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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exercise testing is an important noninvasive method for the exposure of arrhythmias. It provides complementary information to that obtained from ambulatory monitoring or electrophysiologic testing. By producing a number of important physiologic changes, especially activation of the sympathetic nervous system and an increase in circulating catecholamines, exercise testing provides a more complete assessment. On continuous monitoring, exercise-induced ventricular premature beats may be found in up to 34% of healthy subjects, in 60 to 70% of those with heart disease and in all patients who have experienced sustained ventricular tachycardia. Couplets or nonsustained ventricular tachycardia can be found during exercise in 0 to 6% of healthy subjects, in 15 to 31% of patients with heart disease and in 75% of those with sustained ventricular tachycardia. Even in patients with heart disease, there is only a small risk of inducing sustained ventricular tachycardia or ventricular fibrillation during exercise. The prognostic relevance of exercise-induced ventricular arrhythmias in patients with coronary artery disease or cardiomyopathy has not been clearly established. There appears to be an increased risk, however, in patients with ventricular premature beats as well as ST-segment depression or in patients with repetitive forms of ventricular arrhythmias during exercise which cannot be medically controlled. In healthy subjects, exercise-induced ventricular premature beats are of no prognostic relevance. In particular, for patients in whom arrhythmias are induced by exercise, exercise testing should be used to assess the effectiveness of antiarrhythmic drug treatment. Importantly, serious cardiac toxicity, often not observed at rest or during routine activities, may become apparent during exercise testing. It should be a standard part of arrhythmia assessment and management.
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PMID:Evaluation of cardiac arrhythmias by exercise testing. 169 Jan 68

Determining safe and effective antiarrhythmic therapy in paediatric patients requires definition of the mechanism of the arrhythmia, determination of associated risk factors for treatment (such as the presence of congenital cardiac defects, myocarditis or cardiomyopathy), and monitoring for potential drug side effects related to the treatment. A number of modalities for non-invasive evaluation of arrhythmias is available, including ECG, 24-hour ambulatory Holter monitoring, and transtelephonic ECG transmission. Arrhythmias requiring medical treatment in children with normal cardiac anatomy and function include supraventricular tachycardia (SVT), ventricular tachycardia (VT) and primary atrial tachycardias. SVT is treated acutely with vagal manoeuvres or drugs which slow AV conduction [adenosine (adenine riboside), edrophonium, phenylephrine or verapamil]. When medical conversion is not achieved, transoesophageal overdrive pacing or direct current (DC) cardioversion may be required. Long term drug therapy for SVT includes first-line treatment with digoxin, verapamil or propranolol. Ventricular tachycardia is managed acutely with DC cardioversion and intravenous lidocaine (lignocaine). Chronic drug regimens include mexiletine, propranolol or amiodarone. In children with structural congenital heart disease or myocardial dysfunction, hazards of drug therapy for arrhythmias include depression of cardiac function, proarrhythmia (drug-induced worsening of arrhythmias), and conduction abnormalities. Care must be taken to choose medication regimens which are likely to be effective with minimum risk of potentiating abnormal haemodynamics or conduction.
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PMID:Cardiac arrhythmias in childhood. Diagnostic considerations and treatment. 172 43

Pulmonary hypertension in pregnant women is uncommon but is associated with a high mortality. We present the case of a 14-yr-old parturient with pulmonary hypertension and cardiomyopathy who required a Caesarean section. Management goals included: (1) maintaining right ventricular function, (2) avoiding the haemodynamic effects of general endotracheal anaesthesia, and (3) minimizing narcotic-related neonatal respiratory depression. While most authors agree on invasive pulmonary and systemic monitoring, opinions differ as to the optimal method of providing anaesthesia for these patients. The successful use of lumbar epidural anaesthesia with lidocaine and fentanyl is described. When the local anaesthetic was administered slowly and in increments, epidural anaesthesia was safe for both mother and fetus.
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PMID:Pulmonary hypertension and cardiomyopathy: anaesthetic management for caesarean section. 174 13

Experimental studies have demonstrated that myocardium reperfused after reversible ischemia exhibits prolonged depression of contractile function ("stunning"). Despite the multiplicity of clinical situations in which myocardial stunning would be expected to occur, investigation of this phenomenon in humans has been hindered by several major problems, including the limited accuracy of the methods available to measure regional left ventricular function, the inability to quantify regional myocardial blood flow during acute ischemia, the difficulty in establishing with certainty, the beginning and end of an ischemic episode, and the uncontrolled influence of variables (such as preload, afterload, adrenergic tone, and inotropic therapy) that have a major impact on postischemic dysfunction. The main problem is to discern whether a reversible defect of contractility is caused by stunning, silent ischemia, or hibernation (i.e., chronic ischemia). This differential diagnosis requires the simultaneous measurement of regional myocardial function and flow, which thus far has not been generally possible. Despite these limitations, however, numerous clinical observations suggest that stunning does occur in various settings in which the myocardium is exposed to transient ischemia, including coronary angioplasty, exercise-induced angina, angina at rest (unstable or variant), acute myocardial infarction with early reperfusion, open-heart surgery, and cardiac transplantation. Recognition of this entity is important, amongst other reasons, because it is likely to cause significant morbidity and because it is potentially correctable with inotropic therapy or even preventable with antioxidant therapy. In addition, the appreciation of the phenomenon of myocardial stunning should allow the clinician to assess the efficacy of reperfusion therapy with greater accuracy and to recognize that patients should not be denied mechanical revascularization solely because of an abnormal left ventricular wall motion. Perhaps the most intriguing clinical implication of the concept of myocardial stunning is the possibility that in patients who exhibit frequent episodes of ischemia in the same territory, the myocardium may not be able to fully recover between episodes and thus may remain reversibly depressed for prolonged periods of time, or even chronically, which could account for some cases of "ischemic cardiomyopathy." Our understanding of myocardial stunning in humans is still relatively crude and will not significantly improve until studies are performed that measure simultaneously regional myocardial perfusion and function (so that stunning can be differentiated from silent ischemia and hibernation). Future important areas of research should also include the elucidation of whether stunning can become chronic and the evaluation of therapies (such as antioxidant treatments) designed to prevent this contractile abnormality.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical relevance of myocardial "stunning". 175 33

A novel, simple, rapid and reproducible microassay is used for kinetic analysis of Ca-sequestration by homogenates of myocardium of turkeys with furazolidone-induced congestive cardiomyopathy. The assay monitors Ca in real-time using dual-emission ratiometric spectrofluorometry and the Ca-indicator dye indo-1. Using this assay and isolated SR studies we make several novel findings regarding the mechanism of SR failure in furazolidone cardiomyopathy. Qualitative differences in Ca-sequestration were not detected between groups. However, compared to controls the furazolidone treatment resulted in: 1) 50% depression in maximal activities (1.54 +/- 0.36 vs 0.73 +/- 0.12 microM/sec); 2) 2-fold increases in post-sequestration concentrations of ionized Ca (79 +/- 23 vs 141 +/- 13 nmol Ca/L homogenate); 3) 2-fold increases in Ca half-life (415 vs 790 msec); and 4) 25% increased passive Ca-binding capacity of homogenates. The Ca-ATPase specific activity of isolated sarcoplasmic reticulum was 60% increased in congestive cardiomyopathy (543 +/- 140 vs 873 +/- 108 nmol ATP hydrolyzed/min/mg membrane protein) although membrane yield was 20% decreased (0.79 +/- 0.09 vs 0.63 +/- 0.03 mg/g heart). The increased ATPase and decreased Ca-uptake activities in combination with the occurrence of 36% cardiac hypertrophy and 19% decreased body weights resulted in estimates of the relative energy cost to the animal for myocardial Ca transport being 5.5-fold increased with cardiomyopathy (20.5 vs 111 nmol ATP hydrolyzed per microM decrease of sarcoplasmic free Ca/kg body weight). These data indicate that congestive cardiomyopathy is associated with markedly increased permeability of sarcoplasmic reticulum to Ca and compensatorily increased Ca-ATPase activity. Accelerated energy consumption due to the increased energy cost of Ca transport and increased time of myocyte activation are predicted to predispose the myocardium to fatigue and irreversible failure.
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PMID:Myocardial Ca-sequestration failure and compensatory increase in Ca-ATPase with congestive cardiomyopathy: kinetic characterization by a homogenate microassay using real-time ratiometric indo-1 spectrofluorometry. 182 61

To determine whether the development of cardiomyopathies is associated with alterations in creatine kinase function, the functional properties of cardiac contractile apparatus and mitochondria were studied in two different models of cardiomyopathies, the Syrian hamster (hereditary dilated cardiomyopathy, strain UM-X7.1, 200 days old) and the diabetic rat (4-6 weeks after injection of streptozotocin) using ventricular skinned fibers. After Triton X-100 treatment, the hereditary cardiomyopathic fibers demonstrated decreased maximal calcium-activated tension and unchanged calcium sensitivity, whereas fibers from diabetic hearts exhibited unchanged maximal tension and increased calcium sensitivity, when compared with their respective controls. In both cases myofibrillar creatine kinase appeared unchanged. The functional properties of total tissue mitochondria were evaluated using saponin-skinned fibers. Coupling between oxidation and phosphorylation was not altered in cardiomyopathies. Respiration rate (per unit of tissue dry weight) was normal in hereditary cardiomyopathy but was considerably lower in diabetic fibers compared with control fibers. In both models of cardiomyopathies, creatine-stimulated respiration was significantly lower than in controls, thus indicating the depression of functional activity of mitochondrial creatine kinase.
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PMID:Creatine kinase and mechanical and mitochondrial functions in hereditary and diabetic cardiomyopathies. 191 31

This study was done on 113 subjects, 93 men and 20 women, whose ages ranged between 32 and 70 years (average 52.9 years). Males varied between 35 and 70 years (average 53.7) and females between 32 and 67 years (average 49.5). Our objective is: to give an account of the different discriminatory methods with mixed data usually used in medical applications, to apply these methods to all the subjects studied with the purpose of comparing their performance and, to develop a protocol for diagnosing coronary artery disease by noninvasive tests. All the subjects were referred for evaluation of chest pain, and were submitted to an exercise test on an ergometric bicycle, selective coronary angiography and left ventriculography. Patients with prior myocardial infarction, cardiomyopathy, valvular or congenital disease, mitral valve prolapse or intraventricular conduction defect were excluded. Subjects were classified as having coronary artery disease and not having coronary artery disease according to the coronarographic results. We used four clinical variables (age, sex, risk factor and chest pain) and five variables obtained from the stress test (ST depression, appearance of chest pain, appearance of arrhythmias, variations in blood pressure and R wave changes). For the analysis of this set of data we use well known univariate statistical methods, such as chi-squared test, F-test and t-test, and the following multivariate statistical methods: Fisher, Quadratic and Logistic, discriminant methods. To study the relative importance of the different variables in the discrimination of the individuals, we performed a stepwise linear discriminant analysis over the 113 subjects. Of the 9 variables tested R-wave was of little value and excluded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnosis of ischemic cardiopathy in ambulatory care patients. Multivariate analysis of clinical and electrocardiographic data]. 207 36

We performed exercise thallium-201 myocardial scintigraphy in 32 patients with angina pectoris to study the incidence of perfusion defects, who had no significant organic stenosis on coronary angiography. None of them had myocardial infarction or cardiomyopathy. Thallium-201 myocardial scintigraphy and 12-lead ECG recording were performed during supine bicycle ergometer exercise. Perfusion defects in thallium-201 scintigrams in SPECT images were assessed during visual analysis by two observers. In the coronary angiograms obtained during intravenous infusion of nitroglycerin, the luminal diameter of 75% stenosis or less in the AHA classification was regarded as an insignificant organic stenosis. Myocardial perfusion defects in the thallium-201 scintigrams were detected in eight (25%) of the 32 patients. Six of these eight patients had variant angina documented during spontaneous attacks with ST elevations in standard 12-lead ECGs. Perfusion defects were demonstrated at the inferior or inferoposterior regions in six patients, one of whom had concomitant anteroseptal defect. The defects were not always accompanied by chest pain. All but one patient demonstrating inferior or inferoposterior defects showed ST depression in leads II, III and aVF on their ECGs, corresponding to inferior wall ischemia. The exception was a case with right bundle branch block. Thus, 25% of the patients with angina pectoris, who had no evidence of significant organic stenosis on their coronary angiograms, exhibited exercise-induced perfusion defects in their thallium-201 scintigrams. Coronary spasms might have caused myocardial ischemia in these patients.
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PMID:[Exercise-induced thallium-201 myocardial perfusion defects in angina pectoris without significant coronary artery stenosis]. 209 48

Intracellular pH and [Na+] in the heart are regulated by the sarcolemmal membrane Na(+)-H+ exchange pathway. No data are currently available regarding the adaptation of this system to pathological conditions in the heart. Because ionic interactions with the heart are altered in cardiomyopathy during chronic experimental diabetes, it was hypothesized that Na(+)-H+ exchange may become abnormal. In addition, the effects of treating diabetic rats with daily injection of L-propionylcarnitine were investigated to determine whether alterations in lipid metabolism may be involved in any potential changes in ion transport. Rats were injected with streptozotocin (65 mg/kg) and killed 8-10 wk later, and sarcolemmal membrane vesicles were isolated from pooled ventricles. Significant depressions in Na(+)-K(+)-adenosinetriphosphatase (ATPase) activity and Na(+)-Ca2+ exchange were observed in the diabetic preparations in comparison to control. L-Propionylcarnitine treatment of the diabetic rats partially normalized these activities. A striking depression in cardiac sarcolemmal Na(+)-H+ exchange was observed in the diabetic animals in comparison to control, and this was not a result of a nonspecific increase in membrane permeability. L-Propionylcarnitine treatment of the diabetic rats did not improve sarcolemmal Na(+)-H+ exchange.
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PMID:Na(+)-H+ exchange in cardiac sarcolemmal vesicles isolated from diabetic rats. 215 33

Cancer chemotherapy with anthracyclines, of which doxorubicin (DX2) is the main representative, is limited by cardiomyopathy developing in animals and patients after cumulative dosing. The toxicity is probably related to free radical formation by the anthracycline as well as its metabolites with concomitant O2.- and .OH generation resulting in lipid peroxidation and subsequent membrane damage. An in vitro model is required to investigate the individual contribution of each metabolite to cardiotoxicity. For in vivo studies, the species of choice is the mouse because it lacks the DX-induced nephrotic syndrome seen for instance in rats and rabbits. Thus, isolated mouse heart muscle was chosen as an in vitro model. To characterize the model, we used l-isoprenaline/dl-propranolol and metacholine/atropine to measure the beta-adrenergic and the muscarinic responses of (spontaneously beating) right and (paced) left atrium. Dose response curves (n greater than or equal to 4) were highly reproducible: pD2,iso = 8.0 +/- 0.3 (left) and 8.5 +/- 0.4 (right); pD2,met = 6.7 +/- 0.1 (left) and 6.2 +/- 0.3 (right). Propranolol as well as atropine behaved as competitive antagonists, with pA2-values of 8.4 +/- 0.2/8.5 +/- 0.2 (l/r) and 9.1 +/- 0.1/9.1 +/- 0.2 (l/r), respectively. These values corresponded to those obtained with other organ preparations. We tested the effect of DX in two ways: a) by measuring the direct inotropic and chronotropic effect during 60 minutes of incubation with 10-100 microM DX in the organ bath, and b) by determining the remaining beta-adrenergic response to l-isoprenaline after the incubation period. Both variables turned out to be equally affected. For paced left atria an IC50 (causing 50% depression of contractile force) of 35 microM was determined. Right atria stopped beating at concentrations above 50 microM, thus hampering IC50 determination. The results indicate that anthracyclines exert an effect not related to receptor integrity, but directly to the functionality of heart muscle. To check whether radical stress can be involved in the observed negative inotropic effect, incubations with xanthine/xanthine oxidase (to produce reactive oxygen species) were performed. A pronounced negative effect on mouse atrial contraction was indeed observed. However, initially a positive inotropic effect accompanied by an increased resting tension were seen. It can be concluded that mouse atrium can be used as a model to compare anthracyclines and their metabolites with regard to their acute cardiotoxic effects.
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PMID:Isolated mouse atrium as a model to study anthracycline cardiotoxicity: the role of the beta-adrenoceptor system and reactive oxygen species. 216 63


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