Percutaneous Mechanical Circulatory Support for Cardiogenic Shock. 24 th Annual San Diego Heart Failure Symposium Ryan R Reeves, MD FSCAI
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1 Percutaneous Mechanical Circulatory Support for Cardiogenic Shock 24 th Annual San Diego Heart Failure Symposium Ryan R Reeves, MD FSCAI
2 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
3 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
4 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
5 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
6 Clinical Scenarios Procedural Support Coronary Artery Disease and Acute Myocardial Infarction Acute Cardiogenic Shock Chronic Heart Failure Complications of Myocardial Infarction Right Heart Failure
7 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) 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) 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 () min: Art & vein access, pump priming 4-5L Hemolysis, thrombocytopenia, infection, stroke, limb ischemia, perfusionist, LV venting
8 Devices Decrease afterload (E a ) and increase SV Reduce LV pressures and volume Increased LV pressure Rihal CS, et al. CCI 2015
9 DATA- IABP-SHOCK Shock and Acute MI - Randomized, prospective, trial 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
10 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
11 DATA- PROTECT II Hemodynamic Support and PCI - Randomized, prospective, trial patients with 3vd or LM & severely depressed EF (<30-35%) - Non-emergent PCI - PEP: DC/30d MACE - IABP vs Impella Not significant 30d primary end point More aggressive atherectomy in Impella group Trend to less repeat PCI - Larger difference in vs 2008, suggesting increased experience - Non-emergent PCI - PEP: DC/30d MACE - IABP vs Impella 2.5 O Neill WW, et al. Circulation 2012
12 Cases
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