Complications of Myocardial Infarction Rekha Mankad, MD, FACC Assistant Professor of Medicine Mayo Clinic College of Medicine Director, Women’s Heart 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 patients 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 thrombus in a patient 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 therapy 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 Disease ©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 arrhythmia Brown SL et al. Chest 1997; 111:1403-09 ©2016 MFMER | slide-23 Pseudoaneurysm Clinical Characteristics • Congestive heart failure, chest pain, 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 -Hypotension -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, syncope •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) Surgery • 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 Pathology 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.