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Background: Cognitive impairment is common following out-of-hospital cardiac arrest (OHCA), but the nature of the impairment is poorly understood. Our objective was to describe cognitive impairment in OHCA survivors, with the hypothesis that OHCA survivors would perform significantly worse on neuropsychological tests of cognition than controls with acute myocardial infarction (MI). Another aim was to investigate the relationship between cognitive performance and the associated factors of emotional problems, fatigue, insomnia, and cardiovascular risk factors following OHCA., Methods: This was a prospective case-control sub-study of The Targeted Hypothermia versus Targeted Normothermia after Out-of-Hospital Cardiac Arrest (TTM2) trial. Eight of 61 TTM2-sites in Sweden, Denmark, and the United Kingdom included adults with OHCA of presumed cardiac or unknown cause. A matched non-arrest control group with acute MI was recruited. At approximately 7 months post-event, we administered an extensive neuropsychological test battery and questionnaires on anxiety, depression, fatigue, and insomnia, and collected information on the cardiovascular risk factors hypertension and diabetes., Results: Of 184 eligible OHCA survivors, 108 were included, with 92 MI controls enrolled. Amongst OHCA survivors, 29% performed z-score ≤ - 1 (at least borderline-mild impairment) in ≥ 2 cognitive domains, 14% performed z-score ≤ - 2 (major impairment) in ≥ 1 cognitive domain while 54% performed without impairment in any domain. Impairment was most pronounced in episodic memory, executive functions, and processing speed. OHCA survivors performed significantly worse than MI controls in episodic memory (mean difference, MD = - 0.37, 95% confidence intervals [- 0.61, - 0.12]), verbal (MD = - 0.34 [- 0.62, - 0.07]), and visual/constructive functions (MD = - 0.26 [- 0.47, - 0.04]) on linear regressions adjusted for educational attainment and sex. When additionally adjusting for anxiety, depression, fatigue, insomnia, hypertension, and diabetes, executive functions (MD = - 0.44 [- 0.82, - 0.06]) were also worse following OHCA. Diabetes, symptoms of anxiety, depression, and fatigue were significantly associated with worse cognitive performance., Conclusions: In our study population, cognitive impairment was generally mild following OHCA. OHCA survivors performed worse than MI controls in 3 of 6 domains. These results support current guidelines that a post-OHCA follow-up service should screen for cognitive impairment, emotional problems, and fatigue., Trial Registration: ClinicalTrials.gov, NCT03543371. Registered 1 June 2018., (© 2023. BioMed Central Ltd., part of Springer Nature.)

BACKGROUND: The evidence for temperature control for comatose survivors of cardiac arrest is inconclusive. Controversy exists as to whether the effects of hypothermia differ per the circumstances of the cardiac arrest or patient characteristics. METHODS: An individual patient data meta-analysis of the Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest (TTM) and Hypothermia versus Normothermia after Out-of-Hospital Cardiac Arrest (TTM2) trials was conducted. The intervention was hypothermia at 33°C and the comparator was normothermia. The primary outcome was all-cause mortality at 6 months. Secondary outcomes included poor functional outcome (modified Rankin scale score of 4 to 6) at 6 months. Predefined subgroups based on the design variables in the original trials were tested for interaction with the intervention as follows: age (older or younger than the median), sex (female or male), initial cardiac rhythm (shockable or nonshockable), time to return of spontaneous circulation (above or below the median), and circulatory shock on admission (presence or absence). RESULTS: The primary analyses included 2800 patients, with 1403 assigned to hypothermia and 1397 to normothermia. Death occurred for 691 of 1398 participants (49.4%) in the hypothermia group and 666 of 1391 participants (47.9%) in the normothermia group (relative risk with hypothermia, 1.03; 95% confidence interval [CI], 0.96 to 1.11; P=0.41). A poor functional outcome occurred for 733 of 1350 participants (54.3%) in the hypothermia group and 718 of 1330 participants (54.0%) in the normothermia group (relative risk with hypothermia, 1.01; 95% CI, 0.94 to 1.08; P=0.88). Outcomes were consistent in the predefined subgroups. CONCLUSIONS: Hypothermia at 33°C did not decrease 6-month mortality compared with normothermia after out-of-hospital cardiac arrest. (Funded by Vetenskapsrådet; ClinicalTrials.gov numbers NCT02908308 and NCT01020916.)

Targeted temperature management (TTM) exerts substantial impact on hemodynamic function in out-of-hospital cardiac arrest (OHCA) patients. Whole-body oxygen consumption (VO 2 ) and delivery (DO 2 ) have not previously been investigated in a clinical setting during TTM at different levels of temperature after OHCA. A substudy of 151 patients randomized at a single center in the TTM-trial, where patients were randomly assigned TTM at 33°C (TTM33) or 36°C (TTM36) for 24 hours. We calculated VO 2 according to the principle of Fick (VO 2  = cardiac output*arteriovenous oxygen content difference). DO 2 was calculated as cardiac output*arterial oxygen content. Cardiac output was measured by pulmonary artery catheter with thermodilution. Arteriovenous oxygen content difference was calculated from arterial and mixed venous oxygen saturation and hemoglobin. Oxygen extraction ratio = VO 2 /DO 2 . At 24 hours, the VO 2 was 169 ± 59 mL O 2 per minute in TTM33 and 217 ± 53 mL O 2 per minute in TTM36 ( p  < 0.0001). During 24 hours of TTM, the overall difference was 53 mL O 2 minute (95% confidence interval [CI]: 31-74, p group < 0.0001). After rewarming at 36 and 48 hours, there was no difference in VO 2 between the groups. DO 2 was overall 277 mL O 2 per minute (95% CI: 175-379, p group < 0.0001) higher in the TTM36-group during TTM. Oxygen extraction ratio during TTM was not significantly different between the two groups (2% [95% CI: -0.1 to 5, p group  = 0.09]). VO 2 during the first 36 hours after OHCA correlated significantly with temperature, and VO 2 was 19 mL O 2 per minute lower per degree reduction in temperature (95% CI: 15-22), p  < 0.0001. TTM at 33°C compared to 36°C after OHCA is associated with significantly lower VO 2 and DO 2 , however, oxygen extraction ratio was not significantly different. For each degree lower body temperature, the VO 2 fell by 19 mL O 2 per minute.

Aim: Post-cardiac arrest syndrome (PCAS) is characterized by a sepsis-like inflammatory response and hemodynamic instability. We investigated the associations between systemic inflammation, endothelial damage and hemodynamic parameters including vasopressor support in patients with out-of-hospital cardiac arrest (OHCA).Methods: In this post-hoc study, we analysed data from 163 comatose patients included at a single center in the Target Temperature Management (TTM) trial, randomly assigned to TTM at 33°C or 36°C for 24h. Inflammatory biomarkers (interleukin (IL)-6, IL-10, procalcitonin and Tumor Necrosis Factor-α (TNF-α)) and endothelial biomarkers (thrombomodulin, sE-selectin, syndecan-1 and VE-cadherin) were measured at randomization and 24, 48 and 72h after OHCA. Corresponding hemodynamic status, heart rate (HR), mean arterial pressure (MAP) and Cumulative Vasopressor Index (CVI) was reported.Results: At randomization, level of IL-6 correlated negatively with MAP (r=-0.19, p=0.03) and positively with HR (r=0.29, p=0.0002). Serial IL-6 levels correlated consistently with CVI at 24h: (r=0.19, p=0.02) 48h: (r=0.31, p=0.0001) and 72h: (r=0.39, p<0.0001). Thrombomodulin (r=0.23, p=0.004) and syndecan-1 (r=0.27, p=0.001) correlated with CVI at 48h. All inflammatory markers excerpt IL-10 and all endothelial markers correlated with CVI at 72h. Multivariable regression models adjusting for potential confounders confirmed that IL-6 (β=0.2 (95% CI: 0.06-0.3), p=0.004) and TTM-group (TTM36: β=-0.5 (95% CI: -0.9 to 0.1), p=0.01) were associated with CVI at 48h. At 72h after OHCA, IL-6 (β=0.3 (95% CI: 0.03-0.6), p<0.0001), TNF-α (β=-0.4 (95% CI:- 0.5 to 0.2), p<0.0001) and TTM-group (TTM36: β=-0.4 (95% CI: -0.8 to 0.1), p=0.008) were associated with CVI. An overall two-fold increase in levels of IL-6 (β=0.2 (95% CI: 0.1-0.3), p<0.0001) and IL-10 (β=-0.2 (95% CI: -0.3 to 0.06), p=0.005) within 72h after OHCA were significantly associated with CVI. TTM-group modified the interaction between CVI and IL-6 (pinteraction=0.008), but not with IL-10 (pinteraction=0.23).Conclusions: In comatose survivors after OHCA, increasing systemic inflammation and endothelial injury was associated with increased need of vasopressor support. Systemic inflammation, in particular IL-6, was consistently associated with vasopressor support, however endothelial injury may also play a role in PCAS associated cardiovascular dysfunction after OHCA. [ABSTRACT FROM AUTHOR]

Aim: The lectin complement pathway, initiated by mannan-binding-lectin (MBL) plays a role in tissue destruction following ischemia/reperfusion, and MBL deficiency has been associated with favorable outcome in stroke patients. MAp44 is produced in the heart and may theoretically function as an endogenous inhibitor of MBL-mediated activities. The aim of this study was to investigate the possible association between MBL deficiency, MAp44 levels and outcome in comatose survivors of out-of-hospital cardiac arrest (OHCA).Methods: In a single center post hoc analysis of the prospective multicenter randomized Target Temperature Management (TTM) trial, we measured MBL and MAp44 levels at baseline, 24, 48 and 72 h after OHCA in 169 consecutive patients randomly assigned to TTM at 33 °C or 36 °C for 24h. Primary outcome was 30 days mortality and secondary outcome was favorable neurological outcome assessed by Cerebral Performance Category (CPC1-2) and modified Rankin Scale (mRS0-3) 180 days after OHCA.Results: Patients with MBL deficiency (defined as plasma levels ≤100 ngml(-1) at baseline) (n=22) carried a 30-day mortality of 41% compared to 32% in MBL sufficient patient (n=147), p=0.55. Baseline MAp44 levels were not associated with mortality, p=0.25. There was no significant difference in neurological outcome between the two MBL groups assessed by CPC (p=0.69) and mRS (p=0.91). In multivariable models, baseline MBL (OR=1.0, p=0.70), (OR=1.5, p=0.30) and MAp44 levels (OR=1.0, p=0.99), (OR=1.6, p=0.21) were not associated with favorable neurological outcome assessed by CPC and mRS, respectively.Conclusions: In comatose survivors after cardiac arrest, neither MBL deficiency nor levels of MBL and MAp44 were associated with mortality or neurological outcome. [ABSTRACT FROM AUTHOR]

Aim: Post-cardiac arrest syndrome (PCAS) is characterized by systemic inflammation, however data on the prognostic value of inflammatory markers is sparse. We sought to investigate the importance of systemic inflammation, assessed by interleukin-6 (IL-6) in comatose survivors of out-of-hospital cardiac arrest.Methods: A total of 682 patients enrolled in the Target Temperature Management (TTM) trial, surviving >24h with available IL-6 data were included. IL-6 was measured on days 1, 2 and 3 after return of spontaneous circulation. Severity of PCAS was assessed daily by the Sequential Organ Failure Assessment score. Survival status was recorded at 30 days.Results: High levels of IL-6 at day 1-3 (all p<0.0001) were independently associated with severity of PCAS with no interaction of target temperature (all p=NS). IL-6 levels did not differ between temperature groups (p(interaction)=0.99). IL-6 levels at day 2 (p<0.0001) and day 3 (p<0.0001) were associated with crude mortality. Adjusted Cox proportional-hazards analysis showed that a two-fold increase of IL-6 levels at day 2 (HR=1.15 (95% CI: 1.07-1.23), p=0.0002) and day 3 (HR=1.18 (95% CI: 1.09-1.27), p<0.0001) were associated with mortality. IL-6 levels at day 3 had the highest discriminative value in predicting mortality (AUC=0.66). IL-6 did not significantly improve 30-day mortality prediction compared to traditional prognostic factors (p=0.08).Conclusions: In patients surviving >24h following cardiac arrest, IL-6 levels were significantly elevated and associated with severity of PCAS with no significant influence of target temperature. High IL-6 levels were associated with increased mortality. Measuring levels of IL-6 did not provide incremental prognostic value. [ABSTRACT FROM AUTHOR]

Objectives: Whole-body ischemia during out-of-hospital cardiac arrest triggers immediate activation of inflammatory systems leading to a sepsis-like syndrome. The aim was to investigate the association between level of systemic inflammation and mortality in survivors after out-of-hospital cardiac arrest treated with targeted temperature management. Design: Post hoc analysis. Setting: Single-center study of a prospective multicenter randomized study. Patients: One hundred sixty-nine patients (99%) with available blood samples out of 171 patients included in the Target Temperature Management trial, randomly assigning patients to targeted temperature management at 33°C or 36°C. Intervention: None. Measurements and Main Results: At baseline and 24, 48, and 72 hours after out-of-hospital cardiac arrest, blood samples were obtained and screened for a battery of inflammatory markers. Level of interleukin-1β, interleukin-2, interleukin-4, interleukin-5, interleukin-6, interleukin-9, interleukin-10, interleukin-12, interleukin- 13, tumor necrosis factor-α, interferon-γ, C-reactive protein, and procalcitonin were measured. Mortality at 30 days was evaluated by Cox analysis, and the predictive capability of inflammatory markers was evaluated by area under the curve. Level of all inflammatory markers changed significantly within 72 hours after out-of-hospital cardiac arrest (all p values < 0.001), but only procalcitonin levels showed overall differences between nonsurvivors and survivors (p = 0.0002). At baseline, interleukin-6 was independently associated with mortality, whereas both interleukin- 6 levels (hazard ratio = 1.23 [1.01-1.49]; p = 0.04) and procalcitonin levels (hazard ratio = 1.20 [1.03-1.39]; p = 0.02) 24 hours after out-of-hospital cardiac arrest were associated with 30-day mortality with no interactions between targeted temperature management group and levels of interleukin-6 (p = 0.25) or procalcitonin (p = 0.85). None of the other inflammatory markers were independently associated with mortality. Area under the curve for procalcitonin and interleukin-6, 24 hours after out-ofhospital cardiac arrest, were 0.74 and 0.63, respectively. Conclusions: Level of inflammation, assessed by interleukin-6 and procalcitonin, was independently associated with increased mortality with the highest discriminative value obtained 24 hours after out-of-hospital cardiac arrest. Interventions aiming at decreasing level of inflammation as a way to improve outcome may be investigated in future studies. [ABSTRACT FROM AUTHOR]

Objective: To investigate the hemodynamic profile associated with different target temperatures and to assess the prognostic implication of inotropic/vasopressor support and mean arterial pressure after out-of-hospital cardiac arrest. There is a lack of information how different target temperatures may affect hemodynamics. Design: Post hoc analysis of a prospective randomized study. Setting: Thirthy-six ICUs in 10 countries. Patients: Nine hundred twenty patients (97%) with available vasopressor data out of 950 patients from the Target Temperature Management trial randomly assigned patients to a targeted temperature management at 33°C or 36°C. Interventions: None. Measurements and Main Results: Mean arterial pressure, heart rate, and lactate were registered at prespecified time points. The population was stratified according to cardiovascular Sequential Organ Failure Assessment = 4 defining the high vasopressor group and cardiovascular Sequential Organ Failure Assessment less than or equal to 3 defining the low vasopressor group. The targeted temperature management 33 (TTM33) group had a hemodynamic profile with lower heart rate (-7.0 min-1 [95% confidence limit, -8.7, -5.1]; group < 0.0001), similar mean arterial pressure (-1.1 mm Hg [95% confidence limit, -2.3, 0.2]; group = 0.10), and increased lactate (0.6 mmol/L [95% confidence limit, 0.3, 0.8]; pgroup < 0.0001) compared with the targeted temperature management 36 (TTM36) group. A cardiovascular Sequential Organ Failure Assessment score = 4 was recorded in 54% versus 45%, p = 0.03 in the TTM33 and the TTM36 group, respectively. The high vasopressor group carried a 53% mortality rate when compared with a 34% in the low vasopressor group, plog-rank less than 0.0001, with an adjusted hazard ratio of 1.38 (95% CI, 1.11- 1.71; p = 0.004). There was no interaction between vasopressor group and allocated target temperature group (p = 0.40). An inverse relationship between mean arterial pressure and mortality was identified (p = 0.0008). Conclusions: Targeted temperature management at 33°C was associated with hemodynamic alterations with decreased heart rate, elevated levels of lactate, and need for increased vasopressor support compared with targeted temperature management at 36°C. Low mean arterial pressure and need for high doses of vasopressors were associated with increased mortality independent of allocated targeted temperature management. [ABSTRACT FROM AUTHOR]

Aim Survivors after cardiac arrest (CA) exhibits a systemic inflammatory response as part of post-cardiac arrest syndrome (PCAS). We investigated the association between systemic inflammation and severity of PCAS and whether level of targeted temperature management (TTM) modifies level of the inflammatory response. Methods We studied 169 patients included at a single center in the TTM-trial, randomly assigned to TTM at 33 °C or 36 °C for 24 h. Plasma samples were analyzed for inflammatory markers including interleukin (IL) IL-1β,IL-4,IL-6,IL-10, tumor necrosis factor-α (TNF-α), C-reactive protein (CRP) and procalcitonin (PCT) at randomization and 24, 48 and 72 h after CA. Severity of PCAS was assessed by Sequential Organ Failure Assessment (SOFA) score. Results Plasma levels of both IL-6 and IL-10 determined at randomization correlated with severity of PCAS at day 2 ( r = 0.36 and r = 0.27, p < 0.001) and day 3 ( r = 0.32 and r = 0.22, p < 0.001). IL-6 at randomization was an independent predictor of severity of PCAS at day 2 ( p = 0.003) and day 3 ( p < 0.0001) and was a significantly stronger predictor of severity of PCAS at day 3 compared to CRP ( p = 0.04) and PCT ( p = 0.03). Level of TTM did not modify level of the inflammatory markers IL-1β, IL-6, TNF-α, IL-4, IL-10, CRP and PCT, ( p = NS for each inflammatory marker). Conclusions Level of inflammatory response was associated with severity of PCAS with IL-6 being consistently and more strongly associated with severity of PCAS than the inflammatory markers CRP and PCT. The systemic inflammatory response after CA was not modified by TTM at 33 °C or 36 °C. [ABSTRACT FROM AUTHOR]

Cardiovascular dysfunction is common after out-of-hospital cardiac arrest as part of the postcardiac arrest syndrome, and hypothermia may pose additional impact on hemodynamics. The aim was to investigate systemic vascular resistance index (SVRI), cardiac index, and myocardial performance at a targeted temperature management of 33°C (TTM33) versus 36°C (TTM36).Single-center substudy of 171 patients included in the Target Temperature Management Trial (TTM Trial) randomly assigned to TTM33 or TTM36 for 24 hours after out-of-hospital cardiac arrest. Mean arterial pressure ≥65 mm Hg and central venous pressure of 10 to 15 mm Hg were hemodynamic treatment goals. Hemodynamic evaluation was performed by serial right heart catheterization and transthoracic echocardiography. Primary end point was SVRI after 24 hours of cooling and secondary end points included mean SVRI, cardiac index, systolic function, and lactate levels. The TTM33 group had a significant increase in SVRI compared with TTM36 (2595; 95% confidence interval, 2422-2767) versus 1960 (95% confidence interval, 1787-2134) dynes m2/s per cm5; P<0.0001, respectively) after 24 hours of cooling with an overall difference of 556 dynes m2/s per cm5 (Pgroup <0.0001). TTM33 was associated with decreased cardiac index (-0.4 L/min per m2; Pgroup <0.0001), decreased heart rate (Pgroup=0.01), and stroke volume index (Pgroup=0.004) compared with TTM36. Left ventricular ejection fraction (P=0.39) and peak systolic myocardial velocity (P=0.62) did not differ between TTM groups. Lactate levels were significantly higher in the TTM33 group (P=0.0008).Targeted temperature management at 33°C with target mean arterial pressure ≥65 mm Hg is associated with increased SVRI and lower cardiac index because of lower heart rate with unaffected left ventricular systolic function compared with 36°C.URL: http://www.clinicaltrials.gov. Unique identifier: NCT01020916. [ABSTRACT FROM AUTHOR]

Abstract: Aim: Inducing therapeutic hypothermia (TH) in Out-of-Hospital Cardiac Arrest (OHCA) can be challenging due to its impact on central hemodynamics and vasopressors are frequently used to maintain adequate organ perfusion. The aim of this study was to assess the association between level of vasopressor support and mortality. Methods: In a 6-year period, 310 comatose OHCA patients treated with TH were included. Temperature, hemodynamic parameters and level of vasopressors were registered from admission to 24h after rewarming. Level of vasopressor support was assessed by the cardiovascular sub-score of Sequential Organ Failure Assessment (SOFA). The population was stratified by use of dopamine as first line intervention (D-group) or use of dopamine+norepinephrine/epinephrine (DA-group). Primary endpoint was 30-day mortality and secondary endpoint was in-hospital cause of death. Results: Patients in the DA-group carried a 49% all-cause 30-day mortality rate compared to 23% in the D-group, p log-rank <0.0001, corresponding to an adjusted hazard ratio (HR) of 2.0 (95% CI: 1.3–3.0), p =0.001). The DA-group had an increased 30-day mortality due to neurological injury (HR=1.7 (95% CI: 1.1–2.7), p =0.02). Cause of death was anoxic brain injury in 78%, cardiovascular failure in 18% and multi-organ failure in 4%. The hemodynamic changes of TH reversed at normothermia, although the requirement for vasopressor support (cardiovascular SOFA≥3) persisted in 80% of patients. Conclusions: In survivors after OHCA treated with TH the induced hemodynamic changes reversed after normothermia, while the need for vasopressor support persisted. Patients requiring addition of norepinephrine/epinephrine on top of dopamine had an increased 30-day all-cause mortality, as well as death from neurological injury. [Copyright &y& Elsevier]

Aims: Targeted temperature management (TTM) is part of the standard treatment of comatose patients after out-of-hospital cardiac arrest (OHCA) to attenuate neurological injury. In other clinical settings, hypothermia promotes coagulopathy leading to an increase in bleeding and thrombosis tendency. Thus, concern has been raised as to whether TTM can be applied safely, as acute myocardial infarction requiring primary percutaneous coronary intervention (PCI) with the need of effective antiplatelet therapy is frequent following OHCA. This study investigated the influence of TTM at 33 or 36°C on various laboratory and coagulation parameters.Methods and Results: In this single-center predefined substudy of the TTM trial, 171 patients were randomized to TTM at either 33 or 36°C in the postresuscitation phase. The two subgroups were compared regarding standard laboratory coagulation parameters, thrombelastography (TEG), bleeding, and stent thrombosis events. Platelet counts were lower in the TTM33-group compared to TTM36 (p=0.009), but neither standard coagulation nor TEG-parameters showed any difference between the groups. TEG revealed a normocoagulable state in the majority of patients, while approximately 20% of the population presented as hypercoagulable. Adverse events included 38 bleeding events, one stent thrombosis, and one reinfarction, with no significant difference between the groups.Conclusions: There was no evidence supporting the assumption that TTM at 33°C was associated with impaired hemostasis or increased the frequency of adverse bleeding and thrombotic events compared to TTM at 36°C. We found that TTM at either temperature can safely be applied in the postresuscitation phase after acute myocardial infarction and primary PCI. [ABSTRACT FROM AUTHOR]

Purpose: Life threatening arrhythmias are increasingly frequent with lower body temperature. While targeted temperature management (TTM) with mild hypothermia following out-of-hospital cardiac arrest (OHCA) is generally considered safe and has been suggested as a potential antiarrhythmic add-on therapy, it is unknown whether the level of TTM affects the burden of ventricular ectopic activity. We sought to assess the ventricular ectopic burden between patients treated with TTM at 33°C or 36°C for 24h.Methods: Continuous 12-lead digital Holter electrocardiograms performed during the intervention were analyzed blinded to treatment allocation in 115 comatose OHCA-survivors from a single center of the TTM-trial. The main study showed no difference with regards to mortality.Results: Fifty-eight patients were randomized to 33°C and 57 to 36°C. Cardiac arrest characteristics were similar between the groups. The number of isolated ventricular ectopic beats (VEB) per hour was similar at the beginning of the maintenance phase of TTM and decreased over time in both groups (both ptime<0.001). The reduction in VEB per hour was significantly affected by target temperature (pinteraction<0.0001), with fewer VEB in the 36°C-group. The total number of isolated, couplets and number of runs of VEB per hour showed similar results, with less ventricular ectopic activity in the 36°C-group (pinteraction<0.0001). Increasing numbers of pre-hospital defibrillations (log2) were associated with a 46% increase in ventricular ectopic activity (p<0.01), adjusted for potential confounders.Conclusions: Ventricular ectopic activity was reduced in comatose OHCA-survivors treated with TTM at 36°C compared to 33°C. Higher numbers of pre-hospital defibrillations were associated with higher incidence of ventricular ectopic activity. [ABSTRACT FROM AUTHOR]