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

OBJECTIVE--Recent clinical, laboratory, and epidemiological evidence that passive smoking causes heart disease was reviewed, with particular emphasis on understanding the underlying physiological and biochemical mechanisms. DATA SOURCES--Publications in the peer-reviewed literature were located via MEDLINE, citation in other relevant articles, and appropriate reports by scientific agencies. Greatest emphasis was given to work published since 1990. CONCLUSIONS--Passive smoking reduces the blood's ability to deliver oxygen to the heart and compromises the myocardium's ability to use oxygen to create adenosine triphosphate. These effects are manifest as reduced exercise capability in people breathing secondhand smoke. Secondhand smoke increases platelet activity, accelerates atherosclerotic lesions, and increases tissue damage following ischemia or myocardial infarction. The effects of secondhand tobacco smoke on the cardiovascular system are not caused by a single component of the smoke, but rather are caused by the effects of many elements, including carbon monoxide, nicotine, polycyclic aromatic hydrocarbons, and other, not fully specified elements in the smoke. Nonsmokers exposed to secondhand smoke in everyday life exhibit an increased risk of both fatal and nonfatal cardiac events.
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PMID:Passive smoking and heart disease. Mechanisms and risk. 789 90

This paper explains the physiological and biochemical basis of the anaerobic threshold (AT), achieved during physical exercise. The lactate concentration is approximately the same at rest in relatively fit adults, in normal sedentary subjects in adult patients with heart disease. But during exercise, the increase of lactate is inversely related to the physical fitness of the individual. During incremental work, the lactate concentration increases initially very little until a distinct metabolic rate (VO2 AT) is reached at which lactate starts to increase steeply (anaerobic threshold/AT; VO2 AT). Above the anaerobic threshold, accelerated glycolysis increases muscle lactic acidosis. This acidosis is buffered primarily by bicarbonate. The bicarbonate-derived CO2 causes an increased alveolar CO2 output relative to O2 uptake. Oxygen uptake is increased virtually linearly with work rate in healthy subjects with a slope of approximately 10 ml O2/min/Watt. VCO2 starts to increase more steeply in the mid-work-rate range after an initial linear behavior. This steepening is caused by an increased CO2 production from the HCO3-buffering of lactic acid for the range of work rates above the AT. Below the AT, the slope of increase in VCO2 is 1 or slightly less, averaging 0.95. Above the AT, it is greater than 1. The submaximal exercise protocol for the determination of AT includes a period of 2-3 min of unloaded cycling, a ramp program with x Watt increase/minute and a recovery period of 2 min. X is the rate of work rate increase per min, so that the incremental period of the exercise test lasts 8-10 min, stressing the patient for only a short time. The anaerobic threshold can be determined during the ramp program using the following four parameters: 1) steeper increase of VCO2 as compared to VO2 (V-slope-method); 2) respiratory exchange ratio = 0.95; 3) PETO2 increase; 4) VE/VO2 increase. The V-slope-method can be successfully applied, not only in healthy volunteers, but also in patients suffering from cardiac and/or pulmonary (breathing abnormalities) diseases. The so far published data show that the anaerobic threshold in healthy people and patients is a highly reproducible, accurately measurable, securely achievable parameter for the non-invasive evaluation of the individual cardiopulmonary exercise capacity.
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PMID:Determination of the anaerobic threshold by gas exchange: biochemical considerations, methodology and physiological effects. 794 54

Cardiopulmonary exercise capacity is a significant criterion of life quality. The evaluation of the exercise capacity is important to answer patient-questions concerning every day activity, choice of profession, sports-activity etc. We performed cardiopulmonary exercise testing in 38 patients (age 33.6 +/- 12.0 years, 18 women, 20 men) with different congenital heart disease (5 after surgical repair of tetralogy of fallot, 2 after Mustard-operation in transposition of the great arteries (TGA), 1 single ventricle, 14 atrial septal defect (ASD), 8 ventricular septal defect (VSD), 8 pulmonary valve stenosis (PS)) during outpatient routine control. All tests were performed on upright bicycle with continuous ramp program of 20 Watt increase/minute. Ventilatory values as O2-uptake, CO2-production, minute ventilation (VE) were measured breath-by-breath. Max. VO2 was reduced as average value for every patient group (tetralogy of fallot 60.2 +/- 20.3% pred., TGA 53.0 +/- 0.0% pred., single ventricle 35% pred., closed ASD 71.9 +/- 23.8% pred., ASD 62.7 +/- 30.0% pred., VSD 64.1 +/- 11.7% pred., PS 73.2 +/- 16.0% pred.). Anaerobic threshold was reduced in tetralogy of fallot (35.9 +/- 12.2% pred. max. VO2) and in single ventricle (28.3% pred. max. VO2). In comparison with clinical classification of exercise capacity we found for max. VO2 differences in 23/38 patients. 22/23 patients reported no exercise limitation but had reduced max. VO2. One patient had a normal max. VO 2 but complaints of exercise dyspnoea. For anaerobic threshold 18/38 patients had discrepancies in objective and subjective estimation of their exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiopulmonary capacity of patients with congenital heart defects in childhood, adolescence and adulthood]. 794 60

Failure to thrive is a common feature of children with congenital heart disease. Whether this is the result of poor nutrition or an abnormally high basal metabolic rate is unknown, yet the state of nutrition has a profound effect on the metabolic response to injury and strongly influences the outcome of surgical treatment. The aim of this study was therefore to measure the preoperative and postoperative energy requirements of children with congenital heart disease. Eighteen children (aged 4 to 33 months) were given two oral doses of doubly labeled water (H2(18)O and 2H2O), the first 1 week before operation and the second 6 hours after the end of cardiac surgery. By measuring the relative loss of each isotope from the body water pool, we were able to calculate the rate of carbon dioxide production and therefore total energy expenditure. In five patients, energy expenditure was clearly elevated, suggesting that a raised basal metabolic rate is an important factor in the observed failure to thrive in at least a proportion of such children. Postoperatively, energy expenditure fell to values below normal for healthy children (not having an operation), which suggests that the stress of surgery leads to smaller energy requirements than have previously been thought.
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PMID:Energy expenditure in children with congenital heart disease, before and after cardiac surgery. 830 56

The primary function of the circulatory system of both the fetus and newborn is to deliver oxygen to metabolizing organs and return deoxygenated blood to the gas exchange organ to replenish the oxygen and eliminate the waste product CO2. In the fetus, the gas exchange organ is the placenta, and its vascular connections are in a parallel arrangement with the other systemic organs, remote from the pulmonary circulation. In order to supply deoxygenated blood to the placenta and return oxygenated blood to the systemic organs, a series of extracardiac shunts (ductus venosus, ductus arteriosus) and an intracardiac communication (foramen ovale) are necessary. With birth, the function of gas exchange is transferred from the placenta to the lungs, and therefore from the systemic circulation to the pulmonary circulation. The venous and arterial circulations are separated, and not only are the fetal shunts unnecessary, but their persistence may lead to circulatory compromise. The transition from the fetal to the neonatal circulation thus includes elimination of the placental circulation, lung expansion, and increase in lung blood flow so that the entire cardiac output can be accommodated, and closure of the foramen ovale, ductus arteriosus, and ductus venosus. For most congenital structural heart disease, the fetal shunt pathways allow redistribution of ventricular blood flows so that systemic blood flow is adequate and fetal growth and development are usually normal. Uncomplicated VSDs do not alter the circulation significantly in either the fetus or immediate newborn period, with the important exception of premature infants. With severe left heart obstruction, the burden of systemic and pulmonary blood flow is transferred to the fetal right ventricle, with reversal of blood flow at the foramen ovale, and systemic blood flow almost entirely transmitted via the ductus arteriosus. This "ductal-dependent" systemic circulation is poorly tolerated in the newborn, because normal closure of the ductus arteriosus progressively decreases systemic blood flow and progresses to circulatory failure and shock. Severe right heart obstruction is also well tolerated in the fetus, because the combined fetal cardiac output can be transferred to the aorta, with the ductus arteriosus supplying predominantly lung blood flow. After birth, such "ductal-dependent" pulmonary blood flow can lead to critically low levels of pulmonary blood flow and severe cyanosis with closure of the ductus arteriosus. An understanding of fetal hemodynamics and the acute and chronic changes that occur with transition to the newborn circulation are important for the care of normal newborns and are crucial to the recognition, diagnosis, and management of the newborn with significant congenital heart disease.
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PMID:The transition from fetal to neonatal circulation: normal responses and implications for infants with heart disease. 832 1

When in some selected patients, a direct arterial surgery (DAS) procedure or an endoluminal surgery (ES) are required for a chronic arterial ischemia (III or IV degrees), and an arteriography with contrast is absolutely contraindicated (because of severe renal failure without hemodialysis program or a severe congestive heart failure or a hyperthyroidism or a seriously demonstrated hypersensibility against the contrast agents); an angiography by digital subtraction with carbon dioxide (DIVAS-CO2) is indicated. This technique provides good quality images with minimal risks for the patient and an adequate study for ulterior treatment. We report a case of a 67-years-old woman, with diabetes-II, ischemic cardiopathy, arterial hypertension and a demonstrated hypersensibility against the iodide compounds. The patient was admitted because of a chronic ischemia (IV degree) with ischemic ulcerations on some fingers from the left foot. High doses of analgesic drugs were needed. Because the hypersensibility against the iodide compounds, an angiography with CO2 was carried out. The good quality images provided by this technique showed the factibility of a revascularization.
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PMID:[Digital subtraction angiography with carbon dioxide in severe arterial ischemia and allergy to iodinated compounds]. 839 9

Aerobic capacity of patients with different forms of congenital heart disease was serially evaluated in 79 patients and the evolution was correlated with the lesion and the level of daily activity. The patients were divided into six groups: patients with a small ventricular septal defect (VSD) with mini shunt (n = 14), mild pulmonary valve stenosis with gradient < 40 mm Hg (PS) (n = 12), mild to moderate aortic valve stenosis (gradient 36 +/- 17 mmHg) (AS) (n = 12), patients 4.7 +/- 2.1 years after repair of tetralogy of Fallot (PO-TF) (n = 16), patients 2.2 +/- 2.9 years after closure of a high flow/high gradient VSD (PO-VSD) (n = 13), and patients 2.6 +/- 1.7 years after Fontan repair (Fontan-PO) (n = 12). Aerobic capacity was assessed by determination of the ventilatory anaerobic threshold (VAT). VAT reflects the highest aerobic exercise level prior to a disproportionate increase of CO2 and ventilation relative to O2 uptake; it is independent of patient motivation. Data are expressed as percentage of normal O2 uptake at VAT, determined in 234 age/gender matched controls. The habitual level of physical activity was assessed by a standardised questionnaire. Aerobic capacity in all subgroups of patients, even with very mild defects, was at or below the lower limit of normal. Children left unrestricted from physical exercise (VSD, PS, PO-VSD) had no change over the study period. However, aerobic capacity of patients with medically imposed physical restrictions (AS) and significant residual haemodynamic lesions (PO-TF, Fontan) decreased with age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serial cardiorespiratory exercise testing in patients with congenital heart disease. 852 76

The purpose of the present study was to measure oxygen uptake (VO2) at the ventilatory threshold (VT) in patients with congenital heart disease using a progressive exercise protocol on a treadmill and to evaluate the validity and feasibility of this procedure. Eight control subjects and seventeen patients performed a maximal exercise test with breath-by-breath measurement of ventilation and gas exchange variables. VT(VE) was determined by the change in the ventilatory equivalent for VO2 and carbon dioxide output, VT(V-sl) by the V-slope method, and the lactate threshold (LT) by the change in blood lactate concentration; these parameters were determined in 100%, 88%, and 96% of subjects, respectively. The interobserver error among three evaluators was not significant, and LT was correlated with each VT (r = 0.97, 0.92; p = 0.0001) and with peak VO2 (r = 0.91; p = 0.0001). The VTs were correlated with each other when expressed as milliliter per minute and milliliters per kilogram per minute. It was concluded that a progressive exercise protocol on a treadmill was a feasible procedure for determining the VTs in most individuals and that VTs were valid, useful parameters for evaluating submaximal exercise tolerance in patients with congenital heart disease.
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PMID:Measurement and validity of the ventilatory threshold in patients with congenital heart disease. 877 9

Noninvasive measurement of the systolic time intervals is a routine procedure for the determination of myocardial performance, even in subjects without clinical or electrocardiographic signs of cardiopathy. Statistically significant differences in pre-ejection period (PEP) and PEP/left ventricular ejection time (LVET) between days and between observations were demonstrated by Levi et al. A high correlation between systolic time intervals and catecholamines was recorded. The aim of the present study was to evaluate the spontaneous modifications in pulmonary and cardiac parameters during a stressful situation, such as right heart catheterization. Seventeen patients with chronic obstructive lung disease (COLD) underwent right heart catheterization. Heart rate (HR), systemic artery pressure (SAP), pulmonary artery pressure (PAP), cardiac output (Q'c), cardiac index (CI), systolic stroke volume (SV), respiratory rate (RR), minute ventilation (V'E), oxygen consumption (V'O2), carbon dioxide production (V'CO2), their ratio (RQ), arterial and venous O2 and CO2, systolic time intervals (total electromechanical interval (QS2), LVET, PEP, PEP/LVET), total pulmonary resistance (TPR), adrenaline (A), and noradrenaline (NA) were recorded at the beginning of the test and 20, 40, 60 and 80 min thereafter. Analysis of variance (ANOVA) showed significant differences between the observations for systolic pulmonary artery pressure (SPAP), Q'c, V'O2, V'CO2, V'E, PEP/LVET, and NA. In conclusion, it is necessary to take into account spontaneous modifications in pulmonary haemodynamic parameters following a stressful situation, such as a catheterization, when studying the effects of drugs such as vasodilators and vasoactive agents.
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PMID:Respiratory and haemodynamic modifications during right heart catheterization in COLD patients. 883 52

Little is known about occupational risks for coronary heart disease. A few specific toxins encountered occupationally are known to affect the heart, most prominently carbon disulfide, nitroglycerin, and carbon monoxide. Of these, carbon monoxide is the most common occupational exposure; it is also a common environmental exposure due to vehicle exhaust. Environmental tobacco smoke, noise, heat, and cold are suspected occupational risk factors for cardiovascular disease. In addition, stress at work may increase heart disease, although little is known conclusively with this regard. Unemployment may also increase risk of heart disease. Shift work, which disrupts circadian rhythms, has also been linked to heart disease, although there again, the data are far from conclusive. Physical activity at work, either too much or too little, can also be a risk factor for heart disease. While in general, more physical activity results in less heart disease, heavy lifting (in occupational and nonoccupational settings) has been associated with increased risk of heart attack. Further epidemiologic research into all these areas is warranted.
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PMID:Epidemiology of occupation and coronary heart disease: research agenda. 889 56


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