Mechanical Circulatory Support in Cardiogenic Shock
Authors, Journal, Affiliations, Type, DOI
- Werdan K (Martin-Luther-University Halle-Wittenberg), Gielen S, Ebelt H, Hochman JS (NYU Langone Medical Center)
- European Heart Journal (2014) 35, 156–167
- Type: Review article
- DOI: 10.1093/eurheartj/eht248
Overview
Published immediately following the IABP-SHOCK II trial publication (2012), this review reassesses the state of MCS devices for cardiogenic shock due to myocardial infarction (CSMI). It advances the central argument that hemodynamic improvement alone — while necessary — is insufficient for survival benefit if initiated after multi-organ dysfunction syndrome (MODS) is established. It introduces a 4-category device classification framework and provides early pre-DanGer Shock Impella data (EUROSHOCK registry; ISAR-SHOCK trial). Written before DanGer Shock, ECLS-SHOCK, CULPRIT-SHOCK final results, and Altshock-2; specific device recommendations are superseded by subsequent literature, but the mechanistic framework and conceptual arguments remain relevant.
Keywords
Cardiogenic shock, mechanical circulatory support, IABP, Impella, TandemHeart, ECMO, MODS, cardiac power output, LV unloading
Key Takeaways
Prognosis: MODS Predicts Survival Better Than Hemodynamics
- Multivariate mortality predictors (SHOCK trial/registry + TRIUMPH trial; n=1,600): age, anoxic brain damage, end-organ hypoperfusion, stroke work, LVEF, SBP, vasopressor support, creatinine clearance
- Cardiac index itself was unrelated to survival beyond the first 24 h of CSMI in the IABP-Shock study — hemodynamics alone cannot guide prognosis after 24h
- BNP levels were also unrelated to prognosis in the first 96 h of CSMI
- MODS severity (APACHE II / SAPS II scores) and SIRS biomarkers (IL-6, RAGE) predict mortality more accurately than hemodynamic indices
- Cardiac power output/index is the single strongest hemodynamic correlate of mortality in CS (SHOCK trial registry) — more predictive than CI or MAP alone
- Improving CO alone may not reverse MODS if MCS is initiated too late — haemodynamic success ≠ survival benefit
Central Argument: Early MCS to Prevent MODS
Three critical prerequisites for MCS to translate into survival benefit:
- Optimal timing — early initiation before MODS is established
- Optimal support level — adequate restoration of CI and end-organ perfusion
- Complication prevention — device complications (limb ischemia, bleeding, SIRS, infection) can outweigh hemodynamic benefit
MCS should NOT be a last resort in CSMI; it should be considered early in the disease course to minimize high-dose catecholamine toxicity on microcirculation and to prevent MODS progression.
Pharmacological Therapy
- Dobutamine: initial inotrope of choice in CS with low-output syndrome and preserved SBP; does not raise BP per se → often combined with vasopressors; all catecholamine-based inotropes cause tachycardia, ↑MVO₂, arrhythmias; in post-cardiotomy CS, high-dose inotropes → higher in-hospital mortality
- Milrinone (PDE inhibitor): fewer chronotropic/arrhythmogenic effects but causes significant vasodilation → not preferred first-line in CS
- Levosimendan (Ca²⁺ sensitizer): does not increase MVO₂; hemodynamic benefit in small CSMI studies (exceeds dobutamine/enoximone); no survival benefit in acute HF trials; not approved in the US
- Dopamine vs norepinephrine (De Backer et al., n=1,679): no overall 28-day mortality difference; more arrhythmic events with dopamine; in the CS subgroup (n=280), dopamine → increased 28-day mortality vs norepinephrine (P=0.03); norepinephrine preferred
- Istaroxime: novel inotrope/lusitropic agent — inhibits Na⁺/K⁺-ATPase + activates SERCA; HORIZON-HF (AHF with preserved SBP): ↓PCWP, ↑CO, improved diastolic LV function; not yet tested in CSMI
Device Classification Framework (4 Categories)
- LV pressure unloading: IABP — reduces LV afterload via diastolic inflation
- LV volume unloading: TandemHeart (LA-to-aorta) and Impella (transaortic microaxial pump) — offload LV by diverting LV volume
- Biventricular support without oxygenation: modified TandemHeart (RA-to-PA for RV) + Impella/IABP for LV
- Biventricular support with oxygenation: VA-ECMO — full cardiopulmonary support
IABP — Mechanism and Clinical Evidence
Mechanism: balloon inflation in diastole and active deflation in systole; shifts ~40 mL per beat; ↑stroke volume and CO up to 1 L/min (15–30%) with largest increases in severely reduced CO
- Hemodynamic effects: ↑SV, ↑CO, ↑coronary perfusion; ↓LVEDP, ↓PCWP; ↓LV wall stress and MVO₂
- Limitation: in severe coronary stenosis/ACS, increased coronary perfusion pressure may NOT translate into increased coronary blood flow beyond critical stenoses
- Mild improvement in microcirculatory flow noted; microvascular density (better prognosis correlate) remained unchanged
Evidence:
- Cochrane meta-analysis (6 RCTs, n=190 patients): HR 1.04 (95% CI 0.62–1.73) — no survival benefit
- Sjauw meta-analysis (9 STEMI-CS cohorts; n=10,529): thrombolysis-treated → 18% ↓30-day mortality with IABP (but higher revascularization rates confound); PCI-treated → 6% increase in 30-day mortality with IABP (P=0.0008) — revascularization impact > IABP
- IABP-SHOCK II Trial (n=600; AMI-CS; RCT): 39.7% (IABP) vs 41.3% (control) 30-day mortality; RR 0.96 (95% CI 0.79–1.17; P=0.69); no benefit in any subgroup including severe hypotension (<80 mmHg); IABP did not improve hemodynamics, systemic inflammation, or MODS severity
- All major RCT evidence for IABP is negative: CSMI, elective high-risk PCI, anterior STEMI without CS
- Guideline discordance: ACC/AHA (2013): Class IIa for CSMI; European STEMI: Class IIb/B; German-Austrian: no recommendation possible in PCI-treated CSMI
TandemHeart — Mechanism and Evidence
- Continuous flow centrifugal pump; up to 4 L/min; aspirates oxygenated blood from LA (via transseptal puncture, 21 Fr inflow cannula) → injects into femoral artery/iliac aorta
- Hemodynamic superiority over IABP: ↑CI, ↑MAP, ↓PCWP, ↓CVP, ↓PAP, ↑cardiac power index
- Complications (registry; n=117): bleeding at cannula site 29.1%; sepsis/SIRS 29.9%; GI bleeding 19.7%; blood transfusion 71%; stroke 6.8%; coagulopathy 11%; limb ischemia 3.4%
- Cannot be inserted during CPR — requires fluoroscopy-guided transseptal puncture; limits emergency utility
- No mortality-focused RCT or meta-analysis for TandemHeart alone
Impella — Mechanism and Evidence
- Axial flow pump positioned across the aortic valve; aspirates blood from LV and expels into ascending aorta
- Impella 2.5: up to 2.5 L/min; percutaneous; Impella 5.0: up to 5.0 L/min; requires surgical cutdown
- LV unloading: ↓LVEDP, ↓PCWP; ↑coronary perfusion pressure; ↓MVO₂
- EUROSHOCK Registry (n=120 CSMI; Impella 2.5): 30-day mortality 64.2%; lactate decreased from 5.8 → 2.5 mmol/L at 48h (P=0.023) — hemodynamic improvement without proven mortality benefit
- ISAR-SHOCK trial (Impella 2.5 vs IABP): Impella → higher CI and MAP, lower lactate; no mortality difference, no difference in bleeding, limb ischemia, arrhythmias, infections
- Percutaneous LVAD meta-analysis (3 trials; n=100; TandemHeart + Impella 2.5 vs IABP): LVAD → higher CI (+0.35 L/min/m²), MAP (+12.8 mmHg), lower PCWP (−5.3 mmHg); 30-day mortality similar (RR 1.06; CI 0.68–1.66); bleeding significantly more frequent with LVAD (RR 2.35; CI 1.40–3.93)
- IMPRESS and RECOVER II trials (Impella 2.5 in STEMI): terminated due to insufficient enrollment
- Limitation: haemolysis from high rotational speed; femoral bleeding/limb ischemia risk; no pulmonary oxygenation support
VA-ECMO — Mechanism and Evidence
- Full cardiopulmonary support system; centrifugal pump + heat exchanger + membrane oxygenator; venous blood from RA via femoral vein → oxygenated → returned to descending aorta via femoral artery
- Up to ~4 L/min; improves tissue oxygenation + cardiogenic shock + pulmonary edema simultaneously
- ↑LV afterload — retrograde aortic flow increases myocardial oxygen demand; may impede myocardial protection; LV venting strategies (IABP + VA-ECMO, Impella + VA-ECMO, atrial septostomy) proposed
- Microcirculatory improvement documented in observational studies (sidestream dark field/orthogonal polarization imaging)
- Complications: SIRS, renal failure, limb ischemia, bleeding
- No RCTs at time of publication; single-center retrospective comparison (ECMO vs historical controls, n=219+115): 30-day survival 60% vs 35% (P=0.003) — confounded by historical comparison
- Used in cardiac arrest during PCI/TAVI; interhospital transfer; myocarditis; post-cardiotomy
Microcirculation as the Final Common Pathway
- Impaired microcirculation predicts poor outcomes in CSMI
- IABP: microvascular density unchanged despite improved microcirculatory flow
- Future monitoring: microcirculatory assessment (sidestream dark field imaging) may be needed to optimize MCS beyond CI-based targets
Future Directions (2014 Perspective)
- Need for devices providing higher CO (beyond IABP range)
- Device complication reduction (limb ischemia, bleeding, hemolysis, SIRS)
- Early MCS timing (before MODS established) as critical research gap
- CULPRIT-SHOCK trial underway (optimal revascularization strategy)
- Therapeutic hypothermia: promising based on animal data; small human case series; no RCT available
- Microcirculatory monitoring as future outcome measure
Limitations of the Document
- Published 2014; predates DanGer Shock (2024), ECLS-SHOCK (2023), CULPRIT-SHOCK (2017), Altshock-2, and 4-trial VA-ECMO IPD meta-analysis — device recommendations substantially updated
- No prospective RCT data with mortality endpoints for TandemHeart, VA-ECMO, or Impella at time of writing
- Impella data limited to EUROSHOCK registry (n=120) and ISAR-SHOCK (small; surrogate endpoints)
- IABP hemodynamic effects (detailed) now largely historical given uniform clinical non-use recommendation
- Focus exclusively on CSMI; HF-CS, post-cardiotomy CS, and secondary CS not addressed
- Mortality comparisons driven by small underpowered trials; heterogeneous populations
Key Concepts Mentioned
- concepts/Cardiogenic-Shock — MODS vs hemodynamics as mortality predictor; cardiac power output; CS definition
- concepts/Temporary-Mechanical-Circulatory-Support — IABP, TandemHeart, Impella, VA-ECMO device framework and early evidence
- concepts/Invasive-Hemodynamic-Monitoring-CS — cardiac power output/index; CI limitations as sole prognostic target
Key Entities Mentioned
- IABP-SHOCK II Trial — definitive negative IABP RCT; central reference
- EUROSHOCK Registry — Impella 2.5 real-world data (n=120 CSMI; 64.2% mortality)
- ISAR-SHOCK Trial — Impella 2.5 vs IABP; hemodynamics better, mortality neutral
- SHOCK Trial — historical AMI-CS revascularization RCT; mortality risk score development
- TRIUMPH Trial — AMI-CS mortality predictors
Wiki Pages Updated
- wiki/sources/mcs-ehj-2014.md (created)
- wiki/concepts/Temporary-Mechanical-Circulatory-Support.md (updated — source_count 3→4)
- wiki/concepts/Cardiogenic-Shock.md (updated — cardiac power output/MODS note)
- wiki/sourceindex.md (updated)
- log.md (updated)