IHD pt 3/4

unstable angina

transient partially occlusive clot that does not result in myocardial cellular damage or release of biochemical markers

NSTEMI

similar to UA (partially occlusive clot); however, myocardial cellular damage occurs and there is an increase in biochemical markers

STEMI

fully occlusive clot that may result in significant myocardial damage and release of biochemical markers

ACS symptomatology

ischemic chest pain or pressure not reproducible by palpation, not relieved by SL NTG, patient may have Hx of chronic angina or no previous diagnosed disease

P wave represents

atrial depolarization

QRS complex represents

ventricular depolarization

T wave represents

ventricular repolarization

when should ECG be done if someone presents to ER with ischemic chest pain

10 min

STEMI ECG changes

ST elevation or new left bundle branch block

Q wave indicates previously completed STEMI

NSTEMI ECG changes

ST depression or T wave inversion (indicate ongoing ischemia)

lab findings ACS

biochemical markers are released into blood on myocardial cell death

troponin and CK MB are sensitive/specific for myocardial necrosis

which forms of ACS have cardiac biomarkers

NSTEMI and STEMI (not UA)

potential complications (STEMI>NSTEMI)

arrhythemias/sudden cardiac death (SCD)

heart failure

angina

hypertension

cardiogenic shock

embolic stroke

re infarction

initial goal in acute management of STEMI

reperfusion (opening) the infarct related artery

initial pharmacotherapy when clinical suspicion of ACS while waiting for ECG results

aspirin chew and swallow, SL NTG, oxygen (if O2 sat <90)

treatment algorithm for initial management of patients with suspected STEMI

initiate reperfusion therapy: primary PCI preferred, fibrinolysis if D2B time >120min

initiate P2Y12 inhibitor: if primary PCI give prasugrel, ticagrelor, clopidogrel and if fibrinolysis give clopidogrel

consider GP IIb/IIIa inhibitor- if primary PCI performed, no P2Y12 inhibitor prior to PCI and bivalirudin not used

initiate anticoagulation- UFH, bivalirudin, LMWH or fondaparinux

what is prefered reperfusion strategy: PCI or thrombolysis?

PCI

when would fibrinolysis be used (and not PPCI)?

time from FMC to PCI >120min

even so should have routine PCI within 24hr of succesful fibronolysis OR immediate PCI for failed fibrinolysis

thrombolytics agents

altepase or tissue plasminogen activator (tPA)

reteplase (rPA)

tenecteplase (TNK)

streptokinase dosing

IV dose over 1hr

reteplase dosing

bolus dose + 30min later another bolus dose

alteplase dosing

bolus dose + infusion

tenecteplase dosing

single bolus dose

which thrombolytic drug is DOC

tenecteplase

average time to reperfusion with thrombolytics

45-60+ minutes

timeframe for giving thrombolytics in STEMI

can be given usually up to 12hr post onset of symptoms (preferably less than 3hr)

thrombolytic absolute CI

any prior hemorrhagic stroke

ischemic stroke within 3mo (except in past 4.5hr)

intracranial neoplasm or arteriovenous malformation

active internal bleeding

aortic dissection

considerable facial trauma or closed-head trauma in the past 3mo

intracranial or intraspinal surgery within 2mo

severe uncontrolled hypertension (unresponsive to emergency therapy)

for streptokinase, a treatment within the previous 6mo (if considering streptokinase again)

thrombolytic relative CI

BP >180/110 on presentation or history of chronic poorly controlled hypertension

history of ischemic stroke >3mo before

recent major surgery (<3 weeks before)

traumatic or prolonged CPR >10min

recent internal bleeding within 2-4wks

active peptic ulcer

noncompressible vascular punctures

pregnancy

known intracranial pathology (dementia)

oral anticoagulant therapy

ae thrombolytics

bleeding including hemorrhagic stroke

risk factors for intracranial hemorrhage with fibrinolysis

older age, female sex, low body weight (<70kg female and <80kg male), prior stroke, HTN (BP >160-170/95 mmHg, at any time)

thrombolytic monitoring

clinical signs of bleeding

mental status changes for signs of ICH

baseline aPTT, INR, CBC (for Hgb and platelets)

follow up CBC

which P2Y12 inhibitors are preferred in pts undergoing primary PCI

prasugrel, ticagrelor

which P2Y12 inhibitors are prefered in pts undergoing fibrinolytic Tx

clopidogrel (new evidence says ticagrelor)

metabolism of clopidegrol vs prasurgrel/ticagrelor

undergoes more extensive hepatic metabolism relative to the other 2 agents

more susceptible to inter patient genetic variability

CI in poor metabolizers (CYP2C19×2/3)

does prasugrel or clopidegrel have faster onset of platelet inhibition

prasugrel

does prasugrel or clopidogrel have higher bleeding risk

prasugrel

ticagrelor CI

history of intracranial hemorrhage

severe hepatic impairment

concomitant strong CYP3A4 inhibitors

ticagrelor ae

dyspnea, ventricular pauses, headache, dizziness, rash, GI (N/V/D)

monitoring of ticagrelor

bleeding, baseline and periodic CBC

UFH dosing

weight based regimens preferred

usually administered as continuous infesion

titrate to maintain aPTT between range set by local institution

UFH renal dosage adjustment

none

LMWH dosing for ACS

weight based subq injections

LMWH renal dosage adjustment

CrCl <30 go to UFH instead of dose adjusting (usually)

renal dosage adjustment fondaparinux

CI CrCl <30mL/min

direct thrombin inhibitor example

bivalirudin

unique situation when to use bivalirudin

heparin induced thrombocytopenia (HIT)

bivalirudin indications

approved for use during PCI for STEMI/or UA/NSTEMI including pts with heparin induced thrombocytopenia (HIT)

which setting are fibrinolytics NOT used in

NSTEMI/ UA

low risk NSTE-ACS initial management

consider P2Y12 inhibitor (clopidogrel, ticagrelor)

initiate anticoagulant (fonaparinux, LMWH, UFH)

do non invasive stress test to see if need coronary angiography ± PCI

intermediate-high risk NSTE-ACS initial management

initiate P2Y12i:

• prasugrel or ticagrelor if increased cTn levels or ischemic changes on ECG

• clopidogrel, prasugrel, ticagrelor if normal cTn levels and no ischemic changes on ECG

initiate anticoagulation (UFH, LMQH, may switch to bivalirudin during PCI)

coronary angiography, PCI, if appropriate

consider GP IIb/a inhibitor or cangrelor if no P2Y12i prior to PCI

what is ischemia guided approach for acute management of NSTE ACS

medical management

often used in patients found to be low risk

potential strategy for intermediate risk groups who go on to elective PCI later

what is early invasive approach for acute management of NSTE ACS

refers to coronary angiography ± PCI

used in pts with high risk indicators

TIMI risk score 5-7; score=3-4 have also been shown to benefit

what is DAPT

ASA + one of clopidogrel, ticagrelor or prasugrel

ACS DAPT 1 year standard therapy

ASA + ticagrelor or prasurgel (equally prefered)

elective PCI DAPT 1 year standard therapy

ASA + clopidogrel

ACS DAPT 3 years therapy

strong recommendation:ASA + ticagrelor (lower dose than first year) or ASA + clopidogrel

weak recommendation: ASA + prasugrel

ACS DAPT deescalate therapy (1-3mo)

SAPT with P2Y12i or ASA

OR
DAPT asa + clopidogrel

elective PCI DAPT 3yr therapy

ASA + clopidogrel

elective PCI DAPT de escalate (1-3mo) therapy

SAPT with clopidogrel or ASA

pre op antiplatelet therapy for CABG (which agents can be continued, which need to be d/c and when)

d/c clopidogrel 2-7 days before surgery

d/c ticagrelor 2-3 days before surgery

continue ASA for CABG

post op antiplatelet therapy: ACS on/off pump CABG recommendation

ASA + ticagrelor or prasugrel (equally preferred) x up to 12mo

post op antiplatelet therapy: not ACS CABG recommendation

ASA + clopidogrel (equally prefered) x up to 12mo

chronic coronary disease (CCD)

includes:

post ACS pts once stabilized

heart failure (systolic) with CAD

SIHD

angina symptoms due to vasospasm

coronary disease based on screening testing

secondary prevention of ischemic events within first 24hr

initiate aspirin, B blocker, statins asap if no CI

aspirin + statin undefinently

B blocker for atleast 1yr and up to 3yrs + in pts with normal ejection fraction, indefinently in LVEF </=40%

secondary prevention of ischemic events prior to hospital discharge

med rec should include:

DAPT w/ ASA + P2Y12i

statin (if not already initiated)

B blocker (if not already initiated)

consider ACEI (or ARB) in all pts, strongest evidence if LVEF <40 (indefinete), anterior MI (for 3mo)

consider aldosterone antagonist if LVEF </=40%, HF symptoms of DM, and no CI

SL NTG as needed

d/c NSAIDs

assess for SGLT2 or GLP-1RA

secondary prevention of ischemic events at 1mo follow up

emphasize adherence

consider statin, B blocker, ACEI (ARB), AA if indicated + not already on

check lipid panel and add ezetimibe ± PCSK9 inhibitor if LDL-C >1.8mmol/L , according to shared decision making between provider and patient

secondary prevention of ischemic events at 12mo follow up

emphasizes adherence

evaluate for continuation of P2Y12i beyond 1 year

evaluate for continued B blocker beyond 1-3 years (consider LVEF + angina Sx control)

standard post care ACS meds

low dose ASA
P2Y12 inhibitor

B blocker

high intensity statin

ACEI/ARB

If LVEF <40% and symptomatuc or diabetic: MRA

assess use of SGLT2 and GLP-1RA

benefits of DAPT (ASA and P2Y12i)

ASA- decreases risk of death, recurrent infarction, and stroke

P2Y12- inhibitor: decreases risk of death, MI, stroke, and stent thrombosis with PCI

which P2Y12 inhibitor is prefered with PCI

ticagrelor (but more bleeding)

thrombolytic Tx (STEMI) preferred P2Y12i

clopidogrel ( new evidence says ticagrelor over clopidogrel tho)

med management (NSTEMI) preferred P2Y12i

only clopidogrel/ticagrelor

preferred P2Y12 for DAPT without revascularization

clopidogrel preferred over prasugrel (strong recommendation)

ticagrelor preferred over clopidogrel (weak recommendation)

how soon do initiate beta blocker after ACS

within first 24hr except where CI

beta blocker CI

HR <60, SBP <100

mod-severe LV failure

severe COPD

duration for continuing beta blocker after ACS

atleast 1yr with normal LVF

indefinently if reduced EF <40%

may also be used longer term if angina, arrythmias, or htn

who to use aldosterone antagonists in post acs

may be used first 2wk post MI in pts already receiving ACEI (or ARB) and have LV EF <40% and either HF symptoms or DM

who has increased risk of hyperkalemia with aldosterone antagonist

ACEi/ARB therapy - esp with reduced renal function

who are SGLT2i shown to have beneficial effects in

heart failure (± T2DM)

CKD (± T2DM)
ASCVD + T2DM

who are GLP-1RA shown to have beneficial effects in

ASCVD + T2DM

ASCVD risk factors

age

htn

dyslipidemia

tobacco use

DM

obesity

family Hx of ASCVD (first degree relative male <55yrs or female relative <65yrs)

should post menopausal women who have has ACS be continued on/initiated on hormone replacement therapy

should not be started in post menopausal women who had STEMI or NSTEMI/UA for secondary prevention of coronary events

post menopausal women should generally not continue taking after ACS (weigh risks vs benefits)