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Biomedical subjects

A Saadjian

Publications and source records attributed to A Saadjian.

At least 37 records · Page 2Linked to original sources
PubMed1988

Long-term follow-up of patients treated with VVI pacing and sequential pacing with special reference to VA retrograde conduction.

The aim of this prospective study is comparing long-term prognosis in patients implanted with a VVI pacemaker (group A) with those implanted with a sequential pacing device, AAI or DDD, (group B). Both groups of 45 patients each, were comparable as regards to age, sex, pacing indications, underlying heart disease, and technical conditions of implantation and were followed-up over 55 months. Atrial arrhythmias (A.A.) incidence was higher in group A: 24.4% than group B: 8.8% (P less than 0.05). Arterial embolisms (A.E.) occurred in group A patients only. Worsening or occurrence of exercise limitation was more frequent in group A: 35.6% as compared to group B: 13.3% (P less than 0.05) and deaths related to these complications, occurred in seven cases in group A versus four cases in group B. In group A, all patients who experienced a worsening or occurrence of an A.A. or an A.E., had a ventriculoatrial conduction (VAC). No statistical difference was observed in worsening or occurrence of exercise limitation between patients with VAC and those without VAC: nine (42.8%) and seven (29.2%) but they respectively experienced at least one complication in 16 cases (76.2%) and seven cases (29.2%) (P less than 0.01). In conclusion, long-term prognosis in patients implanted with VVI pacing as compared to patients implanted with sequential pacing is poorer. The presence of VAC in patients treated with permanent VVI pacing is a major factor for complications and deaths related to A.E. and cardiac failure. Thus VVI pacing should be avoided in patients with VAC.

Arrhythmias, Cardiac↗
PubMed1988

Hemodynamic effects of a single dose of dopamine and L-dopa in pulmonary hypertension secondary to chronic obstructive lung disease.

Dopamine (DA) has rarely been administered at low dosage to stable patients with pulmonary hypertension (PAH) secondary to chronic obstructive lung disease (COLD). Since L-dopa (L-DA) is metabolized into DA, it might be an oral source of DA. After informed consent 10 patients with PAH, secondary to COLD underwent right catheterization to allow measurements of pressures and cardiac output (CO) as well as arterial and mixed venous oxygen levels before and then 30 and 60 min after the beginning of intravenous DA at a rate of 4 micrograms/kg/min. A week later, the same parameters were remeasured in 5 of these patients after a single oral intake of 1.5 g L-DA. At low doses both DA and L-DA increased CO and decreased pulmonary vascular resistances, suggesting a pulmonary vasodilator effect. They also enhanced oxygen delivery and Pvo2 without decreasing Pao2. A correlation was observed between cardiac index and plasma DA level. Thus though they do have some immediate adverse side effects and their long-term effects are unknown, inotropic and vasodilator drugs may have positive effects on pulmonary circulation.

Administration, Oral↗
PubMed1988

One-year clinical study on nifedipine in the treatment of pulmonary hypertension in chronic obstructive lung disease.

The advantages of long-term administration of vasodilators in the treatment of chronic cor pulmonale were investigated after informed consent in 60 patients with obstructive respiratory insufficiency (56 men, 4 women, mean age 63.5 +/- 1.5 years; mean pulmonary pressure 30.4 mm Hg). They were randomly divided into two groups of 30, a control group and a group treated with nifedipine, 10 mg three times a day. The following parameters were recorded every 3 months for a year: dyspnea, degree of right ventricular failure, number of days spent in hospital, survival and arterial blood gas tension. On the first day of study, no significant difference existed between the control and the treated groups. After 1 year 22 patients in the control group were still followed and 8 were dead. In the treated group 19 were followed, 7 were dead and 4 stopped treatment, generally due to ankle edema. At the end of the study, the only significant modification was improvement of the dyspnea in the nifedipine group (p less than 0.01). In conclusion, in spite of an improvement in the dyspnea index, clinical study for 1 year failed to demonstrate any objective benefit of nifedipine treatment.

Aged↗
PubMed1987

Hemodynamic and oxygen delivery responses to nifedipine in pulmonary hypertension secondary to chronic obstructive lung disease.

The effects of a single dose of nifedipine (20 mg sublingually) on hemodynamics and tissue oxygenation were evaluated in 24 patients suffering from pulmonary hypertension secondary to severe chronic obstructive lung disease. A significant improvement in pulmonary circulation and right ventricular pump function occurred. An increase in the oxygen delivery to the tissue was also demonstrated. A complementary study in 10 patients showed that the effects observed after a single dose were still apparent after oral intake (30 mg/day) for 15 days. For these reasons nifedipine may contribute in the treatment of cor pulmonale.

Adult↗
PubMed1986

Comparative study of the respiratory effects of two beta 1-selective blocking agents atenolol and bevantolol in asthmatic patients.

Seven asthmatic patients were given a single placebo tablet in a first test session and then in two subsequent double blind sessions they randomly received 400 mg bevantolol or 100 mg atenolol, with at least 2 days between each of the sessions. Neither beta-blocker had any significant effect on FVC as compared to the placebo. FEV 1, however, was significantly lower 2 and 3 h after atenolol or bevantolol; there was no significant difference between the effects of the two drugs on FEV 1. Peak expiratory flow rate was reduced by bevantolol but not by atenolol, the difference reaching significance after 3 h. Fenoterol inhalation at the end of each test session always enhanced pulmonary performance, but to a lesser extent after bevantolol than after placebo or atenolol. A slower heart rate was recorded 2, 3, and 4 h after bevantolol and 3 and 4 h after atenolol; the mean 2-h value was significantly lower with atenolol than with bevantolol. No patient suffered any adverse effect. Bevantolol may be slightly less selective than atenolol.

Adrenergic beta-Antagonists↗
PubMed1986

[Nifedipine in the treatment of chronic cor pulmonale].

The effects of a single dose of nifedipine (20 mg sublingual) on the haemodynamics and parameters of tissue oxygenation were assessed by right heart catheterisation and oximetry of mixed arterial and venous blood in 24 patients with pulmonary hypertension secondary to severe chronic obstructive airways disease. The haemodynamic effects of 15 days' oral therapy (30 mg/day) were studied in 10 other patients. Significant improvement in right ventricular pump function (25 p. 100 increase in cardiac index. average reduction of 3 mmHg of right ventricular end diastolic pressure), and lowering of pulmonary hypertension (mean pulmonary artery pressures reduced by an average of 10 p. 100 and total pulmonary resistance by 25 p. 100) were observed after the single dose of nifedipine. This improvement was maintained after oral therapy for 15 days. The significant improvement of tissue oxygenation was reflected by an increase in oxygen transport (+ 24 p. 100), in the coefficient of delivered oxygen (+ 19 p. 100), in the oxygen partial pressure (+ 4 p. 100) and saturation (+ 3 p. 100) in the mixed venous blood. Arterial lactate concentrations fell by about 28 p. 100. In addition, a moderate fall in ppO2 and arterial saturation was observed due to a weak shunt effect which was more than compensated by the increase in cardiac output, and especially by the increase in the coefficient of relieved oxygen. These results show that nifedipine may be a valuable addition in the treatment of cor pulmonale secondary to chronic obstructive airways disease by improving right ventricular haemodynamics and pulmonary circulation and by increasing the quantity of oxygen delivered.

Adult↗
PubMed1985

Two-week nifedipine treatment for pulmonary hypertension complicating chronic obstructive lung disease.

The effects of nifedipine on hemodynamics and blood gases were studied in 10 patients with pulmonary hypertension secondary to chronic obstructive lung disease. Two different sets of test data were recorded. The first set of readings was taken immediately before and during the initial hour after sublingual administration of 20 mg of nifedipine. The second set was taken after 2 weeks of therapy with 3 X 10 mg per day. After the acute sublingual dose, a significant decrease in pulmonary arterial pressure and pulmonary vascular resistance was recorded: 13% and 26% respectively. This decrease was accompanied by a 32% increase in cardiac output. Similar findings were recorded at the end of the 2-week therapy. Moreover, at this time, although blood gas tension had not been significantly altered, oxygen delivery was 35% higher. No adverse side effects were observed. This study suggests that nifedipine therapy can improve hemodynamics and tissue oxygenation in patients with pulmonary hypertension complicating chronic obstructive lung disease.

Administration, Oral↗
PubMed1984

[Effect of captopril on pulmonary arterial hypertension in congestive heart failure associated with chronic obstructive bronchopneumopathy].

Acute hemodynamic effects of oral 25 mg of the angiotensin converting enzyme inhibitor captopril were studied in 8 patients suffering from left ventricular failure and severe chronic obstructive lung disease (COLD) with pulmonary hypertension. In all the patients left ventricular failure resulted from a dilated cardiomyopathy. No significant change in right or left ventricular function and a decrease of 10% in arterial blood pressure and total systemic resistances were observed after administration of captopril. It is suggested that patients suffering from left ventricular failure and severe chronic obstructive lung disease will not benefit from administration of captopril.

Captopril↗
PubMed1983

[Postextrasystolic sinus responses after autonomic blockade in patients with sinus node dysfunction].

The interpretation and significance of postextrasystolic responses obtained in human electrophysiological examinations of patients with sinus node dysfunction has long been a matter of controversy. We carried out programmed atrial stimulation by the method of Strauss et al. in 54 patients with sinoatrial disorder, before and after pharmacologic autonomic blockade (with propranolol 0.2 mg/Kg and atropine sulfate 0.04 mg/Kg intravenously). There were two responses, as follows: computable sinoatrial conduction times and chaotic patterns. Patients were divided into groups on the basis of their intrinsic heart rate (IHR). If the total estimated sinoatrial conduction time over greater than or equal to 200 msec and greater than or equal to 147 msec after autonomic blockade and chaotic pattern were considered to be pathologic, so the ratio of abnormal parameters decreased from 73 to 44% in patients of normal IHR, and increased from 70 to 90% in patients of abnormal IHR. The latter 90% was mostly to the expense of the incalculable chaotic patterns. Interpreting a postextrasystolic curve, the existence of reset zone refers to the functional integrity of the sinoatrial node, to the organisation and synchronism of sinus potentials, which depends on the balance of autonomic nervous system and on the intrinsic electrophysiological integrity of the pacemaker cells.

Adolescent↗
PubMed1981

Relationship of pulmonary diastolic and pulmonary wedge pressures to left ventricular diastolic pressures: role of acute myocardial infarction localization.

Right and left hemodynamics have been simultaneously studied in 127 patients with acute myocardial infarction with respect to electrocardiographic localization. Hemodynamic profiles of the different localizations suggest a high incidence of right ventricular dysfunction in infero-posterior infarcts. The comparison with the other localizations suggests that such a right ventricular dysfunction is likely to be responsible for an additional underestimation of left ventricular end-diastolic pressure when estimated by pulmonary diastolic pressure.

Adult↗
PubMed1980

Flow analysis within the left ventricle using an integral equation method: interest in left ventricular function assessment.

The following parameters are derived from a hydrodynamic analysis of left ventricular ejection: pressure distribution along ventricular long axis and walls, regional and net forces applied to the blood within the ventricle. They are computed from human ventricular contours (angiograms), using an original application of integral equation method and numerical analysis. This technique enables flow analysis inside bodies of any shape. Comparison of each parameter computed from normal and infarcted (akinetic or bulged) ventricles shows that hydrodynamic analysis within the human left ventricle may provide better documented and quantitative assessment of its muscular and pump function than does morphological analysis of cardiac imaging.

Animals↗
PubMed1978

Heat and mass transfer of a thermal indicator in pulsatile flow through the cardio-pulmonary system. I. Modeling.

The construction of a physico-mathematical model which describes the mechanism of indicator dispersion in the circulation and which fits the thermal dilution curves (TDC) is presented. Because of its more evident physical meaning, formulation of the problem in terms of heat and mass transfer is preferred to stochastic theory. Hypotheses necessary to simplify the general system of governing equations are clearly defined and discussed. This deductive method leads to a one-dimensional convective heat transfer model in which pulsatility and form of injection appear naturally. Simulations of TDC in constant and pulsatile flow cases are performed on a digital mini-computer which demonstrates the model's ability to represent different experimental or clinical observations. This will facilitate hemodynamic parameter identification from TD techniques and will increase the accuracy of this identification.

Aorta↗
PubMed1978

Heat and mass transfer of a thermal indicator in pulsatile flow through the cardio-pulmonary system. II. Identification of cardiac output.

Hamilton's celebrated formula for cardiac output measurement is simple but its validity is dependent on several methodologic requirements which are not generally fulfilled, particularly in thermal dilution. A quite different method, based on a physico-mathematical model of the indicator dispersion in the circulation, is proposed. It allows direct derivation of cardiac output once the model's parameters have been identified. Combined deconvolution and least squares procedures are used with truncated data for this identification. Numerical tests and application to clinical observations are presented. Both limitations and possibilities of further developments in estimation of pulsatile flow conditions from TD technique are discussed.

Blood Circulation↗