Hemodynamic Assessment in Cardiogenic Shock Regarding the Etiology
2 other identifiers
observational
64
1 country
1
Brief Summary
The classic physiopathology of cardiogenic shock is explained by a systolic ventricular failure, responsible for a decrease in cardiac output associated with high systemic vascular resistances (SVR). This theory is currently challenged in light of the data collected in the SHOCK study, which assessed outcome of early revascularization versus initial medical stabilization, in cardiogenic shock following myocardial infarction.13 A sub-study highlighted depressed SVR in the population with ischemic cardiogenic shock, related to a systemic inflammatory response syndrome.14 Furthermore, mean FEVG was 30% in the SHOCK trial,13 with a similar distribution with post myocardial infarction heart failure patients without signs of shock.15-19 Thus, alteration of myocardial contractility can be only moderate in cardiogenic shock and isn't the only cause responsible for the hemodynamic instability.20 Recent studies suggest the important roles of the peripheral vascular system and neurohormonal system in the genesis and prolongation of cardiogenic shock.12 Vasodilation caused by nitrous oxide synthase activation27 explains the absence of compensating vasoconstriction observed during the SHOCK trial13, and leads to decreased systemic and coronary perfusion, thus increasing myocardial ischemia and initial ventricular dysfunction. 28,29 Cotter et al. conducted an interesting study of hemodynamic evaluation of various cardiac conditions where they observed a significant variability in the peripheral vascular status, with systemic vascular resistances collapsed in certain patients (similar to those observed in septic shock) and rather close to normal or very high resistances in other patients.21 However these data were obtained from a selected group of patients without differentiating the etiology of cardiogenic shock. Finally, the majority of available studies were limited to cardiogenic shock whose etiology was myocardial infarction. Therapeutic management of cardiogenic shock is based in first intention on an inotropic support by Dobutamine.11,23 However, better outcomes on contractility and microcirculatory state have been observed with the use of a vasopressor support by Norepinephrine, suggesting the importance of SVR decreasing in genesis of cardiogenic shock.14,24 Recent reviews showed very few data on inotropic treatment and association with vasopressor support,22 hence the low level of recommendations in current guidelines.11,23 So far it is crucial to accurately characterize hemodynamic status and in particular the systemic vascular resistance for patients with cardiogenic shock. Important variabilities in hemodynamic profiles observed in Cooter's trial could explain the difficulty in defining an optimal therapeutic strategy. the investigators hypothesize that the hemodynamic profile, particularly SVR, of patients with cardiogenic shock is different depending on their etiology. Ischemic cardiogenic shock should be characterized by lower SVR, in relation to a major role of systemic inflammatory response syndrome. On the contrary, non-ischemic cardiogenic shock could be associated with normal or elevated SVR, and thus could explain the variability in distribution of SVR.
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Trial Relationships
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Study Timeline
Key milestones and dates
Study Start
First participant enrolled
September 6, 2017
CompletedFirst Submitted
Initial submission to the registry
September 13, 2017
CompletedFirst Posted
Study publicly available on registry
September 15, 2017
CompletedPrimary Completion
Last participant's last visit for primary outcome
September 1, 2018
CompletedStudy Completion
Last participant's last visit for all outcomes
March 1, 2019
CompletedApril 11, 2018
April 1, 2018
12 months
September 13, 2017
April 10, 2018
Conditions
Outcome Measures
Primary Outcomes (1)
Monitoring by transpulmonary thermodilution (VolumeView
2 days
Study Arms (4)
cardiogenic shock without SCA
cardiogenic shock with SCA
SCA,
acute left heart failure with severe alteration of LVEF
Interventions
hemodynamic measure
hemodynamic measure
Eligibility Criteria
patients with cardiogenic shock.
You may qualify if:
- Persistent hypotension (systolic blood pressure \<90 mmHg for at least 30 minutes or need for vasopressor support)
- Signs of visceral hypoperfusion (confusion, marbling, oliguria, hyperlactataemia), 11
- Lower heart rate (\<1.8 L / min / m2) Adap Suitable or high filling pressures12
You may not qualify if:
- Pregnant or nursing women
- Major under guardianship
- Person staying in a health or social facility
- Non-beneficiaries of a social security scheme
- Persons deprived of liberty
- No one is able to give consent.
Contact the study team to confirm eligibility.
Sponsors & Collaborators
Study Sites (1)
Assisatnce Publique Hopitaux de Marseille
Marseille, France
MeSH Terms
Conditions
Interventions
Condition Hierarchy (Ancestors)
Intervention Hierarchy (Ancestors)
Study Officials
- STUDY DIRECTOR
jean-olivier ARNAUD
Assistance Publique Hopitaux De Marseille
Central Study Contacts
Study Design
- Study Type
- observational
- Observational Model
- CASE CONTROL
- Time Perspective
- PROSPECTIVE
- Target Duration
- 2 Days
- Sponsor Type
- OTHER
- Responsible Party
- SPONSOR
Study Record Dates
First Submitted
September 13, 2017
First Posted
September 15, 2017
Study Start
September 6, 2017
Primary Completion
September 1, 2018
Study Completion
March 1, 2019
Last Updated
April 11, 2018
Record last verified: 2018-04