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Indices of cardiac function during treatment with betamimetic drugs (fenoterol and hexoprenaline).

The limiting factor in the treatment of preterm labor by betamimetics is the effect of these drugs on heart rate and cardiac action. In this paper we compare these effects produced by hexoprenaline and fenoterol, which are both beta-sympathomimetic drugs now in clinical use. As indices of cardiac action we measured the pre-ejection period (PEP), the left ventricular ejection time (LVET) and their sum, namely total electromechanical systole (QS2) by thoracic impedance cardiography. In 20 individual tests, seven subjects were given both hexoprenaline and fenoterol on separate occasions in a dose relationship of 1 : 12.5. We found a relation between PEP/LVET on the one hand and the Heather-index (an impedance specific parameter of response to stress) on the other. Both parameters represent inotropic effects in cardiac action. With increasing betamimetic stimulation there was a decrease of PEP/LVET (-23% for hexoprenaline and -29% for fenoterol) and an increase in the Heather-index (+98% for hexoprenaline and +117% for fenoterol). These results are not statistically significantly different and so we cannot agree with Lipshitz [19 ]who reported less beta 1-stimulation with hexoprenaline.

Adult↗

The influence of positive end-expiratory pressure on intrapericardial pressure and cardiac function after coronary artery bypass surgery.

The hemodynamic effects of positive end-expiratory pressure (PEEP) were studied in coronary artery bypass patients by recording intrapericardial and intracardiac pressures, measuring cardiac output by thermodilution, and determining left ventricular volumes by nuclear radiography. An elevation of PEEP to 5, 10, and 15 cm H2O led to a decrease in cardiac output (15% decrease at PEEP 15) as intrapericardial pressure increased and transmural left atrial pressure decreased. Modest volume loading (an increase in left atrial pressure of 3 mm Hg) greatly attenuated the deleterious effects of 15 cm H2O PEEP. There was an excellent correlation between pulmonary capillary wedge pressure and left atrial pressure at PEEP 0 and 5 (r = .85 and r = .83). This correlation was not nearly as reliable at PEEP 15 (r = .54). A predictable increase in intrapericardial pressure was observed as PEEP was applied in these patients. The magnitude of this increase can be estimated by multiplying the change in PEEP (in cm H2O) by 0.4 to estimate the change in intrapericardial pressure (in mm Hg). Using this estimation as a guide, modest volume loading can be used to maintain transmural filling pressures (and cardiac output) when PEEP is used after coronary artery bypass surgery.

Coronary Artery Bypass↗

Long-term evaluation of cardiac function in children who received anthracyclines during pregnancy.

BACKGROUND: The use of anthracyclines in patients with cancer has been associated with the presence, even when standard doses were employed, of cardiac toxicity, most frequently after 5 years of therapy. Treatment of cancer during pregnancy remains a dilemma because cytotoxic therapy has been associated with the presence of severe side-effects. The outcome of children that received antracyclines during pregnancy, including during the first trimester, remain unknown because long-term follow-up is not available. PATIENTS AND METHODS: Eighty-one children whose mothers (29 acute leukemia, 33 malignant lymphoma and 19 Hodgkin's disease) were treated with cytotoxic drugs, including anthracyclines, during pregnancy were evaluated to detect cardiac toxicity, including clinical evaluation and echocardiogram [all parameters were evaluated, but fraction shortening (FS) was taking as the best parameter to evaluate cardiac toxicity in children] every 5 years after birth until 29 years of age. RESULTS: Children with actual age of 9.3-29.5 years (mean 17.1) did not show any clinical date of cardiac disfunction, in all cases echocardiogram was normal and FS did not showed any abnormality during the follow-up. CONCLUSIONS: The use of anthracyclines did not show any clinical or echocardiogram evidence of late cardiac toxicity. We hope that the present report increases the number of reports of the long-term follow-up of children who received cytotoxic drugs, in order to define the best treatment in this special patient setting.

Adolescent↗

99mTc SESTAMIBI scintigraphic evaluation of skeletal muscle disease in patients with systemic sclerosis: diagnostic reliability and comparison with cardiac function and perfusion.

The diagnosis of skeletal muscle involvement in patients with systemic sclerosis (SSc) is usually based on clinical, laboratory, electromyographic, and bioptic evidence of muscle disorder, whereas SSc cardiac disease is well established by nuclear medicine techniques (radionuclide ventriculography and myocardial scintigraphy). Previous reports have retrospectively hypothesized a possible relationship between cardiac and muscle involvement in scleroderma patients. In order to improve overall diagnostic accuracy in the qualitative/quantitative assessment of skeletal muscle involvement in these patients and to compare these results with those obtained at the cardiac level, diethylenetriaminepentaacetic acid (DTPA)-99mTc radionuclide ventriculography and 99mTc SESTAMIBI myocardial and muscular scintigraphic examinations were performed in 10 SSc patients and in five healthy subjects. Muscular radioactivity, as assessed at thigh and calf levels by means of a segmental score, was significantly decreased in SSc patients in comparison with healthy subjects (global score value 15.6+/-2.2 vs 22.7+/-1.6, p<0.001), as well as right ventricular ejection fraction (RVEF, 34.3%+/-5.3 vs 53.6%+/-4.2, p<0.001) and myocardial segmental perfusion (global score value, 19.6+/-2 vs 25.9+/-1.1, p<0.01). The results show a high frequency of skeletal muscle involvement in patients with SSc. Moreover, scleroderma patients with muscle disorders, as evidenced by scintigraphy, show a comparable occurrence of cardiac involvement, even in the absence of clinical signs of cardiac dysfunction.

Cardiomyopathies↗

[The value of the diastolic pulmonary arterial pressure for the estimation of the cardiac functional capacity in patients with myocardial infarct].

From 4 weeks to several months after infarction the patients revealed an altogether clearly decreased total physical functional capacity compared with healthy persons. Behaviour of pulse and blood pressure as well as ventilatory indices in comparable Watt-degrees did not reveal any significant differences compared with persons with a healthy heart. The stroke volume pro surface and the heart-time-volume did also not reveal any determinable deviation concerning the mean values compared with normal persons. In patients with compensated infarction the pulmonary arterial pressure in rest was, as a rule, within the normal. However, under load it increased more than in healthy persons. Patients with decompensated infarction revealed a PAEDP in rest between 20 and more than 30 Torr. The question about a critical PAEDP under load should further be pursued. The ECG gives reliable limiting findings in functional examinations.

Adult↗

Improvement of cardiac function by angiotensin converting enzyme inhibition. Sites of action.

BACKGROUND: The discovery of new properties of angiotensin converting enzyme (ACE) inhibitors in addition to their well-known ability to lower blood-pressure, such as antiproliferative actions and antiadrenergic and vagal-stimulating effects, has contributed to the usefulness of this class of agents in the prevention and treatment of cardiovascular diseases. METHODS AND RESULTS: The contribution of an activated endocrine and/or cardiac paracrine renin-angiotensin system to the progression of cardiovascular diseases with the exception of renovascular hypertension is not fully understood. In particular, the following questions were addressed: 1) Is the facilitation of noradrenaline release in the genesis of arrhythmias a target for ACE inhibition? 2) Is an impaired nutritional cardiac blood flow in heart failure a target for ACE inhibition? 3) Is the intimal hyperplasia that results from coronary angioplasty a target for ACE inhibition? 4) Is the diastolic dysfunction associated with left ventricular hypertrophy in essential hypertension a target for ACE inhibition? In an isolated rat heart preparation with ischemia-induced arrhythmias, none of the ACE inhibitors nor an angiotensin II antagonist was able to significantly suppress the incidence or severity of arrhythmias. In 12 patients with New York Heart Association functional class II-IV heart failure, a fall in cardiac filing pressures after ACE inhibition was associated with an immediate rise in cardiac output and an increase in coronary blood flow of almost 30%. In 24 patients with angina at rest, a preceding percutaneous transluminal coronary angioplasty, and a second angioplasty, control angiograms at 6 months revealed a high degree of restenosis in both ACE inhibitor-treated and placebo patients. Luminal narrowing amounted to 72% in the placebo group and 61% in the ACE inhibitor group. The differences between placebo and enalapril were statistically not significant. In 12 patients with essential hypertension treated with 5 mg cilazapril, left ventricular mass was reduced by 30%, which was closely related to the change in mean arterial blood pressure. The concomitant normalization of the diastolic filling pattern by ACE inhibition, however, was not related to the respective changes in blood pressure. CONCLUSIONS: Promising experimental data regarding the antiproliferative effects of ACE inhibitors in preventing restenosis could not be transferred into clinical benefits for patients who underwent repeat coronary angioplasty. Possible antiarrhythmic effects of ACE inhibitors are not likely to be caused by their suppression of noradrenaline release during myocardial ischemia. ACE inhibition was effective in reducing coronary resistance in patients with severe heart failure, thereby augmenting nutritional cardiac blood flow. ACE inhibition also effectively induced a regression of left ventricular hypertrophy in essential hypertension. The associated normalization of diastolic filling pattern may represent an important goal in the treatment of hypertension.

Angioplasty, Balloon, Coronary↗

Effects of hydrogen peroxide on cardiac function and post-ischaemic functional recovery in the isolated 'working' rat heart.

The effects of hydrogen peroxide on the normal and ischaemic myocardium were investigated using the isolated 'working' rat heart preparation. In the range 0-3 microM no changes in heart rate, aortic flow, coronary flow, or aortic pressure were observed. Between 3 and 30 microM, however, there was a dose-dependent fall in aortic flow and an accompanying increase in coronary flow, the total cardiac output remaining unchanged. At concentrations about 30 microM functional failure occurred. Following a 24-min ischaemic period during which time 6 microM hydrogen peroxide was infused via the aorta at a constant rate to remove any vasodilatory effect, all hearts failed to recover. In contrast, 50% of control hearts recovered pump function. In conclusion, therefore, hydrogen peroxide can reduce function in the aerobic working rat heart and may exert a vasodilatory effect. When this effect is eliminated hydrogen peroxide affords no protection during ischaemia and appears to exacerbate tissue injury.

Animals↗

Estimation of cardiac function from computer analysis of the arterial pressure waveform.

This paper presents a method for estimating parameters of a cardiovascular model, including the left-ventricular function, using the sequential quadratic programming (SQP) and the least minimum square (LMS) algorithms. In a first stage, a radial arterial-pressure waveform with corresponding cardiac output are used to automatically seek the set of parameters of the diastolic model. Computer simulation of the model using these parameters generate a pressure waveform and a cardiac output very close to those used for the estimation. In a second stage, the estimated arterial load parameters are used to select the best left-ventricular model function, from four different possibilities, and to estimate its optimum parameter values. The method has been tested numerically and applied to real cases, using data obtained from cardiovascular patients. It has also been subjected to preliminary validation using data obtained from laboratory dogs, in which cardiovascular function was artificially altered.

Algorithms↗

Effect of myo-inositol and T3 on myocardial lipids and cardiac function in streptozocin-induced diabetic rats.

Numerous experimental studies have implied a link between diabetes-induced abnormal lipid buildup in the myocardium and the development of cardiomyopathy. Because the diabetic state in rats is associated with lowered T3 (triiodothyronine) and T4 levels and because diabetic patients excrete large amounts of myo-inositol, a lipotropic agent, we investigated the effects of myo-inositol and T3 on the elevated myocardial lipid levels and depressed cardiac performance of streptozocin (55 mg/kg i.v.)-induced diabetic (STZ-D) rats. myo-inositol (2.5 g.kg-1.day-1 in the drinking water) and T3 (30 micrograms.kg-1.day-1 s.c.) were given for an 8-wk period 3 days after diabetes induction. Untreated diabetic rats were characterized by a decreased rate of body weight gain, hyperglycemia, and hypoinsulinemia, which were not altered after myo-inositol and/or T3 treatment. Thyroid status of diabetic animals was normalized by T3 alone or in combination with myo-inositol but not by myo-inositol alone. The elevations in plasma and myocardial lipids associated with the diabetic state were prevented by myo-inositol treatment. However, the plasma lipid and myocardial cholesterol levels in diabetic rats remained elevated or were further increased with treatment with T3 or myo-inositol plus T3. myo-inositol treatment partially improved cardiac performance in STZ-D rats. T3 treatment alone did not prevent cardiac dysfunction in diabetic rats. There was, however, some improvement in heart function in the groups treated with both myo-inositol and T3, coinciding with a significant decrease in the myocardial triacylglycerol level. The data indicate that a possible correlation may exist between elevated myocardial triacylglycerol levels and cardiac dysfunction in diabetic rats.

Animals↗