Acute MI Complications Jay Gardner Stern Cardiovascular February 28, 2015

Types of Complications Related to the acute MI myocardial death Procedural/Therapy related complications

Acute MI results from occlusion of a coronary artery causing myocardial death

Complications related to Acute MI Cardiac Arrest Heart Failure/Shock Arrhythmia, usually VT/VF Stroke from LV thrombus Structural disruption (free wall rupture, mitral regurgitation from papillary muscle dysfunction, VSD)

Location location location Some complications can be anticipated based on location of infarct

Anterior STEMI - LAD usually large amount of myocardium “widow maker” Post MI complications include shock, low EF/CHF, embolic, and heart block

Inferior STEMI - RCA / Cx Arrhythmias/ bradycardia common RV infarct - drop in pressure with SLNTG, post MI hypotension ischemic MR

Thromboembolic Stroke - 3-6% of large anterior MI 3mos anticoagulation

Cardiac Arrest Usually arrhythmia related from ischemia/scar Dismal prognosis if not witnessed and resuscitated quickly (survival rate 10% approximately Early hypothermia protocol may improve neurologic outcome Source: Heart Disease and Stroke Statistics-2013 Update Circulation 2013

Free Wall Rupture.5% of MI pts in PCI era 5d-2wks post MI sudden onset CP with cough/strain, but may have subacute course high mortality

Mitral Regurgitation/Papillary muscle rupture 7% of pts with CV shock have PMR Acute pulm edema usually Inferior MI

VSD Rare in PCI era.2% usually 24hrs post MI harsh systolic murmur can be treated surgically

Procedural/Therapy Related Complications

Abbreviated List of Things That Can Go Awry Bleeding (Access site vs. non-access site) Sedation Contrast Rare procedural complications (stroke, dissection, perforation/tamponade et. Al.) Bleeding

Treatment of acute MI is a balancing act between bleeding and thrombosis Patients often pre-treated with heparin and aspirin Given full anticoagulation with Angiomax (Bivalirduin) or heparin during intervention Treated with 2 nd potent anti-platelet inhibitor (Plavix, Effient, Brilinta) +/- GP IIBIIIA inhibitor

Lots of Post-PCI bleeding 6% of patients experience bleeding 2/3 is access site bleeding Non-access bleeding usually GI (less frequently intracranial) Bleeding strongly associated with increased mortality Risk Factors include: – increasing age – female gender – shock – renal disease – STEMI – CHF – Larger sheath Source: Rao et. Al. An Updated Bleeding Model to Predict the Risk of Post-Procedure Bleeding Among Patients Undergoing Percutaneous Coronary InterventionA Report Using an Expanded Bleeding Definition From the National Cardiovascular Data Registry CathPCI Registry JACC Interventions 2013

Access Site Complication: Hematoma Due to closure device failure, inadequate manual compression, spontaneous re-bleed, ? pseudoaneurysm Treatment: PUSH!

Pseudoaneurysm Hole in femoral artery allows bleeding and formation of hematoma, constricted by surrounding tissue Treatment: Ultrasound- guided compression, thrombin injection, surgery

AV Fistula Connection between artery and vein, may be associated with thrill on exam Treatment is surgical

Retroperitoneal Bleed Life threatening and tough to diagnose Usually no hematoma Nothing to stop the bleeding! Hypotension usually late sign, tachycardia and back pain earlier symptoms Can be managed with more compression or percutaneously

Best Management for Access Site Bleeding

Other Bleeding Comments Rarely need to continue therapeutic anticoagulation after PCI Manage non-access site bleeds as per usual, discuss anti-platelet strategy as team When in doubt, manual compression and then call, not the other way around

Sedation Standard sedation risks apply: – Hypotension – Respiratory depression – Aspiration – Paradoxical agitation – Allergic reaction

Contrast: Allergic Reaction Anaphylactic reactions- airway compromise, hypotension, rash Anaphylactoid reaction- similar but not as rapid or severe, non-IgE mediated Minor rxn- itching, urticaria, nausea/vomiting Prevent with premedication: – Oral steroids 1-2 days before procedure. – If urgent, 125 solu- medrol IV – Benadryl 50mg IV – Epi IV for anaphylactic rxn, subQ for anaphylactoid

Contrast Nephropathy Creatinine increase starts in hours Peaks around 5 days Normalizes by 10 days Generally requires increase of 0.5 mg/dL to meet criteria Somewhere around 5-10% of patients experience Strong association with mortality

CIN Risk Factors High baseline Cr Diabetes Older Age Female gender EF <40% Hypotension ACS CHF Nephrotoxic drugs Shock Increased contrast volume (PE protocol CT 100mL of dye, PCI around 200mL)

CIN Prevention

What Doesn’t Prevent CIN? Lasix Mannitol Dopamine N-Acetyl-Cysteine (ACT Trial) Bicarbonate controversial CVVT and HD ineffective ACE/ARB therapy possibly increases risk

Probability of death or need for dialysis from the day of randomization (day 0) to day 30 among patients in the acetylcysteine and placebo groups. ACT Investigators Circulation. 2011;124: Copyright © American Heart Association, Inc. All rights reserved.

Effect of acetylcysteine on contrast-induced acute kidney injury according to subgroup. ACT Investigators Circulation. 2011;124: Copyright © American Heart Association, Inc. All rights reserved.

Post MI Practical Office Care 2015 Cardiac Rehab Medical tx – Aspirin - 50% risk reduction – Statin - moderate intensity (Atorva 40 Crestor 20) Post MI EF – <40% independent predictor mortality – BB and ACEI titrated to max doses – ICD if EF < 35%, Life vest Diet: Low Fat is OUT Risk Factors: Smoking cessation, DM, HTN

Questions?