CAD & ACS Flashcards
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
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
What is under the umbrella of Ischemic Heart Disease
-
IHD:
- Chronic Stable Angina
- Acute Coronary Syndromes (ACS)
- Unstable angina
- Non-STEMI
- STEMI
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
Non-Cardiac Conditions Associated with Angina
- anxiety
- anemia
- carbon monoxide poisoning
- PUD, GERD
- PE, pneumothorax, pulmonary HTN, thryotoxicosis
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
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
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
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
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
General Meds/Factors to prevent ACS and death
- Control modifiable risks
- dyslipidemia
- HTN
- DM
- antiplatelet agents
- ace-i/ARBs
- Statins
Meds to Prevent Recurrent Ischemic Symptoms
- Beta-blockers
- CCB
- -long-acting nitrates
- Ranolazine
Meds to Relieve acute symptoms
Short Acting Nitrates
Antiplatelet Classes
ASA and P2Y12 inhibitors
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
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
- but higher doses can cause arterial dilation which reduces afterload and BP
-
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
-
PDE5 inhibitors → ***severe hypotension, syncope or MI****
-
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
- nitro-bid – 2% ointment
- Sublingual spray:
- nitrolingual → 1-2 sprays q5min PRN
- Nitromist
- Sublingual Tab:
- nitrostat = 0.4mg SL q5min prn
- Topical:
-
Long Acting:
-
isosorbide mononitrate
- dosing 1-2x/day
-
isosorbide dinitrate
- dosing 1-3x/day
-
isosorbide mononitrate
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
- short acting dihydropyridines (ie nifedipine, nicardipine)
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
Enoxaparin**
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)
- higher-dose statin before primary PCI
- Option 2:
- Fibrinolysis
- clopidogrel, statin
- then IV UFH or IV & SC enoxaparin
- then Beta-blocker, ACE-i/ARB, eplerenone (spironolactone)
- Option 1:
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
