Elective percutaneous coronary intervention without on-site cardiac surgery: clinical and economic implications

BACKGROUND: Low procedural complication rates, barriers to access, and patient preference have encouraged the development of percutaneous coronary intervention (PCI) programs at centers that are often closer to home but without on-site cardiac surgical capability. OBJECTIVES: We compared clinical and economic outcomes associated with performing low-risk elective PCI at a community hospital without on-site cardiac surgery with those obtained at a more remote tertiary care center with on-site cardiac surgery. DESIGN AND MEASURES: We matched 257 patients undergoing low-risk, elective PCI at a community hospital (Immanuel St. Joseph's Hospital [ISJ] between January 27, 2000, and July 31, 2002) to 514 PCI patients treated at a tertiary care hospital (Saint Marys Hospital [SMH] between January 27, 2000, and April 30, 2002) based on clinical and lesion criteria. Clinical outcomes (in-hospital procedural success and target vessel failure during long-term follow up) and economic outcomes (direct medical costs, billed charges, and hospital length of stay [LOS]) were compared between groups. The Mayo Clinic PCI Registry (containing clinical, angiographic, and follow-up data) and administrative data were used in matching and outcomes assessment. RESULTS: Procedural success was achieved more often among ISJ-treated patients (99% vs. 95%; P = 0.02); however, no difference in target vessel failure rates was observed during a median follow-up time of 3.1 years (estimated 1-year event rate: 15.2% vs. 14.8%; P = 0.46). ISJ-treated patients incurred, on average, $3024 more in estimated total costs ($13,771 vs. $10,746; P < 0.001) and $6084 more in billed charges (P < 0.001), but incurred similar LOS post procedure (1.53 days). CONCLUSIONS: Similar clinical outcomes were achieved at a community hospital without on-site cardiac surgery but at significantly increased direct medical cost. Patients, providers, hospitals, payers, and policymakers should consider whether the benefits associated with locally provided specialized cardiovascular services warrant this additional cost.     

Gastrointestinal hypomotility with loss of enteric nicotinic acetylcholine receptors: active immunization model in mice

Background Autoimmune gastrointestinal dysmotility (AGID) is a limited form of dysautonomia. The only proven effector to date is IgG specific for ganglionic nicotinic‐acetylcholine receptors containing α3 subunits [α3*‐ nicotinic acetylcholine receptor (nAChR)]. Rabbits immunized with recombinant α3‐polypeptide produce α3*‐nAChR autoantibodies, and profound AGID ensues. Human and rabbit α3*‐nAChR‐specific‐IgGs induce transient hypomotility when injected into mice. Here, we describe success and problems encountered inducing gastrointestinal hypomotility in mice by active immunization. Methods We repeatedly injected young adult mice of seven different strains susceptible to autoimmunity (spontaneous diabetes or neural antigen immunization‐induced myasthenia gravis or encephalomyelitis) with: (i) α3‐polypeptide, intradermally or (ii) live α3*‐nAChR‐expressing xenogeneic cells, intraperitoneally. We measured serum α3*‐nAChR‐IgG twice monthly, and terminally assessed blue dye gastrointestinal transit, total small intestinal α3*‐nAChR content (radiochemically) and myenteric plexus neuron numbers (immunohistochemically, ileal–jejunal whole‐mount preparations). Key Results Standard cutaneous inoculation with α3‐polypeptide was minimally immunogenic, regardless of dose. Intraperitoneally injected live cells were potently immunogenic. Self‐reactive α3*‐nAChR‐IgG was induced only by rodent immunogen; small intestinal transit slowing and enteric α3*‐nAChR loss required high serum levels. Ganglionic neurons were not lost. Conclusions & Inferences Autoimmune gastrointestinal dysmotility is inducible in mice by active immunization. Accompanying enteric α3*‐nAChR reduction without neuronal death is consistent with an IgG‐mediated rather than T cell‐mediated pathogenesis, as is improvement of symptoms in patients receiving antibody‐depleting therapies.     

The effects of different alcoholic drinks on lipids, insulin and haemostatic and inflammatory markers in older men

Light to moderate drinking is associated with lower risk of coronary heart (CHD) than non-drinkers. We have examined the relationships between total alcohol intake and type of alcoholic beverage and several potential biological mechanisms. We carried out the study in 3158 men aged 60-79 years drawn from general practices in 24 British towns with no history of myocardial infarction, stroke or diabetes and who were not on warfarin. Total alcohol consumption showed a significant positive dose-response relationship with high density lipoprotein cholesterol (HDL-C), coagulation factor IX, haematocrit, blood viscosity, and tissue plasminogen (t-PA) antigen, and an inverse dose-response relationship with insulin, fibrinogen, von Willebrand factor (vWF) and triglycerides after adjustment for possible confounders. Total alcohol consumption showed weak associations with plasma viscosity and fibrin D-dimer, and no association with factors VII, VIII, or C-reactive protein (CRP). Wine was specifically associated with lower CRP, plasma viscosity, factor VIII and triglycerides. The findings are consistent with the suggestion that HDL-C in particular but also insulin and haemostatic factors may contribute to the beneficial effect of light to moderate drinking on risk of CHD. Wine has effects that may confer greater protection than other alcoholic beverages.     

Prognostic value of circulating pregnancy-associated plasma protein levels in patients with chronic stable angina.

AIMS: Unstable coronary atherosclerotic plaque can be present in patients with chronic stable coronary artery disease (CAD). Our objective was to assess whether measurement of plasma pregnancy-associated plasma protein (PAPP-A) level, a reflection of plaque instability, in patients with chronic stable CAD had an independent prognostic value on the subsequent incidence of death, acute coronary syndrome (ACS), and revascularization. METHODS AND RESULTS: Patients referred for coronary angiography were recruited. A cohort of 103 patients with stable symptoms for at least 6 weeks and with a coronary angiogram showing at least a 50% luminal diameter narrowing formed our study population. Median follow-up was 4.9 years. Mean age was 65+/-10 years. In a multivariable model that included CAD traditional risk factors, ejection fraction, extent of coronary atherosclerosis, prior history of myocardial infarction, prior revascularization, discharge medications, and C-reactive protein, the plasma PAPP-A was found to be significantly associated with the endpoint of future death [adjusted hazard ratio (HR) 5.29; 95% CI 1.27-22.0; P=0.023] and with the endpoint of future death and ACS (adjusted HR 3.56; 95% CI 1.27-10.0; P=0.015), but not with the endpoint of future death and revascularization. CONCLUSION: Measurement of plasma PAPP-A level in patients with chronic stable CAD has an independent prognostic value on the occurrence of death and ACS.     

Road safety - threats and opportunities for poor countries

Chances are that everyone reading this will either have lost a close friend, relative, or work colleague in a road traffic crash in the last couple of years. Chances are, the reports said it was an “accident”. There might even have been police reports giving the “cause of the accident.” Now, think about the meaning of the word “accident” - most people would agree it is an unpredictable event, one for which you could not possibly have prepared - it just happened. Now, think again. Can we predict what will happen when a cyclist''s unprotected head hits the concrete at 100 kms an hour? Can we predict what will happen when a powerful car races down a road a few meters away from the entrance of a primary school, just as the kids are leaving school? Can we predict what will happen when a matatu (commuter mini bus) driver gets behind the wheel at dusk, after a few bottles of alcohol, heading for a destination six hours away? And can we predict what will happen when a mosquito bites a baby, just after feeding on a person sick from malaria? Well - chances are, the first three scenarios will be called accidental, and the last one will be targeted for prevention! The truth is, all four are perfectly predictable, and preventable. The more than 3, 200 persons dying on the world''s road every day have become predictable - we know they will happen, we know where they will happen, and what kind of people will be involved. Yet the majority of communities and governments still call them accidental, and make no concrete provision for their prevention.On April 7 2004, the WHO and its partners will commemorate World Health Day. This time round, the theme is “Road Safety is no Accident.” Road traffic injuries are a huge public health and development problem that kills between 800 000 and 1.18 million people, and injures or disables another 20 to 50 million more every year¹. Data from the WHO and World Bank show that without appropriate response, these injuries will rise dramatically by the year 2020, particularly in rapidly motorizing countries. In addition, apart from the enormous impact on families and communities, road traffic crashes are costing governments between 1 and 3 per cent of their gross domestic product². Health facilities are over-burdened with victims of road traffic crashes, over-stretching their already meager health budgets.Once we acknowledge that Road Safety does not happen by accident, (and that road safety is the state where we have “no accident”) then we are well on the road to finding solutions. The systemic approach being recommended by the WHO moves from defining the burden of the road traffic injuries (size, nature) to understanding the factors that increase risk and vulnerability, to designing interventions, testing them for effectiveness, and finally, to getting the effective interventions implemented wherever they are needed.