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Despite well-documented clinical benefit of the use of statins in patients with coronary artery disease (CAD) and even mild lipid elevations, studies have documented the presence of a significant "treatment gap" between those patients in whom treatment is indicated and those patients who actually receive it. It has been proposed that a prescription for statin therapy given to indicated patients at the time of initial angiographic diagnosis of CAD has the potential to improve long-term medication compliance, but this requires further evaluation. We prospectively followed 600 patients with angiographically demonstrated CAD (diameter stenosis > or = 70%) who met the National Cholesterol Education Project (NCEP) guidelines for statin therapy for an average of 3.0 years (range 2.0 to 4.6). Patients were an average of 65 years of age, 78% were men, 77% presented initially with acute ischemic syndrome, and 64 (10.7%) died during follow-up. Overall, 105 patients (18%) were discharged from the initial hospitalization with a statin prescription. At long-term follow-up, the number of patients taking statins had increased to 47%. However, long-term statin compliance was significantly higher among patients initially discharged with a statin prescription than those who were not (77% vs 40%; p < 0.0001). Additionally, those patients discharged with a statin prescription had significantly reduced mortality rate at long-term follow-up (5.7% vs 11.7%; p = 0.05). Cox hazard regression analysis, controlling for all known clinical baseline variables, confirmed the absence of a prehospital discharge statin prescription to be an independent predictor of increased mortality (hazard ratio 2.4) with a statistical trend (p = 0.06). Thus, this study demonstrates that after angiographic diagnosis of CAD, prescription of appropriate statin therapy at the time of hospital discharge improves long-term statin compliance and may significantly enhance survival. [ABSTRACT FROM AUTHOR]

Objective: We tested whether a common AMPD1 gene variant is associated with improved cardiovascular (CV) survival in patients with coronary artery disease (CAD)., Background: Reduced activity of adenosine monophosphate deaminase (AMPD) may increase production of adenosine, a cardioprotective agent. A common, nonsense, point variant of the AMPD1 gene (C34T) results in enzymatic inactivity and has been associated with prolonged survival in heart failure., Methods: Blood was collected from 367 patients undergoing coronary angiography. Genotyping was done by polymerase chain reaction amplification and restriction enzyme digestion, resulting in allele-specific fragments. Coronary artery disease was defined as > or =70% stenosis of > or =1 coronary artery. Patients were followed prospectively for up to 4.8 years. Survival statistics compared hetero- (+/-) or homozygotic (-/-) carriers with noncarriers., Results: Patients were 66 +/- 10 years old; 79% were men; 22.6% were heterozygous and 1.9% homozygous for the variant AMPD1(-) allele. During a mean of 3.5 +/- 1.0 years, 52 patients (14.2%) died, 37 (10.1%) of CV causes. Cardiovascular mortality was 4.4% (4/90) in AMPD1(-) allele carriers compared with 11.9% (33/277) in noncarriers (p = 0.046). In multiple variable regression analysis, only age (hazard ratio, 1.11/year, p < 0.001) and AMPD1(-) carriage (hazard ratio, 0.36, p = 0.053) were independent predictors of CV mortality., Conclusions: Carriage of a common variant of the AMPD1 gene was associated with improved CV survival in patients with angiographically documented CAD. The dysfunctional AMPD1(-) allele may lead to increased cardiac adenosine and increased cardioprotection during ischemic events. Adenosine monophosphate deaminase-1 genotyping should be further explored in CAD for prognostic, mechanistic and therapeutic insights.

Controversy exists over the role of complement activation in the natural history of decompression illness (DCI), and whether an individual's predisposition to DCI might be influenced by susceptibility to activation of complement by intravascular gas bubbles. Treatment with a soluble complement receptor (sCR-1), which neutralizes activated complement components, is known to be beneficial in other complement-dependent disease processes. This study investigated the effect of treating rats with sCR-1 or saline before decompression from a dive profile known to produce a high incidence of DCI. No statistical difference in the incidence of DCI was observed between the 27 rats treated with sCR-1 and 26 control rats treated with saline. The study was unable to confirm the previously reported observation in rats of a positive correlation between DCI incidence and increasing weight.

In this study, the levels of activated complement fragments C3a and C5a were measured on 11 U.S. Navy divers as they performed a 28-day saturation dive to a pressure equivalent of 1,000 feet of seawater (fsw, 31.3 atm abs). Two subjects developed symptoms consistent with the high pressure nervous syndrome (HPNS) and three were treated for type I DCS (joint pain only). These events allowed us to test two hypotheses: a) alterations in C3a or C5a levels during compression are related to the occurrence of HPNS and b) increases in complement fragments are an indicator of decompression stress associated with type I DCS. There was no correlation between changes in C3a and C5a levels during compression and the diagnosis of HPNS. Our results suggest that an increase in C3a and C5a levels during saturation diving correlates with decompression stress and the clinical diagnosis of type I DCS.

The standard treatment for cerebral arterial gas embolism (CAGE) is an initial recompression to 6 atm abs on air for 30 min followed by oxygen breathing at 2.8 and 1.9 atm abs. It has been suggested that initial recompression to 2.8 atm abs on O2 may be as beneficial, thus avoiding potential treatment complications associated with the deeper depth. To test this hypothesis, we measured the recovery of the somatosensory evoked potential (SEP) following air embolism in anesthetized, ventilated cats. Air was infused into the carotid artery in increments of 0.08 ml until the SEP amplitude was reduced to less than 10% of the baseline value for 15 min. Three groups were studied. A control group (n = 10) received no further treatment after SEP suppression. The second group (6 atm abs/HBO] (n = 8) was compressed to 6 atm abs on air for 30 min followed by O2 breathing at 2.8 atm abs for 100 min. The third group (HBO) (n = 8) was compressed to 2.8 atm abs on O2 for 130 min. The control group recovered 28.8 +/- 18.2% (mean +/- SD) of the baseline amplitude, whereas the 6 atm abs/HBO group recovered 48.6 +/- 22.6%, and the HBO group recovered 62.0 +/- 20.3%. An analysis of variance revealed that only the HBO group had significantly (P less than 0.01) better recovery than the control group. There was no significant difference in SEP recovery between the 2 treatment groups. These results suggest that treating CAGE at 2.8 atm abs with O2 is a viable alternative to the current therapy.

Dexamethasone is often recommended as an adjunct to recompression in the treatment of serious central nervous system decompression accidents. We studied the effects of prophylactic and therapeutic administration of dexamethasone combined with hyperbaric treatment in anesthetized dogs that were subjected to carotid air embolism and a brief episode of arterial hypertension. To assess recovery we measured somatosensory evoked potential (SSEP) amplitude, intracranial pressure, brain water, and cerebral blood flow. Three groups were studied: pre-air treatment (dexamethasone 1 mg/kg 3-4 h before carotid air embolism, and 1 mg/kg immediately after air embolism); post-air treatment (2 mg/kg immediately after air embolism); and control (equivalent volumes of saline pre- and post-air). There was a slight improvement in SSEP early in the course of hyperbaric therapy in the pre-air treated group; the post-air group never differed from control. No differences in intracranial pressure or brain water were found among groups. No blood flows below those lethal to neurons occurred in treated animals but 4 of 7 control animals had low flows. Although prophylactic treatment with dexamethasone produces some improvement in recovery, we cannot confirm that dexamethasone is an effective adjunct to recompression when administered therapeutically.

Decompression sickness (DCS) is usually categorised as type I (mild; peripheral pain, non-neurological) or type II (serious; neurological). Type II is regarded as predominantly a spinal cord disease with infrequent cerebral involvement. Cerebral perfusion was studied by injection of 99Tcm-hexamethylpropyleneamine oxime and single photon emission tomography in 28 divers with confirmed incidents of DCS and cerebral arterial gas embolism (CAGE). Cerebral perfusion deficits were present in all 23 cases of type II DCS and in all 4 cases of CAGE. No deficits were present in the single case of type I DCS. Type II DCS should be recognised as a diffuse, multifocal, central nervous system disease.

This paper reports two cases involving divers who presented with painful hands and were treated for decompression sickness. Although treatment was successful, their symptoms and diving history suggest non-freezing cold injury, the so-called immersion hand, rather than decompression sickness. For long exposures or cases where the diver may have inadequate insulation, thermal protection of hands is recommended even in water as warm as 16 degrees C.

Carbon monoxide causes one third of all poisoning deaths in Britain. In this paper a modern scheme for the assessment and management of victims of carbon monoxide poisoning is outlined, the importance of the direct cellular toxicity of carbon monoxide and the rationale behind hyperbaric oxygen therapy are discussed, and a list of currently available hyperbaric facilities is given.

Many aspects of central nervous system (CNS) decompression sickness (DCS) are poorly understood, including the temporal pattern of its presentation and the pathogenic mechanisms involved in the development of the disease. Using case histories and clinical series published in the literature and retrieved from treatment center records, this study is an attempt to define the interval between surfacing from a hyperbaric exposure and the onset of symptoms of CNS DCS. The results of 1070 cases of human CNS DCS were included in the study. The results show that the disease generally occurs rapidly: over 50% became symptomatic within 10 min of returning to 1 ATA, and in only 15% of cases was the onset of symptoms delayed for more than 1 h. Cerebral DCS had a more rapid onset than spinal cord disease: 50% of cerebral cases became apparent within about 3 min and a similar proportion of spinal cord cases within about 9 min from surfacing. The influence of these results on the diagnosis and treatment of dysbaric illness, on the safety of certain diving practices, and on possible pathogenic mechanisms is discussed.

A disquieting and rarely described feature of the treatment of arterial gas embolism (AGE) is the high incidence of relapse following good to excellent initial responses to recompression therapy. This paper includes a discussion of the issues involved in the etiology and clinical approach to the specific problem of relapse and relates experience from selected clinical cases to a modified therapeutic approach that has been introduced into Royal Navy diving and submarine medicine practice. It illustrates how and why current treatment procedures have been expressly designed to minimize the incidence of relapse and to modify favorably the pathophysiological responses (particularly vasogenic cerebral edema) associated with cerebral AGE.