MGH ACS.pdf

TOC Cardiology Acute Coronary Syndrome DEFINITIONS AND EVALUATION Myocardial injury: defined as any patient with troponin >99th percentile without evidence of myocardial ischemia (sx of ischemia, new ischemic ECG changes, new wall-motion abnormalities, and/or acute coronary thrombus on angio). M...

TOC Cardiology Acute Coronary Syndrome DEFINITIONS AND EVALUATION Myocardial injury: defined as any patient with troponin >99th percentile without evidence of myocardial ischemia (sx of ischemia, new ischemic ECG changes, new wall-motion abnormalities, and/or acute coronary thrombus on angio). May be acute or chronic. Myocardial infarction: myocardial necrosis (trop >99th percentile + ∆) w/ ischemia (4th universal def. of MI, types 1-5: JACC 2018;72:2231) • Type 1 MI: spontaneous plaque rupture, ulceration, fissure, erosion, dissectionintraluminal thrombus • Type 2 MI: supply-demand mismatch that is not atherothrombosis – most commonly due to sepsis/infection, arrhythmias, severe anemia, renal failure, surgery, hypertension, and heart failure; other causes include vasospasm, microvascular ischemia (e.g. Takotsubo), non-plaque thromboembolism (e.g. infectious via PFO), aortic dissection, vasculitis, steal (Circulation 2019;140:1661). o Must have a clear precipitating factor. If not, treat as a type 1 MI until further evaluation o 50-70% have obstructive CAD – reasonable to initiate ASA, BB, and high-intensity statin Evaluation of CP with hsTnT Emergency Department – CP onset ≥3h PTA Inpatient or Emergency – CP onset < 3h Check hsTnT immediately and at 1h Check hsTnT immediately and at 3h Rule in: hsTnT ≥10 (F) or ≥15 (M) AND ∆ ≥7 from baseline Rule in: hsTnT ≥52 OR ∆ ≥5 from baseline AND sx or ECG changes or concerning imaging (CCTA, cath)  consider ACS  consider ACS Rule out: hsTnT <10(F) or <12(M) AND ∆ <3 from baseline  Rule out: no significant ∆ in 3h unlikely ACS  unlikely ACS Intermediate: calculate HEART score, repeat hsTnT in 3h and apply inpatient criteria (right) STEMI NSTEMI Unstable Angina • 1mm STE in two contiguous leads (if V2-V3: >2.5mm in M<40, 2mm in M>40, 1.5mm in F) OR new LBBB AND ⊕ biomarkers • If baseline LBBB, use Sgarbossa’s criteria: ≥1 mm concordant STE, 1 ⊕ ECG or hx, ⊕ ECG or hx, mm STD V1-V3, ≥ 5 mm discordant STE ⊝ biomarkers ⊕ biomarkers • Electrically Silent: LCx or RCA lesions. Consider posterior V7-V9 leads, in which STE>0.5mm is diagnostic. Other changes: large R in V2-V3, STdep in anterior leads (mirror image effect) Clinical Evaluation & Risk Stratification: • Consider pt’s baseline CAD risk. Review prior stress test and cath data. risk of MI w/ resp infxn (esp flu) (NEJM 2018;378:345) • Treat secondary causes of myocardial demand ECG: (NEJM 2003;348:993) • Obtain serial tracings (q15-30min) if initial ECG non-diagnostic in pts with compelling hx & sx • Non-STE ischemic EKG changes: ≥0.5mm STD (horizontal, downsloping), new TWI ≥1mm or normalization (“pseudonormalization”) of prior TWI in s/o sx Cardiac Biomarkers: • hsTnT 99th %ile among normal subjects: M 15ng/L, F 10ng/L • 75% of healthy individuals will have measurable hsTnT • hsTnt peaks within 12-48 hrs, normalizes in 5-14 days REVASCULARIZATION • • • • PCI Indications: recommended over fibrinolysis at a PCI-capable center in patients with STEMI <12h symptom onset o STEMI: door to device ideally <60min at PCI centers. PCI regardless of time from onset for cardiogenic shock, malignant arrhythmia (recurrent sustained VT, VF), persistent STE and/or CP. Late PCI (>48h post-event) not indicated in stable pts (NEJM 2006;355:2395); if PCI delayed (>120min from first medical contact), worse outcomes -- consider fibrinolysis (Eur Heart J 2020;4:858) o NSTEMI/UA: see “Risk Stratification” above PCI Strategies: Access: radial > fem | Stent: DES > BMS (NEJM 2016;375:1242) o STEMI without cardiogenic shock: complete revascularization strategy (culprit + non-culprit) has risk of CV death and MI at 3y (COMPLETE, NEJM 2019;381:1411) o STEMI with cardiogenic shock: culprit-lesion only PCI has a risk of death/RRT (CULPRIT-SHOCK, NEJM 2018;379:1699) CABG: preferred for 3VD (NEJM 2009;360:961), L main disease (Lancet 2016;388:2743; NEJM 2016;375:2223), 2VD with prox LAD stenosis or EF <50%, DM + 2VD w/ involvement of LAD (NEJM 2012;367:2375). (Guideline: Circulation 2022;145:4). Fibrinolysis: inferior to PCI (Lancet 2003;361:9351); consider in STEMI with symptom onset <12 hours (12-24 hours reasonable) if first medical contact to device time anticipated >120 minutes. Contraindicated in ↑bleeding risk (esp ICH), suspected dissection, ischemic stroke <3 months prior, severe HTN (Circulation 2012;127:362). o Door to needle ideally <30 minutes. Tenecteplase (TNK-tpA), reteplase (rPA), alteplase (tPA) > streptokinase. o Adjuncts: Load with ASA (325mg; continued indefinitely at 81mg) and clopidogrel (300mg if ≤75, 75mg if >75; continued for at least 14 days to 1 year at 75mg), AC with heparin or Lovenox for 48 hours (Circulation 2016;134:123). Michael Hendrickson 14 TOC Cardiology RISK STRATIFICATION FOR PCI TIMING IN NSTEMI/UA Acute Coronary Syndrome • Multiple risk models incl GRACE, TIMI, PURSUIT. GRACE score is based on predictors of 6mo mortality (age, HR, SBP, Cr, cardiac arrest at admission, ST deviation, elevated trop) (BMJ 2006;333:1091) • Four subgroups for urgency to revascularization (JACC 2014;64:e139) 1. Very high risk (“immediate invasive,” within 2h): refractory/recurrent angina, hemodynamic, or electrical instability 2. High risk (“early invasive,” within 24h): temporal change in troponin, ECG changes (STD, TWI), high risk pt (GRACE>140) a. Conflicting results between TIMAC (NEJM 2009;360:2165) and VERDICT (Circ 2018;138:2741) trials about outcome benefit of early cath. However, both show improved outcomes with early cath in patients with GRACE >140 3. Intermediate risk (“delayed invasive,” within 72h): none of above but risk factors at baseline (e.g. EF <40%, GFR <60) 4. Low risk (“ischemia guided,” no cath): no risk factors, GRACE <109, TIMI 0-1 ADJUNCTS TO REVASCULARIZATION ASA: established mortality benefit, give to all pts in an immediate load/maintenance strategy (325mg/81mg) (Lancet 1988;2:8607) P2Y12 Inhibitors: (pre-cath load not done at MGH, controversial benefit & may delay CABG by 5-7 days (Circulation 2022;145:4)). o Ticagrelor: mortality compared to clopidogrel w/o increasing major bleeding. Reversible with platelet transfusion. Side effect: dyspnea (14-21%, often mild & transient, but can be severe enough to warrant discontinuation), risk of pneumonitis w/ alveolar hemorrhage. Avoid in liver disease, prior CVA, oral AC (PLATO, NEJM 2009;361:1045). o Prasugrel: death, MI, CVA compared to ticag (NEJM 2019;381:1524). Contraindicated if prior TIA/CVA, wt <60kg, or >75y o Clopidogrel: death, repeat MI when load/maintenance with PCI (Lancet 2001;358:527I). Prodrug, metabolized by CYP219, less effective in those with LOF allele (NEJM 2009;360:354). May benefit from PPI ppx for ↓UGIB (NEJM 2010;363:1909). ↓Bleeding compared to ticagrelor and prasugrel but ↑ischemic events (Circulation 2020;142:150). o Cangrelor: IV reversible inhibitor with immediate onset and return of platelet function in 1h. Used in pts with recent PCI who are unable to take PO or are periprocedure, needs pharmacy approval 3. Nitrates: TNG SL (0.3-0.6mg) x3, if refractory  gtt (start 5-10mcg/min). Nitropaste and gtt have shorter half-life than SL if c/f HoTN. No mortality benefit. Caution in inferior MI/RVMI, SBP<100, or PDEi use in last 48h. If refractory CP indication for earlier cath. 4. Anticoagulation: o UFH: usually stopped after 48h if ECG changes improving and concern for ongoing ischemia resolved (BMJ 1996;313:652). Start gtt w/ bolus and use low intensity PTT goal (63-83). No bolus if giving lytics or if on warfarin and INR<2 o LMWH: possible reduction in death w/ minimal evidence for major bleeding, trials vs UFH largely null (BMJ 2012;344:e553) o Fondaparinux: preferred to UFH/LMWH if medically managed. Contraindicated in PCI catheter thrombosis/complications (JAMA 2006;295:1519) o GPIIb/IIa Inhibitors: eptifibatide (Integrilin) used at MGH. Initiated in cath lab if PCI high-risk (extensive thrombus) o Bivalirudin/Argatroban: direct thrombin inhibitor, preferred for patients w/ HIT, otherwise cost does not outweigh benefit 5. Beta Blockers: start within 24h (1B for STEMI, 1A for NSTE-ACS), mortality benefit. Consider early initiation if ischemic arrhythmias present. Not indicated for stable ischemic heart disease s/p cath, but rec’d after CABG (Circulation 2022;145:4) o Caution in decompensated HF, risk for cardiogenic shock (>70y, SBP <120, HR >110 or <60) o Contraindications: cocaine-induced MI, PR>240ms, 2nd or 3rd degree AVB, severe bronchospasm (Lancet 2005;366:1622) 6. ACEi or ARB: start ACE within 24h in all patients if BP/renal function normal (2a;LOE:A for STEMI) but mortality benefit (1; LOE:A) in anterior STEMI; use ARB if intolerant of ACE. ARB > ACE in patients with HF or LVEF <40% (Circulation 2008; 117:269). 7. Aldosterone antagonist: s/p MI on ACE and BB, and have LVEF<=40 + DM or sx of HF (1;LOE:B) (Circulation 2008; 117:269) 8. Statin: atorvastatin 80mg daily regardless of baseline LDL (NEJM 2004;350:1495) o Early high-dose statin within 24-96h may reduce death/adverse cardiac events if given pre-PCI (JACC 2009;54:2157; JAMA 2018;319:1331). Early anti-inflammatory effect may stabilize plaque (JAMA 2001;285:1711; JAMA 2004;291:1071) 9. Morphine: not recommended. Consider only if unacceptable level of pain refractory to TNG, careful if suspicious for inferior MI/RVMI 10. Discontinue NSAIDs: risk of mortality, re-infarction, HF, and myocardial rupture after ACS 1. 2. SECONDARY PREVENTION 1. 2. 3. 4. 5. 6. 7. Aspirin: 81mg w/o enteric coating indefinitely (should be chewed) (NEJM 2010;363:930) Dual antiplatelet therapy (DAPT): ACS: DAPT for at least 12 months; stable ischemic disease: DAPT after DES for at least 6 months, BMS at least 1 month, CABG 12 months (Circ 2016;134:e123). Use DAPT score to help risk stratify. Evolving movement to shorten DAPT duration (TWILIGHT NEJM 2019;381:2032; TICO JAMA 2020:323:2407; STOPDAPT-2 JAMA 2019;321:2414; SMART CHOICE JAMA 2019;321:2428; GLOBAL LEADERS Lancet 2018;392:940-949; MASTER DAPT NEJM 2021;385:1643-1655). Bottom line: In select patients, single agent P2Y12 inhibitor after 1-3 months (vs. longer duration DAPT) is non-inferior in reduction of cardiovascular events, with reduced bleeding risk. Beta blockers: as above ACEi or ARB: as above Statin: high intensity statin (atorvastatin 40-80mg or rosuvastatin 20-40mg qd) indefinitely for pts ≤75y, moderate intensity in >75y a. If very high risk clinical ASCVD w/ LDL-c>70 mg/dL, add ezetimibe and consider PCSK9i (JACC 2019;73:3168) AF + PCI: P2Y12 inhibitor + DOAC > triple therapy. bleeding and non-inferior for ischemic events (AUGUSTUS NEJM 2019;380;1509; RE-DUAL PCI NEJM 2017;377:1513; NEJM 2016; 375:2423). (Guideline JACC 2021;77:629). See Anticoagulation Management a. Common practice example: initiate triple therapy (ASA/clopidogrel/AC) for 1-4wks and d/c ASA  AC + clopidogrel Lifestyle: smoking cessation, BP <140/90 (if DM or CKD, <130/80), cardiac rehab (1; LOE:B), depression screening M G H P 2 Y 1 2 S W I T C H I N G G U I D E L I N E S (Ellucid policy, does not apply to patients on triple therapy) Michael Hendrickson 15 TOC Cardiology MI Complications M E C H A N I C A L C O M P L I C A T I O N S (JACC 2013;61:e78; JACC Cardiovasc Interv 2019;12:1825) LATE COMPLICATIONS (Weeks – Months) EARLY COMPLICATIONS (Hours – Days) Complication Prevalence / Risk Factors Timing / Clinical Signs Evaluation Treatment  STEMI: 50% develop shock w/in 6h of MI, 75% w/in 24h  NSTEMI: 72-96h after MI  New CP, cold/wet physiology, HoTN, tachycardia, dyspnea, JVD, rales, new murmur  TTE  PAC (CI<2.2, PCWP>18)  End organ hypoperfusion (lactic acidosis, AKI)  Inotropes/pressors  Emergent PCI/CABG (<75y + STEMI + shock w/in 36h of MI). SHOCK trial (NEJM 1999;341:625)  IABP and other MCS  40% w/in 24h, 85% w/in 1w  Tamponade in 85%  Electromechanical dissociation, aberrant T wave evolution, abrupt episodes of HR/BP  TTE (pericardial effusion w/ high acoustic echoes indicating clot)  STAT cardiac surgery consult  Emergent surgery for resection of ruptured myocardium w/ primary reconstruction  TTE w/ doppler (L to R shunt, RV overload)  RHC: increase in O2 sat from RA to PA >5, large V waves  Emergency surgery or transcatheter closure device  Vasodilators (use cautiously) to decrease L to R shunt (nitroprusside or nitroglycerin)  IABP  No reperfusion: 2-7d  With reperfusion: median 13h  Abrupt dyspnea, pulmonary edema, hypotension  Hyperdynamic LV, holosystolic murmur at apex (radiates to LSB w/ posterior pap muscle rupture), murmur may be absent in torrential MR or severe HF  TTE (MR)  CXR: edema (can be asymmetric to RUL if MR jet directed at right pulmonary veins)  Tall c-v wave in PCWP tracing  Aggressive afterload reduction (nitroprusside or nitroglycerin)  IABP  Emergent surgery  Days to weeks  Acute: diffuse, displaced PMI, S3 and/or S4, MR murmur, CHF  Chronic: HF, VT/VF, systemic embolization, may be asymptomatic  ECG w/ persistent STE  TTE, other imaging (CMR, CT, ventriculography) LV Thrombus  5% of AMI patients postPCI  Usually in LV apex  Large infarct size, severe apical akinesis or dyskinesis, LV aneurysm, anterior MI  Can form 24-72h post MI  90% of thrombi are formed by 2w  Embolization risk persists for 6mo but most by 3-4mo; risk 10% if not on warfarin  TTE w contrast  CMR or CT Pericarditis  5% of pts in the ED w/ CP and no MI, M > F  85-90% idiopathic (viral/post viral), infectious, post-MI, uremic, autoimmune, malignancy, XRT, drugs  10% at 2-4d post-transmural MI  May be focal or diffuse  Dressler’s syndrome (1-6wks): malaise, fever, leukocytosis, late autoimmune carditis, rare  ECG (diffuse STE, PR depressions)  TTE (effusion)  CMR and/or cardiac CT  ASA + colchicine  Avoid NSAIDs and steroids post MI as can impair infarct healing  Most cases occur within 30d of PCI irrespective of stent type  ACS symptomatology  ECG  Biomarkers (troponin/CKMB)  PCI  Long term anti-platelet therapy, adherence to therapy  STEMI ~6%  NSTEMI ~3% Cardiogenic Shock  Anterior MI, LBBB, prior MI, 3VD, age, HTN, DM, (see Inpatient HF) mechanical complications  50% of post-MI death  0.01% STEMIs & Myocardial Free NSTEMIs  Transmural MI, 1-vessel Wall Rupture MI, 1st MI (poor (Pseudoaneurysm: collaterals), anterior & LV defect contained lateral MI, HTN, late by only pericardium, thrombolysis (>14h), scar, more prone to fibrinolysis>>PCI, NSAIDs, rupture than true female, age >70 aneurysm)  10% post-MI death Interventricular Septal Rupture (VSD)  0.21% STEMIs, 0.04% NSTEMIs  Bimodal: 24h & 3-5d to up to 2w  1st MI, 1-vessel MI (esp. from event LAD), CKD, anterior  New, harsh holosystolic murmur infarct w/ inferior STE due (50% w/ thrill), S3, loud P2, to wrap-around LAD, older hypotension, BiV failure (R>L) age, female  5% of post-MI death Papillary Muscle Rupture (leading to acute MR)  0.05% STEMIs, 0.01% NSTEMIs  Posteromedial (supplied by PDA, with inf. or post. MI) >> anterolateral (dual blood supply by LAD and LCx)  5% of post-MI death LV Aneurysm (discrete,  No reperfusion: 10-30% dyskinetic area of  Apical-anterior wall >> inferior posterior LV with broad  Steroids, NSAIDs neck, rarely ruptures)  Highest risk is absence of Coronary Artery P2Y12 inhibitor In-Stent  1% at 1 year, then ~0.2% Thrombosis per year thereafter  Acute: management of CHF, ACEi, avoid NSAIDs/steroids, start heparin (if EF<35%)  Chronic: ACEi, digoxin, diuretics, warfarin (if EF<35%)  Surgical repair  Warfarin (INR 2-3); DOAC may be a reasonable alternative (Circ. 2022;146:e205–e223)  When to stop AC unclear, check for resolution of thrombus on TTE at 36mo Aditya Achanta 16 TOC Cardiology U R G E N T A S S E S S M E N T O F P O S T - M I C O M P L I C A T I O N (page Cardiology) • • • MI Complications Assess VS for hemodynamic instability, focused physical exam (new murmur, pericardial friction rub, elevated JVP, crackles, access site/s) Stat labs (troponin, PT/INR, PTT, T&S, BMP, lactate), ensure adequate vascular access (≥2 PIVs) Run telemetry, repeat ECG, STAT TTE, consider STAT CTA if concern for RP bleed/aortic dissection, notify interventionalist Circuit SA Node AV Node Bundle of His RBB LBB LAFB LPFB Coronary Vessel Supply 60% from RCA, 40% from LCx 90% from distal RCA, 10% from distal LCx AV nodal artery (RCA), LAD septal perforators LAD septal perforators, collaterals from RCA/LCx LAD, collaterals from RCA/LCx LAD septal perforators (single supply, sensitive to ischemia) AV nodal arteries proximally, distally dual supply from LAD/PDA septal perforators Ecgwaves.com ELECTRICAL COMPLICATIONS Overview • Bradyarrhythmia/conduction block: may be due to coronary artery occlusion (see below) or baroreceptor reflexes (Anes 2003;98:1250) • Tachyarrhythmia: related to creation of re-entrant circuit from scar formation and/or automaticity from adrenergic surge Arrhythmia Bradyarrhythmia Sinus bradycardia First degree AV block Second degree AV block: Mobitz Type I Second degree AV block: Mobitz Type II Third degree AV block Ventricular Tachyarrhythmias Supraventricul ar Arrhythmias Intraventricular Conduction Blocks Sinus tachycardia Atrial fibrillation, Atrial flutter Premature Ventricular Contraction Accelerated Idioventricular Rhythm (AIVR) Location/Mechanism  Inferior and posterior MI  Beneficial: myocardial O2 demand  Inferior: vagal tone or AV node ischemia (RCA), narrow QRS  Anterior: septal necrosis below AV node, RBBB, wide QRS  Usually inferoposterior MI (vagal tone, narrow QRS) or AV node ischemia  Usually anterior MI with infranodal conduction injury, wide QRS, HR often <30, 33% progress to CHB  If inferior MI: intra-nodal lesion; narrower QRS escape  If anterior MI: infra-nodal lesion; wide, unstable escape rhythm  50% already present on first ECG, may represent antecedent disease of conduction syndrome  Suggests more extensive infarct  May be compensatory for LV dysfunction, common in anterior MI  Pain, anxiety, pericarditis, fever Incidence/Timing  Atropine, pacing if unstable, dopa/epi if HoTN  More common in inferior MI  If due to inferior MI, transient (vagal)  Continue CCB or BB unless PR interval >240ms  Usually within first 24h of MI  Usually transient; observe  Atropine if symptoms or HR <45  Usually within first 24h of MI  3-7% acute MI  Inferior: gradual, stable  Anterior: sudden, 12-24h after MI  2-5% of MI  25% of acute MI  Early: may be transient due to sympathetic; atrial ischemia  Late: due to atrial stretch/HF  6-8%, may be >30% of acute MI  Due to electrical instability and increased sympathetic tone  Variable  50-110bpm, higher V- vs A-rate; in 40%, considered a reperfusion rhythm Ventricular Tachycardia  Monomorphic VT <170bpm is unusual early after STEMI, suggests pre-existing arrhythmogenic scar; recurrent ischemia usually polymorphic VT Ventricular Fibrillation  Risk factors: age, prior MI (scar), anterior MI, cardiogenic shock, LVEF, CKD  VF >48h post-MI may indicate LV dysfunction Treatment/Outcome  Up to 40% of acute MI  Occurs early in STEMI  Up to 20% of STEMI  Usually within 12-48h, can occur after reperfusion  NSVT 1-7%, sustained VT (2-3% of STEMI, <1% NSTEMI)  Usually 48h post STEMI, late VT (>48h) has very poor prognosis  5% of STEMI  1% of NSTEMI  Consider temporary pacing  In infranodal block, atropine may paradoxically worsen AV block  Recovery 3-7d; temp pacing required  Inferior: transient, resolves on own  Anterior: carries high mortality rate (80%) and indicates extensive necrosis  Patients w/ BBB are more likely to have comorbid conditions, less likely to have received therapies, have larger area infarcts, and have high mortality  Undesirable as myocardial oxygen demand, diastole time causes coronary perfusion time  Treat underlying cause  A/w mortality, particularly if late (>30d) AF (Circ 2011;123:2094)  If unstable, cardioversion; consider BB, amiodarone, digoxin, anticoagulation  Correct electrolyte deficits, BB. Do NOT treat with anti-arrhythmics as can mortality (NEJM 1991;324:781)  Do not treat unless symptomatic or hemodynamically unstable, usually short duration & does not affect prognosis  Antiarrhythmic agents (amio, lidocaine)  Urgent revasc if due to ischemia  Cardioversion/defibrillation to prevent VF and restore hemodynamic stability  Correct underlying abnormalities (pH, K, Mg, hypoxemia)  ACLS/defibrillation  Anti-arrhythmic infusion (24-48h amiodarone post-defibrillation)  Maintain K>4, Mg>2.2 Aditya Achanta 17 TOC Cardiology Cardiac Catheterization LEFT VS RIGHT HEART CATHETERIZATION • LHC (often used to describe Cor Angio): Arterial access (radial, fem). Assess coronary anatomy/lesions, LV & Ao pressures. PCI. • RHC: Venous access (IJ, fem). Assess hemodynamics (see Pulmonary Artery Catheterization); cardiac biopsies (usually RV) CO RO NARY ANATO MY • LCA and RCA & their branches create two rings around the heart: RCA + LCX in AV groove; LAD + PDA in IV groove • 80% of PDA arises from RCA (right dominant), thus inferior MI more likely due to RCA lesion; 10% from LCx; 10% co-dominant PREPARATIO N FO R CA TH ETER IZ A TIO N • NPOpMN; INR<2; monitor Cr, no ppx abx. Continue ASA, statin, BB. UFH gtt (hold when on call), LMWH (hold 24h prior; see PeriProcedural AC), hold DOACs >48hr or >72hr if CrCl<30. Hold metformin (usually 1d pre-, 2d post-proc), may hold/delay starting ACEi • Document b/l radial, femoral, popliteal, DP pulses, & Allen’s test. Check for bruits. Note history of HIT, PVD, Ao aneurysm/dissection • Contrast allergy: pre-tx w/ steroids & benadryl if patient has documented allergy. See Contrast Allergy for MGH protocols. Consult Allergy for expedited protocol if the cath is required emergently • Respiratory distress: patient will need to lie flat; consider intubation if prohibitive hypoxemia/pulmonary edema • Pre-hydration w/ crystalloids and NAC/bicarb have not been shown to prevent CIN in most patients with moderate CKD (Lancet 2017;389:1312; NEJM 2018;378:603); CIN risk calculator; See Contrast PERCUTANEOUS CORONARY INTERVENTION CONSIDERATIONS • Access: fewer bleeding/vascular complications if radial (vs femoral), possible death in ACS (JACC 2018;71:1167); due to radial vasospasm, CCB and/or nitrogylcerin is administered along with UFH to prevent arterial occlusion • BMS vs DES: in-stent thrombosis with DES with subsequent MI/revascularization andCV death; however, risk of late stent restenosis so requires longer duration of DAPT (JAHA 2021;10:e018828; Lancet 2019; 393; 2503) • Can identify HD significant lesions via: fractional flow reserve (FFR), Instant Wave Free Ratio (iFR), intravascular ultrasound (IVUS) • Contraindications to stents: predicted DAPT non-adherence, anticipated major surgery within treatment time, elevated bleeding risk • Antiplatelet: 81mg ASA indefinitely (Circ 2016;134:e123). P2Y12 inhibitor added after cath (prasugrel, ticagrelor or clopidogrel) o Not high bleeding risk: ACS, 12mo DAPT (DES/BMS); stable IHD, ≥6mo DAPT if DES or ≥1mo if BMS o High bleeding risk: ACS, 6mo DAPT (DES/BMS). In select patients, DAPT 1-3 months followed by P2Y12 monotherapy (NEJM 2019; 381:2032); stable IHD, ≥3mo DAPT if DES or ≥1mo if BMS (also consider 1-3mo DAPT followed by P2Y12 monotherapy) o Triple therapy: see ACS. Usually, 1 wk triple therapy and transition to P2Y12 inhibitor + DOAC. POST-PROCEDURE CARE • Femoral access: 4-6h bedrest after procedure. Closure devices decrease time needed for bedrest o Groin checks immediately, 6h, 8h post-procedure: check b/l pulses, palpate for pulsatile masses, auscultate for bruits o Sheaths: usually removed when PTT<60, confirm with interventional fellow; only fellows (page access fellow) remove  Radial access: TR band for 4-6h. Driven by RN protocol; if paresthesias/numbness, examine, check finger sat probe for perfusion. Can remove several mLs of air from band if necessary and if no complications. NOTE: if hematoma do not remove until fellow assesses. PO ST-CATHETERIZATIO N CO MPLICAT IO NS • Access site complications: always inform the interventional fellow who performed the procedure, diagnose by exam and US o Hematoma: mass w/o bruit. Apply compression. If unable to control, may require Fem-Stop device to apply external pressure o Pseudoaneurysm: pulsatile mass with bruit at access site. Tx w/ compression; if <2cm, may require thrombin injection or surgery if >2 cm. Urgent US & Vascular Surgery consult o AV fistula: continuous bruit with no mass. Evaluate w/ US. Surgical repair usually necessary o Limb ischemia: from thrombus, dissection, or malpositioned closure device. Evaluate pulses, limb warmth, & PVR o Retroperitoneal bleed: presents within hours post-cath, often with hemodynamic instability ± flank pain ± ecchymoses. STAT CT A/P if stable. Transfuse, IV fluids, discuss with attending about stopping/reversing anticoagulation • Other complications: o Infection: more common in setting of vascular closure devices o Atheroembolism: eosinophilia; livedo reticularis; blue toes; mesenteric ischemia; acute, subacute, or chronic renal dysfunction o CIN: occurs within 24-72h with peak Cr 1-5d post contrast load, risk correlated with contrast load and initial GFR o Tamponade: post-cath hypotension from coronary/cardiac perforation. Check pulsus (>10 mmHg), STAT TTE, alert cath fellow. o MI/CVA: due to in-stent thrombosis (MI) or distal embolization post-cath (CVA). Discuss all CP/neuro changes with cath fellow o Radiation injury: more common in CTO cases. Occurs days to weeks after PCI. Ranges from erythema to skin ulceration Will Pohlman 18 TOC Cardiology Non-Invasive Cardiac Testing STRESS TESTING BASICS • • • • • Indications: o Diagnose CAD: sx of stable angina in pts with intermediate-high risk of CAD. Not indicated for low risk or asymptomatic pts o Evaluate new or changing sx concerning for ischemia in pts with known CAD o Post-revascularization: evaluate pts with angina or asymptomatic pt if incomplete revasc or >2y post-PCI/5y post-CABG o Pre-op risk assessment: if indicated (see Perioperative Medicine) o Newly diagnosed HF or cardiomyopathy likely secondary to ischemia, functional capacity (for exercise prescription), viability testing, valvular disorders, dobutamine stress echo in LFLG AS, quantify microvascular disease (PET) Contraindications: untreated ACS, MI within 2d, high risk or LM CAD, uncontrolled arrhythmia, ADHF, severe AS or HOCM, recent DVT/PE, acute myo-/peri-/endocarditis, aortic dissection, uncontrolled HTN Preparation: NPO 3h prior, longer if imaging or adenosine. Must reverse DNR/DNI for test. o If the question is “Does the patient have CAD?”  hold BB and nitrates o If the question is “How well are meds working in known CAD?”  continue BB and nitrates o Hold BB >24h for dobutamine stress test; hold caffeine >12h for adenosine Caveats: o Majority of vulnerable plaques are angiographically insignificant (<70% stenosis)  stress testing unable to identify the presence of these plaques (CCTA more sensitive) o Angiographically significant (>70% stenosis) 3VD may produce false-negative vasodilator stress test  ”balanced ischemia”  Can see transient ischemic dilatation (apparent enlargement of LV cavity during stress) which can occur in 3VD Positive test results: optimize medical tx. Decision re: angiography/revascularization varies by pt (degree of sx, known stenosis, current meds). In ISCHEMIA trial, initial revascularization did not reduce the risk of ischemic CV events for pts with moderate to severe stable ischemic heart disease (NEJM 2020;382:1395). ROLE OF NONINVASIVE CARDIAC TESTING IN CHEST PAIN EAVLUATION Source: 2021 ACC/AHA Guidelines for Evaluation and Diagnosis of Chest Pain (Circ 2021;144:e368-e454) When deciding between CCTA (anatomic) and stress (functional) imaging in an intermediate risk patient: • If known <50% nonobstructive CAD, or age<65 years old, prior functional study without conclusive results, bypass graft assessment, and to rule out obstructive CAD, consider evaluation with CCTA FFR • If >50% obstructive CAD, age>65, to assess for specific areas of ischemia, or prior CCTA without conclusive results, consider evaluation with stress imaging. If high concern for ischemia after inconclusive stress, consider CCTA for balanced ischemia. Stress Testing Modality Exercise (treadmill) Vasodilator (adenosine, regadenoson) Inotropy (dobutamine) Imaging Modality ECG, TTE, SPECT TTE, SPECT, PET, MRI Aditya Achanta 19 TOC Cardiology Non-Invasive Cardiac Testing STRESS TESTS Exercise Tolerance Test (ETT)  ECG or imaging (TTE, SPECT) • Exercise preferred over pharmacologic testing if pt is able to reach goal exertion • Assesses exercise duration, METs, BP/HR response, HR recovery, double product (HR x SBP), Duke Treadmill Score (estimates risk of CAD in pts w/ chest pain undergoing exercise stress testing (Circ 1998;98:1622)) • Protocols: Bruce (large changes in workload between stages), modified Bruce (for less fit pts  adds stages of lower workload) • Diagnostic if >85% max-predict HR (220-age), peak double product (HRxBP) >20k, HR recovery (HRpeak – HR1min post-exercise) >12 • Increased probability of ischemia:  # of leads with STD, degree of max STD, METs when ECG changes occur, ventricular ectopy during recovery, increased time to recovery of ECG, failure of SBP to rise with exercise • Exercise ECG has much lower sensitivity than exercise imaging testing Pharmacologic Stress Test  imaging only (TTE, SPECT, PET, MRI) • Choosing an agent: o Adenosine/Regadenoson: detects ischemia by coronary steal (vasodilation via cAMP). Stenosed coronary arteries are unable to further dilate to adenosine  limited flow reserve to distal areas and relative perfusion deficit  Side effects: wheezing, bradycardia, HoTN. Caution if ACTIVE bronchospasm, high grade AVB, SSS, severe AS  Regadenoson: decreased respiratory/conduction side effects, more cost-effective in obese pts. Caution if seizure hx (reversal agent aminophylline seizure risk)  False negative can occur in 3VD: no relative perfusion deficit when all 3 vessels affected equally (“balanced ischemia”) o Dobutamine: workload induced by positive inotropy and chronotropy via β-1 receptor agonism  Extremely high dose of dobutamine is given, dose titrated up to 40mcg/kg/min  Side effects: tachyarrhythmias. Caution if MI <48h, hx of malignant arrhythmia, severe AS, HOCM, severe HTN, severe PAH, aortic dissection • Choosing an imaging modality: o TTE: preferred if primary objective is to exclude CAD (76% Sn, 88% Sp). Can give info regarding hemodynamics/valve disorders  Do not use in pts with LBBB, V-pacing or extensive wall motion abnormalities at rest o Nuclear imaging: utilizes a radioactive tracer to detect areas of perfusion between rest and stress states. More expensive than TTE & high amount of radiation (SPECT > PET)  PET is more Sn & Sp than SPECT with faster image acquisition, quantitative. Less widely available & most expensive. Additional uses for imaging in rheumatologic (i.e. cardiac sarcoid) and oncologic contexts (i.e. cardiac myxoma, metastases) VIABILITY TESTING • • Indication: determine viability of ischemic myocardial tissue (“hibernating myocardium”) Imaging modalities: SPECT (thallium or sestamibi), PET, TTE, MRI o SPECT is performed using exercise or pharmacologic stress. PET/TTE/MI performed using pharmacologic stress only REST IMAGING Coronary CTA: used to evaluate for presence and extent of CAD, provides anatomic information (JACC 2010;55:2663) • Requires cardiac gating (goal HR 60-70, may need to give BB) and respiratory gating (breath hold for 5+ sec) • Indications: o Should NOT be used to screen asymptomatic pts o Low risk pts: has high NPV (99%) for CAD rule-out (JACC 2008;52:1724) o Moderate risk pts: reasonable to further risk stratify pts at intermediate risk of CAD or pts with equivocal stress test results • Findings: 2y ACS risk significantly elevated if high-risk plaque (16%) and/or stenotic disease (6%) (JACC 2015;28:337) o Higher Sn & Sp for coronary stenosis compared to cMRI (Annals 2010;152:167) o CT-Fractional Flow Reserve (FFR): can be computed on CCTA to determine hemodynamics of stenosis • Less useful in pts with extensive calcifications or stented vessels due to “blooming” artifact (cannot evaluate patency) Coronary Artery Calcium (CAC) Scans: CT modality that provides risk assessment score (CAC or “Agatston” Score) for CAD and ASCVD risk stratification. Either performed alone or concurrently with coronary CTA. Non-gated, non-contrast chest CT scans can be used to provide a qualitative estimation of CAC score • Indications: to guide decision making for primary prevention for asymptomatic adults ≥40y at intermediate risk (7.5-19.9% 10y ASCVD risk) if statin therapy decision remains uncertain. Do NOT use as a stand-alone test in evaluation of symptoms of myocardial ischemia. Do NOT use in high risk patients, including those with familial hypercholesterolemia • Findings: o If CAC (Agatston) scores ≥100 or >75 %ile for age & gender independent of ASCVD risk, recommend aggressive therapeutic lifestyle changes, ASCVD RF modification (BP, smoking cessation, diabetes treatment), & statin therapy (JACC 2019;73:285) o For those with calcium score of 0 without significant risk factors, reasonable to defer statin therapy for up to 5 years (Circ 2019;140:496) o MESA score accounts for CAC score and is able to refine 10 year risk estimates Cardiac MRI: • Modality of choice for assessment of funtional & tissue properties of the heart that cannot be adequately assessed w/ echocardiography or CCTA (inflammation, infiltration, cardiac tumors, pericardial disease) • Preferred for post-CABG vessel imaging, evaluation of suspected or known congenital or acquired coronary abnormalities Aditya Achanta 20 TOC Cardiology View/Description Position PARASTERNAL LONG AXIS • • • LV size, function, wall thickness (septum/posterior wall) MV/AoV function/flow (w/ Doppler) LVOT diameter, aortic root size • • • View* Cross-sectional views of the heart from base to apex, at level of AoV, MV and midventricle/papillary muscles APICAL 4 CHAMBER • • Patient: lying on left side, with left arm under head Probe: 2-3 inches left of sternum at 3rd-4th intercostal space, indicator at 10 o’clock (facing R shoulder) Patient: same as above Probe: from long axis view, turn probe clockwise until indicator at 2 o’clock (facing L shoulder) PARASTERNAL SHORT AXIS • Echocardiography RV/LV size, function, thrombus TV/MV function/flow (w/ Doppler) Septal size/motion Pericardial effusion In 5-chamber view, can see AoV and proximal ascending aorta Patient: lying flat on back or left decubitus Probe: at PMI w/ probe indicator at 3 o’clock (to the pt’s L). For 5-chamber view, tilt probe upward Patient: laying flat on back, can slightly bend legs Probe: below xyphoid process, indicator to pt’s R SUBXIPHOID • • RV/LV size, function Pericardial effusion Patient: same as above Probe: rotate probe 90°, indicator to patient’s head INFERIOR VENA CAVA • IVC diameter and respiratory variation gives estimate of volume status and RA pressure REVIEWING • • • • • THE Valvulopathy: stenosis/regurgitation (valve area, gradients, severity), leaflets, vegetations Structure/chamber dimensions: aorta, LVIDd & LVIDs (LV internal diameter in diastole, range: 42 – 58mm & systole, range: 25 – 40mm), IVS (septum, 6-10mm), PWT (posterior wall thickness, 6-10mm,  in LVH, diastolic dysfunction), LV volume (ULN: 74ml/m2 in men 61 in women, <40 suggest restrictive), LA volume (ULN: 34ml/m2, in MR/MS, diastolic dysfunction, AF) EF: “preserved” EF ≥50%, “borderline” EF 40-50%, “reduced” EF <40% WMA: territory correlates w/ coronary vessels (anterior + septal = LAD, inferior = RCA, lateral = LCx). If global WMA, r/o diffuse ischemia vs non-ischemic insult (sepsis, stress) RVSP: RVSP=4v2 + RAP. RAP assumed to be 10 mmHg and v = TR jet velocity CLINICAL QUESTIONS • • • • • • *Images from: Soni, N. J., Arntfield, R., &amp; Kory, P. (2020). Point of care ultrasound. Elsevier. M G H R E P O R T : for questions or clarification of findings, call Echo Lab (x6-8871) or page on-call Echo Fellow AND Indications for STAT TTE: - Eval hemodynamic instability of suspected cardiac etiology - Eval for early MI complication - Suspected MI w/ non-diagnostic biomarkers and EKG - Identify potential cause of cardiac arrest ASSOCIATED TTE FINDINGS Right heart strain in acute PE: RV WMA or hypokinesis, RV dilation (RV:LV ratio >1), interventricular septal bowing, IVC collapse, “D-sign”: septal flattening, “McConnell’s sign”: RV free wall akinesia w/ normal RV apex motion (77% Sn, 94% Sp for acute PE) Tamponade: large effusion, swinging heart, R-sided chamber collapse, interventricular septal bowing, dilated IVC (no  w/ inspiration) ACS/mechanical complications of ACS: regional WMA, septal/free wall rupture, acute MR, LV thrombus Stress (Takotsubo) cardiomyopathy: LV apical ballooning and akinesis/hypokinesis; Heart failure: depressed EF, RV/LV hypertrophy and/or dilation Diastolic dysfunction: LA enlargement, E/e’ >14, LVH (note: diastolic dysfunction not typically called on MGH TTE reports) Constrictive pericarditis: thickened or hyperechoic pericardium, abnormal septal motion, respiratory variation in ventricular size, dilated IVC Sharon Grossman 21