PubMed Health⌕ Search

Biomedical subjects

E Doria

Publications and source records attributed to E Doria.

At least 37 records · Page 2Linked to original sources
PubMed1993

Sustained cardiac diastolic changes elicited by ultrafiltration in patients with moderate congestive heart failure: pathophysiological correlates.

OBJECTIVE: To investigate the pathophysiological (cardiac function and physical performance) significance of clinically silent interstitial lung water accumulation in patients with moderate heart failure; to use isolated ultrafiltration as a means of extravascular fluid reabsorption. DESIGN: Echocardiographic, Doppler, chest x-ray evaluations, and cardiopulmonary tests at baseline, soon after ultrafiltration (veno venous extracorporeal circuit), and four days, one month, and three months later. SETTING: University institute of cardiology. SUBJECTS: 24 patients with heart failure due to idiopathic dilated cardiomyopathy or ischaemic myocardial disease with sinus rhythm and ejection fraction less than 35%. Twelve were randomised to ultrafiltration and 12 were taken as controls. MAIN OUTCOME MEASURES: Left ventricular systolic function (from ultrasonography); Doppler evaluation of mitral, tricuspid, and aortic flow and echo-Doppler determination of cardiac output; radiological score of extravascular lung water; right and left ventricular filling pressures; oxygen consumption at peak exercise and exercise tolerance time in cardiopulmonary tests. RESULTS: Soon after ultrafiltration (1976 (760) ml of fluid removed) the following was observed: a reduction in radiological score of extravascular lung water (from 15(1) to 9(1)) and of right (from 7.1 (2.3) to 2.3 (1.7) mm Hg) and left (from 17.6 (8.8) to 9.5 (6.4) mm Hg) ventricular filling pressures; an increase in oxygen consumption at peak exercise (from 15.8 (3.3) to 17.6 (2) ml/min/kg) and of tolerance time (from 444 (138) to 508 (134) s); a slight decrease in atrial and ventricular dimensions; no changes in the systolic function of the left ventricle; a reduction of the early to late filling ratio in both ventricles (mitral valve from 2 (2) to 1.1 (1.1)); (tricuspid valve from 1.3 (1.3) to 0.69 (0.18)) and an increase in the deceleration time of mitral and tricuspid flow, reflecting a redistribution of filling to late diastole. Variations in the ventricular filling pattern, lung water content, and functional performance persisted for three months in all cases. None of these changes was detected in the control group. CONCLUSIONS: Reduction of interstitial lung water was probably the mechanism whereby ultrafiltration modified the pattern of filling of the two ventricles and improved functional performance.

Aged↗
PubMed1993

Modification of exercise performance by sharp reduction of blood pressure. A study in patients with uncomplicated hypertension.

We evaluated exercise performance in 14 patients with uncomplicated essential hypertension 1 h after the administration of a single dose of placebo, nifedipine (20 mg), captopril (50 mg), and propranolol (80 mg). Drugs were administered at the same time of day following a randomized, double-blind protocol. Mean resting blood pressure (+/- SE) was 135 +/- 3 mm Hg with placebo administration, 118 +/- 4 with captopril, 110 +/- 4 with nifedipine, and 115 +/- 5 with propranolol and increased with exercise to 163 +/- 4, 146 +/- 3, 136 +/- 4, 136 +/- 4, respectively. Oxygen consumption at peak exercise and at ventilatory anaerobic threshold (VAT) was 25.2 +/- 1.1 and 18.1 +/- 1.0 ml/min/kg with placebo. Only propranolol (-2.3 ml/min/kg) decreased peak exercise oxygen consumption. Oxygen consumption at VAT was reduced by nifedipine and propranolol but unaffected by captopril. The effects on exercise capacity of blood pressure reduction in hypertensive patients are dependent on the drug utilized and are not related to the amount of blood pressure reduction. The lowered oxygen consumption at VAT observed with nifedipine and propranolol, and not with captopril, might be due to an excessive downward shift of the muscle perfusion pressure--oxygen consumption relationship which might take place during exercise.

Anaerobic Threshold↗
PubMed1993

[Changes in the physical characteristics of the lung can account for the improvement observed after ultrafiltration in patients with moderate heart failure].

Ultrafiltration improves the clinical condition of patients with moderate congestive heart failure. Ultrafiltration (1895 +/- 120 ml of plasma water, rate 600 ml/h, veno-venous bypass) was performed in 30 patients with moderate congestive heart failure in stable clinical conditions. The effects of ultrafiltration were assessed through pulmonary function and cardiopulmonary exercise tests performed before and 30 days after the procedure. Vital capacity, forced expiratory volume (1 s) and maximal voluntary ventilation improved as improved exercise performance (increase in oxygen consumption at peak exercise and at anaerobic threshold). Tidal volume at anaerobic threshold and at peak exercise increased by 10% with no changes in respiratory rate. This suggests that ultrafiltration induces changes at the physical characteristics of the lungs probably related to changes in lung water content.

Aged↗
PubMed1993

[The improvement of the Doppler echocardiographic method for the estimation of pulmonary systolic pressure].

The formulas currently utilized for noninvasive evaluation of right ventricular systolic pressure (RVSP) include right ventricular-right atrial pressure gradient (RV-RAG) and right atrial pressure (RAP). The former is expressed by trans-tricuspid systolic flow velocity, the latter is generally assumed. We recently observed that ultrasound estimation of RAP through inferior vena cava collapsibility index (CI) may help in the choice of the more appropriate formula for the evaluation of RVSP. However, these traditional methods (method A:RV-RAG + 10; method B:RV-RAG x 1.1 + 14) have limitations, particularly when RAP is low. The present study was undertaken to improve noninvasive estimation of RVSP through new formulas based on CI prediction of RAP. One hundred and four patients, in whom tricuspid regurgitation was adequately documented with CW-Doppler, were included in this study. They were classified into 3 groups: Group 1 with CI > 45%, Group 2 with CI < or = 35%, Group 3 with CI 35-45%. RVSP was evaluated by 3 different methods: A, B, and C. Method C was based on CI, assigning 6, 16, or 9 mmHg to RAP (respectively, the mean values in the 3 groups of our previous study). Results indicate that method C improves noninvasive estimation of RVSP in Group 1 and Group 2, with respect to other methods, with reduction of the SEE and of the mean difference of the t-test between hemodynamic and echographic values. In Group 3, Doppler estimation by method A and C, and catheter measurements are comparable, whereas method B significantly overestimates the actual value.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Exercise performance in patients with uncomplicated essential hypertension. Effects of nifedipine-induced acute blood pressure reduction.

In untreated patients with uncomplicated essential hypertension, exercise induces an abnormal increase in blood pressure; the influences of this increase on exercise were evaluated by a cardiopulmonary exercise test (CPX) performed in control conditions (step 1) and during acute blood pressure reduction (step 2). Patients were classified as (1) normotensive (resting diastolic blood pressure [BPd] less than 90 mm Hg; n = 14), (2) mildly hypertensive (BPd of 90 to 104 mm Hg; n = 9), and (3) moderately to severely hypertensive (BPd greater than or equal to 105 mm Hg; n = 16). For the three groups, peak mean blood pressure during exercise was 125 +/- 5 mm Hg (mean +/- SEM), 144 +/- 3 mm Hg (p less than 0.01 vs normotensive), and 161 +/- 4 mm Hg (p less than 0.01 vs normotensive and p less than 0.01 vs mild hypertension), respectively. Oxygen consumption (VO2) at peak exercise and at ventilatory anaerobic threshold was 26.1 +/- 1.1 and 17.2 +/- 0.5 ml/min/kg, 25.4 +/- 1.1 and 16.9 +/- 0.8 ml/min/kg, and 26.4 +/- 1.3 and 17.5 +/- 1.2 ml/min/kg in normotensive subjects, those with mild hypertension, and those with moderate to severe hypertension, respectively. Fourteen normotensive subjects, six with mild hypertension, and nine with moderate to severe hypertension participated to step 2 (nifedipine vs placebo, double-blind crossover). Nifedipine reduced blood pressure at rest and at peak exercise in those with hypertension. Peak exercise VO2 was unaffected by nifedipine in both normotensive subjects and those with hypertension. With nifedipine, ventilatory anaerobic threshold occurred earlier and at a lower VO2 in mild and in moderate to severe hypertension (delta VO2 = -1.9 and -2.4 ml/min/kg, respectively). These findings might be due to nifedipine-induced redistribution of blood flow during exercise and might be the reason for the complaint of weakness after blood pressure reduction in hypertensive subjects.

Blood Pressure↗
PubMed1992

[Better efficacy of K-strophanthidin versus digoxin in subjects with dilated cardiomyopathy and chronic heart insufficiency].

We evaluated the efficacy of K-strophanthidin and digoxin in 20 patients with stable, severe congestive heart failure. In this aim, we studied the left ventricular pump function at rest and following manipulation of the cardiac load (cold pressor test and nitroprusside infusion), the exercise performance (cardiopulmonary exercise test), and the level of circulating norepinephrine. The study was double-blind and cross-over and comprehended 4 periods of 1-week each during which patients received in random order: placebo (oral+intravenous), K-strophanthidin (intravenous + oral placebo), digoxin (oral+intravenous placebo and, in 8 patients, intravenous + oral placebo). The efficacy of the various compounds was tested at the end of each period 1 and 10 hours after drug dosing. Comparable results were obtained by the 2 sets of measurements. Both digoxin and K-strophanthidin showed a positive inotropic effect. This is shown by an upward shift of the ejection fraction/end-systolic stress. In spite of this, only K-strophanthidin significantly increased exercise performance: tolerance time (+153 s), peak oxygen consumption (+1.2 ml/kg/min) and oxygen consumption at anaerobic threshold (+2.3 ml/kg/min). Norepinephrine plasma level at rest was significantly lowered only by K-strophanthidin. Results were comparable when digoxin was given intravenously. We conclude that both glycosides elicit an increase of the inotropic cardiac state but only K-strophanthidin improves exercise performance.

Administration, Oral↗
PubMed1992

[The improvement in physical exercise capacity in dilated cardiomyopathy during short-term treatment with L-thyroxine].

Reduced left ventricular function and other factors, such as vascular resistances, redistribution of cardiac output and impaired muscular metabolism, limit exercise performance in chronic heart failure. Thyroid hormones have a positive cardiac inotropic effect, stimulate protein synthesis (particularly at muscular level) and reduce peripheral vascular resistances with consequent increase of cardiac output. Therefore, it is possible that thyroid hormones can improve exercise performance in chronic heart failure. We have administered L-thyroxin (100 mcg/die) for 1 week to 9 patients affected by primary dilated cardiomyopathy. All the patients were euthyroid (T3 = 1.06 +/- 0.1 mcg/ml, T4 = 8.5 +/- 1.9 mcg/dl, TSH = 1.32 +/- 0.7 mU/ml) and in II-III NYHA functional class. Before starting the treatment and at the end of it, we performed the cardiopulmonary exercise test and the echocardiogram. We also evaluated the resting hemodynamic parameters through catheterization and the plasmatic values of thyroid hormones and noradrenaline. At the end of the treatment all patients were euthyroid, despite a significant (p less than 0.05) increase of T4 (10.5 +/- 3.2 mcg/dl) and a decrease of TSH (1.1 +/- 0.1 mU/ml). Mean values of effort parameters changed as follows: peak oxygen consumption from 19.6 +/- 1.6 to 20.6 +/- 1.3 ml/min/kg, tolerance time from 460 +/- 61 to 481 +/- 60 s. These variations were not associated with changes in resting hemodynamic parameters and noradrenaline. Left ventricular ejection fraction, calculated by echocardiography, increased from 26 +/- 6 to 28.9 +/- 8% (p less than 0.05). We conclude that in dilated cardiomyopathy short term treatment with L-thyroxin significantly improves patient's response to cardiopulmonary exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Acute and chronic efficacy of felodipine in congestive heart failure.

In 13 patients with congestive heart failure we tested the acute hemodynamic effects of 5 vs. 10 mg felodipine tablets, in a double-blind, cross-over study. One hour after felodipine 5 mg, echocardiographic ejection fraction (%), cardiac index (thermodilution-ml/min/m2), and pulmonary wedge pressure (mm Hg) significantly changed (from 21 +/- 2 to 26 +/- 2, 2350 +/- 150 to 2790 +/- 160, 24 +/- 4 to 17 +/- 4) while they remained steady after felodipine 10 mg. The greatest stroke index increases were associated with felodipine 5 mg in 12 patients and 10 mg in 1 patient. Therefore we evaluated (open study) the long-term (2 months- 1 year) clinical and hemodynamic efficacy following the treatment with the acutely most effective dose (twice daily). After 2 months ejection fraction, cardiac index and pulmonary wedge pressure were respectively 24 +/- 2, 2550 +/- 150, and 18 +/- 4 (12 hours after the last drug administration, n = 11, P less than 0.02 from baseline). These parameters further increased one to two hours after the following administration of felodipine. Clinical improvement (reduction of 1 functional class, according to the New York Heart Association) was observed in 8/13 patients. These 8 patients participated to the one year follow-up. In 5 patients follow-up was interrupted because of acute cardiovascular events. However, before study interruption (5 patients) or ending (3 patients) clinical status did not worsen and ejection fraction remained higher than in the pretreatment period. Therefore, low dose felodipine might be used in the treatment of congestive heart failure.

Double-Blind Method↗
PubMed1991

Systemic to pulmonary bronchial blood flow in mitral stenosis.

We measured systemic to pulmonary bronchial blood flow [Qbr(s-p)] during total cardiopulmonary bypass in 15 patients with mitral stenosis and elevated pulmonary venous pressure (group A, mean pulmonary wedge pressure = 22.2 +/- 5.4 mm Hg, mean +/- SD) and in 15 patients with coronary artery diseases and normal pulmonary venous pressure (group B). Qbr(s-p) is the volume of blood accumulating in the left side of the heart in the absence of pulmonary and coronary flows. This blood was vented through a cannula introduced into the left atrium and measured. Qbr(s-p) was 76.3 +/- 13.9 ml/min (2.18 +/- 0.37 percent of extracorporeal circulation pump flow) and 22.3 +/- 2.1 (0.63 +/- 0.15) in group A and B, respectively (p less than 0.01). During total cardiopulmonary bypass, pulmonary venous pressure is approximately atmospheric pressure, and no differences in systemic blood pressure, extracorporeal circulation pump flow, and airways pressure were observed between group A and B. Therefore, vascular resistance through the bronchial vessels draining into the pulmonary circulation is reduced in patients with mitral stenosis and elevated pulmonary venous pressure.

Adult↗
PubMed1990

Doppler assessment of left ventricular filling pattern in silent ischemia in patients with Prinzmetal's angina.

Spontaneous angina is an ideal condition in which to study left ventricular (LV) dysfunction induced by acute myocardial ischemia. In 6 patients with Prinzmetal's angina, LV diastolic function during 16 episodes of spontaneous angina was studied by simultaneous recordings of electrocardiographic (ECG), echocardiographic and hemodynamic parameters. In particular, pulsed Doppler echocardiography measured peak velocity of early (E) and late (A) transmitral flow and E/A ratio, as indexes of relative early versus late LV filling. During the ischemic attacks, the time sequence of pulsed Doppler echocardiographic and ECG changes showed 3 distinct phases: (1) "waxing phase: transmitral flow changes with minimal ECG modifications (E/A = 0.85 +/- 0.1); (2) "steady" phase: maximal ECG changes (E/A = 0.9 +/- 0.1); and (3) "waning" phase: regression of the ECG changes (E/A = 1.26 +/- 0.15). In each phase, E/A ratio showed a significant difference from the baseline value (E/A = 1.17 +/- 0.2) as a result of changes in E, suggesting that myocardial ischemia affects mainly the early phase of diastole. In the waxing phase, LV diastolic dysfunction preceded systolic abnormalities, as documented by a significant reduction of E/A ratio in the absence of alterations in LV ejection fraction, as well as in systemic arterial and pulmonary wedge pressures. Finally, all the recorded parameters were consistent with LV "contractile rebound" occurring in the waning phase and affecting both diastole and systole.

Angina Pectoris, Variant↗
PubMed1990

Cardiac tamponade produced by a loculated pericardial hematoma simulating a right atrial mass.

We report a case of cardiac tamponade due to thrombosis of a loculated pericardial effusion which occurred after open heart surgery. The loculated hematoma was highly echogenic and mimicked a right atrial mass. Cross-sectional echocardiography, in association with color Doppler flow imaging, was extremely useful in identifying this rare complication of cardiac surgery and, therefore, in determining the subsequent surgical approach.

Cardiac Surgical Procedures↗
PubMed1990

Inspired gas relative humidity affects systemic to pulmonary bronchial blood flow in humans.

To our knowledge, the effects of humidity of inspired air on bronchial blood flow in humans are unknown. During total cardiopulmonary bypass, we measured systemic to pulmonary bronchial blood flow (Qbr[s-p]) which is the volume of blood accumulating into the left side of the heart in the absence of pulmonary and coronary flow. A cannula was introduced into the right upper pulmonary vein and advanced into the lowermost portion of the left side of the heart. From this cannula Qbr(s-p) was vented by gravity and measured. Inspired gas (10 L/min, endotracheal tube, 50 percent O2 + 50 percent N2O) relative humidity was less than 20 percent and greater than 85 percent in group A (n = 25) and in group B (n = 25), respectively. Mean (+/- SE) Qbr(s-p) was 40.7 +/- 0.06 ml/min or 1.32 +/- 0.12 ml/min (percent cardiac output) in group A and 21.7 +/- 1.8 ml/min or 0.68 +/- 0.06 ml/min in group B. These data indicate that under these conditions Qbr(s-p) is increased by dry gas lung inflation in humans.

Cardiopulmonary Bypass↗
PubMed1989

Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure.

1. In systemic hypertension the pulmonary vessels show an excessive tone at rest and hyper-react to adrenoceptor stimulation. Alterations in Ca2+ handling by the vascular smooth muscle cells seem to underlie these disorders. Alveolar hypoxia also constricts pulmonary arteries, increasing the intracellular Ca2+ availability for smooth muscle contraction. This suggests the hypothesis that hypoxic pulmonary vasoconstriction depends on similar biochemical disorders, and that the response to the hypoxic stimulus may be emphasized in high blood pressure. 2. In 21 hypertensive and 10 normotensive men, pulmonary arterial pressure and arteriolar resistance have been evaluated during air respiration and after 15 min of breathing 17, 15 and 12% oxygen in nitrogen. Curves relating changes in pulmonary arterial pressure and arteriolar resistance to the oxygen content of inspired gas had a similar configuration in the two populations, but in hypertension were steeper and significantly shifted to the left of those in normotension, reflecting a lower threshold and an enhanced vasoconstrictor reactivity. 3. This pattern was not related to differences in severity of the hypoxic stimulus, degree of hypocapnia and respiratory alkalosis induced by hypoxia, and plasma catecholamines. 4. The association of high blood pressure with enhanced pulmonary vasoreactivity to alveolar hypoxia could have clinical implications in patients who are chronically hypoxic and have systemic hypertension.

Adult↗
PubMed1989

Nifedipine reduces pulmonary pressure and vascular tone during short- but not long-term treatment of pulmonary hypertension in patients with chronic obstructive pulmonary disease.

We evaluated in patients suffering from COPD-related pulmonary hypertension whether nifedipine therapy lowers acutely and chronically pulmonary vascular pressure and resistance and whether pulmonary transmural pressure may be further lowered by the combined use of nifedipine and oxygen. Changes of the pulmonary vascular tone were determined on the pulmonary driving pressure/flow curve, which was generated by upright exercise. Fifteen patients with COPD and mean pulmonary pressure greater than or equal to 20 mm Hg were studied at control (Week 0) and after 1 wk of nifedipine treatment (180 mg daily, Week 1). It was possible to pursue the same nifedipine daily dosage for 2 months in 10 patients, who were re-evaluated after 8 wk of treatment and after nifedipine withdrawal the following week. At Week 1, mean pulmonary transmural pressure was reduced (32.8 +/- 4.1 versus 27.3 +/- 2.8 mm Hg, mean +/- SE, p less than 0.05) via active pulmonary vasodilation because the pulmonary driving pressure/flow curve was shifted right and downward. Both mean transmural pulmonary pressure lowering effect and active pulmonary vasodilatation regressed during long-term nifedipine treatment. Oxygen reduced pulmonary transmural pressure (32.8 +/- 4.1 versus 28.6 +/- 2.9 mm Hg, p less than 0.05, Week 0); however, this effect always disappeared during nifedipine treatment. We conclude that nifedipine should not be used as long-term treatment for COPD-related pulmonary hypertension and that nifedipine inhibits the oxygen capability to reduce pulmonary pressure.

Adult↗
PubMed1989

Accessory thyroid tissue in the right ventricle.

In an asymptomatic 66-year-old woman presenting a systolic murmur in the pulmonic area, echocardiography evidenced a voluminous mass in the right ventricular outflow tract resembling a cardiac tumor. Histologic finding was that of aberrant normal thyroid. Although the occurrence of ectopic thyroid tissue in the heart is rare, it should be considered in the differential diagnosis whenever a mass is located at the level of the interventricular septum and encroaches on the right ventricular outflow tract. In these cases, a thyroid scintiscan may avoid an unnecessary surgical intervention.

Aged↗
PubMed1989

Increase of alveolar pressure reduces systemic-to-pulmonary bronchial blood flow in humans.

We studied the effect of positive alveolar pressure (PA) on systemic to pulmonary bronchial blood flow, Q?? in humans. The Q?? was measured during total cardiopulmonary bypass as the volume of blood accumulating in the left heart. This blood was vented by gravity from the left heart via a cannula introduced in the right upper pulmonary vein and advanced to the lowest portion of the left heart. In group A (n = 10) the Qbr(s-p) was measured for 25 to 95 min with constant PA (4.0 +/- 0.2 cm H2O, mean +/- SE). In group B (n = 10) Qbr(s-p) was measured for 20 min with PA = 4.1 +/- 0.2 cm H2O and for a further 20 min with PA = 14.1 +/- 0.4 cm H2O. The Qbr(s-p) ranged between 0.32 and 2.76 percent of cardiac output (pump flow) and remained constant with time (group A). The increase of PA from 4.1 +/- 0.2 to 14.1 +/- 0.4 cm H2O reduced Qbr(s-p) by approximately 40 percent (p less than 0.01, group B). We conclude that positive PA reduces Qbr(s-p) during total cardiopulmonary bypass. Therefore, we advise using low PA during assisted ventilation to preserve bronchial blood flow.

Bronchi↗
PubMed1989

[Positive alveolar pressure reduces bronchial systemic-to-pulmonary blood flow in man].

We studied in humans during total cardio-pulmonary by-pass the effects of positive alveolar pressure on systemic to pulmonary bronchial blood flow. Systemic to pulmonary bronchial blood flow is the entire bronchial blood flow to the lung and was measured as the volume of blood which accumulates in the left heart when there is no pulmonary flow. Systemic to pulmonary bronchial blood flow was vented by gravity via a cannula (18 French) introduced in the upper superior pulmonary vein and advanced into the lower most portion of the left heart. In Group A (10 patients) systemic to pulmonary bronchial blood flow was measured with alveolar pressure constant at 4.0 +/- 0.4 cm H2O for 53.5 +/- 6.2 min (range 25 to 95 min), and ranged between 0.32 and 2.76% of cardiac output (pump flow) remaining constant with time. In Group B (10 patients) systemic to pulmonary bronchial blood flow was measured for 2 periods of 20 min each with alveolar pressure equal 4.1 +/- 0.2 and 14.1 +/- 0.4 cm H2O respectively. The increase of alveolar pressure reduced systemic to pulmonary bronchial blood flow by almost 40%. The reduction of systemic to pulmonary bronchial blood flow we observed may be deleterious for the survival of the lung parenchyma particularly in some circumstances. This is the case of pulmonary embolism, when bronchial blood flow is the major source of blood to the lung parenchyma and serves to prevent pulmonary infarction, or the case of acute respiratory distress syndrome, when pulmonary flow is compromised and systemic to pulmonary bronchial blood flow increases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗