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

Oxygen uptake efficiency slope is a new index of cardiorespiratory functional reserve derived from the logarithmic relation between oxygen uptake (VO(2)) and minute ventilation during incremental exercise. The oxygen uptake efficiency slope represents how effectively oxygen is extracted and taken into the body from the air, and then ventilated. The physiologic backgrounds of the index are based on: 1) the development of metabolic acidosis that is controlled by the distribution of blood to the skeletal muscles; 2) the physiologic dead space that is affected by the perfusion to the lungs; and 3) arterial carbon dioxide partial pressure. One of the greatest advantages of the oxygen uptake efficiency slope is that it can be calculated by exercise data of submaximal levels. Another advantage is that it is mathematically determined from a set of gas analysis data and, therefore, is completely an objective measurement. Moreover, the oxygen uptake efficiency slope is shown to be highly reproducible. Clinical applications of the oxygen uptake efficiency slope have been reported initially from a population of pediatric patients with heart disease, then from adult patients with chronic heart failure, and finally from elite endurance athletes. Further applications are expected with the use of this sophisticated index. (c)2000 by CHF, Inc.
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PMID:The oxygen uptake efficiency slope and its value in the assessment of cardiorespiratory functional reserve. 1218 86

Periodic breathing is often associated with heart disease or stroke, and commonly Cheyne-Stokes breathing has a period of about a minute. Periodic breathing also commonly occurs in healthy subjects at high altitude, and here the periods may be much shorter, of the order of 15-20 s. In this paper we study such periodic breathing using the classical model of Grodins et al. (1967, J. Appl. Physiol. 22, 260-276), together with a prescription for the dependence of ventilation on the blood CO2 concentration, modulated by the reduced oxygen pressure (the 'Oxford fan'). The model focusses on the fast dynamics of the arterial blood CO2, and differs in this respect from our previous work which emphasised the brain CO2 concentration; in this sense our model is in fact a generalization of the conceptually simpler Mackey-Glass model.
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PMID:Periodic breathing at high altitude. 1282 66

Several recent epidemiologic studies investigating the short-term effects of particulate matter (PM) concentrations have shown carbon monoxide (CO) to have the strongest and most consistent statistical relationship with hospital admissions for cardiac diseases. This article suggests a potential hypothesis for these epidemiologic observations. Oxygen (O2) is transported, in reversible combination with hemoglobin, from the lungs to the tissues, where it diffuses into cardiac myocytes. Within the myocyte a portion of the O2 diffuses directly to the mitochondria, while the remaining O2 is transported by facilitated diffusion bound to myoglobin, a heme protein found in muscle. Within the mitochondria, O2 reacts to produce adenosine triphosphate (ATP), a high-energy phosphate compound that provides energy for all cell functions. Accordingly, the sustained production of ATP depends on the continuous delivery of O2 to the mitochondria, and failure at any point in the O2 transport system will compromise ATP production and myocardial function. Myoglobin, a fundamental constituent of cardiac muscle is essential for delivering O2 to the mitochondria. Myoglobin concentrations in cardiac tissue were 50% lower in patients with heart failure than in patients dying from noncardiac causes. Myoglobin concentrations are also severely depressed in animal models of congestive heart failure. Consequently, the role of myoglobin as a cellular transporter of O2 is seriously impaired by heart disease. Carbon monoxide reduces O2 transport to the tissues and, within the tissues, binds with myoglobin to form carboxymyoglobin (COMb). Thus, in cardiac patients CO further exacerbates the disease-related loss of myoglobin function. This further disrupts O2 transport and promotes adverse consequences for the compromised heart. Moreover, during hypoxia CO has the propensity of leaving the blood and binding with myoglobin in the intracellular compartment. Elderly persons with preexisting cardiopulmonary disorders appear to be at maximum risk of harmful health effects due to ambient air pollution exposure. Many of these disorders result in generalized or regional hypoxia. It is reasonable to hypothesize that CO also moves out of the blood of these patients and into the heart tissue whenever they are under hypoxic stress, such as exercise. Accordingly, CO binds with the marginal myoglobin concentrations present in the hearts of cardiac patients and further compromises cardiac function, resulting in poor tolerance of activity. Therefore, reduced cardiac myoglobin in people with heart disease, further exacerbated by CO moving into the cardiac tissue during episodes of hypoxia, may account for the positive association between ambient CO concentrations and hospitalization for heart disease.
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PMID:Biological plausibility for carbon monoxide as a copollutant in PM epidemiologic studies. 1288 88

Chronic obstructive pulmonary disease (COPD) often leads to massive oedema and the development of what is usually called cor pulmonale. The mechanisms by which patients with COPD retain salt and water are not completely understood. Several abnormalities have been found including reduced renal blood flow with relatively preserved glomerular filtration rate and elevated levels of renin, aldosterone, arginine vasopressin and atrial natriuretic peptide. Generally, these abnormalities worsen with the severity of COPD and are most marked during the oedematous phases. Cardiac output is remarkably normal, suggesting that "cor pulmonale" is not primarily a cardiac disorder but rather a condition of volume overload due to activation of sodium-retaining mechanisms. The stimulus for this activation could be underfilling of the arterial system (reduced effective circulating volume) secondary to a fall in total peripheral vascular resistance. The latter is caused by hypercapnia-induced dilation of the precapillary sphincters. Apparently, the massive sodium retention by the kidney is not able to restore the circulating volume and a vicious cycle ensues ultimately leading to a clinical picture which resembles right-sided heart failure. Predictably, only blockade of the effects of carbon dioxide at the level of the precapillary sphincters would be able to halt this process.
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PMID:Fluid homeostasis in chronic obstructive lung disease. 1462 Nov 5

Sitaxsentan may benefit patients with pulmonary arterial hypertension by blocking the vasoconstrictor effects of endothelin-A while maintaining the vasodilator/clearance functions of endothelin-B receptors. Patients with pulmonary arterial hypertension that was idiopathic, related to connective tissue disease or congenital heart disease, were randomized to receive placebo (n = 60), sitaxsentan 100 mg (n = 55), or sitaxsentan 300 mg (n = 63) orally once daily for 12 weeks. The primary endpoint was change in peak VO(2) at Week 12. Secondary endpoints included 6-minute walk, New York Heart Association class, VO(2) at anaerobic threshold, VE per carbon dioxide production at anaerobic threshold, hemodynamics, quality of life, and time to clinical worsening. Although the 300-mg group increased peak VO(2) compared with placebo (+3.1%, p < 0.01), none of the other endpoints derived from cardiopulmonary exercise testing were met. However, both the 100-mg dose and the 300-mg dose, compared with placebo, increased 6-minute walk distance (100 mg: +35 m, p < 0.01; 300 mg: +33 m, p < 0.01); functional class, cardiac index, and pulmonary vascular resistance also improved (p < 0.02 for each parameter at both doses). The incidence of elevated aminotransferase values (> three times normal) was 3% for the placebo group, 0% for the 100-mg group, and 10% for the 300-mg group.
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PMID:Sitaxsentan therapy for pulmonary arterial hypertension. 1476 56

Numerous recent epidemiologic studies report increases in the daily incidence of cardiovascular disease mortality and morbidity related to increases in daily levels of fine particulate matter (PM)* air pollution. This study sought to evaluate the possible association between the occurrence of out-of-hospital sudden cardiac arrest (SCA) and daily PM levels in the Seattle metropolitan area. The underlying hypothesis was that PM exposure may act as a cardiovascular trigger for SCA. A case-crossover study was conducted among 362 SCA cases identified by paramedics from October 1988 through June 1994. Cases were King County WA residents who were married, aged 25 to 74 years at the time of their SCA, with no prior history of clinically recognized heart disease or other life-threatening comorbid conditions. Daily averages of regional PM monitoring data for nephelometry measures of PM (reported in units of bsp, referred to as coefficient of light scattering) and PM10 (particulate matter 10 microm or smaller in aerodynamic diameter) from three monitoring sites were used as indicators of exposure. In the case-crossover analysis, PM levels during index times of cases within the five days preceding an SCA were compared with PM levels at referent days, defined as the same days of the week during the month of SCA occurrence. Lag periods for index days of 0 to 5 days were investigated. The estimated relative risk (RR) at a lag of 1 day for an interquartile range (IQR) change in nephelometry (0.51 bsp) was 0.893 (95% confidence interval [CI] 0.779-1.024). Varying the lag period had only minimal change on the observed association. The estimated relative risk at a lag of 1 day for an IQR change of PM10 (19.3 microg/m3) was 0.868 (95% CI 0.744-1.012). There was no evidence of confounding by ambient daily exposures to carbon monoxide or sulfur dioxide. Analysis of effect modification by individual-level variables, including age, cigarette smoke exposure, physical activity, and other risk or protective factors for cardiovascular disease did not reveal any susceptible subgroups. The null results of this study may be due to several factors; these include: the highly selected nature of this SCA case series; the fact that cases were free of prior clinically recognized heart disease or major life-threatening comorbidity; and the possibility that PM exposures at the relatively low levels seen in the Seattle metropolitan area do not trigger cardiovascular toxic mechanisms that culminate in SCA.
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PMID:A case-crossover analysis of fine particulate matter air pollution and out-of-hospital sudden cardiac arrest. 1547 96

Tobacco smoking is the main risk factor associated with chronic destructive periodontal disease. No other known factor can match the strength of smoking in causing harm to the periodontium. The harmful effects manifest themselves by interfering with vascular and immunologic reactions, as well as by undermining the supportive functions of the periodontal tissues. The typical characteristic of smoking-associated periodontal disease is the destruction of the supporting tissues of the teeth, with the ensuing clinical symptoms of bone loss, attachment loss, pocket formation, and eventually tooth loss. A review of the international literature that has accumulated over the past 20 years offers convincing evidence that smokers exhibit greater bone loss and attachment loss, as well as more pronounced frequencies of periodontal pockets, than non-smokers do. In addition, tooth loss is more extensive in smokers. Smoking, thus, considerably increases the risk for destructive periodontal disease. Depending on the definition of disease and the exposure to smoking, the risk is 5- to 20-fold elevated for a smoker compared to a never-smoker. For a smoker exposed to heavy long-life smoking, the risk of attracting destructive periodontal disease is equivalent to that of attracting lung cancer. The outcome of periodontal treatment is less favorable or even unfavorable in smokers. Although long-term studies are rare, available studies unanimously agree that treatment failures and relapse of disease are predominantly seen in smokers. This contention is valid irrespective of treatment modality, suggesting that smoking will interfere with an expected normal outcome following commonplace periodontal therapies. The majority of available studies agree that the subgingival microflora of smokers and non-smokers are no different given other conditions. As a consequence, the elevated morbidity in smokers does not depend on particular microflora. The mechanisms behind the destructive effects of smoking on the periodontal tissues, however, are not well understood. It has been speculated that interference with vascular and inflammatory phenomena may be one potential mechanism. Nicotine and carbon monoxide in tobacco smoke negatively influence wound healing. Smoking research over the past two decades has brought new knowledge into the domains of periodontology. Even more so, it has called into question the prevailing paradigm that the disease is primarily related to intraoral factors such as supra- and subgingival infection. Smoking research has revealed that environmental and lifestyle factors are involved in the onset and progression of the disease. Being the result of smoking, destructive periodontal disease shares a common feature with some 40 other diseases or disorders. As a consequence, periodontal disease should be regarded as a systemic disease in the same way as heart disease or lung disease. Thus, chronic destructive periodontal disease in smokers is initiated and driven by smoking. Its progression may or may not be amplified by unavoidable microbial colonization.
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PMID:Tobacco smoking and chronic destructive periodontal disease. 1549 Feb 98

A carbon dioxide laser was used through a bronchoscope to split the posterior aspect of complete tracheal rings in the distal trachea of a 16-month-old boy previously palliated for cyanotic congenital heart disease. After laser division of the complete tracheal rings, the patient was successfully extubated. Subsequently, the boy had granulation tissue develop, which required bronchoscopic resection, and then severe posterior tracheal impingement developed from the esophageal herniation, which required placement of a distal tracheal stent. Although unsuccessful in this case, carbon dioxide laser division of complete tracheal rings may be a safe and effective method of treating congenital tracheal stenosis in selected cases.
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PMID:Endoscopic carbon dioxide laser division of congenital complete tracheal rings: a new operative technique. 1568 Aug 63

End-tidal CO2 (ET(CO2)) monitoring and transcutaneous (TC) CO2 monitoring were prospectively compared in 53 patients, 1 month to 16 years of age, with congenital heart disease (CHD). There were 32 patients with cyanotic CHD and 21 with acyanotic CHD. The TC-Pa(CO2) difference was 2 +/- 1 mm Hg and the ET-Pa(CO2) difference was 5 +/- 3 mm Hg (P < .0001). The TC-Pa(CO2) difference was < or = 2 mm Hg in 30 of 53 patients and < or = 5 mm Hg in 53 of 53 patients. The ET-Pa(CO2) difference was < or = 2 mm Hg in 9 of 53 patients and < or = 5 mm Hg in 30 of 53 patients (P < .001). No variation in the TC-Pa(CO2) difference was noted based on the type of CHD (acyanotic vs cyanotic) or age. The ET-Pa(CO2) difference was greater in patients with cyanotic versus acyanotic CHD (7 +/- 3 mm Hg vs 4 +/- 2 mm Hg, P < .0001) and in patients < or = 1 year of age versus patients > or = 1 year of age (6 +/- 3 mm Hg vs 4 +/- 2, P = .008). In infants and children with CHD, TC monitoring provides a more accurate estimation of Pa(CO2) than ET monitoring.
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PMID:Noninvasive monitoring of carbon dioxide in infants and children with congenital heart disease: end-tidal versus transcutaneous techniques. 1614 21

We evaluated how Paco(2) and respiratory variables relate during and after exercise and derived a new noninvasive estimation of Paco(2) in children and postoperative patients with congenital heart disease. We randomly selected 8 subjects from each of three categorized groups from our previous studies: 15 control subjects (8 to 21 years old), 16 Fontan procedure patients (9 to 22 years old), and 13 patients after right ventricular outflow tract reconstruction (RVOTR) [7 to 21 years old], and used their respiratory variables during exercise testing to estimate Paco(2) (study 1). In a stepwise multiple regression analysis, end-tidal carbon dioxide tension (Petco(2)), age, ventilatory equivalent for carbon dioxide (minute ventilation [Ve]/carbon dioxide production [Vco(2)]), and gas exchange ratio (R) were major determinants of Paco(2) in control subjects: Paco(2) = 12.0 + 0.54 Petco(2) + 0.15 Ve/Vco(2) - 3.6 R + 0.22 age (r = 0.86). In addition to Petco(2) and Ve/Vco(2), arterial oxygen saturation and tidal volume were additional major determinants for Fontan procedure and RVOTR patients, respectively. We derived equations to predict the Paco(2) (r = 0.92 for Fontan procedure and r = 0.74 for RVOTR). These equations were applied to the remaining study subjects to estimate Paco(2) (study 2). Estimated values correlated with the measured Paco(2) (r = 0.71 to 0.86), and the mean differences for the control subjects, Fontan procedure, and RVOTR patients were - 0.1, - 0.1, and - 1.0, with limits of agreement of +/- 3.3, +/- 4.4, and +/- 3.1, respectively. Although estimated Paco(2) based on the Jones equation correlated with the measured Paco(2) in all groups, their slopes were significantly flatter than ours. Paco(2) throughout exercise testing may be estimated in control children and postoperative pediatric patients. The Jones equation should be applied with great care in pediatric subjects.
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PMID:Estimation of PaCO2 during exercise in children and postoperative pediatric patients with congenital heart disease. 1630 16


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