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Biomedical subjects

A Barsotti

Publications and source records attributed to A Barsotti.

At least 19 recordsLinked to original sources
PubMed1999

Usefulness of a tilt training program for the prevention of refractory neurocardiogenic syncope in adolescents: A controlled study.

BACKGROUND: Recurrent syncope represents a debilitating disorder and quality of life deteriorates as a function of recurrence of symptoms. Although the administration of beta-blockers, vasoconstrictors, fludrocortisone, and serotonin reuptake inhibitors may be helpful in preventing episodes, many patients are intolerant of or respond poorly to these agents. Orthostatic training has been reported to be effective in preventing refractory syncope. Thus, to determine whether a tilt training program could prevent symptoms in adolescents, the following controlled study was undertaken. METHODS AND RESULTS: Forty-seven consecutive adolescents (18 male and 29 female, mean age 16.0+/-2.2 years) with recurrent syncope and positive head-up tilt test refractory to previous traditional therapies were distributed between 2 groups, depending on their consent (24 patients) or refusal (controls, 23 patients) to enter the program. Orthostatic training was started, in the presence of a family member, with a series of 5 in-hospital sessions. The 24 patients and their relatives were then instructed to perform the tilt training at home by standing against a wall twice a day for a planned duration of up to 40 minutes, depending on the in-hospital orthostatic tolerance. Head-up tilt response was reevaluated after 1 month, and the clinical effect was noted over a mean follow-up of 18. 2+/-5.3 months (range 15 to 23); 26.1% of patients in the control group and 95.8% of patients in the training group became tilt-negative (P<0.0001). Spontaneous syncope was observed in 56.5% versus 0% in the control and training group, respectively (P<0.0001). CONCLUSIONS: Orthostatic training was found to significantly improve symptoms of adolescents with neurocardiogenic syncope unresponsive to or intolerant of traditional medications. Twice-a-day training sessions of 40 minutes were well accepted by patients.

Adolescent↗
PubMed1999

Effects of paroxetine hydrochloride, a selective serotonin reuptake inhibitor, on refractory vasovagal syncope: a randomized, double-blind, placebo-controlled study.

OBJECTIVES: The purpose of the study was to determine whether the well tolerated serotonin reuptake inhibitor paroxetine hydrochloride could prevent vasovagal syncope in patients resistant to or intolerant of previous traditional therapies. BACKGROUND: Serotonergic mechanisms play a major role in the processes leading to neurocardiogenic vasovagal syncope, and serotonin reuptake inhibitors have been reported to be effective in preventing refractory syncope. METHODS: Sixty-eight consecutive patients (26 men and 42 women, mean age 44.7+/-16.5 years) with recurrent syncope and positive head-up tilt test and in whom standard therapies with beta-adrenergic blocking agents, vagolytic, negative inotropic or mineral corticoid agents were ineffectual or poorly tolerated were referred for study. Patients randomly received either paroxetine at 20 mg once a day or a placebo. A head-up tilt test was then reperformed after one month of treatment, and the clinical effect was noted over a mean follow-up of 25.4+/-7.9 months. RESULTS: The response rates (negative tilt test) after one month of treatment were 61.8% versus 38.2% (p < 0.001) in the paroxetine and placebo groups, respectively. During follow-up spontaneous syncope was reported in six patients (17.6%) in the paroxetine group as compared to 18 patients (52.9%) in the placebo group (p < 0.0001). Only one patient (2.9%) asked to be discontinued from the drug for severe side effects. CONCLUSIONS: Paroxetine was found to significantly improve the symptoms of patients with vasovagal syncope unresponsive to or intolerant of traditional medications and was well tolerated by patients.

Acute Disease↗
PubMed1999

Surgical treatment of dilated cardiomyopathy with conventional techniques.

OBJECTIVE: We review our surgical experience using different conventional surgical techniques in the surgical treatment of the dilated cardiomyopathy (DCMP) in non-transplant eligible patients. METHODS: In this series we included patients who fit the following criteria: ejection fraction < 35%; end diastolic volume > or = 110 ml/m2; enlargement of the base of the heart (maximal mitral diameter > or = 22 mm/m2) with functional mitral regurgitation; mitral surgery to be performed in every case. Moreover, two groups were considered. (A) Normal or moderately impaired right ventricular function; PAP < 45 mmHg; elective or semielective surgery. (B) Severely impaired right ventricular function; PAP > or = 45 mmHg; severe organ failure; dependency on IABP and/or inotropes; need of ICU stay. From January 1990 to September 1998, 66 patients underwent isolated mitral valve surgery (n = 30); in the remaining 36 the Batista operation (n = 21) or exclusion of akinetic areas (n = 15) were associated. The etiology was ischemic in 42, idiopathic in 23 and post-valvular in one. RESULTS: When isolated mitral valve surgery was performed, early mortality in group A (n = 22) was 0, in group B (n = 8) 50%. Overall 5-year survival was 70.0 +/- 8.4. in group A 81.8 +/- 8.2, and in group B 37.5 +/- 17.1. When the Batista operation was performed, early mortality in group A (n = 13) was 23.1%, in group B (n = 8) 75%. Overall 2-year survival was 42.9 +/- 10.8 in group A 61.5 +/- 13.5 and in group B 25.0 +/- 15.3. When akinetic areas were excluded, early mortality in group A (n = 11) was 18.2% and in group B (n = 4) 100%. Overall 1-year survival was 53.3 +/- 12.9, in group A 72.7 +/- 13.4. CONCLUSION: Group A patients have better results in every cohort of patients considered. Even if patients selection seems to be the most important variable for early mortality and late survival, isolated mitral valve surgery, when feasible, provides the best early and late results.

Adult↗
PubMed1999

Shock waves (SW) noninvasive extracorporeal thrombolysis treatment (NISWT).

A group of 24 patients were considered for noninvasive shock waves thrombolysis (NISWT). Of these, 15 patients gave their informed consent. NISWT was attempted in eight patients (while seven patients were randomized for follow-up only). NISWT was possible in six of seven patients. In one patient randomized for NISWT, local inguinal scarring, due to previous surgery, made impossible the visualization of the femoral vein, and therefore focusing of shock waves (SWs). No side effects were reported in the days after SWs administration during the 4-month follow-up. In patients treated with NISWT it was possible to observe just after the SWs session the presence of echolucent "acoustic holes" and flow (by color and power Doppler) within the "holes." All "echolucent holes" produced at the first session were still present at 4 months, and color flow imaging also detected new flow channels in echogenic areas of thrombi previously not visible. In one patient thrombolysis was achieved after the first treatment, but at 3 and 4 months the thrombus was completely avascular. In conclusion, thrombolysis using SWs was obtained in selected cases and it was still persisting at 4 months in six of the seven treated patients. NISWT appears feasible and promising. These results should be confirmed by larger, prospective trials.

Adult↗
PubMed1999

Comparison of low-molecular-weight heparin, administered primarily at home, with unfractionated heparin, administered in hospital, and subcutaneous heparin, administered at home for deep-vein thrombosis.

In this study, 294 patients with acute proximal DVT (deep venous thrombosis) were randomly assigned to receive intravenous standard heparin in the hospital (98 patients) or low-molecular-weight heparin (LMWH) (nadroparin 0.1 mL [equivalent to 100 AXa IU] per kg of body weight subcutaneously twice daily) administered primarily at home (outpatients) or alternatively in hospital (97 patients) or subcutaneous calcium heparin (SCHep) (99 patients, 0.5 mL bid) administered directly at home. The study design allowed outpatients taking LMWH heparin to go home immediately and hospitalized patients taking LMWH to be discharged early. Patients treated with standard heparin or LMWH received the oral anticoagulant starting on the second day, and heparin was discontinued when the therapeutic range (INR 2-3) had been reached. Anticoagulant treatment was maintained for 3 months. Patients treated with SCHep were injected twice daily for 3 months without oral anticoagulants. Patients were evaluated for inclusion and follow-up with color duplex scanning. Venography was not used. In case of suspected pulmonary embolism (PE) a ventilatory-perfusional lung scan was performed. Endpoints of the study were recurrent or extension of DVT, bleeding, the number of days spent in hospital, and costs of treatments. Of the 325 patients included, 294 completed the study. Dropouts totaled 31 (10.5%); six of the 325 included patients (1.8%) died from the related, neoplastic illness. Recurrence or extension of DVT was observed in 6.1% of patients in the LMWH group, in 6.2% in the standard heparin group, and in 7.1% in the SCHep group. Most recurrences (11/17) were in the first month in all groups. Bleedings were all minor, mostly during hospital stay. Hospital stay in patients treated with LMWH was 1.2+/-1.4 days in comparison with 5.4+/-1.2 in those treated with standard heparin. There was no hospital stay in the SCHep group. Average treatment costs in 3 months in the standard heparin group (US $2,760) were considered to be 100%; in comparison costs in the LMWH group was 28% of the standard heparin and 8% in the SCHep group. This study indicated that LMWH and SCHep can be used safely and effectively to treat patients with proximal DVT at home at a lower cost.

Ambulatory Care↗
PubMed1999

[Simvastatin and ischemia-reperfusion damage: its effects on apoptotic myocyte death and on the endothelial expression of nitric-oxide synthetase in an experimental model of the isolated rat heart].

Recent studies have suggested that simvastatin may exert endothelial-protective and anti-ischemic effects via nitric oxide (NO) mechanisms. The aim of this study was to evaluate, in isolated working rat hearts, the effect of acute simvastatin administration on endothelial and inducible NO-synthase (eNOS and iNOS) mRNA and on myocytic apoptosis after ischemia-reperfusion. We used isolated working rat hearts submitted to 15 min global, no-flow, normothermic ischemia and 180 min reperfusion. To detect myocytic apoptosis we used DNA agarose gel electrophoresis and Tunel technique; eNOS and iNOS expression were evaluated by multiplex reverse transcriptase-polymerase chain reaction; glyceraldehyde-3-phosphate dehydrogenase (G3PDH) was used as standard. The eNOS and iNOS mRNAs were expressed as G3PDH/eNOS and G3PDH/iNOS densitometric ratio (BioRad Gel Doc 1000). Hearts were divided into four groups: A) hearts excised and used as histological controls; B) untreated hearts submitted to ischemia and reperfusion; C) actinomicin D-treated (1.5 mg/kg) hearts, perfused with 25 microM simvastatin, subjected to ischemia and reperfusion; D) hearts treated with simvastatin 25 microM and submitted to ischemia and reperfusion. In Group B we evidenced a significant myocytic apoptotic damage, reduced in groups C and D. In Group B an increase in G3PDH/eNOS ratio vs Group A was detected; in Group D a reduction in G3PDH/eNOS ratio vs Group B occurred; no significant changes were observed between groups C and D. As for G3PDH/iNOS ratio, it was significantly increased in Group D with respect to groups A and B. Our data suggest that simvastatin in acute may modulate NO-synthase mRNA expression (induction of eNOS mRNA by means of post-transcriptional mechanisms and inhibition of iNOS postischemic overexpression) and reduce myocytic apoptosis.

Acute Disease↗
PubMed1999

[Single coronary artery with a right origin: angiography identification of the R-II subgroup].

This case report illustrates the clinical and angiographic findings of 2 patients undergoing coronary angiography for ischemic heart disease and with the unexpected presence of anomalous origin of the left coronary artery from the right aortic sinus. The angiographic classification of the different subgroups of single coronary artery is reviewed and the 2 cases are identified as type R-II with septal and anterior course of the left main stem.

Aged↗
PubMed1999

A simple test to monitor oxidative stress.

BACKGROUND: The role of oxygen free radicals is considered important in the development of cardiovascular disease. However, until recently determination of free radicals plasma levels and the effect of antioxidant therapy on these levels has been difficult. The aim of the study was to determine the oxidative stress and the effect of the antioxidant compound AR(D) Stenovit on this stress in normal subjects and patients with intermittent claudication after oral administration for one week. METHODS: A portable, free radicals (FRs) determination system (D-Roms test, Diacron, Grosseto, Italy) was used. This test is based on the ability of transition metals to catalyse in the presence of peroxides with formation of FRs which are trapped by an alchilamine. The alchilamine reacts forming a coloured radical detectable at 505 nm. The reagents utilised are the cromogen (R1, an alchilamine) and a pH 4.8 buffer (R2). Ten microl of hemolysis-free serum are to 1 ml of R2 and to 10 microl of R1. The sample is mixed, incubated (1 min; 37 degrees C) and read for optical density. After another minute, the sample is read again. The average delta A/min is multiplied by a K factor and calculated using serum with defined value. RESULTS: In normal subjects the mean (+/-SD) levels of free radicals were 312+/-49 U.CARR (Carratelli units) before treatment and 218+/-33 U.CARR after treatment (p<0.05). A decrease of at least 10% was detected in every subject. In patients with peripheral vascular disease the mean (+/-SD) levels of free radicals were 404+/-42 U.CARR before treatment and 278+/-33 U.CARR after treatment (p<0.02). A decrease of at least 15% was detected in every patient (medium value 31%). CONCLUSIONS: The D-Roms test provides a simple, inexpensive and practical method to identify subjects with a high level of oxidative stress and to demonstrate the effect of treatment. The compound AR(D) Stenovit is effective in reducing circulating free radicals. Its action on the progression of atherosclerotic disease should be assessed in future studies.

Adult↗
PubMed1999

[The effects of verapamil on the postischemic changes in the coronary microcirculation: the role of nitric oxide].

BACKGROUND: The aim of this study was to evaluate, in the model of isolated working rat heart, the effects of verapamil on postischemic changes in cardiac mechanical function and microvascular coronary permeability, and the possible role of nitric oxide. METHODS: We used 72 male Wistar rats, weighing 250-300 g, divided into six groups: Group A, hearts perfused with modified Krebs-Henseleit solution (KH); Group B, hearts perfused with KH + verapamil 0.25 microM; Group C, hearts perfused with KH + verapamil 0.5 microM; Group D, hearts perfused with KH + verapamil 1 microM; Group E, hearts perfused with KH + NG-nitro-L-arginine methyl ester (L-NAME) 30 microM; Group F, hearts perfused with KH + verapamil 0.25 microM + L-NAME 30 microM. Hemodynamic parameters, necrosis enzyme release and fluoroscein isothiocyanate-albumin extravasation were evaluated. RESULTS: We observed a clear preservation of cardiac mechanical function and microvascular function in Group B (low dose verapamil) compared to groups A (control), C and D (high dose verapamil); the inhibition of nitric oxide-synthase in the presence of verapamil, obtained in Group F, elicited a loss of myocardial protective effects of verapamil. CONCLUSIONS: Our data suggest that low dose verapamil is effective on postischemic damage reduction and most probably nitric oxide plays a determinant role in this effect.

Animals↗
PubMed1998

Shock waves in vascular diseases: an in-vitro study.

UNLABELLED: Three human aortic specimens were used for this in-vitro study on the effects of shock waves on the arterial wall. Specimen one was from a normal (for age) healthy aorta. The full abdominal length was used (including mesenteric and renal arteries and the aortoiliac bifurcation), divided into six pieces (3 cm). The pieces were placed and fixed into degassed water. Shock waves (SW) were focused onto the aortic wall by means of a B-mode ultrasound imager. An SW generator (Minilith SL1, Storz Medical AG, Kreuzlingen, Switzerland) was used for setting of energy flux density between 0.03 and 0.5 mJ/mm2. The six aortic pieces (excluding piece 1, placed in water and left untreated as control) were treated with SW at increasing energy levels. A second aortic specimen of a man with arteriosclerotic plaques was also used and the experiment repeated at energy levels 1, 5, and 8. Another specimen of normal thoracic aorta was exposed at energy levels 1 and 8 only. Energy levels delivered onto the aortic walls were selected from theoretically destructive levels to minimal levels known not to alter vascular tissues. High-resolution ultrasounds of the aortic segments were performed with a 10 MHz high-resolution, broad-band (ATL 3000, USA) probe in water before and after SW application to detect structural changes in the wall after SW. Histology was performed with a standard hematoxylin-eosin staining. RESULTS: The aortic pieces did not show macroscopic damages at visual examination, and at the ultrasound examination no visible changes were observed even at higher levels of SW energy. Also no effects were seen by histology. In conclusion, no damaging effects were observed, visually, by ultrasound, or by histology. At these energy levels SW appear to be safe and do not produce any damage to the aortic wall. Therefore, SW could be considered a safe, nondamaging procedure for potential treatment (ie, thrombolysis) in which vessel walls could be involved. Theoretically it is possible that functional changes could be observed in vivo including cell permeability modifications and other alterations (including changes in the potential of the cells in SW fields to modify themselves and to divide). At the energy levels described in this study SW could, theoretically be, safely used for vascular applications (ie, treating venous and arterial thrombi or in arterial plaques modification) without altering major, structural, arterial wall characteristics. Lesions or alterations that have a different density from the normal wall (thrombi or plaques) could be differently sensitive to the same dosage of SW. These differences in acoustic impedance characteristics could be used for potential treatments with SW without damaging the arterial wall.

Aorta↗
PubMed1998

Treatment of severe intermittent claudication with PGE1--a short-term vs a long-term infusion plan--a 20 week, European randomized trial--analysis of efficacy and costs.

The efficacy, safety, and cost of prostaglandin E1 (PGE1) in the treatment of severe intermittent claudication was studied by comparing a long-term treatment protocol (LTP) with a short-term treatment protocol (STP) in a randomized 20-week study. The study included 109 patients (96 completed the study) with an average total walking distance of 65.5 +/- 8 m (range 20-109). Phase 1 was a 2-week run-in phase (no treatment) for both protocols. In LTP, phase 2 was the main treatment phase. In the LTP, treatment was performed with 2-hour infusions (60 microg PGE1, 5 days each week for 4 weeks). In phase 3 (4-week interval period) PGE1 was administered twice a week (same dosage). In phase 4 (monitoring lasting 3 months, from week 9 to 20) no drugs were used. In STP, phase 2 treatment was performed in 2 days by a 2-hour infusion (1st day: morning 20 microg, afternoon 40 microg; 2nd day morning and afternoon 60 microg). The reduced dosage was used only at the first cycle (week 0) to evaluate reduced tolerability or side effects. Full dosage (60 microg b.i.d.) was used for all other cycles. The same cycle was repeated at the beginning of weeks 4, 8, and 12. The observation period was between weeks 12 and 20. A treadmill test was performed at inclusion, at the beginning of each phase, and at the end of the 20th week. A similar progressive physical training plan (based on walking) and a reduction in risk factors levels plan was used in both groups. Intention-to-treat analysis indicated an increase in walking distance, which improved at 4 weeks (101.5% in STP vs 78.3% in LTP), at 8 weeks (260.9% STP vs 107.3% LTP), and at 20 weeks (351% STP vs 242% LTP). Comparable increases in pain-free walking distance were observed in the two groups. No serious drug-related side effects were observed. Local, mild adverse reactions were seen in 7% of the treated subjects in the LTP and 5% in the STP. Average cost of LTP was approximately 6,588 ECU; for STP the average cost was approximately 1,881 ECU. The cost to achieve an improvement in walking distance of 1 m was 35.6 ECU with the LTP and 9.45 ECU with the STP (26% of the LTP cost; p<0.02). For an average 100% increase in walking distance the LTP cost was 1,937 ECU vs 550 ECU with STP (p<0.02). The cost of PGE1 (including infusion and operative costs) was 25% of the total cost for LTP (24.9% for STP). In summary, between-group-analysis favors STP, in terms of walking distance and costs. Results indicate good efficacy and tolerability of PGE1 treatment. With STP less time is spent in infusion and more can be spent in the exercise program. STP reduces costs, speeds up rehabilitation, and may be used in a larger number of nonspecialized units available to follow the protocol.

Alprostadil↗
PubMed1998

[Nonobstructive cor triatriatum].

Our experience refers to a 50-years-old man with isolated nonobstructive cor triatriatum sinistrum. He was evaluated casually for essential hypertension.

Cor Triatriatum↗
PubMed1998

[Effect of A1 adenosine receptor blockade on postischemic damage to the coronary microcirculation].

Recent studies suggest that A1 adenosine receptor antagonists may prevent reperfusion injury in the lung and heart. The pathophysiology of this protective effect is unclear; a possible inhibition of superoxide anion release from neutrophils, or leukocyte activation and platelet aggregation are reported. We tested the hypothesis of a blood-independent cardioprotection following A1 adenosine receptor antagonism with 1,3 dipropyl,8-cyclopentylxanthine (DPCPX). Isolated working rat hearts were submitted to 10 and 20 min global ischemia in order to assess functional alterations, necrosis enzyme and purine release in coronary effluent, arrhythmias, heart weight, ultrastructural morphometry and microvascular permeability by FITC-albumin diffusion technique. DPCPX (100 nM) was administered to the perfusion buffer before ischemia. In untreated hearts we detected a significant impairment of function, associated with a significant enzyme and purine release, myocardial edema and ultrastructural damage. In DPCPX-treated hearts functional and histological damage was significantly reduced compared to controls. Moreover, a significant reduction in postischemic endothelial permeability (FITC-albumin diffusion, p < 0.02) and ultrastructural damage was observed. Our data suggest that A1 adenosine receptor antagonism with DPCPX significantly reduces ischemia-reperfusion damage in isolated, crystalloid perfused rat heart by a direct reduction of endothelium damage, fluid diffusion within the interstitium and improvement of coronary microcirculation.

Adenosine↗