Vasoactive pharmacologic therapy in cardiogenic shock: a critical review

Figures & data

Figure 1. Flow diagram of study selection and exclusion.

Table 1. Summary of retrieved studies.

First author Acronym Sample size (N) Sites number (S)	Objective	Inclusion criteria	Interventions	Main outcome measures (Group 1 vs. Group 2)	Conclusion
Vasopressors and inotropes
De Backere^a^69 SOAP II N = 1679 S = 8 Europe	To evaluate whether the choice of NE over dopamine as the first-line vasopressor agent could reduce the rate of death among patients in shock	Shock requiring vasopressor MAP <70 mmHg or SBP <100 despite adequate fluids, unless CVP >12 or PCWP >14 mmHg Signs of hypoperfusion	Group1: Dopamine Dose adjusted to target BP decided by physician Max. 20 mcg/kg/min Group 2: Norepinephrine Dose adjusted to target BP decided by physician Max. 0.19 mcg/kg/min	EF: NR F/U: 28 d All-cause mortality: 52.5% vs. 48.5% (OR 1.17; 95% CI 0.97–1.42; p = .10) CS subgroup (n = 280; 17%): higher mortality in dopamine group (p = .03)	No significant difference in death Dopamine use was associated with a greater number of adverse events Dopamine use was associated with higher mortality rate in CS subgroup
Levy^70 N = 30 S = 1 France	To compare epinephrine and NE-dobutamine in dopamine-resistant CS without ACS	Acute or chronic HF with EF <30% and CI <2.2 L/min/m^2 PCWP >14 mmHg SBP <90 mm Hg or MAP <60 mm Hg or a drop in MAP of >30 mm Hg UOP <0.5 mL/kg/h Lactate >2 mmol/L Signs of hypoperfusion	Group 1: Epinephrine Dose titrated to obtain MAP of 65–70 mmHg with a stable or increased CI Group 2: NE - Dobutamine Dose titrated to obtain MAP of 65–70 mmHg with a stable or increased CI	EF: 24% F/U: 26 months Hemodynamic: HR, MAP, CO, CVP, PAP, and PAOP Tonometric: Gastric mucosal PCO2 measured by tonometry Metabolic: lactate and pyruvate	Epinephrine was as effective as NE-dobutamine in term of global hemodynamic effects Epinephrine was associated with a transient lactic acidosis, higher HR and arrhythmia, and inadequate gastric mucosa perfusion NE-dobutamine appears to be a more reliable and safer strategy
Levy^71 OptimaCC N = 57 S = 9 France	To compare efficacy and safety of epinephrine and NE in patients with CS after AMI	CS due to AMI after PCI SBP <90 mm Hg or MAP <65 mm Hg cardiac index <2.2 L/min/m^2 without vasoactive agent PCWP >15 mmHg EF <40% Evidence of hypoperfusion	Group 1: Epinephrine Dose titrated to obtain MAP of 65–70 mmHg Group 2: Norepinephrine Dose titrated to obtain MAP of 65–70 mmHg	EF: 34% F/U: 60 d Change in CI: no difference (p = .43) Incidence of refractory CS: 37 vs. 7% (p = .011)	Use of epinephrine compared with NE was associated with similar effects on arterial pressure and CI and higher incidence of refractory shock
Inodilators
García-González^c^72 N = 22 S = 1 Spain	To evaluate hemodynamic effects of levosimendan compared to dobutamine in AMI patients revascularized by PPCI, who developed CS secondary to severe LV systolic dysfunction	STEMI treated with PPCI CS diagnosed according to published criteria^b	Group 1: Levosimendan 24 mcg/kg over 10 min, then 0.1 mcg/kg/min × 24 h Group 2: Dobutamine 5 mcg/kg/min × 24 h, titrated to response	EF: 29% F/U: at 30 h ≥30% increase in CPO after 24 h of therapy: consistently better with levosimendan p < .05 CI after 24 h of therapy: consistently better with levosimendan p < .05	Levosimendan improved CPO Levosimendan could be a better choice than dobutamine in this setting Further investigation is warranted before its general recommendation
Dominguez-Rodriguez^c^73	To evaluate effects of levosimendan compared to dobutamine on LV diastolic function in AMI patients revascularized by PPCI, who developed CS secondary to severe LV systolic dysfunction	As above	As above	F/U: at 24 h E/A ratio: 1.4 vs. 0.9 (p < .001) DT (ms): 198 vs. 188 (NS) IVRT (ms): 70.4 vs. 102.8 (p < .001)	Levosimendan compared to dobutamine caused significant reduction of the IVRT, and significant increase of the E/A ratio
Samimi-Fard^c^74	To assess effect on long-term survival of levosimendan compared to dobutamine in AMI patients revascularized by PPCI, who developed CS secondary to severe LV systolic dysfunction	As above	As above	F/U: 12 months Cardiac death: p = .24^d	Levosimendan compared to dobutamine did not improve long-term survival
Fuhrmann^75 N = 32 S = 1 Germany	To investigate effects of levosimendan compared with enoximone in refractory CS complicating AMI, on top of current therapy	AMI with hypotension and peripheral hypoperfusion Refractory CS (despite therapy) within 2 h after PCI SBP <90 mm Hg CI <2.5 L/min/m^2 PCWP >18 mm Hg Signs of hypoperfusion	Group 1: Levosimendan 12 mcg/kg over 10 min, then 0.1 mcg/kg/min × 50 min, and 0.2 mcg/kg/min × 23 h Group 2: Enoximone Fractional bolus of 0.5 mcg/kg over 30 min, then 2–10 mcg/kg/min	EF: 25% F/U: at 30 d Overall survival rate: 68.7 vs. 37.5% (p = .023)	Levosimendan as add-on therapy may contribute to improved survival compared with enoximone
Husebye^a^76 LEAF N = 61 S = 1 Norway	To evaluate efficacy and safety of levosimendan in patients with PPCI-treated STEMI complicated by symptomatic HF	STEMI subjected to PPCI Opening of IRA Signs of decreased wall motion in LV Clinical HF defined CS subgroup: SBP <90 mmHg or 90–100 mmHg despite inotrope Signs of hypoperfusion	Group 1: Levosimendan 0.2 mg/kg/min for 1 h followed by 0.1 mg/kg/min × 24 h Group 2: Matching placebo	EF: 41% F/U: up to 42 d Change in WMSI from baseline to days 5 and 42: 1.66 vs. 1.83 (p = .031) and 1.61 vs. 1.73 (p = .18), respectively MACE or HF hospitalization: NS CS subgroup (n = 9; 15%): similar results for safety and efficacy	Levosimendan improved contractility in post-ischemic myocardium Levosimendan was well tolerated, without any increase in arrhythmias
Nitric oxide synthase inhibitors
Cotter^77 LINCS N = 30 S = 1 Israel	To evaluate effect of L-NAME in treatment of refractory CS after ACS	ACS with hypotension and peripheral hypoperfusion Progressive decrease in SBP <100 mmHg Signs of hypoperfusion >1 h after PCI (despite therapy)	Group 1: Supportive care Plus: L-NAME 1 mg/kg bolus, then 1 mg/kg/h × 5 h Group 2: Supportive care only (no treatment)	EF: 24% F/U: at 30 d All-cause mortality: 27% vs. 67% (p = .008) MAP at 24 h: 86 vs. 66 mmHg (p = .004) UOP at 24 h: +135 mL/h vs. −12 mL/h (p < .001)	NOSi are beneficial in the treatment of patients with refractory CS
Dzavík^e^78 SHOCK-2 N = 79 S = 22 North America and Europe	To assess preliminary safety and efficacy, pharmacokinetics, and biological activity of L-NMMA To assess feasibility of a randomized trial in AMI complicated by persistent CS	AMI complicated by persistent CS despite open IRA SBP <100 mmHg despite vasoactive agent CI <2.2 L/min/m^2 (if off IABP), or  < 2.5 L/min/m^2 (if on IABP) PCWP ≥15 mmHg	Group 1: L-NMMA in 5 regimens 0.15 mg/kg IV bolus, then 0.15 mg/kg/h × 5 h 0.5 mg/kg IV bolus, then 0.5 mg/kg/h × 5 h mg/kg IV bolus, then 1.0 mg/kg/h × 5 h 1.5 mg/kg IV bolus, then 1.5 mg/kg/h × 5 h Group 2: Placebo Normal saline IV bolus, then infusion x 5 h	EF: 26% F/U: 30 d Change in MAP at 2 h: NS Change in MAP at 15 min: significant increase in all groups except 1.0 mg/kg group 30-d mortality: NS	L-NMMA resulted in modest increases in MAP at 15 min compared with placebo but no differences at 2 h
Alexander^f^79 TRIUMPH N = 398 S = 130 North America and Europe	To examine effects of nonselective NOSi in patients with MI and refractory CS despite opening of IRA	MI with patency of IRA Refractory CS <24 h Signs of hypoperfusion and SBP <100 mmHg despite vasoactive agent Elevated LV filling pressure EF <40%	Group 1: Tilarginine (L-NMMA) 1-mg/kg bolus, then 1-mg/kg/h × 5 h Group 2: Matching Placebo	EF: 27% F/U: 6 months 30-d mortality: 48 vs. 42%; RR, 1.14; 95% CI 0.92–1.41; p = .24	Tilarginine did not reduce mortality rates Early mortality rates are high Further research is needed

A: Late diastolic flow; ACS: Acute coronary syndrome; AMI: Acute myocardial infarction; BP: Blood pressure; CI: Cardiac index; CO: Cardiac output; CPO: Cardiac power; CS: Cardiogenic shock; CVP: Central venous pressure; DT: Deceleration time; E: Early diastolic flow; EF: Ejection fraction; F/U: Follow-up duration; H: Hour; HF: Heart failure; HR: Heart rate; IRA: Infarct-related artery; IVRT: Isovolumetric relaxation time; L-NAME: N^G-Nitro-L-Arginine-Methyl Ester; L-NMMA: L-N-monomethyl-arginine; LV: Left ventricular; MACE: Major adverse cardiac events; MAP: Mean arterial pressure; max: Maximum; MI: Myocardial infarction; NE: Norepinephrine; NOS: Nitric oxide synthase; NOSi: Nitric oxide synthase inhibitor(s); NR: Not reported; NS: Non-significant; OR: Odds ratio; PAOP: Pulmonary artery occlusion pressure; PAP: Pulmonary artery pressure; PCI: Percutaneous coronary intervention; PPCI: Primary PCI; RR: Risk ratio; SBP: Systolic blood pressure; STEMI: ST elevation myocardial infarction; UOP: Urine output; WMSI: Wall motion score index.

^aCS patients as predefined subgroup analysis of the study.

^bAlexander RW, Pratt CM, Ryan TJ, Roberts R. Diagnosis and management of patients with acute myocardial infarction. In: Fuster V, Alexander RW, O’Rourke RA, editors. Hurst’s the heart, 10th ed. New York’ McGraw-Hill Company, Inc.; 2001. p. 1275– 359.

^cOne study in 3 publications reporting different outcomes.

^dNot primary endpoint.

^ePhase II dose-ranging study.

^fEnrollment was terminated at 398 patients based on a prespecified futility analysis.

Table 2. Jadad scale.

Study	Jadad scale				Modified Jadad scale
	Randomization (0–2)	Blinding (0–2)	Dropouts (0–1)	3-Item scale (0–5)	Inclusion/exclusion (0–1)	AE (0–1)	Statistics (0–1)	6-Item scale (0–8)
SOAP II^68	2	2	1	5	1	1	1 AC: yes ITT: yes SS: yes	8
[69]	1	0	1	2	1	0	1 AC: no ITT: unclear SS: no	4
OptimaCC^70	2	2	1	5	1	1	1 AC: yes ITT: yes SS: yes	8
Mean (SD)	–	–	–	4 (1.73)	–	–	–	6.66 (2.30)
[71]^b	0	0	1	1	1	1	1 AC: no ITT: unclear SS: no	4
[74]	2	0	1	3	1	0	1 AC: yes ITT: unclear SS: yes	5
[75] LEAF	2^a	2	1	5	1	1	1 AC: yes ITT: yes SS: yes	8
Mean (SD)	–	–	–	3 (2)	–	–	–	5.66 (2.08)
LINCS^76	1	0	0	1	1	1	1 AC: no ITT: yes SS: no	4
SHOCK-2^77	2	1	1	4	1	1	1 AC: yes ITT: yes SS: yes	7
TRIUMPH^78	2	1	1	4	1	1	1 AC: yes ITT: yes SS: yes	7
Mean (SD)	–	–	–	3 (1.73)	–	–	–-	6 (1.73)

AC: Allocation concealment; AE: Adverse effects; ITT: Intention-to-treat; SD: Standard deviation; SS: Sample size.

^aPatients with cardiogenic shock were stratified by block randomization.

^bSubsequent publications^72,73 of the study on different outcomes are not presented in this table.

Bold values represent quality score calculations for each study.

Table 3. Registered clinical trials.

Trial identifier^a	Trial brief title (acronym)	Agent (s)	Design (phase)	Enrollment	Primary outcome (time frame)	Start date	Status
NCT04325035	The safety and efficacy of istaroxime for pre-CS (SEISMiC)	Istaroxime vs. placebo	Randomized, double-blind (II)	60	Change from baseline in SBP and AUC	June 2020	Not yet recruiting
NCT03340779	NE vs. NE and Dobutamine in CS (SHOCK-NORDOB)	NE vs. NE/dobutamine	Randomized, cross-over, open-label (III)	40	Obtention of an optimal cardiac output defined as presence of 2 efficacy criteria without any side effects from 0 to 6.5 h	January 2018	Unknown
NCT04020263	Effect of early use of levosimendan vs. placebo on top of a conventional strategy of inotrope use on a combined morbidity-mortality endpoint in patients With CS	Levosimendan vs. placebo	Randomized, double-blind (III)	610	Composite of all-cause mortality, ECLS, and/or dialysis at 30 d	December 2019	Not yet recruiting
NCT02591771	Study of multisite pharmacological and invasive management for CS	Adrenaline	Single-group, open-label (II)	24	Survival at 60 d	October 2015	Completed
NCT03727282	LV volume index in adjustment of initial dose of dobutamine in HF and CS	Dobutamine: Adjust according to ejection volume index vs. attending physician	Randomized, open-label (−)	30	Multiple measures at 24 h, such as base excess levels, bicarbonate levels, SBP/DBP, CO, systolic volume, UOP, lactate levels, arterial lactate levels, and troponin levels	January 2019	Not yet recruiting
NCT04141410	Global longitudinal strain assessment in cardiogenic shock during sepsis (GLASSES-1)	Levosimendan vs. ECHO	Prospective, observational, case-control (−)	35	Global longitudinal strain ≥ 15%; up to 1 week	October 2019	Recruiting
NCT00093301	Levosimendan vs. dobutamine in shock patients (LICI)	Levosimendan vs. dobutamine	Randomized, double-blind (II and III)	40	Resolution of shock state	October 2004	Unknown
NCT03207165	Milrinone vs. dobutamine in critically Ill patients	Milrinone vs. dobutamine	Randomized, double-blind (VI)	192	Composite of all-cause in-hospital death, non-fatal MI, TIA, or CVA, renal failure, need for cardiac transplant or new mechanical support, any atrial or ventricular arrhythmia leading to cardiac arrest and resuscitation (up to 12 months)	August 2017	Recruiting
NCT04224103	Nitric oxide in venoarterial extracorporeal membrane oxygenation (VA ECMO) (NOVICE)	Inhaled nitric oxide	Prospective, observational, case-only (−)	10	Participant recruitment and multiple right heart-related outcomes, e.g. qualitative function, TAPSE, and the changes from baseline	August 2019	Recruiting
NCT02118467	Vasoactive drugs in intensive care unit	NE/epinephrine as add-on vs. Phenylephrine/vasopressin as add-on	Randomized, double-blind (IV)	836	Hospital mortality (6 months)	May 2014	Recruiting
Terminated
NCT00782652	The effects of nitric oxide for inhalation in right ventricular infarction patients	Inhaled nitric oxide vs. nitrogen gas	Randomized, double-blind (II)	3	Survival to hospital discharge or Day 30, whichever occurs first without need for renal replacement therapy or RVAD	March 2006	Terminated (due to slow enrollment)

AUC: Area under the curve; CO: Cardiac output; CS: Cardiogenic shock; CVA: Cerebrovascular accident; DBP: Diastolic blood pressure; ECLS: Extra corporeal life support; ECHO: Echocardiography; MI: Myocardial infarction; N/A: Not applicable; NE: Norepinephrine; RVAD: Right ventricular assistance device; SBP: Systolic blood pressure; TAPSE: Tricuspid annular plane systolic excursion; TIA: Transient ischemic attack; UOP: Urine output

^aFrom http://clinicaltrials.gov/- accessed on 20/5/2020.

Figure 2. Targets of vasoactive agents^11,13,22.

Table 4. Vasoactive agents^{10,12,18,91,92}.

Agent	Mechanism	Effect	Indication/considerations	Comment
Vasopressor/inotropes
Norepinephrine	Agonist: α1 (++++) β1 (++), and β2 (+)	Inotropy, chronotropy, dromotropy, and vasoconstriction ↑ CO ↑↑SVR	CS phenotypes: classic wet and cold, euvolemic cold and dry, vasodilatory warm and wet or mixed CS RV shock, pericardial tamponade	Most common first-line agent in shock Most benefits demonstrated in septic shock
Dopamine	Agonist: α1, β1, and β2 D (++ to +++) Dose-dependent agonism	Inotropy, dromotropy, chronotropy, and vasoconstriction ↑ to ↑↑ CO ↑ to ↑↑ SVR	CS phenotypes: classic wet and cold, euvolemic cold and dry RV shock	Second-line agent in most forms of shock
Epinephrine	Agonist: α1(++++) β1 (++++), and β2 (+++)	Inotropy, chronotropy, dromotropy, and vasoconstriction ↑↑ CO ↑↑ SVR	Add-on if rise in BP is not achieved Anaphylactic shock	Surviving Sepsis Guidelines has most data for epinephrine as second-line agent
vasopressin	Agonist: V1 receptors in vascular smooth muscle	Vasoconstriction ↑↑ SVR ↔ PVR	Add-on to avoid high doses of NE Unstable heart rhythm when high dose NE is unsafe RV shock	Second-line agent in most forms of shock On or Off dosing, can cause hyponatremia
Inodilators
Dobutamine	Agonist: α1 (+) β1 (++++), and β2 (++)	Inotropy and mild vasodilation ↑↑ CO ↓ SVR, ↓ PVR, ↓ MAP	Predominant low CO Isolated LV dysfunction	Commonly used in CS May contribute to hypotension Most commonly used inotrope
Levosimendan	Myofilament Ca^+ sensitizer and K^+ channel modifier	Inotropy and inodilator ↑ CO ↓ SVR, ↓ PVR, ↓ MAP	Acutely decompensated chronic HF Chronic β-blocker therapy Elevated pulmonary resistance and RV dysfunction	Minimal effect on myocardial oxygen consumption Not suitable when SBP < 85 mmHg or CS unless in combination with other vasoactive agents
Enoximone Milrinone	PDEi	Inotropy and inodilator ↑ CO ↓ SVR, ↓ PVR, ↓ MAP	Chronic β-blocker therapy Elevated pulmonary resistance and RV dysfunction	Not recommended in STEMI patients

BP: Blood pressure; CO: Cardiac output; CS: Cardiogenic shock; D: Dopamine; HF: Heart failure; LV: Left ventricular; LVOT: Left ventricular outflow tract; MAP: Mean arterial pressure; PDEi: Phosphodiesterase inhibitor; PVR: pulmonary vascular resistance; RV: Right ventricular; SBP: Systolic blood pressure; STEMI: ST-segment elevation myocardial infarction; SVR: Systemic vascular resistance; V: Vasopressin.

Table 5. First-line vasoactive agent in guidelines.

Guidelines	STEMI				HF		CS
	2013 STEMI (AHA/ACC)^23	2017 STEMI (ESC)^18	2018 (ESC) Revascularization^93	2020 ACVC (ESC)^92	2013 HF (AHA/ACC)^94	2016 HF (ESC)^12	2017 Scientific Statement (AHA)^10
First-line agent	Individualized use	Inotrope/vasopressor	Inotropic support	Vasopressor: NE Inotrope	Inotropic support	Vasopressor: NE Inotrope: DB	Individualized use
Grade	None	Class IIb, Level C	None	V: Class IIb, Level B I: Class IIb, Level C	Class I, Level C	V: Class IIb, Level B I: Class IIb, Level C	None

ACVC: Acute cardiovascular care association; AHA/ACC: American Heart Association/American College of Cardiology; CS: Cardiogenic shock; DB: Dobutamine; ESC: European Society of Cardiology; HF: Heart failure; I: Inotrope; NE: Norepinephrine; STEMI: ST-segment elevation myocardial infarction; V: Vasopressor.

Figure 3. SCAI shock stages^20,104.

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