Laure Hammer

Night-time and diastolic hypertension are common and underestimated conditions in newly diagnosed apnoeic patients

Background In newly diagnosed apnoeic patients without a history of hypertension, clinical hypertension is underdiagnosed in at least 40% of the cases. An increase in diastolic blood pressure is the most frequent pattern encountered. Objective To assess clinic and 24-h blood pressure, baroreflex sensitivity and left ventricular mass for identifying the prevalence, the type and the consequences of hypertension in newly diagnosed apnoeic patients. Patients and methods Fifty-nine unselected patients (age = 48 ± 12 years, body mass index = 28.1 ± 4.5 kg/m2) referred to a university hospital sleep laboratory for symptoms suggesting obstructive sleep apnoea were included. Diagnosis of apnoea was accepted when respiratory disturbance index was ≥15/h of sleep. Blood pressure was considered as normal by their general practitioner and all of them were free of any medication for hypertension. Echocardiography, 24-hour ambulatory blood pressure monitoring and assessment of the baroreflex sensitivity were performed. Results Forty-two percent of the apnoeic patients demonstrated a clinical hypertension, 34 subjects (58%) had a daytime hypertension, and 45 patients (76%) had a night-time hypertension, using 24-h monitoring. All the daytime hypertensives also had night-time hypertension. Forty-seven of the 59 patients (80%) were hypertensive either in the clinic or using 24-h recording. Diastolic and systolo-diastolic hypertension were the prominent types of hypertension observed both by clinic or ambulatory measurements. Respiratory disturbance index was significantly higher in apnoeic patients suffering isolated diastolic hypertension than in the normotensives (50.9 ± 26.5/h versus 36.0 ± 12.3/h, respectively; P = 0.02). The prevalence rate of left ventricular hypertrophy was high (between 15 and 20%) and occurred independently of associated hypertension. Baroreflex sensitivity was altered whatever the type of hypertension and decreased with the severity of obstructive sleep apnoea. Conclusion Hypertension is hugely underdiagnosed in apnoeic patients unknown to be hypertensive. Use of 24-h blood pressure monitoring allowed the diagnosis of twice as much hypertension than did clinical measurement. Even at the beginning of their history of hypertension, apnoeic patients exhibited chronic adaptations of their cardiovascular system, as shown by early changes in baroreflex sensitivity and an increased prevalence of left ventricular hypertrophy.

Immediate prehospital hypothermia protocol in comatose survivors of out-of-hospital cardiac arrest

Therapeutic hypothermia (TH) improves the outcomes of cardiac arrest (CA) survivors. The aim of this study was to evaluate retrospectively the efficacy and safety of an immediate prehospital cooling procedure implemented just after the return of spontaneous circulation with a prehospital setting. During 30 months, the case records of comatose survivors of out-of-hospital CA presumably due to a cardiac disease were studied. A routine protocol of immediate postresuscitation cooling had been tested by an emergency team, which consisted of an infusion of large-volume, ice-cold intravenous saline. We decided to assess the efficacy and tolerance of this procedure. A total of 99 patients were studied; 22 were treated with prehospital TH, and 77 consecutive patients treated with prehospital standard resuscitation served as controls. For all patients, TH was maintained for 12 to 24 hours. The demographic, clinical, and biological characteristics of the patients were similar in the 2 groups. The rate of patients with a body temperature of less than 35 degrees C upon admission was 41% in the cooling group and 18% in the control group. Rapid infusion of fluid was not associated with pulmonary edema. After 1 year of follow-up, 6 (27%) of 22 patients in the cooling group and 30 (39%) of 77 patients in the control group had a good outcome. Our preliminary observation suggests that in comatose survivors of CA, prehospital TH with infusion of large-volume, ice-cold intravenous saline is feasible and can be used safely by mobile emergency and intensive care units.

Conséquences cardiovasculaires du syndrome d’apnées obstructives du sommeil

Resume Propos. – Cet article fait le point sur les donnees passees et actuelles des relations existantes entre syndrome d’apnees obstructives du sommeil et maladies cardiovasculaires. Actualites et points forts. – Le syndrome d’apnees obstructives du sommeil est une pathologie frequente mais sous-estimee qui ne se resume pas a l’association ronflements et obesite. Il est evoque par l’interrogatoire mais son diagnostic de certitude est obtenu par la polysomnographie. De nombreuses etudes ont retrouve des relations significatives entre la presence d’un syndrome d’apnees obstructives du sommeil et la survenue d’evenements cardiovasculaires. Cependant, le lien de causalite n’est etabli de facon formelle que pour l’hypertension arterielle. Les stimuli a l’origine de la reponse cardiovasculaire, aigue et chronique, sont multiples. Les mecanismes physiopathologiques pouvant expliquer l’association morbide entre syndrome d’apnees obstructives du sommeil et maladies cardiovasculaires sont egalement nombreux, en premier lieu l’hyperactivite sympathique. Le pronostic vital de cette pathologie est etroitement lie a la survenue d’accidents cardiovasculaires. Perspectives et projets. – L’existence d’une relation independante entre syndrome d’apnees obstructives du sommeil et atherosclerose n’est pas demontree. L’effet benefique de la pression positive continue nocturne, traitement de reference du syndrome d’apnees obstructives du sommeil, sur l’incidence des maladies cardiovasculaires reste egalement a etablir malgre les resultats des etudes recentes qui suggerent que la prise en charge du syndrome d’apnees obstructives du sommeil par cette therapeutique est a meme de reduire le risque cardiovasculaire, en particulier d’hypertension arterielle.

Model for predicting short-term mortality of severe sepsis.

IntroductionTo establish a prognostic model for predicting 14-day mortality in ICU patients with severe sepsis overall and according to place of infection acquisition and to sepsis episode number.MethodsIn this prospective multicentre observational study on a multicentre database (OUTCOMEREA) including data from 12 ICUs, 2268 patients with 2737 episodes of severe sepsis were randomly divided into a training cohort (n = 1458) and a validation cohort (n = 810). Up to four consecutive severe sepsis episodes per patient occurring within the first 28 ICU days were included. We developed a prognostic model for predicting death within 14 days after each episode, based on patient data available at sepsis onset.ResultsIndependent predictors of death were logistic organ dysfunction (odds ratio (OR), 1.22 per point, P < 10-4), septic shock (OR, 1.40; P = 0.01), rank of severe sepsis episode (1 reference, 2: OR, 1.26; P = 0.10 ≥ 3: OR, 2.64; P < 10-3), multiple sources of infection (OR; 1.45, P = 0.03), simplified acute physiology score II (OR, 1.02 per point; P < 10-4), McCabe score ([greater than or equal to]2) (OR, 1.96; P < 10-4), and number of chronic co-morbidities (1: OR, 1.75; P < 10-3, ≥ 2: OR, 2.24, P < 10-3). Validity of the model was good in whole cohorts (AUC-ROC, 0.76; 95%CI, 0.74 to 0.79; and HL Chi-square: 15.3 (P = 0.06) for all episodes pooled).ConclusionsIn ICU patients, a prognostic model based on a few easily obtained variables is effective in predicting death within 14 days after the first to fourth episode of severe sepsis complicating community-, hospital-, or ICU-acquired infection.

Efficacy and safety of glycoprotein IIb/IIIa receptor antagonists for patients undergoing percutaneous coronary intervention within twelve hours of fibrinolysis†

Objective: To compare clinical outcomes between glycoprotein IIb/IIIa receptor antagonist recipients and nonrecipients who underwent percutaneous coronary intervention (PCI) within 12 hr of fibrinolysis. Background: Despite limited evidence, glycoprotein IIb/IIIa receptor antagonists are widely used in ST‐elevation myocardial infarction (STEMI) patients undergoing routine early or rescue PCI after fibrinolysis. Methods: We evaluated 87 and 556 glycoprotein IIb/IIIa receptor antagonist recipients and nonrecipients enrolled in a regional registry of STEMI between October 2002 and December 2005. The primary efficacy endpoint was a composite of death from any cause, reinfarction, and stroke at 1 year of follow‐up. The primary safety endpoint was the rate of in‐hospital major bleeding that was not related to coronary artery bypass grafting. Results: The primary efficacy endpoint occurred in 12% (10 of 81) and 13% (72 of 525) of glycoprotein IIb/IIIa receptor antagonist recipients and nonrecipients, respectively (P = 0.74). The corresponding rates of major bleeding during index hospitalization were 4.8% (4 of 84) and 5.1% (28 of 544) (P = 0.88), respectively. Two glycoprotein IIb/IIIa receptor antagonist recipients and five nonrecipients experienced intracranial hemorrhage. After adjusting for propensity score, the odds of primary efficacy (odds ratio, 0.79; 95% confidence interval, 0.34–1.83) and safety (odds ratio, 0.75; 95% confidence interval, 0.22–2.62) endpoints did not differ according to the use of glycoprotein IIb/IIIa receptor antagonists. Conclusion: In this observational cohort study of unselected patients with STEMI, the administration of glycoprotein IIb/IIIa receptor antagonists provided no additional benefit to PCI performed within 12 hr of fibrinolysis, nor did it compromise patient safety.

Early Cooling in Cardiac Arrest: What is the Evidence?

Cardiac arrest is a major cause of unexpected death in developed countries, with survival rates ranging from less than 5% to 35% [1, 2]. In patients who are initially resuscitated, anoxic neurological injury is an important cause of morbidity and mortality [3]. For successful resuscitation, rapid return to spontaneous circulation is mandatory, but overcoming post-resuscitation tissue injury is necessary as well [4, 5]. Various treatment strategies have been used to attenuate ischemic-related pathophysiological damage and behavioral deficits. Prolonged therapeutic hypothermia is the only post-resuscitation therapy clinically demonstrated to improve the outcome of cardiac arrest survivors [6, 7, 8, 9]. Therapeutic hypothermia is recommended by the International Liaison Committee on Resuscitation (ILCOR) [8].