The blood pressure targets in survivors of cardiac arrest: a systematic review and meta- analysis

doi:10.21203/rs.3.rs-2634189/v1

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The blood pressure targets in survivors of cardiac arrest: a systematic review and meta- analysis

https://doi.org/10.21203/rs.3.rs-2634189/v1

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Background

The patients with return of spontaneous circulation post cardiac arrest have a mortality rate of up to 30-50%. Hemodynamic support is a key component of out-of-hospital cardiac arrest (OHCA) management and is essential to ensure survival. The meta-analysis was performed to investigate the optimizing blood pressure targets in survivors of OHCA.

Methods

Studies were searched in electronic databases from January 1, 2015 to January 13, 2023. Results were pooled using random effects model and fixed effects model and are presented as odd ratios (ORs) with 95% confidence intervals (CI). The primary outcome was all-cause death and the secondary outcome were severe bleeding, arrhythmia, renal replacement therapy, cerebral performance category (CPC) score≥3, modified Rankin Scale (mRS) score≥4 and the level of serum norepinephrine, neuron-specific enolase (NSE), troponin T.This study was registered with INPLASY 2022120065.

Results

Four studies involving 1,327 participants were included. No significant differences of the risk of all-cause death were found between the low-target blood pressure and high-target blood pressure strategy (OR 0.93 [95% CI 0.73–1.17], I²=0%, P=0.55). Meanwhile, the low-target blood pressure therapy had a higher proportion of mRS score≥4 (OR 0.43 [95% CI 0.20–0.94], I²=0%, P=0.03) ≥4 compared with the high-target blood pressure therapy. No significant between-group differences were identified among patients in the level of the serum NSE (SD 0.82 [95% CI -1.50–3.13], I²=28%, P=0.49), troponin T (SD 0.54 [95% CI -0.03–1.12], I²=0%, P=0.07), renal replacement therapy (OR 1.09 [95% CI 0.71–1.69], I²=49%, P=0.69), severe bleeding(OR 1.18 [95% CI 0.85–1.65], I²=0%, P=0.33) and arrhythmia(OR 0.84 [95% CI 0.57–1.24], I²=0%, P=0.38).

Conclusions

The higher mean arterial pressure (MAP) is not associated with improved outcome when compared to conventional target, but may be associated with worse neurological outcome.

Blood pressure

Cardiac arrest

Mortality

Meta-analysis

Cardiac arrest is defined as the cessation of cardiac mechanical activity, with signs of absence of circulation[1]. The incidence of emergency medical services treated out-of-hospital cardiac arrest (OHCA) is 88.8 individuals per 100 000 population in the United States in 2020. Despite a trend of improvement, the overall survival rate of cardiac arrest patients remains limited[2, 3]. The survival rate to hospital discharge is only 9.0% overall, and as low as 29.2% even in witnessed collapse and shockable rhythm[3]. The in-hospital mortality in patients with return of spontaneous circulation (ROSC) post cardiac arrest (PCA) is high, and estimated to be 30–50%[4, 5]. The low survival rate highlighted the importance of advancing the knowledge on the overall management.

Circulatory failure or shock is common in PCA patients. It accounts for the major cause of death in survivors PCA in intensive care unit during the first 3 days, and hypoxic ischemic brain injury as another major cause in a later phase[6]. Hence, the hemodynamic support is the key component in OHCA management, and vital in ensuring survival. Vasopressors, inotropes and fluids are used to ensure adequate vital organ perfusion, especially brain, heart, and the kidney. In the meantime, as the increase of vasopressor and inotrope dose, the blood pressure and afterload increase, the risk of myocardial ischemia and life-threatening ventricular arrhythmia increases[7, 8]. In order to balance vital organ perfusion with the consequences of high dose vasopressor, the mean arterial pressure (MAP) needs to be closely monitored and titrated to ensure survival. Some society guidelines recommended to avoid hypotension (MAP < 65 mmHg or systolic blood pressure < 90mmHg)[9, 10]. A few observational studies suggested that a higher MAP target might be beneficial in maintaining cerebral perfusion and coronary blood supply, especially in patients with history of hypertension [11–13]. One retrospective study demonstrated that higher MAP (> 90 mmHg) was associated with good neurological function (modified Rankin Scale ≤ 3) compared to MAP at 70–90 mmHg[12]. But this remains controversial. Other observational studies did not find the association[14]. To evaluate the influence of blood pressure target directed treatment on mortality, neurological outcome and surrogate biomarkers, a few randomized controlled studies were delivered, but also failed to provide supportive evidence[15, 16]. More recently, adding to previous studies, Kjaergaard et al. conducted a randomized controlled trial aimed to study the effect of a higher MAP target (77 mmHg) on 90 days survival, which showed no difference in survival and neurological outcome when compared with lower MAP target (63 mmHg). Thus, it was an instrumental time for an updated and a comprehensive meta-analysis to shed some light on these issues.

The aim of this prespecified meta-analysis is to evaluate the optimal blood pressure targets in PCA care, by pooling data from on all clinical randomized controlled trials (RCTs) available to increase power to testify. In this meta-analysis, including four RCTs, the effects of maintaining a higher MAP target on all-cause mortality, neurological outcome, biomarkers and related adverse events were estimated.

We carried out the meta-analysis in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines[17]. Our protocol has been registered on the International Platform of Registered Systematic Review and Meta-analysis Protocols database (Inplasy protocol: INPLASY202310037), and is available in full on inplasy.com (https://inplasy.com/inplasy-2023-1-0037). Ethics approval was not required for our work.

Search strategy

Four independent researchers (Ying Xie, Yu Geng and Tong Gao) conducted extensive electronic searches for relevant articles published from Jan 1, 2013 to Jan 13, 2023. The database includes PubMed, Embase and the Cochrane database. The relevant RCTs were manually selected. The search strategy of the literature was shown in the supplement (Supplement Table S1).

Inclusion and exclusion

EndNote (X9 version) software is selected for document management, two investigators independently evaluated the eligibility of the identified items. The title and summary are filtered for the first time, and qualified articles are reserved for full-text review. Inclusion criteria for studies meeting the following requirements include: (1) Patients survivors of cardiac arrest. (2) Outcomes Indicators: All cause death, severe bleeding, arrhythmia, renal replacement therapy, (cerebral performance category) CPC score ≥ 3, (modified Rankin Scale) mRS score ≥ 4, the level of serum norepinephrine, neuron-specific enolase (NSE) and troponin T, including one. We excluded studies enrolling patients < 18 years old, and there was not enough data to extract, such as the summary of some meetings, literature materials such as review and pharmacological introduction. We contacted the authors if associated data from their studies were required. The primary outcome was all-cause death and the secondary outcome were severe bleeding, arrhythmia, renal replacement therapy, cerebral performance category (CPC) score ≥ 3, modified Rankin Scale (mRS) score ≥ 4 and the level of serum norepinephrine, neuron-specific enolase (NSE), troponin T.

Bias & quality assessment

The two researchers independently evaluated, preliminarily selected and checked the literature data according to the unified and standardized method, and included them in the literature in strict accordance with the admission and exclusion criteria, and then collected information. We evaluated the quality of selected articles according to the quality evaluation standard of Cochrane Reviewer Handbook 5.1.0 [18].

Data synthesis and analysis

Revman 5.3 were used for meta-analysis. Data which met homogeneity (P > 0.10 and I²⩽ 50%) through heterogeneity test were meta-analyzed using fixed effect model. If homogeneity (P ⩽0.10 or I² > 50%) was not met, and heterogeneity cannot be ruled out, random effect model can be used to combine effects[19]. While it should be noted that sensitivity analysis and subgroup analysis should be considered for this type of analysis data. For the continuous outcomes, mean differences (MD) and 95% CIs were estimated as effective. Some included RCTs reported median as the measure of treatment effect, with interquartile range (IQR). We estimated the mean from median and standard deviations (SD) from IQR using the methods described in the previous studies[20]. A P value < 0.05 was considered statistically significant.

The flow chart (Fig. 1) summarizes the search and study selection process. A total of 1,350 studies were identified through the electronic searches, of which 886 were excluded due to duplication. 464 studies were also excluded after reading the titles and abstracts. The remaining 14 studies were assessed by reading the full texts. Data from 4 trails evaluating the efficacy and safety in acutely ill adults of cardiovascular disease treated with liberal versus conservative oxygen therapy were included.

The main features of the included trials are presented in Table 1. A total of 1,327 patients’ survival of cardiac arrest allocated to the low-target blood pressure therapy or the high-target blood pressure therapy were included in our analyses. Four RCTs were included and the follow-up time lasted from 3 months to 6 months. No differences were observed in terms of the proportion of patients lost to follow up between the low-target blood pressure therapy and high-target blood pressure therapy groups across trials.

Table 1

Design and Outcomes of the Studies Included in the Meta-Analysis
Num	Author/Year	Country	Intervention assignments		Participants				Outcomes
Num	Author/Year	Country	The low- target group	the high- target group	Sample size, n	Mean age, years	Men, n (%)	Follow up	Outcomes
1	Grand/2019	Denmark	mean arterial pressure target < 70 mmHg	mean arterial pressure target > 80 mmHg	369	64	80%	6 months	Primary outcome: brain injury, which was defined as the serum level of NSE. Secondary outcomes: the cognitive function after 6 months assessed in survivors by the MMSE.
2	Grand/2020	Denmark	mean arterial pressure target of 65 mmHg	mean arterial pressure target of 72 mmHg	49	61	88%	6 months	Primary outcome: sTM after 48h. Secondary outcomes: the biomarkers indicative of endothelial activation.
4	Kjaergaard/2022	Denmark	mean arterial pressure target of 63 mmHg	mean arterial pressure target of 77 mmHg	789	63	81%	3 months	Primary outcome: a composite of death from any cause or discharge with a CPC of 3 or 4. Secondary outcomes: death from any cause, renal-replacement therapy, neuron-specific enolase levels, the MCA score, the mRS and CPC score.
8	Ameloot/2020	Belgium	mean arterial pressure target of 65 mmHg	mean arterial pressure target of 80–100 mmHg	120	63	87%	6 months	Primary outcome: myocardial injury as assessed by the area under the 72-h hs-cTnT curve. Secondary outcomes: new-onset atrial fibrillation, re-arrest, all-cause mortality, and CPC score.
CPC = Cerebral Performance Category; hs-cTnT = high-sensitive cardiac troponin T; MMSE = mini-mental state examination; mRS = modified Rankin scale; MCA = Montreal Cognitive Assessment; NSE = neuron-specific enolase; sTM = Soluble thrombomodulin.

The data of all cause death was available from 4 RCTs, which are summarized in Fig. 2. No significant differences of the risk of all-cause death were found between the low-target blood pressure and high-target blood pressure strategy (OR 0.93 [95% CI 0.73–1.17], I²=0%, P = 0.55). Meanwhile, similar results were found in these patients of the cognitive function after 6 months assessed in survivors by the CPC score (OR 1.11 [95% CI 0.85–1.46], I²=0%, P = 0.42) while the low-target blood pressure therapy had a higher proportion of mRS score ≥ 4 (OR 0.43 [95% CI 0.20–0.94], I²=0%, P = 0.03) ≥ 4 compared with the high-target blood pressure therapy.

The biomarkers indicative of endothelial activation and cerebral cortex function and the adverse event were generalized in Fig. 3–4. The results showed that the level of the serum norepinephrine was lower in patients who received a the low-target blood pressure therapy than those who received a the high-target blood pressure therapy (SD -0.09 [95% CI -0.17–-0.02], I²=88%, P = 0.02). No significant between-group differences were identified among patients in the level of the serum NSE (SD 0.82 [95% CI -1.50–3.13], I²=28%, P = 0.49) and troponin T (SD 0.54 [95% CI -0.03–1.12], I²=0%, P = 0.07). Similarly, no differences were observed between groups among patients in the risk of renal replacement therapy (OR 1.09 [95% CI 0.71–1.69], I²=49%, P = 0.69), severe bleeding (OR 1.18 [95% CI 0.85–1.65], I²=0%, P = 0.33) and arrhythmia (OR 0.84 [95% CI 0.57–1.24], I²=0%, P = 0.38).

We used Revman to investigate the influence of a single study on the overall pooled estimate of each predefined outcome. We found that the removal of any one study would not affect the following results. The results of the risk of bias assessment with the RoB2 of randomized control trials are summarized in the Figure S1 and four studies were considered at low risk for overall risk of bias.

We performed a meta-analysis to evaluate the optimal blood pressure target after successful resuscitation from cardiac arrest. This resulting synthesis of existing data and outcomes of the meta-analysis represents a contemporary review of the evidence. This meta-analysis pooled data from four available RCTs that included 1,327 OHCA patients and demonstrated no mortality or neurological outcome benefit from high-target group. Regarding the level of biomarkers of brain function and myocardium injury, our results did not show any significant difference between the two groups. At the same time, despite higher serum norepinephrine in high-target group, the adverse effects including the risk of renal replacement therapy, severe bleeding or arrhythmia was similar.

Previous observational studies have suggested an association of higher MAP target and improved outcome[11, 12]. However, the following RCTs did not find supportive evidence for targeting a higher MAP. This meta-analysis showed similar results, that higher MAP did not improve the outcomes of all-cause death during admission or neurological function in survivors. Jakkula et al. and Ameloot et al. conducted two pilot studies, compared the impact of higher MAP target (80/85 to 100 mmHg) with lower MAP target (65 mmHg). Both trials failed to detect any difference in survival or neurological outcomes[15, 16]. A patient-level pooled post-hoc analysis of these two trials also found no different between groups in terms of neurological outcome and all-cause mortality[21]. Following the open-label randomized studies, Grand et al. used modified blood pressure modules with a -10% offset to enable double-blind study. In this study, they randomized 50 patients into higher MAP (72 mmHg) group and lower MAP (65 mmHg) group. Similarly, they did not find improvement in the all-cause death[22]. The most recent double-blind study using similar strategy and widened the difference between the intervention and controlled group, to 77 mmHg as the higher MAP target, and 63 mmHg as the lower, and still failed to prove the benefit.

Our findings in this meta-analysis were consistent with the previous results in severe bleeding and arrhythmia. Kjaergaard et al. assessed the adverse events during PCA care, including severe bleeding, arrythmia, infection, electrolyte disorder, metabolic disorder and seizure, which are all similar in the two groups[23]. Grand et al. also found no difference in severe bleeding, arrhythmia, and biomarkers of organ injury, including soluble thrombomodulin and neuron-specific enolase between two groups[22].

Results from observational studies showed decreased renal replacements therapy needs in higher MAP patients[24]. However, this was not observed by Grand et al. and Kjaergaard et al[22, 23]. Similar to our findings, a meta-analysis of RCTs in shock, non-cardiac, and cardiac surgery patients. However, in a subgroup of shock patients with premorbid hypertension, higher MAP target (> 70 mmHg) resulted in significantly lower renal replacement therapy needs[25].

Notably, our meta-analysis showed the high MAP target treatment had a higher proportion of negative neurological outcome as indicated by mRS ≥ 4. Similarly, Grand et al. also found high MAP may related to even higher rate of mRS ≥ 4 in the survivors[26]. In the other study that used mRS, the high MPA group showed a tendency of improvement, however, this did not reach statistical significance[22]. The other neurological function assessment score, CPC did not differ in the two groups in both the meta-analysis or in the RCTs included. In general, the organ-perfusion pressure is related to MAP and autoregulation of the organs. The lower threshold of organ autoregulation may shift rightwards in OHCA patients[27], so the hypothesis is that they may benefit from a higher MAP in the short period after the primary event. For cerebral circulation, the perfusion pressure was the difference between the inlet (the arterial) and the outlet (the venous) pressure. The inlet pressure may be influenced by MAP, arterial stenosis, or vasoconstriction, while the affecting factors of outlet pressure includes central venous pressure and intracranial pressure that reflects changes in intracranial blood, cerebrospinal fluid, and brain parenchyma, etc. The influence of MAP on cerebral perfusion pressure might be divergent and a same MAP may result in both hypoperfusion and hyper-perfusion, depending on different premorbid diseases, metabolic influences, and stage of the pathophysiological changes, etc. These results together point out, targeting higher MAP may not provide additional benefit when compared to the conventional target of 65 mmHg, and may even have a harmful effect on brain function in some patients. Hence, a static MAP may not provide a whole picture for the treatment target. Considering using individualized monitoring of cerebral perfusion as target of hemodynamic management might be considered in future studies.

To our knowledge, this current meta-analysis is the first of this topic, but it still carries some limitations. First of all, there’s heterogeneity in the studies that we involved. The definition of high and low target MAP differs between studies. Secondly, the overall sample size is relatively small in our meta-analysis.

In conclusion, this meta-analysis of patients admitted to intensive care unit post OHCA showed that treatment strategy targeting a higher MAP is not associated with improved outcome when compared to conventional target, but may be associated with worse neurological outcome indicated by mRS ≥ 4.

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Availability of data and materials

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

Conflict of interest

All the authors declare no potential conflict of interest.

Funding

The work was supported by the Beijing Municipal Administration of Hospitals’ Ascent Plan (Code: DFL20190902), Tsinghua University Spring Breeze Fund, and the Beijing Tsinghua Changgung Hospital Fund (Grant No. 12019C1009).

Author Contributions

Xie Ying, Yu Geng and Tong Gao searched the scientific literature and drafted the manuscript. Lei Bi and Siyuan Li helped to collect the data and performed statistical analysis. Yintang Wang, Ping Zhang contributed to the conception, design, data interpretation, manuscript revision for critical intellectual content, and supervision of the study. All authors read and approved the manuscript.

Acknowledgements

Not applicable.

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No competing interests reported.

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The blood pressure targets in survivors of cardiac arrest: a systematic review and meta- analysis

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Abstract

Figures

Introduction

Methods

Search strategy

Inclusion and exclusion

Bias & quality assessment

Data synthesis and analysis

Results

Discussion

Conclusion

Declarations

References

Additional Declarations

Supplementary Files

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