BackgroundCardiovascular disease and cancer increasingly coexist, yet relationships between cancer and long-term cardiovascular outcomes post–percutaneous coronary intervention (PCI) are not well studied.Methods and ResultsWe examined stented PCI patients at Duke (1996–2010) using linked data from the Duke Information Systems for Cardiovascular Care and the Duke Tumor Registry (a cancer treatment registry). Our primary outcome was cardiovascular mortality. Secondary outcomes included composite cardiovascular mortality, myocardial infarction, or repeat revascularization and all-cause mortality. We used adjusted cause-specific hazard models to examine outcomes among cancer patients (cancer treatment pre-PCI) versus controls (no cancer treatment pre-PCI). Cardiovascular mortality was explored in a cancer subgroup with recent (within 1 year pre-PCI) cancer and in post-PCI cancer patients using post-PCI cancer as a time-dependent variable. Among 15 008 patients, 3.3% (n=496) were cancer patients. Observed rates of 14-year cardiovascular mortality (31.4% versus 27.7%, P=0.31) and composite cardiovascular death, myocardial infarction, or revascularization (51.1% versus 55.8%, P=0.37) were similar for cancer versus control groups; all-cause mortality rates were higher (79.7% versus 49.3%, P<0.01). Adjusted risk of cardiovascular mortality was similar for cancer patients versus controls (hazard ratio 0.95; 95% CI 0.76 to 1.20) and for patients with versus without recent cancer (hazard ratio 1.46; 95% CI 0.92 to 2.33). Post-PCI cancer, present in 4.3% (n=647) of patients, was associated with cardiovascular mortality (adjusted hazard ratio 1.51; 95% CI 1.11 to 2.03).ConclusionsCancer history was present in a minority of PCI patients but was not associated with worse long-term cardiovascular outcomes. Further investigation into PCI outcomes in this population is warranted.
We describe a miniature electrochemically driven, wrist-worn infusion pump. Generation of gas by an electrolytic reaction compresses a reservoir containing medication and provides a predictable and controllable infusion rate. The pump was used for patient-controlled analgesia (PCA) in women who required analgesia after Caesarean section. It was accepted readily and was convenient for both patients and nursing staff. This portable system, using a novel motive force, has advantages of convenience over larger systems and has sophisticated features not present in existing small systems. It has potential as a routine PCA device and it may have uses in other situations requiring convenient infusion or intermittent injection in an ambulatory setting.
Plasma digoxin concentrations on admission to hospital have been compared with levels on day 8 in a group of 50 patients who were maintained on their preadmission digoxin doses for 7 days. In the absence of a change in renal function, 18 patients (36%) had higher levels on day 8 and were considered to be non-compliant: a further 7 patients (14%) had lower levels on day 8 suggesting that before admission they had been taking more than their prescribed digoxin dose. Fifty per cent were, therefore, taking their digoxin improperly. In addition, an incorrect dose of digoxin may have been prescribed in 14 patients (28%) with plasma digoxin concentrations either below 0-8 ng/ml (1.02 nmol/l) or above 2-0 ng/ml (2 56 nmol/l) on day 8. Long-term compliance was assessed by comparing day 8 'steady state' digoxin levels with those obtained at outpatient follow-up. Thirty of the originalgroup were studied at 4 weeks when 27per cent were considered non-compliant, and 20 at 3 months when 30 per cent were non-compliant. These results have serious implications both for drug prescribing andfor the treatment of disease, and suggest that a problem of communication exists between doctors and their patients.In a previous study of patients already taking digoxin when admitted to hospital as emergencies (Carruthers et al., 1974), it was found that only 42 per cent had plasma digoxin concentrations within the normal therapeutic range of 08 to 2-0 ng/ml (1-02-2*56 nmol/l) (Whiting et al., 1973); 33 per cent had levels below 08 ng/ml (1P02 nmol/l) and were presumably under-treated and 25 per cent had levels greater than 2-0 ng/ml (2-56 nmol/l) and may have been potentially at risk from digoxin toxicity (Chamberlain et al., 1970;Whiting et al., 1973). Factors responsible for the wide scatter of digoxin concentrations were not identified. A further group of patients have now been studied in which serial inpatient and outpatient plasma digoxin concentrations were used to investigate non-compliance as a possible explanation of the fact that so many levels lie outside the 'therapeutic range'. Patients and methodsConsecutive patients admitted as emergencies to a general medical ward in the Belfast City Hospital and receiving maintenance digoxin treatment before admission were studied. For each patient, a careful history relating to digoxin treatment was taken with particular reference to the dose, the
Plasma myocardial, and skeletal muscle digoxin concentrations were measured in 32 patients undergoing cardiopulmonary bypass who were on long-term treatment with digoxin. The patients were divided into 4 groups according to the daily digoxin dose and the interval between discontinuation of the drug and operation. Before bypass, the mean digoxin concentrations were 1.58 nmol/l (1.24 ng/ml) in plasma 65.2 nmol/kg (50.9 ng/g) in the atria, 121.4 nmol/kg (94.98 ng/g) in 11 papillary muscles, and 16.6 nmol/kg (13.0 ng/g) in skeletal muscle. Mean atrial digoxin concentrations were significantly lower tham mean papillary muscle concentrations in 11 patients. Ratios of plasma of myocardial or skeletal muscle digoxin concentrations were very variable. Generally digoxin concentrations were higher in patients on the larger digoxin dose and with the shorter discontinuation time before surgery. These differences attained significance only with plasma digoxin concentrations. There was a slight fall in plasma digoxin concentration during cardiopulmonary bypass but no significant differences were observed between plasma, atrial, or skeletal muscle digoxin concentrations before and at the end of bypass. No clear relation was seen between plasma or atrial digoxin concentrations and postoperative cardiotoxicity. Stopping digoxin 48 hours before operation appeared to account for pre- or post-bypass plasma digoxin concentrations of less than 1.0 nmol/l (0.8 ng/ml) in most of the instances encountered, whereas the 3 patients who developed pulsus bigeminus postoperatively had received 0.5 mg digoxin only 24 hours before operation.
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