Complications of

Rekha Mankad, MD, FACC

Assistant Professor of Mayo Clinic College of Medicine Director, Women’s Clinic Mayo Clinic, Rochester, MN [email protected] @RMankadMD DISCLOSURE

Relevant Financial Relationship(s) None

Off Label Usage None

©2016 MFMER | slide-2 Objectives •Review subacute and acute presentations of complications related to an acute coronary event •Review how echocardiography can be used to determine the etiology of a complication post-MI

©2016 MFMER | slide-3 Case • 54 year old male • Smoker; no other significant PMH • 3 weeks of intermittent chest tightness • 3 days prior to presentation severe pain (curled up into a fetal position): didn’t come into hospital; pain resolved and he went to work • Then recurrence of pain- lasted 4 hours and finally decided to come to hospital

©2016 MFMER | slide-4 Case • In ER: pain ongoing although milder; diaphoretic • Vitals: HR 114 (sinus tachycardia), BP 141/100 • Exam: No evidence of heart failure; no murmurs

©2016 MFMER | slide-5 EKG

©2016 MFMER | slide-6 Coronary Angiogram • 100% proximal LAD • In addition, high grade proximal RCA lesion (90%), diagonal 1 with 70% lesion • Successful PTCA of the LAD- 3.0 x 38 mm DES • Does well with the procedure • No hemodynamic compromise • Troponin T: 0.96, 0.88, 0.95

©2016 MFMER | slide-7 What is the next best step?

A. Perform RCA intervention prior to dismissal B. Dismiss in a 2 days with outpatient follow up C. Perform a low level stress ekg prior to dismissal D. Perform an echocardiogram E. Perform a stress echocardiogram prior to dismissal

©2016 MFMER | slide-8 Role of Echocardiography after a STEMI

• Class I • LVEF should be measured in all with a STEMI (Level of evidence: C)

©2016 MFMER | slide-9 Echocardiography

LV

©2016 MFMER | slide-10 What would you do next? A. Repeat angiography B. Dismiss to home with close outpatient follow up C. Initiate VKA D. Initiate DOAC E. Perform contrast echocardiography

©2016 MFMER | slide-11 ©2016 MFMER | slide-12 What is the incidence of an LV in a such as ours?

A. ≤2% B. 2-5% C. 10-15% D. ≥25%

©2016 MFMER | slide-13 Am J Cardiol 2010;106:1197–1200 •Conclusion:100 patients LV thrombus formation is •aDual frequent anti-platelet finding in patientspost primary with PCI •anteriorSerial imaging wall studiesST elevation (Stem Cell myocardial protocol) •infarctionLV thrombi detectedtreated inacutely 15 patients withduring PCI the and first dual3 months, antiplatelet 2/3 of them therapy within the and first should week be • Associated with lower EF (43.0% vs 46.0%, p<0.03) assessedand larger infarct by echocardiography size (p<0.01) within the first week. LV Thrombus Post-MI

• Static flow in region of akinesis or dyskinesis • Apical MI location • Reduced EF (<30%) • Risk of Emboli • Differentiate from trabeculation (multiple planes) STEMI Guidelines: 2013 • Class IIa: • Anticoagulant therapy with a Vitamin K antagonist is reasonable with patients with STEMI and asymptomatic LV mural thrombi (LOE: C) • Class IIb: • Anticoagulant therapy may be considered for patients with STEMI and anterior apical akinesis or dyskinesis (LOE: C) • Targeting vitamin K antagonist therapy to a lower INR (2.0-2.5) might be considered in patients with STEMI who are receiving DAPT O’Gara, P et al. Circulation 2013; 127: e362-e425

©2016 MFMER | slide-16 LV Aneurysm vs LV Pseudoaneurysm

Images Courtesy of Dr. W. Edwards MD

©2016 MFMER | slide-17 LV Apical Aneurysm

©2016 MFMER | slide-18 LV Pseudoaneurysm

LV

©2016 MFMER | slide-19 LV Pseudoaneurysm

©2016 MFMER | slide-20 Left Ventricular Pseudoaneurysm

Video by Dr. Roger Click ©2016 MFMER | slide-21 LV Aneurysm vs Pseudoaneurysm

From Braunwald’s Textbook of Heart

©2016 MFMER | slide-22 LV Aneurysm vs LV Pseudoaneurysm • Post-MI LV pseudoaneurysm occurs when a rupture of the LV free wall is contained by overlying, adherent pericardium → usual treatment is urgent surgical repair • Post-MI LV aneurysm is caused by scar formation resulting in thinning and expansion of the myocardium → usual treatment is conservative unless refractory angina, heart failure or ventricular

Brown SL et al. Chest 1997; 111:1403-09

©2016 MFMER | slide-23 Pseudoaneurysm Clinical Characteristics

• Congestive heart failure, , dyspnea most common • ~10% without any symptoms • EKG nonspecific; 20% with ST elevation • Inferior infarcts > anterior infarcts

Frances C et al. JACC 1998; 32(3): 557-561 ©2016 MFMER | slide-24 Not Always Easy: LV Aneurysm

• It can sometimes be tricky to determine the size of the neck to body ratio as demonstrated in this short-axis view. The posteromedial papillary muscle makes it seem like the neck is narrow, but on closer inspection there is a wide neck to base ratio in this basal infero-septal LV aneurysm.

©2016 MFMER | slide-25 Case • 78 year old female • Presented with chest pain and evidence of “NSTEMI” by biomarkers • EKG - nonspecific • Echocardiogram: Preserved EF, lateral HK • Cath: occluded diagonal, 70% RCA and LCx  planned medical tx • Worsening dyspnea and atypical chest pain 48 hours after admission

©2016 MFMER | slide-26 Stat Echo

LV RV

Taken Emergently to OR

©2016 MFMER | slide-27 Myocardial Free Wall Rupture

30-40% of patients may have “subacute” free wall rupture - -Nausea/emesis -Pericardial chest pain

©2016 MFMER | slide-28 ©2016 MFMER | slide-29 Myocardial Free Wall Rupture • Occurs in approximately 1% of MI’s • Accounts for up to 8-17% of deaths • Second most common cause of death after MI following pump failure • More common in women, hypertensive and older patients • Typically 5-7 days post infarct • Single CAD • Usually no clinical warning signs • Sudden death

©2016 MFMER | slide-30 More Typical Scenario for Myocardial Rupture •65 year old male •Inf Lat MI, PCI with DES, EF 45%

©2016 MFMER | slide-31 2 days later •Patient in bathroom, •Stat Echo during code •Echo reveals rupture with coagulum

©2016 MFMER | slide-32 Myocardial Rupture  Tamponade  Death

Image Courtesy of William Edwards, MD ©2016 MFMER | slide-33 Etiology of Cardiogenic Shock After Acute MI 251 patients from 19 centers LV failure 85%

8% 5% VSD or MR

Others RV infarct (2%)

Hochman JS et al. Circulation 1995; 91:873-881 ©2016 MFMER | slide-34 Post-MI Ventricular Septal Rupture or Defect

©2016 MFMER | slide-35 Post MI VSD: GUSTO-I Study

• Incidence 0.2% (84 of 41, 021 patients) • Onset 1 day • Mortality 74% (47% vs 94%) • Association with Medical Tx •Age •Anterior MI •Female sex •Nonsmoker •Higher HR on admission •Greater heart failure on admission Crenshaw BS et al: Circulation 2000; 101:27 ©2016 MFMER | slide-36 Case: Apical VSD •84 year old female, post-MI day 5 •Sudden onset, pulmonary edema, loud murmur

©2016 MFMER | slide-37 • CHF improved with medical treatment • Multidisciplinary discussion, not felt to be a good surgical candidate, VSD closed in cath lab with device

©2016 MFMER | slide-38 Post Infarct VSD

• Poor Location and size for device closure in Cath Lab

©2016 MFMER | slide-39 66 yo man – Single vehicle MVA Multiple injuries : - Loss of consciousness, confusion - Open, compound fracture of right leg (mid tibia, lateral malleolus) - Closed fracture of left leg - L3 and L5 burst fractures - Initial BP 130/80 mmHg, pulse 102 bpm - Lactate level 6.8 In Trauma bay after pan CT : c/o severe chest pain - SBP decreased to 80 mm Hg - 66 yo man with chest pain : EKG How would you manage this patient next? 1. Supportive medical therapy, including ASA but no heparin or clopidogrel 2. Emergent coronary angio and POBA; ASA but no heparin or clopidogrel 3. Emergency coronary angio with PCI; dual antiplatelet Rx and heparin 4. Prayer 66 yr man – Single vehicle MVA

- Anterior ST elevation MI - Cath lab activated Agreement between cardiology, ortho, trauma, and neurosurgery that MI care superseded injury management - Rx in ED: aspirin, ticagrelor, heparin - Emergency coronary angiography Coronary Angiography Successful Revascularization 66 year old man – Anterior STEMI In cath lab, then CCU - Shock, SBP as low as 50 mm Hg - Intubated, sedated - Intra-aortic balloon pump - IV dopamine, norepinephrine - IV blood and fluids - Persistent hypotension (SBP 70-90 mmHg) - Quick-look Transthoracic Echo TTE – Subcostal View

small IVC, tiny pericardial effusion What would you do next? 1.Repeat ECG 2.Repeat CT chest, abdomen 3.Cardiac MRI 4.TEE 5.Supportive medical care in CCU TEE - LV Function TEE TEE - LVOT CW Doppler LVOT

Peak velocity 5.8 m/s, Peak gradient 135 mm Hg TEE - LVOT Before After

1. Stopped IV norepinephrine 2. Stopped IV dopamine 3. Removed IABP 4. Given intravascular volume CW Doppler LVOT

Before After

Peak LVOT velocity 5.8 m/s Peak LVOT velocity 1.6 m/s TEE – LV Function (after) 66 yr man Anterior STEMI, Dynamic LVOT Obstruction

Hospital course (15 days): - Remained on dual antiplatelet Rx - 2 days later – Ortho surgery (fasciotomies and bilateral external fixation of leg fractures) - Eventually recovered and doing well ©2016 MFMER | slide-57 62 yo woman with chest pain and severe pulmonary edema

Courtesy John Gorcsan, MD ©2016 MFMER | slide-58 Papillary Muscle Rupture 3D TEE and Gross

Courtesy John Gorcsan, MD ©2016 MFMER | slide-59 Papillary Muscle Rupture

• Loss of papillary muscle integrity • Typically occurs 3-7 days after infarct • Hemodynamically, the most serious MV complication • Most commonly involves small infarct of RCA or Circumflex (inferior, inferolateral MI) → posteromedial papillary muscle • Rupture of RV papillary muscle rare

©2016 MFMER | slide-60 Partial Papillary Muscle Rupture

©2016 MFMER | slide-61 Partial Papillary Muscle Rupture

LV RV

©2016 MFMER | slide-62 Partial Papillary Muscle Rupture Severe Eccentric Mitral Regurgitation

Patient underwent successful mitral valve repair

©2016 MFMER | slide-63 Late survival in operative survivors

©2016 MFMER | slide-64 Differential Diagnosis of a New Loud Systolic Murmur Following MI VSD Pap Musc Rupt. LVOT Obst. Location Anterior or Inferior > Usually Anterior Inferior Anterior (Apical)

Signs Low Cardiac Pulmonary Hypotension Output Edema

Hemodynamics O2 step-up V wave on Dynamic LVOT (RA→PA) > 10% PCWP tracing Obstruction

Treatment Operation Operation Fluids, β - blocker, - agonist

Adapted from Oh JK et al. Echo Manual 3rd Edition ©2016 MFMER | slide-65 Conclusions: Echo for MI Ruptured complications papillary muscle

Dynamic LV Free wall rupture Outflow Tract Obstruction

Ventricular septal rupture False aneurysm

Right ventricular True infarction aneurysm

Pericardial effusion Mural thrombus

©2016 MFMER | slide-66 Thank You! [email protected] @RMankadMD

©2016 MFMER | slide-67