Orthopedic-geriatric cocare for the older patients with HF was associated with significant reductions in morbidity and mortality, and increases in optimal postoperative care. Options for further improvement of orthopedic-GM cocare need to be investigated.
Objective To synthesise the literature on the effects of fish oil-docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA)-on mortality and arrhythmias and to explore dose response and formulation effects. Data extraction The primary outcomes of interest were the arrhythmic end points of appropriate implantable cardiac defibrillator intervention and sudden cardiac death. The secondary outcomes were all cause mortality and death from cardiac causes. Subgroup analyses included the effect of formulations of EPA and DHA on death from cardiac causes and effects of fish oil in patients with coronary artery disease or myocardial infarction. Data synthesis 12 studies totalling 32 779 patients met the inclusion criteria. A neutral effect was reported in three studies (n=1148) for appropriate implantable cardiac defibrillator intervention (odds ratio 0.90, 95% confidence interval 0.55 to 1.46) and in six studies (n=31 111) for sudden cardiac death (0.81, 0.52 to 1.25). 11 studies (n=32 439 and n=32 519) provided data on the effects of fish oil on all cause mortality (0.92, 0.82 to 1.03) and a reduction in deaths from cardiac causes (0.80, 0.69 to 0.92). The dose-response relation for DHA and EPA on reduction in deaths from cardiac causes was not significant. Conclusions Fish oil supplementation was associated with a significant reduction in deaths from cardiac causes but had no effect on arrhythmias or all cause mortality. Evidence to recommend an optimal formulation of EPA or DHA to reduce these outcomes is insufficient. Fish oils are a heterogeneous product, and the optimal formulations for DHA and EPA remain unclear.
Pericarditis has been noted as a potential complication of pacemaker implantation. This study evaluated the risk of developing pericarditis following pacemaker implantation with active-fixation atrial leads. Included were 1,021 consecutive patients (mean age 73.4+/-0.4 years, range 16-101 years; 45.2% women) undergoing new pacemaker system implantation between 1991 and 1999 who were reviewed for the complication of pericarditis. The incidence and outcomes of postimplantation pericarditis in patients receiving active-fixation atrial leads were compared to those not receiving these leads. Of 79 patients who received active-fixation atrial leads, 4 (5%) developed pericarditis postpacemaker implantation. Of 942 patients with passive-fixation atrial leads or no atrial lead (i.e., a ventricular lead only), none developed pericarditis postoperatively (P < 0.001). Of patients receiving active-fixation ventricular leads only (n = 97), none developed pericarditis. No complications were apparent at the time of implantation in patients who developed pericarditis. Pleuritic chest pain developed between 1 and 28 hours postoperatively. Three patients had pericardial rubs without clinical or echocardiographic evidence of tamponade. They were treated conservatively with acetylsalicylic acid or ibuprofen and their symptoms resolved without sequelae in 1-8 days. One patient (without pericardial rub) died due to cardiac tamponade on postoperative day 6. Postmortem examination revealed hemorrhagic pericarditis with no gross evidence of lead perforation. Pericarditis complicates pacemaker implantation in significantly more patients who receive active-fixation atrial leads. It may be precipitated byperforation of the atrial lead screw through the thin atrial wall. Patients developing postoperative pericarditis should befollowed closely due to the risk of cardiac tamponade.
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