PUMP FAILURE COMPLICATING AMI: ISCHAEMIC VSR

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1 PUMP FAILURE COMPLICATING AMI: ISCHAEMIC VSR Dr Susanna Price MD PhD MRCP ESICM FFICM FESC Consultant Cardiologist & Intensivist Royal Brompton & Harefield NHS Foundation Trust

2 DECLARATIONS Educational contract: Medtronic

3 Key messages VSR with cardiogenic shock: almost invariably fatal New chest pain/ecg changes should prompt clinical examination & echo If diagnose VSR refer & intervene before shock supervenes Be aware that standard supportive guideline therapies for acute HF may be harmful

4 Mortality: cardiogenic shock in AMI Goldberg NEJM 1999; 340:1162

5 Aetiology: cardiogenic shock % LV failure Acute MR SHOCK Trial and Registry (N=1160) 8.3% 4.6% 3.4% 1.7% 8% VSD RV Infarct Cardiac Rupture Hochman Circ 1995; 91: Other

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7 Physiology in ischaemic VSD Size of infarct LV +/- RV (does not correlate with outcome) LV dysfunction (does not correlate with outcome) Inter-ventricular shunt (size does not correlate with outcome) Progressive RV dilatation & failure (correlates with outcome) CI <1.75L/min/m2 most powerful predictor of survival Contribution of septum complex (inferior vs anterior infarcts) Complex vs simple defects Anatomy of the IVS vs septal rupture Not solely dependent upon coronary artery disease and ischaemia Increased (and reactive) PVR Moore, Circulation 1986

8 Historical perspective Brunn A-M diagnosis Sager Clinical signs described Cooley First successful surgical repair Proudfoot First surgical series

9 Historical perspective /

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11 55% mortality within 1 week 4 survived >8 days without surgery Of those operated: 9/19 (47% survival to discharge) 4/4 late repair (>10 days) survived 5/15 early repair survived

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13 Effects on VSR? 6678 consecutive patients, 425 free wall rupture, 145 VSR

14 Changing interventions for CR?

15 Effects on mortality? Reduction in mortality thought to be multifactorial (& despite significant increase in age; 66.5 vs 75.4yrs) Rates of death from EMD reduced (71.8 vs 47.2%) Rates of death from CS increased (25.6 vs 49%) Operated VSR: mortality less if later than 5 days (27 vs 73%)

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17 Associated factors in heart rupture History: Older, female, history of CVA Presentation: Increased: STEMI, elevated biomarkers, higher GRACE score, higher creatinine Lower: SBP, Killip class I, medication for IHD Treatment: Primary PCI not related to cardiac rupture Time delay from onset of symptoms to thrombolysis increased in cardiac rupture patients

18 Do cardiology interventions increase rupture risk? Usually transmural infarction with haemorrhagic transformation Rather than contained, begins at epicardium/continues through to epicardium Increased haemorrhage postthrombolysis esp if delayed Decreased risk <7h, increased risk >17h (delay in thrombolysis) Confirmed by GISSI-2, not by LATE NB incomplete revascularisation also associated with increased rupture Honan et al., JACC 1990

19 Factors related to heart rupture (GRACE)

20 Mortality (GRACE) 60, 198 patients enrolled 0.45% heart rupture (0.25% VSR) 0.9% STEMI, 0.15% NSTEMI Mortality 41% VSR vs 4.5% no VSR (p<0.001)

21 Post-rupture intervention? Intravenous drugs Renal support Devices Surgery Diuretics Vasodilators Inotropes / vasopressors Ultrafiltration Haemofiltration Peritoneal dialysis or haemodialysis CRT IABP; Impella (micro-axial pump) Ventricular assist devices, total artificial heart AMI (ischaemic VSD, papillary muscle rupture) Aortic dissection CABG in unstable coronary syndromes Percutaneous valve replacements Ventricular assist devices, Transplantation

22 Supportive interventions? Recommendations ESC guidelines on AHF: Reserve intubation/ventilation for hypercapnia? Judicious use of inotropes and vasoactive agents? IABP ESC/ESCTS guidelines 2010, Ic (effects maximal within first 24h)

23 Copyright 2008 The Society of Thoracic Surgeons Epidemiology: contemporary surgical series 64 patients (10 years) Mean age 70 +/-7yrs Median time to onset 5 days Survival (surgical): 30d: 71% 1yr: 48% 5yr: 32% Survival (medical): 0% Early repairs: lower BP CS on admission/developing after: 100% mortality Poulsen S. H. et al.; Ann Thorac Surg 2008;85:

24 Outcomes Early survival: medical vs surgical Late survival: timing of surgery Late survival: age Poulsen S. H. et al.; Ann Thorac Surg 2008;85:

25 VSD post-mi: surgeon s perspective Unoperated: 25%/24 hours 50%/1 week 65%/2 weeks 80%/4 weeks >>90% 1year Mortality in presence of CS: VSR: 100% vs 38% (G R A C E r e g i s t r y ) (Free wall rupture: 85% vs 79%)

26 Device therapies N=29; patients underwent primary transcatheter VSD closure Median follow-up time of surviving patients: 730 days Median time between VSD occurrence and closure: 1 day [IQR 1 3] Procedure-related complications such as major residual shunting, left ventricular rupture, and device embolization: 41% Overall 30-day survival rate:35% Mortality was higher for cardiogenic shock vs non-shock patients (88 vs. 38%, P, 0.001) Long-term mortality for CS %

27 Current recommendations The natural history [sic] is characterized by a rapid downhill course and medical treatment alone results in close to 100% mortality With persistent haemodynamic deterioration despite the presence of an intra-aortic balloon pump (IABP), surgery should be performed as soon as possible (Ib) There is limited evidence to support percutaneous attempts at defect closure either transiently using balloons or durably with implantation of closure devices Pre-operative coronary angiography is recommended. Achieving complete revascularization in addition to correcting the mechanical defect improves the clinical outcome (Ib)

28 Why is the mortality of ischaemic VSR in CS still so high?

29 Cardiogenic shock: a systemic disease Vasoplegia VA uncoupling Neurohormonal activation Oxidative stress Progressive MOF if cause not reversed

30 Why is the mortality in CS still so high? Premise of successful management of CS: reverse the underlying cause: in treating VSD, converting one cause to another In the context of RV infarction and/or dysfunction plus abnormal pulmonary vascular resistance, contribution of the IVS to maintaining CO is crucial

31 Additional measures? Earlier detection of inadequate cardiac output state(regional oxygen delivery/consumption) Extracorporeal support (LVAD, RVAD, BiVAD, VA ECMO, percutaneous VAD) Delayed surgical/catheter intervention whilst avoiding systemic inflammatory response from CS Learning from elderly hearts: identification and modulation of cardiac remodelling

32 Key messages VSR with cardiogenic shock: almost invariably fatal New CP/ECG changes should prompt clinical examination & echo If diagnose VSD refer & intervene before shock supervenes Be aware that supportive therapies may be harmful

33 Shock, a momentary pause in the Act of Death Warren JC. Surgical Pathology and Therapeutics. Philadelphia: Lea & Febiger; 1895 Dr. J. Collins Warren ( ), circa 1890

34 THANK YOU Dr Susanna Price MD PhD MRCP ESICM FFICM FESC Consultant Cardiologist & Intensivist Royal Brompton & Harefield NHS Foundation Trust