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Biomedical subjects

A Fortini

Publications and source records attributed to A Fortini.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Changes in the wall motion of left ventricle in dipyridamole-induced ischemic cardiopathy studied by nuclear magnetic resonance. A comparison with myocardial scintigraphy with 99mTc MIBI].

To investigate whether magnetic resonance imaging (NMR) can detect alterations in LV contractility during myocardial ischemia, ten patients aged 32-72 with coronary artery disease underwent ECG gated NMR performed at 0.5 Tesla after intravenous infusion of high dose dipyridamole (DP) (0.7 mg/Kg) over 5 minutes. LV contraction in planes similar to echo short axis projection was imaged under condition, 3' and 15-20' after infusion of DP by fast multiphasic imaging (FMI), multiple angulated cine-NMR sequence with a temporal resolution of 50 m/sec. Entity and size of perfusion defects after DP were determined by Tc 99m MIBI myocardial scintigraphy. In all patients changes in LV contractility appeared at NMR in the same site of perfusion impairments revealed with MIBI. In 8 patients the alterations lasted even more than 20' after the first NMR scan. NMR provides the opportunity of performing long-lasting assessment of ventricular wall contractility and enables to exactly localize the site and extension of kinetic changes as well as their time of onset and time duration.

Contrast Media↗
PubMed1991

Anaerobic threshold in patients with exercise-induced myocardial ischemia.

The aim of the present study was to investigate the ventilatory anaerobic threshold in patients with exercise-induced myocardial ischemia. Ventilatory volumes and gas exchanges were measured during treadmill stress testing in 36 patients (11 with previous myocardial infarction) with electrocardiographic criteria of myocardial ischemia during the test and in 23 healthy, untrained control subjects of equivalent age. The anaerobic threshold was detected in 32 of 36 patients (89%) and in 22 of 23 control subjects (96%). The anaerobic threshold was significantly lower in patients than in control subjects (13.5 +/- 1.9 versus 19.7 +/- 1.7 ml/kg per minute VO2, p less than 0.001). In the 21 patients without previous myocardial infarction, the anaerobic threshold was also significantly lower than in the control subjects (13.9 +/- 1.6 versus 19.7 +/- 1.7 ml/kg per minute VO2, p less than 0.001). Among the 21 patients without previous myocardial infarction, the 12 with a low ischemic threshold, which occurred during the first three steps of the modified Bruce protocol, had an anaerobic threshold significantly lower than the other nine patients (13.1 +/- 1.5 versus 14.9 +/- 1.0 ml/kg per minute VO2, p less than 0.01). However, even in the patients with a moderate to high ischemic threshold, the anaerobic threshold was significantly lower than in the control subjects (p less than 0.001). These data show that the anaerobic threshold can be measured in the great majority of patients with exercise-induced myocardial ischemia. The low anaerobic threshold level indicates a relevant functional impairment in these patients.

Adult↗
PubMed1990

Insulin secretion in polycystic ovarian disease: effect of ovarian suppression by GnRH agonist.

Nine obese and ten non-obese women with polycystic ovarian disease (PCO), and seven obese and eight non-obese normal women, had an oral glucose tolerance test (OGTT) before and after treatment with GnRH agonist (buserelin 400 micrograms/day s.c. for 8 weeks) in order to investigate the effect of ovarian suppression on their insulinaemic secretion. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), oestradiol (E2), androstenedione (A), testosterone (T), DHEAS, cortisol and insulin (I) were measured at time 0 of OGTT; in all samples of OGTT, E2, T, A and I were also assayed. PCO patients showed higher basal androgen levels than control patients. All subjects showed a normal glycaemic response to OGTT. The mean fasting and areas under the curve (ISA) of plasma I were significantly greater in the obese PCO women than in non-obese PCO, the normal obese and non-obese women. All PCO patients showed significantly higher fasting I and ISA values in respect to all control patients. Hyperinsulinaemic responses were 89% in PCO obese, 30% in non-obese PCO and 29% in obese control patients. After buserelin treatment, these values did not change significantly in respect to pretreatment in all groups, in spite of a significant decrease of androgen secretion. During OGTT, no variations of steroid plasma concentrations were seen in both normal or hyperinsulinaemic PCO patients. The data of this study show that hyperandrogenism, hyperinsulinism and obesity were associated with different modalities in PCO patients and that a marked decrease of androgen secretion did not restore a normal insulinaemic response to OGTT, suggesting that hyperandrogenism does not produce hyperinsulinism.

Adult↗
PubMed1990

Low-dose heparin as an antithrombotic agent.

Heparin, after subcutaneous administration, has been found to be able to bind to endothelial receptors both in rabbits and in humans. N-sulphonate 35S-heparin remains bound in rabbits for at least 24 h and is able to enhance the inactivation process of thrombin and factor Xa. Heparin subcutaneously (200 U/kg) injected for 2 weeks resulted in an enhanced inactivation of thrombin and factor Xa by the endothelium. The antithrombin-enhancing activity persists longer than the anti-Xa activity. In man, daily subcutaneous administration of heparin (12,500 U/day) for 2 weeks significantly reduces the increased fibrinopeptide A plasma levels and normalizes the increased 125I-fibrinogen turnover. The present work indicates that heparin administration at a low dose represents a treatment able to remarkably enhance the antithrombotic properties of the vessel wall, independently of the presence of detectable heparin levels in the circulating blood.

Animals↗
PubMed1987

Acute reversible reduction of PGI2 platelet receptors after iloprost infusion in man.

Platelet sensitivity to PGI2 and platelet PGI2 receptors were investigated in eight subjects with peripheral artery disease (stage IV according to Fontaine) treated for 14 consecutive days with six hour iv infusion of Iloprost (Schering, FRG) 2 ng/kg/min. Platelet studies were performed on the 1st, the 2nd, the 7th and the 14th day of therapy, immediately before infusion (between 8.00 and 9.00 a.m.), at the end and 6 and 18 hours (the following morning) after the end of the infusion. Platelet sensitivity to PGI2 was assessed by determining the PGI2 inhibitory dose 50(ID 50) on platelet aggregation induced by 5 microM ADP. PGI2 platelet receptors were investigated by a direct radioligand binding assay. PGI2 ID 50 after the infusion was significantly higher than that at baseline(p less than 0.01) and six hours later the baseline sensitivity was restored. After the six hour Iloprost iv infusion a significant reduction in the number of high affinity PGI2 platelet receptor (HAR) was observed (p less than 0.005) without any change in their affinity for the ligand. Six hours after the end of the infusion the number of the HAR was still significantly reduced (p less than 0.05). The following morning the receptor number of HAR was restored. The baseline values of PGI2 HAR, when reassessed after seven and fourteen days of treatment, were not significantly different from those recorded on the first day of therapy. These data indicate that the reduction of platelet PGI2 sensitivity following short-term Iloprost infusion is rapidly reversible and is related to a contemporary down-regulation of PGI2 platelet receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1987

Effectiveness of low-dose heparin in prevention of myocardial reinfarction.

728 patients aged 50-75 years who had had Q-wave myocardial infarction 6-18 months previously were enrolled in a randomised, multicentre trial of low-dose heparin in prevention of reinfarction. The control group (365 patients) received their study centres' usual therapy; the heparin group (363 patients) also received subcutaneous calcium heparin (12,500 IU daily). Mean (SD) follow-up was 708 (265) days in the heparin group and 687 (251) in the control group. The reinfarction rate was 63% lower in the heparin than in the control group (4/303, 1.32% v 13/365, 3.56%). The difference in cumulative reinfarction rate between the groups was significant by both drug-efficacy (chi 2 = 3.99, p less than 0.05) and intention-to-treat analysis (chi 2 = 3.84, p = 0.05). Heparin treatment reduced the cumulative general mortality rates by 48% on drug-efficacy analysis (chi 2 = 3.88, p less than 0.05) and by 34% on intention-to-treat analysis (chi 2 = 2.05, not significant). Cardiovascular mortality was also reduced (33%) but not significantly. However, fatal events attributable to thromboembolism (fatal reinfarction, stroke, pulmonary embolism) were significantly less frequent in the heparin than in the control group (1 v 7, p less than 0.05). 60 patients (16.5%) discontinued heparin treatment, but only 23 patients (6.3%) stopped because of side-effects. Low-dose heparin appears to be effective, safe, well tolerated, and free from haemorrhagic risk for the prevention of myocardial reinfarction.

Aged↗
PubMed1987

[Changed diastolic function at rest in patients with perfusion defects in exertion myocardial scintigraphy with TI-201].

Myocardial perfusion scintigraphy with TI-201 after exercise allows distinction between areas of scar (irreversible defect) and areas of ischemia (reversible defects). Accordingly 4 major groups of patients can be identified: with normal perfusion pattern (Group I); with reversible ischemia (Group II); with scar of previous myocardial infarction (Group III); with both evidence of scar and ischemia (Group IV). Sixty-nine patients (59 m; 10 f; mean age 55.7 +/- 9 years) with suspected or demonstrated ischemic heart disease underwent stress TI-201 myocardial scintigraphy and on the basis of the scintigraphic results were assigned as follows: 11 to group 1, 14 to group II, 31 to group III and 13 to group IV. In order to investigate the behaviour of ventricular diastolic function in these different subsets, all the patients underwent subsequently a radionuclide angiography at rest (both first pass and equilibrium gated blood pool studies), which allowed the assessment of left ventricular ejection fraction (EF), peak filling rate (PFR)--as expression of diastolic function--and regional wall motion pattern. The values of EF and PFR were significantly reduced (p less than 0.05) in the patients with defects of perfusion (Groups II, III and IV) in comparison to the patients with normal perfusion (Group I); abnormal wall motion was found in 0 (I), 8 (II), 22 (III) and 7 (IV) patients. The diastolic function was more frequently altered (PFR less than 2.5 EDV/sec) than the systolic function (EF less than 50%) or regional wall motion, mainly in patients with reversible scintigraphic defects (prevalence of alterations in the groups II and IV: PFR: 78%, EF: 22%, abnormal wall motion: 56%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Heparin does not interfere with prostacyclin and prostaglandin D2 binding to platelets.

Heparin has been reported to antagonize the platelet antiaggregating activity of prostacyclin (PGI2) and prostaglandin D2 (PGD2). To investigate whether heparin interferes with PGI2 and/or PGD2 binding to the specific membrane platelet receptors, the number and the affinity of binding sites for tritiated PGI2 and PGD2 were determined in 8 healthy subjects (aged 25-32; 4 for PGI2 and 4 for PGD2 studies) in the absence and in the presence of heparin. Preliminary aggregation tests indicated that the heparin concentration tested (2 I.U./ml) reduced the antiaggregating activity of PGI2 and PGD2. Heparin, when preincubated with platelet suspension, did not induce any significant change in the number/platelet (bs/plt) and affinity (Kd) of PGI2 and PGD2 binding sites (bs) in comparison to control values (PGI2 high affinity bs: bs/plt = 106 +/- 12 vs 107 +/- 17 - Kd = 9.7 +/- 3.1 vs 10.0 +/- 2.3 nM; PGI2 low affinity bs: bs/plt = 3551 +/- 233 vs 3670 +/- 465 - Kd = 877 +/- 125 +/- 125 vs 833 +/- 104 nM; PGD2 bs: bs/plt = 228 +/- 14 vs 234 +/- 24 - Kd = 68 +/- 10 vs 73 +/- 7 nM; p greater than 0.4 for all the differences). No significant binding modification was also observed when heparin was preincubated with 3H-PGI2 and 3H-PGD2. The present demonstration that heparin does not interfere with PGI2 and PGD2 binding to platelets is consistent with the hypothesis that heparin reduces the antiaggregating effects of PGI2 and PGD2 by directly potentiating platelet aggregation.

Adenosine Diphosphate↗
PubMed1985

Decreased number of PGD2 binding sites on platelets from patients with type IIa hyperlipoproteinemia.

Platelets from patients with familial hypercholesterolemia (type IIa hyperlipoproteinemia), a condition associated with a high prevalence of atherosclerosis and its ischemic complications, are claimed to be hyperresponsive to aggregating stimuli. We investigated the platelet responsiveness to and the binding of PGD2, a potent endogenous inhibitor of platelet aggregation via stimulation of adenylate cyclase, in a group of 7 patients affected by IIa hyperlipoproteinemia (IIa HLP) and in a control group of 10 healthy subjects. Inhibition by PGD2 of ADP-induced platelet aggregation was significantly lower in IIa HLP patients than in controls. The number of binding sites for PGD2 of platelets from IIa HLP patients was significantly reduced in comparison with that from controls (93 +/- 19 and 232 +/- 23 receptors/platelet, respectively), whereas the affinity for PGD2 was comparable to that of controls (Kd = 68.8 +/- 19.8 nM in patients and 66.1 +/- 15.9 nM in controls). The reduced number of platelet PGD2 binding sites in IIa HLP patients may account for the impaired sensitivity to PGD2 shown in vitro by platelets and may contribute to the increased tendency to thrombotic manifestations observed in IIa HLP.

Adolescent↗
PubMed1985

Age related changes of platelet prostacyclin receptors in humans.

Platelet receptors for PGI2 were investigated in eighteen healthy volunteers divided in two classes of age: nine were 18-40 years old and nine were 41-65 years old. PGI2 platelet receptors were found to decrease significantly with age; the young subjects had 106 +/- 16 (mean +/- SD) high affinity receptors/platelet and 3509 +/- 529 low affinity receptors/platelet whereas the old subjects had 86 +/- 14 high affinity receptors/platelet (P less than 0.02) and 2471 +/- 640 low affinity receptors/platelet (P less than 0.005). The cumulated data from all the subjects yielded a significant negative correlation with age (r = -0.71, P less than 0.001 for the high affinity class and r = -0.65, P less than 0.01 for the low affinity class). The affinity of receptor sites for the ligand did not statistically change with aging (P less than 0.30 and P less than 0.90 respectively for high and low affinity receptors).

Adolescent↗
PubMed1984

Reduction in prostacyclin platelet receptors in active spontaneous angina.

The number and affinity of binding sites for tritiated prostacyclin (PGI2) in platelets were investigated in twenty-eight patients with spontaneous angina (fourteen in the active and fourteen in the inactive phase) and in nine healthy controls of similar age. Active-phase patients had significantly lower numbers of both classes of platelet PGI2 receptors (high affinity and low affinity) than controls or inactive-phase patients. In contrast, the affinity for PGI2 was not significantly different in the three groups. In six active-phase patients restudied in the inactive phase the previously low number of PGI2 receptors had returned to normal. These results suggest that the instability of angina is associated with functional changes not confined to the coronary vasculature.

Angina Pectoris↗