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Background: While the short-term prognosis of cardiac arrest patients - nearly 250,000 new cases per year in Europe - has been extensively studied, less is known regarding the mid and long-term outcome of survivors., Objective: The aim of the DESAC study is to describe mid- and long-term survival rate and functional status of cardiac arrest survivors, and to assess the influence of pre and intra hospital therapeutic strategies on these two outcomes., Methods: Between Jul 2015 and Oct 2018, adult patients over 18 years who were discharged alive from any intensive care units (public and private hospitals) in the Ile-de-France area (Paris and suburbs, France) after a non-traumatic cardiac arrest were screened for participation in this multicentric study. Survivors were included after they signed (or the proxies) an informed consent before discharge during initial hospitalisation. We calculated that including 600 patients in total would allow an 80% power to demonstrate a 2 years survival rate difference of 10% between patients who did and those who did not receive therapeutic hypothermia after resuscitation. Pre- and in-hospital data related to the circumstances surrounding the event and to the therapeutic interventions (such as cardio-pulmonary resuscitation, defibrillation, emergent coronary revascularization, neuroprotective therapeutics) were collected. After discharge, patients were interviewed at 3 months, 6 months and every year thereafter for a minimum follow-up of 26 months and a maximum follow-up of 48 months. Information on vital status, occurrence of cardiovascular events, medications and a comprehensive assessment of the functional status (qualitive of life as assessed by the Short-Form General Health Survey (SF36) scale, activities of daily living (ADL) scale, neurological Cerebral Performance Categories (CPC) and Overall Performance Categories (OPC) scales, socio-professional activities) were collected at follow-up interviews., Discussion: The DESAC study should provide important information regarding several dimensions of the mid and long-term prognosis of cardiac arrest survivors and on the benefit (and potentially harm) of early therapeutic strategies., Competing Interests: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: [Antoine Vieillard-Baron declares being member of a research advisory board for Air Liquide Company. Alain Cariou received fees from Bard for lectures and conferences]., (© 2023 The Authors.)

Background: Data on the possible association between depressive disorders and inflammatory markers are scarce and inconsistent. We investigated whether subjects with depressive mood had higher levels of a wide range of inflammatory markers involved in coronary heart disease (CHD) incidence and examined the contribution of these inflammatory markers and depressive mood to CHD outcome., Methods and Results: We built a nested case-referent study within the Prospective Epidemiological Study of Myocardial Infarction (PRIME) study of healthy middle-aged men from Belfast and France. We considered the baseline plasma sample from 335 future cases (angina pectoris, nonfatal myocardial infarction, coronary death) and 670 matched controls (2 controls per case). Depressive mood characterized men whose baseline depression score (13-item modification of the Welsh depression subscale) was in the fourth quartile (mean score, 5.75; range, 4 to 12). On average, men with depressive mood had 46%, 16%, and 10% higher C-reactive protein, interleukin-6, and intercellular adhesion molecule-1 levels, respectively, independently of case-control status, social characteristics, and classic cardiovascular risk factors; no statistical difference was found for fibrinogen. The odds ratios of depressive mood for CHD were 1.35 (95% CI, 1.05 to 1.73) in univariate analysis and 1.50 (95% CI, 1.04 to 2.15) after adjustment for social characteristics and classic cardiovascular risk factors. The latter odds ratio remained unchanged when each inflammatory marker was added separately, and in this analysis, each inflammatory marker contributed significantly to CHD event risk., Conclusions: These data support an association of depressive mood with inflammatory markers and suggest that depressive mood is related to CHD even after adjustment for these inflammatory markers.

Background: Abdominal (visceral) and overall obesity are both related to coronary heart disease mortality risk; however, the relative contribution of these 2 components of fat deposit in the etiology of sudden death is unknown., Methods and Results: We used the data from 7079 asymptomatic men of the Paris Prospective Study I who were free of ischemic heart disease and who were 43 to 52 years of age at first clinical examination between 1967 and 1972. Body mass index (BMI) and sagittal abdominal diameter (SAD) were measured at baseline and used as markers of overall and abdominal obesity. During a follow-up of 23 years, there were 118 sudden deaths and 192 fatal myocardial infarctions. After adjustment for baseline level of cardiovascular risk factors, trunk subcutaneous fat, and thoracic diameter, the ratio of the fifth over the first quintile of SAD was 2.6 (95% CI 1.0 to 6.7) and 2. 6 (95% CI 1.3 to 5.1) for sudden death and fatal myocardial infarction, respectively, and the risk of sudden death increased proportionally with SAD level. The corresponding ratios for BMI were 2.0 (95% CI 1.1 to 3.8) and 1.0 (95% CI 0.6 to 1.7), respectively. Compared with men with low SAD (first tertile) and normal BMI (<25 kg/m2), men with elevated SAD (third tertile) were at increased risk of sudden death but not of fatal myocardial infarction, whether they were of normal weight (multivariate adjusted relative risk 3. 0 [95% CI 1.3 to 6. 9]) or overweight (BMI > or =25 kg/m2; 1.9 [95% CI 1.0 to 3.9])., Conclusions: In asymptomatic French middle-aged men, larger SAD was associated with a particularly increased risk of sudden death, independent of BMI level and known cardiovascular risk factors.

Aims: To assess whether the Framingham and PROCAM risk functions were applicable to men in Belfast and France., Methods and Results: We performed an external validation study within the PRIME (Prospective Epidemiological Study of Myocardial Infarction) cohort study. It comprised men recruited in Belfast (2399) and France (7359) who were aged 50 to 59 years, free of CHD at baseline (1991 to 1993) and followed over 5 years for CHD events (coronary death, myocardial infarction, angina pectoris). We compared the relative risks of CHD associated with the classic risk factors in PRIME with those in Framingham and PROCAM cohorts. We then compared the number of predicted and observed 5-year CHD events (calibration). Finally, we estimated the ability of the risk functions to separate high risk from low risk subjects (discrimination). The relative risk of CHD calculated for the various factors in the PRIME population were not statistically different from those published in the Framingham and PROCAM risk functions. The number of CHD events predicted by these risk functions however clearly overestimated those observed in Belfast and France. The two risk functions had a similar ability to separate high risk from low risk subjects in Belfast and France (c-statistic range: 0.61-0.68)., Conclusion: The Framingham and PROCAM risk functions should not be used to estimate the absolute CHD risk of middle-aged men in Belfast and France without any CHD history because of a clear overestimation. Specific population risk functions are needed.