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Biomedical subjects

A Barsotti

Publications and source records attributed to A Barsotti.

At least 19 recordsLinked to original sources
PubMed2001

MR evaluation of coronary stents with navigator echo and breath-hold cine gradient-echo techniques.

The aim of this study was to evaluate coronary artery stents with MR. Thirty-eight patients underwent MR imaging 48.1 +/- 6.6 days (range 38-60 days) after placement of 47 coronary stents of 11 different types, using navigator echo (NE) and cine gradient-echo (GE) techniques. For both sequences the low signal artifact was used to localize the stent, whereas the flow-related high signal before and distal to the stent was considered as a patency sign. Exercise electrocardiographic test (EET) had been performed 1-7 days before MR. No adverse event with possible relation to the MR examination was observed. All the stents were recognized as signal void with GE, and all but one with NE. Of the 2 patients with positive EET, the first one, with a stent on the left anterior descending coronary artery, presented low signal distal to the stent at both MR sequences, suggesting dysfunction [60% stenosis at conventional coronary angiography (CCA)]; the second one, with two sequential stents on the right coronary artery, presented lack of signal distal to the stents at both MR sequences, suggesting occlusion (97% stenosis at CCA). For the 44 remaining stents in 36 patients with negative EET, MR high signal before and distal to the stent suggested patency at both sequences. MR seems to be a safe and promising technique for non-invasive evaluation of coronary stents.

Adult↗
PubMed2001

Simvastatin reduces reperfusion injury by modulating nitric oxide synthase expression: an ex vivo study in isolated working rat hearts.

OBJECTIVE: We tested the hypothesis of beneficial effects of the 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA)-reductase inhibitor simvastatin in a model of ischemia-reperfusion, and investigated potential mechanisms. METHODS: Isolated working rat hearts were subjected to 15 min global ischemia and 22-180 min reperfusion in the presence or absence of simvastatin (10-100 microM). We evaluated creatinephosphokinase and nitrite levels in coronary effluent, heart weight changes, microvascular permeability (extravasation of fluoresceine-labeled albumin), ultrastructural alterations, and the expression of endothelial (e) and inducible (i) nitric oxide synthase (NOS) (by reverse-transcribed polymerase chain reaction and Western blotting) in the presence or absence of the transcriptional inhibitor actinomycin-D. RESULTS: Simvastatin (25 microM) significantly reduced myocardial damage and vascular hyperpermeability, concomitant with a reduction in endothelial and cardiomyocyte lesions. Protection became less evident at 50 microM and reverted to increased damage at 100 microM. At 25 microM, simvastatin significantly increased eNOS mRNA and protein compared with untreated hearts, probably due to a post-transcriptional regulation since unaltered by animal pretreatment with actinomycin D. Simvastatin also significantly decreased iNOS mRNA and protein, as well as nitrite production after ischemia-reperfusion. The addition of the NOS inhibitor N(pi)-nitro-L-arginine methylester (L-NAME, 30 microM) to 25 microM simvastatin-treated hearts significantly reduced cardioprotection against ischemia-reperfusion. CONCLUSIONS: In this model, in the absence of perfusing granulocytes, the acute administration of a pharmacologically relevant simvastatin concentration reduces ischemia-reperfusion injury and prevents coronary endothelial cell and cardiomyocyte damage by cholesterol-independent, NO-dependent mechanisms.

Analysis of Variance↗
PubMed2001

MK-954 (losartan potassium) exerts endothelial protective effects against reperfusion injury: evidence of an e-NOS mRNA overexpression after global ischemia.

BACKGROUND: the cardiac Renin-Angiotensin system (RAS) plays an important role in the regulation of coronary flow and cardiac function and structure in normal and pathological conditions such as ischemia-reperfusion (I/R) injury. The aim of this study was to investigate the effects of the Angiotensin II type 1 (AT-1) receptor antagonist MK-954 (losartan potassium) on postischemic endothelial dysfunction and NOS mRNA expression (inducible nitric oxide synthase, iNOS; endothelial nitric oxide synthase, eNOS) in isolated working rat hearts. METHODS: isolated working rat hearts were subjected to 15 min global ischemia and 180 min reperfusion. MK-954 was added to perfusion buffer (a modified Krebs-Henseleit solution) at 1 microM concentration. We assessed functional parameters, creatin kinase (CK) release, heart weight changes, microvascular postischemic hyperpermeability (FITC-albumin extravasation) and morphological ultrastructural alterations. eNOS and iNOS mRNA levels were also detected by the means of multiplex RT-PCR technique using glyceraldehyde-3-phosphate dehydrogenase (G3PDH) gene as internal control; results were expressed as densitometric ratio. RESULTS: in Losartan-treated hearts we observed a significant reduction of postischemic contractile dysfunction, CK release and myocardial ultrastructural damage; postischemic FITC-albumin extravasation was significantly reduced respect to controls. Moreover, 1 microM Losartan produced a significant reduction of eNOS/G3PDH respect to untreated hearts submitted to I/R. Regarding iNOS/G3PDH ratio, no significant changes were detected in Losartan-treated hearts compared with controls. CONCLUSIONS: our study revealed that Losartan treatment before ischemia, and during reperfusion, is able to reduce the reperfusion injury of the rat heart by reducing mechanical and microcirculatory dysfunction and necrotic cell death, ameliorating cardiac ultrastructure and endothelial protection, probably inducing eNOS over-expression and reducing post-ischemic hyperpermeability of coronary microcirculation.

Angiotensin Receptor Antagonists↗
PubMed2001

Carotid and femoral ultrasound morphology screening and cardiovascular events in low risk subjects: a 10-year follow-up study (the CAFES-CAVE study(1)).

BACKGROUND: Subclinical arteriosclerotic lesions at the carotid and femoral bifurcations may be related to the occurrence of future cardiovascular events and of occult arteriosclerotic coronary disease. B-mode ultrasound of carotid and femoral arteriosclerotic bifurcation lesions may provide a simple screening method to select asymptomatic subjects at risk of future events. METHODS AND RESULTS: 13221 low-risk, healthy, asymptomatic individuals were included in a 10-year, prospective, follow-up based on carotid and femoral bifurcation morphology defined by B-mode ultrasound. Four classes were considered at inclusion (I: normal wall, II: wall thickening, III: non-stenosing plaques, IV: stenosing plaques). When 10000 subjects (75.6% of included subjects; 6055 males, 3945 females) completed the 10-year follow-up the study was concluded. At 10 years there were 10 events (out of 7989 subjects) in class I and 81 events in II (930 subjects; incidence=8.6%); 239 events were observed in class III (611 subjects; 39.28%) and 381 events (470 subjects; 81.06%) in IV; 61 deaths occurred in classes III+IV (1081 subjects) producing a death rate within these two classes of 5.5% (51 out of 61=81.5% in class IV). The increased event rates in classes III and IV were significant (log rank; P<0.02) in comparison with I and II. CONCLUSIONS: Carotid and femoral morphology identified 2011 subjects (20.1% of the population) in classes II,III,IV including 98.6% of cardiovascular events and deaths in the following 10 years. A higher (P<0.05) rate of progression in classes III and IV in comparison with I and II was also observed. The ultrasound carotid and femoral classification was useful in selecting subjects at very low risk of cardiovascular events (class I), those at limited risk (class II) and a group at moderate risk (class III). A subpopulation at high risk of cardiovascular events (IV) was identified.

Adult↗
PubMed2001

Age-dependence of risk factors for carotid stenosis: an observational study among candidates for coronary arteriography.

In order to identify subjects at higher risk for carotid stenosis and to provide insights into mechanisms of disease development at different age-intervals, a color duplex ultrasound of extracranial arteries was performed in 624 consecutive patients (mean age 62.9+/-10.7, 483 males) undergoing coronary angiography. Significant carotid atherosclerosis (> or =50% stenosis) was documented in 87 patients (14%): the disease was moderate (50/69% stenosis) in 51 patients (8%), severe (> or =70% stenosis) in 36 patients (6%). Age (P<0.0001), smoking (P<0.0001), diabetes (P=0.0002), renal dysfunction (P=0.0119) and hypertension (P=0.0202) were independent predictors of significant carotid atherosclerosis; age (P=0.0001), smoking (P=0.0009) and diabetes (P=0.0201) were independent predictors of severe disease. Among 262 candidates for cardiac surgery, significant carotid artery disease was identified in 57 cases (2.63 Relative Risk, 95% Confidence Intervals: 1.32/5.24). Correlation and regression tree analysis demonstrated that diabetes was associated with greater severity of carotid stenosis in younger patients and hypertension in older ones. In conclusion age is the primary determinant of carotid artery disease; diabetes and smoking accelerate progression of atherosclerosis in younger patients, hypertension and smoking in older ones. Among patients undergoing coronary angiography, carotid ultrasonography should be recommended in high risk subgroups of patients.

Age Factors↗
PubMed2001

Maximal endothelial tissue plasminogen activator release is not impaired in patients with acute coronary syndromes before heparin treatment.

Procoagulant and fibrinolytic disturbances are described in patients with acute coronary syndromes (ACS), but whether defective maximal tissue plasminogen activator (t-PA) release from the endothelium is also present is still controversial. Previous studies did not take into consideration the contribution of heparin, which strongly affects fibrinolysis. Accordingly, in this study, we measured maximal t-PA release in patients with ACS before, during, and after heparin treatment. Maximal t-PA release was measured by the venous occlusion test in 38 hospitalized patients with confirmed ACS (18 acute myocardial infarctions and 20 unstable anginas) before starting heparin, during heparin treatment, and 4 and 12 h after discontinuation. Plasma plasminogen activator inhibitor type 1 (PAI-1), D-dimer and prothrombin fragment F1 + 2 were also measured. Eighteen age-matched subjects with no evidence of coronary disease were used as controls. At admission, patients showed significantly higher plasma levels of t-PA, PAI-1, and F1 + 2 than controls. Before heparin, maximal t-PA release was similar in patients and controls. Heparin treatment was associated with a significant increase of plasma t-PA, while it did not affect maximal t-PA release. Coagulative and fibrinolytic disturbances are present in patients with ACS, but these do not include maximal t-PA release. Among our patients, maximal t-PA release appears stable over time and is not affected by heparin treatment.

Aged↗
PubMed2001

Oxygen-free radical decrease in hypertensive patients treated with lercanidipine.

BACKGROUND: The relationship between oxidative stress, lipoproteins, cardiovascular risk factors and vascular disease progression has recently attracted fresh attention due to the possibility of measuring free radicals (FRs). The aim of this study was to evaluate blood plasma variations in oxygen FRs in hypertensive patients treated with lercanidipine, a drug acting on blood pressure and microcirculation. METHODS: Twenty-two patients with moderate hypertension (M:F=12:10; age=52) and no vascular disease (evaluated by high-resolution ultrasound) were treated for 24 weeks with Lercanidipine (10 mg/day or 20 mg/day if BP values did not decrease at least 15 percent after four weeks of treatment). BP was measured at inclusion and after 4, 8, 12 and 24 weeks of treatment. FRs measurements (using the D-Roms test) were made at inclusion, at the 8th, 12th and 24th week. RESULTS: All patients completed the treatment which was well tolerated and without side effects. Systolic and diastolic BP decreased after 8, 12 (p<0.05) and 24 weeks (at 24 weeks systolic pressure was decreased by 21.1 percent, and diastolic by 11.1 percent; p<0.02). FRs levels progressively decreased from 541 Carr Units (SD 54) at inclusion to 411 (SD 56) at eight weeks (p<0.05), to 401 (SD 35) (p<0.05) at 12 weeks and finally to 398 (SD 33), (p<0.02) at 24 weeks of treatment (72.2 percent of the initial value). CONCLUSIONS: The possibility of measuring FRs in vivo with a simple, inexpensive test allows the identification of subjects with a high level of oxidative stress, and the monitoring of the effects of treatments. Lercanidipine, acting on blood pressure, on the microcirculation and decreasing oxidative stress and Frs plasma levels may effectively decrease the rate of progression of cardiovascular diseases offering the advantage of an increased level of protection in patients with high levels of oxidative stress.

Adult↗
PubMed2000

Endothelial NOS expression and ischemia-reperfusion in isolated working rat heart from hypoxic and hyperoxic conditions.

Induction of endothelial nitric oxide synthase (eNOS) contributes to the mechanism of heart protection against ischemia-reperfusion damage. We analyzed the effects of hypoxia and hyperoxia on eNOS expression in isolated working rat hearts after ischemia-reperfusion damage. Adult male Wistar rats were submitted to chronic hypoxia (2 weeks) and hyperoxia (72 h). The hearts were submitted to 15 min of ischemia and reperfused for 60 min, then we evaluated hemodynamic parameters and creatine phosphokinase (CPK) release. eNOS expression was estimated by RT-PCR; enzyme localization was evaluated by immunohistochemistry and the eNOS protein levels were detected by Western blot. All hemodynamic parameters in hypoxic conditions were better with respect to other groups. The CPK release was lower in hypoxic (P<0.01) than in normoxic and hyperoxic conditions. The eNOS deposition was significantly higher in the hypoxic group versus the normoxic or hyperoxic groups. The eNOS protein and mRNA levels were increased by hypoxia versus both other groups. Chronic hypoxic exposure may decrease injury and increase eNOS protein and mRNA levels in heart subjected to ischemia-reperfusion.

Animals↗
PubMed2000

Nomograms used to define the short-term treatment with PGE(1) in patients with intermittent claudication and critical ischemia. The ORACL.E (Occlusion Revascularization in the Atherosclerotic Critical Limb) Study Group. The European Study.

Infusional, cyclic PGE1 treatment is effective in patients with intermittent claudication and critical limb ischemia (CLI). One of the problems related to chronic PGE1 treatment in vascular diseases due to atherosclerosis is to evaluate the variations of clinical conditions due to treatment in order to establish the number of cycles per year or per period (in severe vascular disease reevaluation of patients should be more frequent) needed to achieve clinical improvement. In a preliminary pilot study a group of 150 patients (mean age 67+/-12 years) with intermittent claudication (walking range from 0 to 500 m) and a group of 100 patients with CLI (45% with rest pain, and 55% gangrene; mean age 68 +/-11 years) the number of PGE1 cycles according to the short-term protocol (STP) needed to produce significant clinical improvement was preliminarily evaluated. Considering these preliminary observations, the investigators established a research plan useful to produce nomograms indicating the number of cycles of PGE1-STP per year needed to improve the clinical condition (both in intermittent claudication and CLI). A significant clinical improvement was arbitrarily defined as the increase of at least 35% in walking distance (on treadmill) and/or the disappearance of signs and symptoms of critical ischemia in 6 months of treatment in at least 75% of the treated patients. With consideration of the results obtained with the preliminary nomograms a larger validation of the nomograms is now advisable. A cost-effectiveness analysis is also useful to define the efficacy of treatment on the basis of its costs. The publication of this report in two angiological journals (Angeiologie and Angiology) will open the research on nomograms to all centers willing to collaborate to the study. The data are being collected in the ORACL.E database and will be analyzed within 12 months after the publication of this report.

Aged↗
PubMed2000

PGE(1) treatment of severe intermittent claudication (short-term versus long-term, associated with exercise)--efficacy and costs in a 20-week, randomized trial.

The efficacy, safety, and cost of prostaglandin E1 (PGE1) in the treatment of severe intermittent claudication was studied comparing a long-term treatment protocol (LTP) with a short-term treatment protocol (STP) in a randomized 20-week study. The study included 980 patients (883 completed the study) with an average total walking distance of 85.5 +/-10 m (range 22-119). 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 (first day: morning 20 microg, afternoon 40 microg; second day morning and afternoon 60 microg). The reduced dosage was used only at the first cycle (week 0) to evaluate tolerability or side effects. Full dosage (60 microg bid) 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 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 and at 20 weeks in the STP more than in the LTP group. At 4 weeks the variation (increase) in pain-free walking (PFWD) was 167.8% (of the initial value) in the LTP group and 185% in the STP group (p<0.05). At 4 weeks the variation (increase) in total walking distance (TWD) was 227.6% of the initial value in the LTP group and 289% in the STP group (p<0.05). At 20 weeks the increase in PFWD was 496% of the initial value in the LTP group vs 643% in the STP group (147% difference; p<0.02). The increase in TWD was 368% in the LTP group and 529% in the STP group (161% difference; p<0.02). In both groups there was a significant increase in PFWD and TWD at 4 and 20 weeks, but results obtained with STP are better considering both walking distances. No serious drug-related side effects were observed. Local, mild adverse reactions were seen in 6.3% of the treated subjects in the LTP and 3% in the STP. Average cost of LTP was 6,664 Euro; for STP the average costs was approximately 1,820 E. The cost to achieve an improvement in walking distance of 1 m was 45.8 E with the LTP and 8.5 E with the STP (18% of the LTP cost; p<0.02). For an average 100% increase in walking distance the LTP cost was 1,989 E vs. 421 E with STP (p<0.02). Between-group analysis favors STP considering walking distance and costs. Results indicate good efficacy and tolerability of PGE, treatment. With STP less time is spent in infusion and more in the exercise program. STP reduces costs, speeds rehabilitation, and may be easily used in a larger number of nonspecialized units.

Aged↗
PubMed2000

Coronary aneurysms and stenosis detected with magnetic resonance coronary angiography in a patient with Kawasaki disease.

Coronary artery abnormalities in Kawasaki syndrome develop in about 15-25% of young patients, mostly as aneurysms. In the long-term evolution of coronary artery disease thrombotic occlusion of aneurysms, premature atherosclerosis, and stenosis, are observed. Magnetic resonance is an emerging modality in the angiographic assessment of coronary arteries. The authors report a case of coronary artery aneurysms and stenosis in a 26-year-old patient with Kawasaki disease detected by magnetic resonance coronary angiography and confirmed by conventional coronary angiography.

Adult↗
PubMed2000

[Is a totally non-invasive assessment of the hemodynamic profile possible in patients with chronic heart failure?].

Relevant hemodynamic information can be obtained by a comprehensive Doppler echocardiographic examination in patients with various cardiac diseases. The assessment of left heart hemodynamics by Doppler echocardiography has been addressed by several investigators. The feasibility and the accuracy of methods for the estimation of left ventricular filling pressure and cardiac output have been validated by comparative right heart catheterization. Studies have shown that Doppler echocardiography can allow the measurement of pulmonary artery pressures from the pressure gradients across the tricuspid and pulmonary valves. The possibility of completely characterizing cardiac hemodynamics noninvasively has recently been documented: in patients with acute myocardial infarction, automated cardiac output measurement along with the assessment of left ventricular filling by Doppler echocardiography may be used for the identification of hemodynamic subsets. Although Doppler echocardiography can provide noninvasive measures of hemodynamic indices, its value has been disputed since the technique is patient-dependent, time-consuming and requires meticulous acquisition and interpretation by skilled operators. The use of contrast agents may improve the accessibility of both right-sided and left-sided Doppler signals, potentially increasing the number of patients to whom the noninvasive hemodynamic assessment could be applied.

Chronic Disease↗