Percutaneous Mechanical Circulatory Support for Cardiogenic Shock. 24 th Annual San Diego Heart Failure Symposium Ryan R Reeves, MD FSCAI

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Percutaneous Mechanical Circulatory Support for Cardiogenic Shock 24 th Annual San Diego Heart Failure Symposium Ryan R Reeves, MD FSCAI

The Need for Circulatory Support Basic Pathophysiologic Problems: End-organ hypoperfusion Coronary hypoperfusion High myocardial oxygen demand and wall stress High cardiac filling pressures Consequential Problems: Multi-organ failure Myocardial ischemia and infarction Progressive systolic dysfunction Pulmonary and peripheral congestion

Starling Curves Steady State Myocardial Ischemia Cardiogenic Shock E max - Load independent contractility E a - Arterial elastance, ratio of LVESP and SV. Rihal CS, et al. CCI 2015

Pharmacologic Support Target + Activity Beta 1 agonist Beta 2 agonist Alpha 1 agonist Contractility Increase Afterload Decrease Blood pressure Neutral slight increase -- Decrease Decrease -- Increase Increase V1 agonist -- Increase Increase Myocardial O 2 demand Increase (direct) Decrease (indirect) Increase (indirect) Increase (indirect) Agent Dobutamine Dopamine Norepinephrine Phenylephrine Epinephrine Receptor selectivity β1 ag > β2 ag +/- isomers α1 ag & ant Low dose Dopa ag Medium (2-10) β1 ag High (>10) α1 ag α1 ag > β1 ag α1 ag High α1 ag = β1 ag PDE3 antagonist Increase Decrease Neutral slight decrease Increase (direct) Vasopressin Milrinone V1 ag PDE3 ant

Pharmacologic Support Agent Receptor Selectivity Detrimental Effects Dobutamine Dopamine β1 ag > β2 ag +/- isomers α1 ag & ant Low dose Dopa ag Medium (2-10) β1 ag High (>10) α1 ag Hypotension, arrhythmia, direct increase myocardial O 2 demand Arrhythmia, direct/indirect increase myocardial O 2 demand, coronary vasoconstriction Norepinephrine α1 ag > β1 ag Indirect increase myocardial O 2 demand, coronary vasoconstriction Phenylephrine α1 ag Indirect increase myocardial O 2 demand, coronary vasoconstriction Epinephrine High α1 = β1 ag Arrhythmia, direct/indirect increase myocardial O 2 demand, coronary vasoconstriction Vasopressin V1 ag Indirect increase myocardial O 2 demand, coronary vasoconstriction Milrinone PDE3 ant Hypotension, < arrhythmia, direct increase myocardial oxygen demand

Clinical Scenarios Procedural Support Coronary Artery Disease and Acute Myocardial Infarction Acute Cardiogenic Shock Chronic Heart Failure Complications of Myocardial Infarction Right Heart Failure

Devices Device Access Placement Output Post-Placement Concerns IABP Femoral or axillary artery (7-8F) 5-20 min: Art access, X-ray/fluoro 0.5-1L Ineffective with tachycardia, device fracture/malfunction, aortic regurgitation Impella Femoral, axillary, subclavian (14, 21F) 15-30 min: Art access, cross aortic valve, Fluoro 2.5, 4 (CP), 5.0L Hemolysis, mitral valve interactions, VT, no oxygenation capability, not optimal for LV VT ablation, limb ischemia, contraindicated if LV thrombus Tandem Heart Femoral artery (15-17F), femoral vein (21F) 30-60 min: Art & vein access, trans-septal, pump priming, Fluoro & TEE/ICE 4-5L Limb ischemia, contraindicated in LA thrombus, may place oxygenator, perfusionist VA-ECMO Femoral artery (), femoral/jugular vein () 25-60 min: Art & vein access, pump priming 4-5L Hemolysis, thrombocytopenia, infection, stroke, limb ischemia, perfusionist, LV venting

Devices Decrease afterload (E a ) and increase SV Reduce LV pressures and volume Increased LV pressure Rihal CS, et al. CCI 2015

DATA- IABP-SHOCK Shock and Acute MI - Randomized, prospective, trial - 600 patients with NSTEMI/STEMI - Shock (SBP <90mmHg for >30min, pulmonary congestion, end-organ hypoperfusion) - Early PCI expected - PEP: 30d mortality - IABP vs no IABP - 30 crossovers to IABP group (26 protocol deviations, not done for mechanical complications) - Selection bias: Rapidly deteriorating patients may not have been enrolled; biasing the study population towards patients exhibiting signs of stability with vasopressor and inotropic support. Thiele H, et al. NEJM 2012

DATA- IABP vs Impella Shock after Acute MI - Meta-analysis of three randomized controlled trial of patient with shock and acute myocardial infarction Ouweneel DM, et al. JACC 2017

DATA- PROTECT II Hemodynamic Support and PCI - Randomized, prospective, trial - 452 patients with 3vd or LM & severely depressed EF (<30-35%) - Non-emergent PCI - PEP: DC/30d MACE - IABP vs Impella 2.5 - Not significant 30d primary end point More aggressive atherectomy in Impella group Trend to less repeat PCI - Larger difference in 2009-10 vs 2008, suggesting increased experience - Non-emergent PCI - PEP: DC/30d MACE - IABP vs Impella 2.5 O Neill WW, et al. Circulation 2012

Cases