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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A Commercially available, non-invasive system for estimation of cardiac output by the CO2-rebreathing method (Sensormedicus MMC4400) was evaluated to determine its reliability in clinical practice. Values of cardiac output were obtained at rest and during mild to moderate bicycle ergometer work in patients with ischemic heart disease or hypertension. Cardiac output measured by the CO2-rebreathing method was significantly correlated with that measured simultaneously by dye dilution or thermodilution methods. Cardiac output values determined by the CO2-rebreathing method were the same as those obtained by the two invasive methods in reproducibility. When cardiac output and Vo2 were normalized for body weight, they were significantly correlated with each other. This result was obtained both by the CO2-rebreathing method, and by the two invasive methods. These results indicate that MMC4400 will provide a value for cardiac output substantially the same as that obtained by using more laborious invasive methods. Clinical use of the CO2-rebreathing method has been limited by technical difficulties. However, the recently developed non-invasive cardiac output measurement system (MMC4400) uses a microcomputer to analyze the results, and the operator can determine the values for cardiac output easily. Furthermore, it simultaneously measures VO2, VCO2 and VE, so the operator can estimate the measured values for cardiac output with background information on ventilatory gas analysis. Determination of cardiac output through the use of the CO2-rebreathing method is suitable particularly for exercise studies, and it is expected to be a useful device, in the near future, for evaluating cardiac function of patients with primary cardiac diseases.
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PMID:[Non-invasive measurement of cardiac output by the CO2 rebreathing method and its reliability in clinical practice]. 190 14

The relationship between smoking and ischemic heart disease was discussed, in terms of the smoking habit and the mechanisms of acute and chronic effects of smoking on the cardiovascular system as one of the coronary risk factors, with reference to exercise capacity and coronary flow reserve. The smoking habits of 1000 consecutive patients with ischemic heart disease, who were evaluated with coronary angiography, were analyzed. High percentages of smokers were observed in the younger generation. It was up to 86% in the 4th decade, though it was only 48% in the 8th decade. There was no large difference in other risk factors between smokers and non-smokers. The exercise capacity with and without smoking was evaluated with treadmill exercise test in 6 healthy volunteers. The exercise time was decreased with smoking, compared to without smoking, indicating a decrease in exercise capacity due to smoking. The elevated concentration of carbon monoxide in blood decreased the ability of oxygen transport. The increased lactic acid level in blood with smoking suggested anaerobic energy production acting as a part of the energy source. The smoking increased the myocardial oxygen consumption in relation to increase in heart rate and blood pressure. It decreased coronary flow reserve, shown by a peak to resting flow velocity ratio measured with the Doppler flow velocimeter. In coronary heart disease, therefore, the threshold of myocardial ischemia was decreased by smoking. The decrease in coronary flow reserve recovered with cessation of smoking for more than 2 days.
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PMID:[Smoking habit and cardiovascular diseases]. 203 94

The purpose of this study was to determine whether low doses of carbon monoxide (CO) exacerbate myocardial ischemia during a progressive exercise test. The effect of CO exposure was evaluated using the objective measure of time to development of electrocardiographic changes indicative of ischemia and the subjective measure of time to onset of angina. Sixty-three male subjects (41-75 years) with well-documented coronary artery disease, who had exertional angina pectoris and ischemic ST-segment changes in their electrocardiograms, were studied. Results from three randomized, double-blind test visits (room air, low and high CO) were compared. The effect of CO exposure was determined from the percent difference in the end points obtained on exercise tests performed before and after a 1-hr exposure to room air or CO. The exposures resulted in postexercise carboxyhemoglobin (COHb) levels of 0.6% +/- 0.3%, 2.0% +/- 0.1%, and 3.9% +/- 0.1%. The results obtained on the 2%-COHb day and 3.9%-COHb day were compared to those on the room air day. There were 5.1% (p = 0.01) and 12.1% (p less than or equal to 0.0001) decreases in the time to development of ischemic ST-segment changes after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. In addition, there were 4.2% (p = 0.027) and 7.1% (p = 0.002) decreases in time to the onset of angina after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. A significant dose-response relationship was found for the individual differences in the time to ST end point and angina for the pre- versus postexposure exercise tests at the three carboxyhemoglobin levels. These findings demonstrate that low doses of CO produce significant effects on cardiac function during exercise in subjects with coronary artery disease.
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PMID:Effects of carbon monoxide on myocardial ischemia. 204 Feb 54

The effect of acute exposure to carbon monoxide on ventricular arrhythmias was studied in a previously described chronically maintained animal model of sudden cardiac death. In 60 percent of dogs with a healed anterior myocardial infarction, the combination of mild exercise and acute myocardial ischemia induces ventricular fibrillation. The events in this model are highly reproducible, thus allowing study by internal control analysis. Dogs that develop ventricular fibrillation during the test of exercise and acute myocardial ischemia are considered at high risk for sudden death and are defined as "susceptible"; dogs that survive the test without a fatal arrhythmia are considered at low risk for sudden death and are defined as "resistant." In the current study, the effects of carboxyhemoglobin levels ranging from 5 to 15 percent were tested in resistant and susceptible dogs. A trend toward higher heart rates was observed at all levels of carboxyhemoglobin, although significant differences were observed only with 15 percent carboxyhemoglobin. This trend was observed at rest and during exercise in both resistant and susceptible dogs. In resistant animals, in which acute myocardial ischemia is typically associated with bradycardia even under the control condition, this reflex response occurred earlier and was augmented after exposure to carbon monoxide. This effect may depend on the increased hypoxic challenge caused by carbon monoxide, and thus on an augmentation of the neural reflex activation or a sensitization of the sinus node to acetylcholine induced by hypoxia. In both resistant and susceptible dogs, carbon monoxide exposure induced a worsening of ventricular arrhythmias in a minority of cases. This worsening was not reproducible in subsequent trials. These data indicate that acute exposure to carbon monoxide is seldom arrhythmogenic in dogs that have survived myocardial infarction. Nevertheless, the observation that carbon monoxide exposure increases heart rate at rest and during moderate exercise may have clinical implications relevant to patients with coronary artery disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Carbon monoxide and lethal arrhythmias. 209 24

The effects of intermittent coronary sinus occlusion (ICSO) on the size of myocardial infarction and reperfusion hemorrhage was evaluated. In Protocol 1, 8 dogs with ICSO and 8 controls underwent 4h of occlusion of the left anterior descending coronary artery. The same number of dogs underwent 4h of occlusion followed by 1h reperfusion in Protocal 2. The ICSO was started 1h after the ligation and continued through the occlusion period. There was no difference between the ICSO and the control group in hemodynamics and regional myocardial blood flow using hydrogen clearance method. However, ICSO did accelerate the rate of decline in intramyocardial CO2 tension. The half life of CO2 tension was 256 +/- 106 min in the control group but 139 +/- 34 min in the ICSO group (p less than 0.01). Lactate extraction rate showed the improving tendency during ICSO period. The ICSO resulted in a 50% and 80% reduction on an average in the size of infarct and reperfusion hemorrhage, respectively. We conclude that ICSO has prospective effects on myocardial ischemia with promise for clinical application.
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PMID:Effects of intermittent coronary sinus occlusion on experimental myocardial infarction and reperfusion hemorrhage. 212 46

After failure of external defibrillation, return of cardiac activity with spontaneous circulation is contingent on rapid and effective reversal of myocardial ischemia. Closed-chest cardiopulmonary resuscitation (CPR) evolved about 30 years ago and was almost universally implemented by both professional providers and lay bystanders because of its technical simplicity and noninvasiveness. However, there is growing concern since the limited hemodynamic efficacy of precordial compression accounts for a disappointingly low success rate; especially so if there is a delay of more than 3 minutes before resuscitation is started. There is also increasing concern with the lack of objective hemodynamic measurements currently available for the assessment and quantitation of the effectiveness of resuscitation efforts. Accordingly, the resuscitation procedure proceeds without confirmation that it increases systemic and myocardial blood flows to levels that would be likely to restore spontaneous circulation. Continuous monitoring of end-tidal carbon dioxide (PETCO2) now appears to be a practical measurement which provides a noninvasive quantitative indication of both systemic blood flow and coronary perfusion pressure. Consequently, PETCO2 predicts the likelihood of successful resuscitation and guides the operator who may modify the technique of precordial compression to improve systemic and myocardial perfusion. Among the large polypharmacy for cardiac resuscitation, only alpha-adrenergic agents (which increase coronary perfusion pressure) and especially epinephrine are of proven benefit. Neither buffer agents nor calcium salts appear to improve outcome except under unique conditions. To the contrary, there is increasing awareness of adverse effects of pharmacologic interventions such that they may hinder the return of viable myocardial and cerebral function. This has constrained the routine use of all drugs except for the use of alpha-adrenergic agonists. More invasive interventions by which blood flow is restored such as open-chest cardiac massage or extra-corporeal pump oxygenation (ECPO) are consistently more effective than conventional CPR. Experimentally, both methods promptly restore systemic and myocardial perfusion to viable levels and thereby increase the likelihood that spontaneous circulation is restored even after prolonged cardiac arrest or failure of conventional CPR.
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PMID:The clinical rationale of cardiac resuscitation. 219 75

The objective of this project was to determine the effects of acute carbon monoxide exposure on cardiac electrical stability. To obtain a comprehensive assessment, diverse biological models were employed. These involved cardiac electrical testing in the normal and ischemic heart in anesthetized and conscious dogs. The experimental plan was designed both to examine the direct effects of carbon monoxide exposure on the myocardium and to evaluate possible indirect influences through alterations in platelet aggregability or changes in central nervous system activity in the conscious animal. Our results indicate that exposure to relatively high levels of carbon monoxide, leading to carboxyhemoglobin concentrations of up to 20 percent, is without significant effect on ventricular electrical stability. This appears to be the case in the acutely ischemic heart as well as in the normal heart. It is important to note that the total exposure period was in the range of 90 to 124 minutes. The possibility that longer periods of exposure or exacerbation from nicotine in cigarette smoke could have a deleterious effect cannot be excluded. We also examined whether or not alterations in platelet aggregability due to carbon monoxide exposure could be a predisposing factor for cardiac arrhythmias. A model involving partial coronary artery stenosis was used to simulate the conditions under which platelet plugs could lead to myocardial ischemia and life-threatening arrhythmias. We found no changes either in the cycle frequency of coronary blood flow oscillations or in platelet aggregability during carbon monoxide exposure. Thus, carbon monoxide exposure does not appear to alter platelet aggregability or its effect on coronary blood flow during stenosis. In the final series of experiments, we examined the effects of carbon monoxide exposure in the conscious state. The rationale was to take into consideration possible adverse consequences mediated by the central nervous system. We found no adverse effects on cardiac excitable properties in response to either a 2-hour or 24-hour-exposure paradigm. This appears to argue against major deleterious influences of carbon monoxide exposure as a result of direct myocardial actions or indirect actions mediated through effects on central nervous system activity.
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PMID:Acute effects of carbon monoxide on cardiac electrical stability. 229 16

For a study of the natural history of coronary artery lesions after Kawasaki disease and their effect on myocardial blood flow reserve with exercise, five such patients underwent exercise testing on a bicycle. Oxygen consumption, carbon dioxide production, minute ventilation, and electrocardiograms were monitored continuously. Thallium-201 scintigraphy was performed for all patients. One patient stopped exercise before exhaustion of cardiovascular reserve but had no evidence of myocardial perfusion abnormalities. Four patients terminated exercise because of exhaustion of cardiovascular reserve; one had normal cardiovascular reserve and thallium scintiscans, but the remaining patients had diminished cardiovascular reserve. Thallium scintigrams showed myocardial ischemia in two and infarction in one. No patient had exercise-induced electrocardiographic changes. These results indicate that patients with residual coronary artery lesions after Kawasaki disease frequently have reduced cardiovascular reserve during exercise. The addition of thallium scintigraphy and metabolic measurements to exercise testing improved the detection of exercise-induced abnormalities of myocardial perfusion.
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PMID:Myocardial performance and perfusion during exercise in patients with coronary artery disease caused by Kawasaki disease. 229 63

It is traditional practice to treat acute hyperventilation (thought to be due to anxiety) by having patients rebreathe into a brown paper bag. The author reports three cases in which this treatment, erroneously applied to patients who were hypoxemic or had myocardial ischemia, resulted in death. This clinical experience motivated a study of the effects of paper bag rebreathing in normal volunteers. Subjects deliberately hyperventilated to an average end-tidal CO2 concentration of 21.6 (SD, 3.2) mm Hg and then continued to hyperventilate into a no. 4 Kraft brown paper bag containing the calibrated sensors for a Hewlett-Packard 47210A capnograph and a Teledyne TED 60J digital oxygen monitor. Fourteen men and six women with an average age of 36 years (SD, 6.1) were tested. Results are reported as mm Hg. After 30 seconds of rebreathing, mean change in O2 from room air was -15.9 (SD, 4.6) and mean CO2 was 38.7 (SD, 6.2); at 60 seconds, -20.5 (6.0) and 40.2 (6.4); at 90 seconds -22 (6.8) and 40.5 (6.4); at 120 seconds -23.6 (6.8) and 40.7 (6.5); at 150 seconds -25.1 (1.2) and 41 (7.3); and at 180 seconds -26.6 (8.4) and 41.3 (7.5). A few subjects achieved CO2 levels as high as 50, but many never reached 40. The mean maximal drop in O2 was 26 (8.8); seven subjects had drops in oxygen of 26 mm Hg at three minutes, four had drops of 34 mm Hg, and one had a drop of 42 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoxic hazards of traditional paper bag rebreathing in hyperventilating patients. 249 28

A group of 75 patients with a history of myocardial infarction and repeated myocardial infarction were subjected to treatment involving dry carbon dioxide baths. Its results demonstrated normalization of IHD manifestations, such as coronary and heart failure, functional state of the cardiovascular system, its reserve potentialities and adaptation to physical effort. Under the influence of a course treatment with dry carbon dioxide baths hemodynamic parameters of cardiac output (cardiac and stroke volume) underwent favourable changes, rhythm slowed down, diastole became longer and systolic and diastolic arterial pressure decreased. The data obtained substantiate application of dry carbon dioxide baths in the recovery period to I-III functional classes patients with a history of myocardial infarction.
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PMID:["Dry" carbon dioxide baths in treating patients with myocardial infarction at the sanatorium stage of rehabilitation]. 252 25


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