone) * Option 2: * Fibrinolysis * clopidogrel, statin * then IV UFH or IV & SC enoxaparin * then Beta-blocker, ACE-i/ARB, eplerenone (spironolactone)

After initial Tx: STEMI ≥ 12 hours

Secondary PCI or CABG or fibrinolysis then BAAAS (beta-blocker, ACE-i/ARB, aspirin, eplerenone (spironolactone) * for secondary PCI during hospitalization, admin bivalirudin alone or UFH or enoxaparin with optional GP IIb/IIIa inhibitor at time of PCI

NSTEMI tx Chart = early conservative therapy or Early invasive strategy

Glycoprotein IIb/IIIa receptor inhibitors

MOA: prevent aggregation * abciximab * eptifibatide * tirofiban * _Contraindications_: * active bleeding, thrombocytopenia, prior stroke, renal dialysis (eptifibatide)

PCI

also called **percutaneous coronary intervention**, is a procedure that uses a catheter (thin, flexible tube) and small balloon threaded through a blood vessel in the groin or arm and guided to heart to open a blocked or narrowed coronary artery

CABG

Surgery in which a healthy blood vessel taken from another part of the body is used to make a new path for blood around a blocked artery leading to the heart. This restores the flow of oxygen and nutrients to the heart. Also called aortocoronary bypass and **coronary artery bypass grafting**