inpatient / Cardiology

Acute Coronary Syndrome (ACS) and Myocardial Infarction (MI)

Last Updated: 1/1/2023

# Acute Coronary Syndrome
# STEMI / NSTEMI / Unstable Angina ***

-- ABCs:
 is the patient in cardiogenic shock requiring ICU or do they need to go straight to the cath lab?
-- STEMI -
1mm STE in two contiguous leads unless V2-V3, or LBBB --> cath lab goal <60 minutes from the door if <12 hours from sx onset)
-- NSTEMI - TIMI Score and GRACE score: Very High Risk - PCI within 2 hours - hemodynamic instability and ongoing angina; High Risk - PCI within 24 hours - GRACE >140 or continued rise trop and dynamic EKG changes; Intermediate Risk - within 72 hours - baseline risk factors (HFrEF, GFR <60); Low Risk - no cath - no risk factors, TIMI 0-1
-- Chart Check: last echo, stress test, heart cath
-- HPI Intake: onset, quality, radiation, worse, relieving, other symptoms, sildenafil use
-- Can't Miss: STEMI or cardiogenic shock, complications after MI
-- Admission Orders: trops, EKG, BNP, echo, telemetry
-- Initial Treatment to Consider: Nitrates, ASA load, atorvastatin, heparin drip, analgesia

-- Onset: ***
-- Quality: *** 
crushing, pressure, sharp
-- Radiation: ***
one arm, both arms, neck
-- Worse With: *** 
exertion, pleuritic, reproducible
-- Relieving: *** 
rest, SL nitro
-- Other Sxs: *** nausea, diaohoresis,
-- Sildenafil Use: *** 

-- History: *** co-morbidities: PAD LR 2.1, CAD LR 2.0, DM, CVA, HLD LR 1.4
-- Clinical: *** radiate to both arms LR 2.6, “typical chest pain” LR 1.9, pleuritic LR 0.35-0.61
-- Exam: *** warm/wet vs cold/dry, hypotension, diaphoresis, Frank's sign, new murmur, S4, overload (S3, crackles, JVP), pain with palpation, signs of PAD, radial/femoral pulses
-- Data: *** troponin, EKG, POCUS/Echo, CXR
-- Etiology/DDx: *** Type 1 MI (plaque rupture), Type 2 MI “MINOCA” (vasospasm, Takotsubo, dissection, vasculitis, steal) infectious emboli, treat as type 1 until sure of precipitating factor; HF, tamponade, PE, PTX, aortic dissection, esoph dx, PNA, MSK pain, GERD, referred pain

The patient's HPI is notable for ***. Exam showed ***. Labwork and data were notable for ***. Taken together, the patient's presentation is most concerning for ***, with a differential including ***.

Differential for Troponinemia:
Decreased Supply of Oxygen to Myocardium
Type 1 MI (plaque rupture)
-- MINOCA or NOMI - vasospasm, dissection, vasculitis, steal
-- Takotsubo (microvascular)
Increased Myocardial Oxygen Demand (increased wall stress)
Increased HR
-- Heart Failure (off starling curve)
-- Hypertension
-- Aortic Stenosis
-- Acute Pulmonary HTN - pulmonary embolism
Other (slow steady rise in troponin)
ESRD (reduced clearance)
-- Myocarditis
-- Infiltrative Disease (amyloidosis, sarcoidosis, hemochromatosis)

-- Trend troponin and EKG *** based on ***
-- Continuous telemetry
-- PCI: goal within *** based on ***; NPOmn, INR <2, monitor Cr, hold UFH on call
-- Non-invasive testing: *** based on *** pain resolved, low-med risk (NPO, hold BB)
-- Monitor for early post-MI complications (shock, arrhythmia, free wall/septal/pap muscle rupture, stent thrombosis, pericarditis)
-- Monitor for post cath complications (hematoma, pseudoaneurysm - pulsatile w/ bruit, AV fistula - bruit with no mass, limb ischemia, retroperitoneal bleed, CIN)

-- Nitrates: *** SL x3 → gtt 5-10mcg/min titrated to pain (avoid in inferior MI, RV dsfx, PDEi use)
-- Pain: *** morphine 4mg IV, increase q10-15mins
-- ASA: *** 325mg load, then 81mg daily
-- AC: *** heparin bolus and gtt for 48 hours or until PCI, goal PTT 60-80 checked q6
-- Lipids: *** atorvastatin 80mg daily; consider ezetimibe; f/u lipid screen
-- P2Y12: *** clopidogrel 600mg then 75mg daily < ticagrelor 180mg load then 90mg BID (causes dyspnea) < prasugrel (if <75 and no h/o CVA); hold on P2Y12 load if might get CABG
-- BB: *** within 24 hours, usually start metop tartrate q6 unless decompensated HF, HR <60, heart block, cocaine)
-- ARB: *** as BP and renal function allows
-- Lifestyle: *** smoking cessation, cardiac rehab, HTN goal <140/90
-- Risk Factors: *** f/u HbA1c, lipid panel, TSH, LFTs; avoid NSAIDs and steroids

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If You Remember Nothing Else

Many patients present with or develop chest pain, and diagnosing ACS and distinguishing between etiologies can be challenging. ACS is an umbrella term for a process that acutely blocks blood flow to the heart muscle. MI implied ischemia whereas injury just means trop leak but not ischemia. Type 1 MI is due to plaque rupture, Type 2 MI is any other reason for reduced flow to heart and ischemia. STEMIs go straight to the cath lab within 60 minutes of presentation. NSTEMIs are triaged based on risk (TIMI and GRACE score)- in general, unless the patient is unstable, you have 24 hours or more. Typical angina is substernal crushing pain with exertion, relieved by rest or nitrates. It is not the most reliable in women and eldery patients who may present with other symptoms like nausea. You can't miss STEMI or cardiogenic shock. Ischemic changes on EKG are not the most sensitive finding for ACS, radiation of pain to both arms has a likelihood ratio of 2.6. Give nitrates, morphine, ASA, hpearin, statin before PCI. After PCI depending on findings, can give P2Y12, BB, ARB. Avoid steroids and NSAIDs. Post-MI complications include shock, arrythmiam muscle rupture, stent thrombosis, pericardidits.

Clinical Pearls

  • ACS is an umbrella term for a process that acutely blocks blood flow to the heart muscle - includes STEMI, NSTEMI, and Unstable Angina (UA)
  • Stable Angina is chest pain with exertion that is relieved with rest and last 3-5 minutes (no more than 30 minutes) - implies underlying blockage/stenosis in coronaries but not an acute event, and thus is not ACS; anginal equivalents include dyspnea, fatigue, lightheadedness, N/V, MAS; depending on risk factors, can be worked up outpatient or inpatient with stress testing
  • Myocardial Infarction is necrosis with trop leak caused by ischemia vs Myocardial Injury which has trop leak but no ischemia)
  • Type 1 MI - spontaneous plaque rupture; Type 2 MI - any other reasons for ischemia (increased demand or decreased supply) - vasospasm, takotsobu (microvascular), non-plaque embolism, dissection, vasculitis; Type 3 is SCD, Type 4a iso PCI, Type 4b stent thrombosis, Type 5 with CABG
  • STEMI due to coronary plaque rupture with transmural ischemia which is the etiology of the ST elevations; NSTEMI can be caused by plaque rupture without complete occlusion of the vessel lumen, but commonly also a Type 2 event
  • There is a push to replace STEMI with "OMI" or occlusive MI, and NSTEMI to "NOMI" or non-occlusive MI - since relying on EKG findings is fraught and does not get at the etiology of the MI itself (also noting that the only real way to tell the difference between OMI and NOMI is to do a cath and look at the coronaries), but this transition will likely take time
  • STEMI criteria (cause for immediate cath lab activation): >1mm elevation in two contiguous leads (if V2-V3, >2mm men or 1.5mm women), New depressions in two leads V1-V4, New depressions with elevation in aVR, New LBBB with symptoms
  • STEMI goes to cath lab (goal within 60 minutes of presentation) if <12 hours after sx onset (unless shock, sustained VT, persistent STE or pain
  • TIMI and GRACE scores can attempt to risk-stratify patients with NSTEMI and UA - if GRACE >140 do PCI within 24 hours, if TIMI 0-1 or GRACE <109 can forgo cath
  • ASA, P2Y12 Inhibitors, Beta-Blockers, ACE/ARB, and statin all reduce mortality; nitrates and morphine alleviate sxs
  • Most Type 2 MI have some obstructive CAD - always worth just giving ASA, BB, atorva
  • HEART Score - used in the ED when patient presents with chest pain to assess risk of ACS - helps determine home vs obs vs cath lab; TIMI Score - estimates mortality for patients with NSTEMI and UA, used as a risk-stratification tool to determine need for stress vs PCI; GRACE Score - estimates 6 month mortality if have ACS
  • Ischemia can be considered symptoms (typical chest pain), new EKG changes, new MWA, evidence of thrombus on cath
  • Ischemic EKG changes are only 32% sensitive for the diagnosis of ACS
  • Discontinue NSAIDs in ACS - increase mortality, re-infarction, CHF, rupture
  • If already inpatient and patient starts having chest pain c/f ACS, get hsTNT immediately and at 3 hours - if >7 change from baseline, sxs consistent, or EKG with changes, rule in ACS 
  • The 99th percentile for hsTNT in men is 15 and in women is 10; 75% of healthy subjects will have a measurable hsTNT
  • Troponin rises over 3-12 hours, peaks 24-48 hours, goes down over 5-14 days
  • Nitrates decrease preload and efterload via vasodilation which increased myocardial blood flow and decreases myocardial demand - be cautious if hypotensive or concern for inferior MI with RV failure; contraindicated if used sildenafil in last 24 hours
  • Beta Blockers - lowers myocardial oxygen demand by lowering HR and contractility; avoid if AV block, hypotension/shcok, severe bradycardia, decompensated heart failure
  • Heparin - prevent further coagulation by blocking thrombin and factor Xa; given for 48 hours or until PCI; may not actually improve outcomes in patients especially those who don't ultimately get PCI, and bleed risk can be serious in certain patients, so use judgement - in such cases, fondaparinux may be the better option based on OASIS-6 Trial; watch for HIT
  • P2Y12 Inhibitors - usually hold off until after cath, as can delay CABG if needed (needs to wash out); DAPT is usually recommended for 6-12 months after DES; Clopidogrel - reduces mortality and repeat MI with PCI, metabolized by CYP219; Ticagrelor - better mortality than clopidogrel, but can cause dyspnea, $$$; Prasugrel - better mortality and repeat MI than ticagrelor, don’t give if prior TIA/CVA (leads to increased risk of intra-cranial hemorrhage), or >75yo, $$$
  • Anticoagulation - almost always UFH drip for 48 hours - bolus with PTT goal 60-80; LMWH largely no difference, fondaparinux increases PCI complications, bivalirudin can be used if HIT ($$$)
  • ACE/ARB - within 24 hours if BP and renal function normal; most useful for HFrEF or anterior MI; continue indefinitely but best for those with HTN or DM
  • Statin - atorva 80mg given immediately (even before PCI) regardless of LDL, thought to possibly help stabilize plaque; continue high-intensity if <75yo, otherwise moderate
  • PCI - Avoid placing stents in patients who are likely to non-adhere to DAPT, who will require holding DAPT for major surgery, or have elevated bleeding risk; also be cautious in patients with renal dysfunction since the aterial contrast load from PCI can cause nephrotoxicity (vs venous load from CT scans which really do not)
  • DAPT - in general, 6-12 months after DES for ACS (12 months if low bleed risk), though many trials are trying to see about shortening duration - based on early results it seems like a single P2Y12 inhibitor after 1-3 months of DAPT is probably fine
  • If have Afib + PCI → P2Y12 Inhibitor + DOAC is better than triple therapy (with ASA)
  • Post-Cath Hypotension Differential - bleeding (femoral, RP), MI, tamponade, arrhythmia; call fellow, give fluid, get EKG/trop, and POCUS
  • Post-MI Complications - acute mitral regurgitation (new murmur, pulm edema, shock - treat with surgery); pericarditis (friction rub, worse supine and better leaning forward, pleuritic, may have effusion - treat with ASA and colchicine consider NSAIDS is >4 weeks after MI); Free Wall Rupture (commonly anterior wall, within first 24 hours, TTE evidence of tamponade, RHC with equalization of pressures - treat with pericardiocenteiss and surgery is only option); Pseudoaneurysm (risk of rupture - surgery to fix); Septal Rupture (new pan-systolic murmur, echo to see left-to-right shunt, oxygen step up at level of RV - surgery to close rupture); LV Thrombus (stroke, limb ischemia, renal infarction, mesenteric ischemia - treat warfarin, maybe DOAC for at least 3 months); RV Failure (proximal RCA, triad of hypotension/JVD/clear lung fields has high specificity, nitrates and BB can make worse - give fluid and inotropes);
  • Stress Cardiomyopathy or Takotsubo Cardiomyopathy is transient LV dysfunction from a catecholamine surge in the setting of physical or emotional stress - catecholamines lead to calcium excess, injury to contractile proteins, and myocyte hypertrophy; heart apex has more B-adrenergic receptors which may explain why it is vulnerable to catecholamines; most patients recover EF witin 4-6 weeks, treated like heart failure (ACE, B-blockers, etc)
  • A patient with angina who has clean coronaries (non-obstructive disease) can still have microvascular angina - only way to address this is to focus on reducing risk factors through lifestyle change and treating co-morbidities
  • Frank’s Sign - diagonal crease in earlobe - weak link with CAD, but studies done in those getting PCI; possible useful if <60yo as may indicate premature aging via loss of dermal and also vascular elastic fibers
  • Sinus tachycardia in ACS can be compensatory for new LV dysfunction, pain, anxiety
  • The SA node is supplied by both RCA and LCx; most AV nodes are supplied by RCA
  • Bundle of His supplied by LAD and septal perforators - reason LBBB counts as criteria for STEMI
  • Diabetes and PAD are equivalent risk factors to CAD for cardiovascular outcomes
  • CABG > PCI if 3 vessel disease, left main disease, 2 vessels with proximal LAD stenosis

Trials and Literature

  • Does this Patient with Chest Pain Have Acute Coronary Syndrome? Rational Clinical Exam (JAMA, 2015)
  • Differential Diagnosis of Elevated Troponin (Heart, 2006)
  • COMPLETE Trial - in STEMI w/o shock, PCI to culprit AND non-culprit vessel decreased risk of death and MI at 3 years (NEJM, 2019)
  • CUPLRIT SHOCK Trial - in STEMI with shock, PCI ONLY to culprit vessel decreased risk of death or dialysis within 30 days and 1 year (NEJM , 2018)
  • NORSTENT Trial - Drug Eluting Stents better than Bare Metal Stents - but only for repeat revascularization within 6 years (16.5% vs 19.8%) and stent thrombosis; (increase late stenosis so require longer DAPT) (NEJM, 2016)
  • ISCHEMIA Trial - 2020 - in pts with stable CAD, revascularization did not decrease ischemic events (NEJM, 2020) 
  • SYNTAX Trial - CABG > PCI if 3 vessel disease - cardiac or CVA events at 12 months 17.8% vs 12.4% (driven by the need for revascularization, death and MI similiar, CVA higher in CABG) (NEJM, 2019)
  • ISIS 2 Trial - ASA alone reduces 5-week vascular and 15-month all-cause mortality in ACS; thrombolysis (streptokinase) also works but increases bleeding risk (Lancet, 1988)
  • PCI CURE Study - adding clopidogrel to ASA leads to decreased mortality/MI/revasc composite 4.5% vs 6.4% within 30 days of PCI with no increased bleed risk; however overall events before and after PCI (CV death/MI) was 12.6% and 8.8%; NNT for adding clopidogrel to ASA with PCI is 27 for non-fatal MI and stroke, and NNH (bleed) was 114 (Lancet, 2001)
  • Cochrane Analysis (2011) of adding clopidogrel to ASA after PCI
  • PLATO Trial - in ACS patients ticag > clopidogrel, reduced mortality composite 9.8% vs 11.7%, no diff in bleeding (NEJM, 2009)
  • ISAR-REACT Trial - in ACS patients prasugrel > ticag, reduced mortality composite 9.3% vs 6.9%, no diff in bleeding; note thatTRITON previously showed higher risk bleed with prasugrel (NEJM, 2019)
  • Meta-analysis of heparin use in ACS suggests it does not add much to ASA and increased bleeding risk - the reason it is stopped after 48 hours
  • OASIS-6 Trial - fondaparinux > enoxaparin given for 6 days in ACS; reduced mortality and lower bleed risk; however has higher thrombosis risk with PCI (JAMA 2006)
  • PROVE IT Trial - sig reduced CVD events after MI with high-dose atorva vs pravastatin (22.4% vs 26.3%) for those already on statin; LFT elevation in 3.3% vs 1.1% (NEJM, 2004)
  • IMRPOVE-IT Trial - ezetimibe added to simvastatin 40mg (lol) improved composite outcome driven by MI and stroke (NEJM, 2015) 
  • COMMIT Trial - metoprolol is significantly beneficial if started day 1 onwards, but increases shock (which usually happens on the first day) (Lancet, 2005)
  • Cardiac Arrythmia Suppression Trial - We don’t treat PVCs with antiarrhythmics (encainide, flecainide) because it increases mortality, so just limit them by fixing electrolytes (NEJM, 1991)
  • REALITY Trial - Hgb transfusion target >8 in patient with acute MI was non-inferior to >10 in major adverse cardiovascular events (MACE; composite of all-cause death, stroke, recurrent myocardial infarction, or emergency revascularization prompted by ischemia) at 30 days (JAMA, 2021)

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