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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The thickening of alveolar basement membrane is found in autopsies, along with microvascular pathologies, in Type 1 and 2 diabetes mellitus (DM). To detect the function and permeability of alveolar basement membrane, carbon monoxide diffusion capacity (DLCO) and technetium 99m-diethyltriaminepentaaceticacid ((99m)Tc-DTPA) aerosol scintigraphy methods can be used. The aim of this study was to determine alveolar basement membrane damage using these two methods. Nineteen women and 6 men, nonsmoking, Type 2 DM cases, without any lung and/or heart disease and who had neither anemia nor obesity, made up the patient group. They were compared with six female and nine male healthy cases who had the same characteristics with the diabetes cases. All of the cases DLCO were measured by single-breath method and (99m)Tc-DTPA aerosol scintigraphy was performed. DLCO showed no difference between the two groups. Aerosol scintigraphy was significantly decreased in the diabetic group (P=.01). In cases with >5 years of diabetic duration (P<.01), in cases with glycolized hemoglobin (HbA(1c)) </=8% (P<.05) and >8% (P<.05), and in microangiopathic cases (P<.01), alveolo-capillary permeability was significantly decreased than in the control group. Among the same groups, no significant difference could be detected for DLCO. The permeability of alveolar basement membrane can reduce in respect to diabetes duration and poor metabolic control. According to our investigation, (99m)Tc-DTPA aerosol scintigraphy method is more sensitive than DLCO method for determining these pathologies.
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PMID:Evaluation of pulmonary alveolo-capillary permeability in Type 2 diabetes mellitus: using technetium 99mTc-DTPA aerosol scintigraphy and carbon monoxide diffusion capacity. 1679 70

We reviewed the performance of a new polymethylpentene oxygenator (DIDECMO, Dideco, Mirandola, Italy) in terms of clinical safety and efficiency in priming, oxygenation, and oxygenator resistance in neonatal and pediatric extracorporeal membrane oxygenation (ECMO) patients. Between March 2005 and January 2006, 14 patients required ECMO in the San Vincenzo Hospital. Of these, 8 (median age, 9 days; range, 3 days to 15 months) received normothermic ECMO for postcardiotomy heart failure after surgery for congenital heart disease. The DIDECMO oxygenator was used in all patients (median weight, 2.4 kg; range, 2 to 7 kg). According to our previous experience, all patients received the same anticoagulation management. DIDECMO is a new phosphorylcholine-coated, polymethylpentene hollow-fiber oxygenator recommended for a maximum blood flow of 2300 ml/min with a membrane surface area of 0.67 m2 and validated to be used up to 5 days. Static priming was 100 ml and mean support time 05 hours (range, 36 to 198 hours). No oxygenators were changed during support. Median pressure drop during overall assistance was 24 mm Hg. Carbon dioxide elimination was obtained with a 1:1 blood flow/air flow ratio. Neither oxygenator-related major nor minor adverse events occurred during support. In our initial experience, the new polymethylpentene DIDECMO oxygenator provided adequate gas exchange and offered technical advantages in terms of low priming volume and acceptable hemodynamic resistance despite pulsatile flow regimen. Also, we used this device for more than 8 days without any technical problems.
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PMID:DIDECMO: a new polymethylpentene oxygenator for pediatric extracorporeal membrane oxygenation. 1696 47

Hypercapnic cerebrovascular reactivity is decreased in obstructive sleep apnoea and congestive heart disease perhaps as a result of repeated apnoeas. To test the hypothesis that repeated apnoeas blunt cerebrovascular reactivity to hypercapnia, we studied breath hold divers and determined cerebrovascular reactivity by measuring changes in middle cerebral artery velocity (MCAV, cm s(-1)) per mmHg change in end-tidal partial pressure of CO2(PET,CO2 ) in response to two hyperoxic hypercapnia rebreathing manoeuvres (modified Read protocol) in elite breath-hold divers (BHD, n=7) and non-divers (ND, n=7). In addition, ventilation and central (beat-to-beat stroke volume measurement with Modelflow technique) haemodynamics were determined. Ventilatory responses to hypercapnia were blunted in BHD versus ND largely due to lower breathing frequency. Cerebrovascular reactivity did not differ between groups (3.7 +/- 1.4 versus 3.4 +/- 1.3% mmHg(-1) in BHD and ND, respectively; P=0.90) and the same was found for cerebral vascular resistance and MCAV recovery to baseline after termination of the CO2 challenge. Cardiovascular parameters were not changed significantly during rebreathing in either group, except for a small increase in mean arterial pressure for both groups. Our findings indicate that the regulation of the cerebral circulation in response to hypercapnia is intact in elite breath-hold divers, potentially as a protective mechanism against the chronic intermittent cerebral hypoxia and/or hypercapnia that occurs during breath-hold diving. These data also suggest that factors other than repeated apnoeas contribute to the blunting of cerebrovascular reactivity in conditions like sleep apnoea.
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PMID:Cerebrovascular reactivity to hypercapnia is unimpaired in breath-hold divers. 1741 71

Hazardous chemicals escape to the environment by a number of natural and/or anthropogenic activities and may cause adverse effects on human health and the environment. Increased combustion of fossil fuels in the last century is responsible for the progressive change in the atmospheric composition. Air pollutants, such as carbon monoxide (CO), sulfur dioxide (SO(2)), nitrogen oxides (NOx), volatile organic compounds (VOCs), ozone (O(3)), heavy metals, and respirable particulate matter (PM2.5 and PM10), differ in their chemical composition, reaction properties, emission, time of disintegration and ability to diffuse in long or short distances. Air pollution has both acute and chronic effects on human health, affecting a number of different systems and organs. It ranges from minor upper respiratory irritation to chronic respiratory and heart disease, lung cancer, acute respiratory infections in children and chronic bronchitis in adults, aggravating pre-existing heart and lung disease, or asthmatic attacks. In addition, short- and long-term exposures have also been linked with premature mortality and reduced life expectancy. These effects of air pollutants on human health and their mechanism of action are briefly discussed.
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PMID:Human health effects of air pollution. 1764 40

Obesity and climate change are two problems currently challenging humanity. Although apparently unrelated, an epidemiological approach to both shows a similar environmental aetiology, based in modern human lifestyles and their driving economic forces. One way of analysing this is through inflammation (defined as '. . . a disturbance of function following insult or injury') of both the internal (biological) and external (ecological) environments. Chronic, low-grade, systemic inflammation has recently been shown to accompany obesity, as well as a range of biological pathologies associated with obesity (diabetes, heart disease, some cancers, etc.). This is influenced by the body's inability to soak up excess glucose as a result of insulin resistance. In a broader sense, inflammation is a metaphor for ecological 'pathologies', manifest particularly in unnatural disturbances like climate change, ocean acidity, rising temperatures and species extinction, associated with the inability of the world's environmental 'sinks' to soak up carbon dioxide ('carbon resistance'?). The use of such a metaphorical analysis opens the possibilities for dealing with two interdisciplinary problems simultaneously. Strategies for managing climate change, including personal carbon trading, could provide a 'stealth intervention' for reducing population levels of obesity by increasing personal energy expenditure and decreasing energy-dense food intake, as well as reducing the carbon emissions causing climate change.
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PMID:Dousing our inflammatory environment(s): is personal carbon trading an option for reducing obesity--and climate change? 1828 77

This review is intended to stimulate interest in the effect of increased expression of heme oxygenase-1 (HO-1) protein and increased levels of HO activity on normal and pathological states. The HO system includes the heme catabolic pathway, comprising HO and biliverdin reductase, and the products of heme degradation, carbon monoxide (CO), iron, and biliverdin/bilirubin. The role of the HO system in diabetes, inflammation, heart disease, hypertension, neurological disorders, transplantation, endotoxemia and other pathologies is a burgeoning area of research. This review focuses on the clinical potential of increased levels of HO-1 protein and HO activity to ameliorate tissue injury. The use of pharmacological and genetic probes to manipulate HO, leading to new insights into the complex relationship of the HO system with biological and pathological phenomena under investigation, is reviewed. This information is critical in both drug development and the implementation of clinical approaches to moderate and to alleviate the numerous chronic disorders in humans affected by perturbations in the HO system.
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PMID:Pharmacological and clinical aspects of heme oxygenase. 1832 2

Cigarette reduction has been proposed as a treatment goal for smokers who are not interested in stopping completely. This randomized controlled trial was designed to determine the effect of a smoking reduction intervention on smoking behavior, symptoms of heart disease, and biomarkers of tobacco exposure. It included 152 patients with heart disease who did not intend to stop smoking in the next 30 days. Participants were randomly assigned to smoking reduction (SR) or usual care (UC). SR subjects received counseling and nicotine replacement therapy to encourage > or =50% reduction in cigarettes per day (CPD). They were followed at 1, 3, 6, 12 and 18 months to assess smoking, heart disease symptoms, quality of life and nicotine, cotinine, carbon monoxide (CO), white blood cell (WBC) count, fibrinogen, hs-C-reactive protein (hs-CRP), F2-isoprostane, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL), and 1-hydroxypyrene (1-HOP). At 6 months SR participants reduced by 10.9 CPD, compared with 7.4 CPD in UC (difference NS). At 18 months, 9/78 SR vs. 9/74 UC participants quit smoking. There were no significant differences between treatment groups in angina, quality of life or adverse events, nicotine, cotinine, CO, WBC count, fibrinogen, hs-CRP, F2-isoprostane, total NNAL or 1-HOP levels at any time point. To determine if smoking reduction, regardless of treatment condition, was associated with improved outcomes, we compared all subjects at 6 months to baseline (mean reduction in CPD from 27.4 to 18.1, p<.01). There were no significant changes in outcome variables except CO, which decreased by 5.5 ppm (p<.01). There were also no significant improvements considering only subjects who reduced by > or =50%, or those who had no history of reduction prior to enrollment in the study. The SR intervention did not significantly reduce CPD or toxin exposure, or improve smoking cessation or clinical outcomes compared to UC. These results emphasize the importance of abstinence for smokers with heart disease to minimize health risks from tobacco.
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PMID:Smoking reduction fails to improve clinical and biological markers of cardiac disease: a randomized controlled trial. 1832 66

Recent data suggest potential benefits of cardiac resynchronization therapy in the management of right ventricular (RV) dysfunction in congenital heart disease. The aim of this study was to determine the nature, prevalence, and functional implications of mechanical RV dyssynchrony in patients after Senning or Mustard procedures for transposition of the great arteries. Twenty-eight patients (mean age 21.1 +/- 3.5 years) at 19.9 +/- 3.2 years after atrial switch operations and 29 healthy controls were studied. The times from the onset of QRS to peak systolic strain (T epsilon) at the base of and the mid RV free wall, the ventricular septum (VS), and the left ventricular (LV) free wall were determined using tissue Doppler echocardiography. Intraventricular mechanical delay was defined as Delta T epsilon(RV-VS) and interventricular mechanical delay as Delta T epsilon(RV-LV). In patients, the magnitude of RV intra- and interventricular mechanical delay was correlated with cardiac magnetic resonance-derived RV volumes and ejection fractions (n = 26) and treadmill exercise testing parameters (n = 20). Compared with controls, patients had significantly longer Delta T epsilon(RV-VS) (48.1 +/- 50.9 vs 17.0 +/- 16.1 ms, p <0.001) and Delta T epsilon(RV-LV) (63.1 +/- 49.5 vs 19.0 +/- 12.9, p <0.001). Nine patients (32%) exhibited RV dyssynchrony (Delta T epsilon(RV-VS) >49 ms, control mean +/- 2SD), and 16 patients (57%) showed interventricular dyssynchrony (Delta T epsilon(RV-LV) >45 ms). In patients, RV intra- and interventricular mechanical delay was correlated negatively with the RV ejection fraction (both r = -0.42, p = 0.03) and percentage predicted maximum oxygen consumption (r = -0.50, p = 0.03, and r = -0.52, p = 0.02, respectively) and positively with minute ventilation/carbon dioxide production slope (r = 0.49, p = 0.03, and r = 0.56, p = 0.01, respectively). In conclusion, RV dyssynchrony is common in young adults after atrial switch operations and is associated with RV systolic dysfunction and impaired exercise performance.
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PMID:Mechanical right ventricular dyssynchrony in patients after atrial switch operation for transposition of the great arteries. 1832 57

Bushfire fighting is a hazardous occupation and control strategies are generally in place to minimize the hazards. However, little is known regarding firefighters' exposure to bushfire smoke, which is a complex mixture of toxic gases and particles. In Australia, during the prescribed burning season, firefighters are likely to be exposed on a regular basis to bushfire smoke, but whether these exposures affect health has yet to be determined. There are a number of factors that govern whether exposure to smoke will result in short-term and/or long-term health problems, including the concentrations of air pollutants within the breathing zone of the firefighter, the exposure duration, and health susceptibility of the individual, especially for pre-existing lung or heart disease. This paper presents measurements of firefighters' personal exposure to bushfire smoke, the first step within a risk management framework. It provides crucial information on the magnitude, extent and frequency of personal exposure to bushfire smoke for a range of typical scenarios. It is found that the primary air toxics of concern are carbon monoxide (CO), respirable particles and formaldehyde. Also, work activity is a major factor influencing exposure with exposure standards (both average and short-term limits) likely to be exceeded for activities such as suppression of spot fires, holding the fireline, and patrolling at the edge of a burn area in the urban-rural interface.
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PMID:Australian firefighters' exposure to air toxics during bushfire burns of autumn 2005 and 2006. 1882 14

The last decade has witnessed an explosion in the elucidation of the role that the heme oxygenase system plays in human physiology. This system encompasses not only the heme degradative pathway, including heme oxygenase and biliverdin reductase, but also the products of heme degradation, carbon monoxide, iron, and biliverdin/bilirubin. Their role in diabetes, inflammation, heart disease, hypertension, transplantation, and pulmonary disease are areas of burgeoning research. The research has focused not only on heme itself but also on its metabolic products as well as endogenous compounds involved in a vast number of genetic and metabolic processes that are affected when heme metabolism is perturbed. It should be noted, however, that although the use of carbon monoxide and biliverdin/bilirubin as therapeutic agents has been successful, these agents can be toxic at high levels in tissue, e.g., kernicterus. Care must be used to ensure that when these compounds are used as therapeutic agents their deleterious effects are minimized or avoided. On balance, however, the strategies to target heme oxygenase-1 as described in this review offer promising therapeutic approaches to clinicians for the effective management of hypertension and renal function. The approaches detailed may prove to be seminal in the development of a new therapeutic strategy to treat hypertension.
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PMID:Physiological significance of heme oxygenase in hypertension. 1902 71


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