Biomedical subjects
Publications and source records attributed to M Ciavatti.
Constrictive pericarditis is an infrequent complication of cardiac surgery. We report the case of a young woman who developed dyspnea and ascites 3 years after surgical closure of an atrial septal defect, and the findings at chest X-ray, computed tomographic scan and Doppler echocardiography are described. Epidemiology of the disease, new pathophysiologic concepts, diagnostic features, and therapeutic targets are reviewed.
OBJECTIVES: We sought to determine the relative prognostic power of several clinical and dobutamine stress test variables in patients after a first uncomplicated acute myocardial infarction (AMI). BACKGROUND: The value of dobutamine echocardiography (DE) for determining prognosis after AMI is not yet defined. In particular, the influence of dobutamine stress test response on the outcome of these patients is unknown. METHODS: A graded predischarge DE (from 5 to 40 microg/kg/min, plus atropine if needed) was performed in 245 patients (mean age 60 +/- 10 years) with a first uncomplicated AMI. RESULTS: At follow-up (17 +/- 13 months), an adverse outcome occurred in 40 patients: cardiac death in 7, nonfatal myocardial infarction in 9 (hard events = 16) and unstable angina requiring hospital readmission in 24. Significant predictors of adverse outcome by univariate analysis were positive DE, ischemic wall motion score index (WMSI), angina during DE and diabetes for all events, and positive DE, ischemic WMSI and age for hard events. At multivariate analysis, the only independent predictors of adverse outcome were positive DE, diabetes and angina during DE for all events, and positive DE and age for hard events. The presence of both age >60 years and a history of diabetes identified patients at high risk of cardiac events (event rate 37%), compared with patients <60 years and no diabetes (event rate 11%). In patients with intermediate risk (only one clinical risk factor, event rate 18%), DE added prognostic information (event rate 10% in the negatives, 25% in the positives and 35% in the positives with angina). CONCLUSIONS: After uncomplicated AMI, dobutamine stress test variables offer additional prognostic information to clinical data.
Twenty-nine obese female Zucker rats (fa/fa) were fed with a laboratory chow supplemented or not with a selenium-rich yeast (Selenion), or Selenion + vitamin E, or vitamin E alone. Twelve lean female Zucker rats (Fa/Fa) of the same littermates fed with the same diet were used as control. After 32 wk of diet, obesity induced a large increase in plasma insulin and lipid levels. A significant decrease in the plasma vitamin E/triglycerides ratio (p<0.005) and an increase in plasma thiobarbituric reactive substances (TBARS) (p<0.005) were also observed. Plasma selenium and vitamin E increased in all supplemented rats. The plasma insulin level was decreased by selenion supplementation and the vitamin E/triglycerides ratio was completely corrected by double supplementation with Selenion + vitamin E. TBARS were also efficiently decreased in two obese groups receiving vitamin E. In plasma, adipose tissue and aorta, obesity induced an increase in palmitic acid (C16:0), a very large increase in monounsaturated fatty acids (palmitoleic acid C16:1, stearic acid C18:1) associated with a decrease in polyunsaturated n-6 fatty acids (linoleic acid C18:2 n-6, arachidonic C20:4 n-6). These alterations in fatty acid distribution were only partly modulated by Se and vitamin E supplements. However, in the aorta, antioxidant treatment in obese rats significantly reduced the increase in C16:0 and C16:1 (p<0.05 and p<0.01, respectively) and the decrease in arachidonic acid (p<0.05). These changes could be beneficial in the reduction of insulin resistance and help to protect the vascular endothelium.
The protective role of selenium (Se), given as a Se-rich yeast, selenomethionine or selenomethionine + vitamin E supplement, toward changes in lipid, peroxide, and fatty acid distribution in tissues of streptozotocin-induced diabetic rats, was investigated, after 24 wk of disease. Diabetes increased liver thiobarbituric acid-reactive substances and conjugated dienes; Se supplement completely corrected these changes. In kidney, as in heart, the peroxide levels were not significantly changed by diabetes. In diabetic rat liver, a significant drop in triglycerides and phospholipids (P < 0.05) was observed; this was modulated by Se + vitamin E supplementation. Se + vitamin E supplementation also inhibited the decrease in 18:2n-6 and the increase in 22:6n-3 observed in liver of diabetic rats, changes which reflect altered glycemic control. In kidney, heart, and aorta, diabetes produced some changes in lipid content and fatty acid distribution, especially an increase in heart triglycerides which was also corrected by the Se supplement. Se supplementation to diabetic rats also increased 18:0 ether-linked alcohol, 20:4 n-6, and 22:5 n-3 in cardiac lipids. In aorta, Se + vitamin E significantly increased 20:5 n-3. These polyunsaturated fatty acids are precursors, in situ, of prostaglandin I2 (PGI2) and PGI3 which may protect against cardiovascular dysfunction. In kidney, conversely, Se decreased 20:4 n-6, the precursor of thromboxane A2 implicated in diabetic glomerular injury. Thus Se, and more efficiently Se + Vitamin E supplementation, in experimental diabetes could play a role in controlling oxidative status and altered lipid metabolism in liver, thereby maintaining favorable fatty acid distribution in the major tissues affected by diabetic complications.
OBJECTIVES: This study sought to assess the relative prognostic power of dobutamine echocardiography and exercise electrocardiography after acute myocardial infarction. BACKGROUND: The prognostic value of dobutamine echocardiography early after acute myocardial infarction has not yet been reported. METHODS: One hundred seventy-eight patients (mean age 58 +/- 9 years) with a first uncomplicated acute myocardial infarction underwent predischarge dobutamine echocardiography (5 to 40 micrograms/kg body weight per min, plus atropine if needed) and symptom-limited bicycle exercise electrocardiography and were followed up for 17 +/- 13 months. Stress-induced dyssynergy and ST segment depression > 1 mm were considered criteria of positivity for dobutamine echocardiography and exercise electrocardiography, respectively. RESULTS: Dobutamine echocardiography was positive in 83 patients and exercise electrocardiography in 60. At follow-up there were 5 deaths, 6 nonfatal myocardial infarctions (11 hard events) and 20 cases of unstable angina. Dobutamine echocardiography and exercise electrocardiography had similar negative predictive values both for all events (88% and 86%, respectively) and for hard events (98% and 95%, respectively). The hard events rate was significantly higher in patients with positive rather than negative dobutamine echocardiography (relative risk [RR] 5.15, 95% confidence interval [CI] 1.14 to 23.16), although there was no difference between patients with positive and negative exercise electrocardiograms. When Cox analysis was performed, dobutamine echocardiography had an independent prognostic value both for all events (RR 2.88, 95% CI 1.37 to 6.08) and for hard events (RR 6.56, 95% CI 1.42 to 30.46). CONCLUSIONS: After uncomplicated acute myocardial infarction, dobutamine echocardiography and exercise electrocardiography have a similar high negative predictive value for both all events and hard events only. Positive dobutamine echocardiography, but not positive exercise electrocardiography, identifies a group of patients at higher risk of subsequent cardiac events.
OBJECTIVES: The aims of this study were: 1) to assess the relative prognostic value of predischarge dobutamine echocardiography (DE) and exercise electrocardiography (EE) in patients after a first uncomplicated acute myocardial infarction (AMI), and 2) to evaluate the optimal prognostic strategy by using the two tests in different combinations. METHODS: DE (dobutamine infusion 5 to 40 micrograms/kg/min plus atropine 0.25 to 1 mg, if needed) and symptom-limited bicycle EE were performed in 208 patients (mean age 58 +/- 9 years, 90% males), on different days and in random order, 12 +/- 4 days after a first uncomplicated AMI and after pharmacological washout. A stress-induced dyssynergy and ST segment depression > 1 mm were considered criteria of positivity for DE and EE, respectively. Only spontaneous cardiac events were considered: cardiac death, reinfarction (= hard events), and unstable angina requiring hospitalization (= soft events). RESULTS: Thirty-eight events occurred during follow-up (16 +/- 13 months; range: 1-44 months); 5 cardiac deaths, 6 reinfarctions and 27 unstable angina. Patients with a positive DE had a twofold increase in all event rates (26 vs 12%, p < 0.01) and a fourfold increase in the rate of hard events (9 vs 2%, p < 0.05). In contrast, no statistically significant difference was observed in the distribution of the same events between patients with positive and negative EE. Both tests showed similar negative (DE 88%, EE 85%) and positive (DE 26%, EE 24%) predictive values. Among six different strategies (performing either DE or EE only in all patients; EE in all patients; EE in all patients and DE only in those with a positive EE; and DE only in those with a negative EE; EE in all patients and DE only in those with anterior AMI), EE only in patients with inferior or non-Q AMI and DE only in those with anterior AMI), performing DE only in patients with a positive EE gave the highest predictive accuracy-74% (95% confidence intervals 68 to 80) for all events and 77% (95% confidence intervals 71 to 83) for hard events. CONCLUSIONS: In patients with a first uncomplicated AMI, DE is useful in identifying patients at high and low risk of future spontaneous cardiac events. The optimal strategy for prognostication of these patients is to perform EE in all and DE only in the ones with a positive EE.
BACKGROUND: Due to the increased utilization of this test for the evaluation of chest pain and for prognostic stratification in patients with a recent myocardial infarction, the results of 235 consecutive tests have been analyzed to evaluate the incidence and clinical significance of side effects induced by dobutamine. A potential limitation to the clinical utilization of dobutamine stress echocardiography is the higher incidence of side effects comparison with to other non invasive tests for the diagnosis of coronary artery disease reported by some authors. METHODS: Dobutamine/atropine stress echocardiography was performed in 256 patients affected by acute myocardial infarction. Dobutamine was infused starting with the dose of 5 micrograms/kg/min over 3 minutes with incremental steps of 10-20-30-40 micrograms/kg/min over 3 minutes and atropine, in cases of poor chronotropic response, under 2D-echocardiographic and 12-lead electrocardiographic monitoring. RESULTS: The test was interrupted only in 4 cases for atrial fibrillation (2 patients) and symptomatic hypotension. Patients were divided according to the absence (G1) or presence (G2) of cardiac arrhythmias during the test. Patients of G2 differred from patients of G1 only in respect of the maximal dose of dobutamine infused and the incidence of a wall motion abnormality in the basal echocardiogram. CONCLUSIONS: Dobutamine/atropine echo stress test may be considered a safe test for the evaluation of the presence and severity of coronary artery disease in patients with a previous or recent myocardial infarction.
In vitro 30 min of incubation with selenomethionine (Sm) + vitamin E multiplied by about five platelet selenium (Se) decreased significantly platelet thrombin and ADP-induced aggregation decrease. Four groups of streptozotocin-induced diabetic rats were fed with a supplemented purified diet with an Se-rich yeast (Selenion): DSel, Sm: DSm, Sm alpha-tocopherol: DSmE or unsupplemented diet: D. After 24 wk of supplementation, only a decrease in thrombin-induced aggregation in group DSel compared to DSm and DSmE and D was observed. However, after 24 wk of diet compared to 14 wk, in group D and DSm, a significant increase in thrombin-induced aggregation occurred (p < 0.0001), whereas a significant decrease in groups DSel and DSmE (p < 0.0001, p < 0.03) was noted. After 21 wk of diet, in DSmE, platelet adhesion to fibronectin was significantly decreased compared to group D (p < 0.05). These changes in DSmE were associated with a significant decrease in platelet sorbitol (p < 0.02) and a very significant increase in platelet Se (p < 0.0005). Sm associated with vitamin E would appear more efficient to prevent oxidative damage of diabetic platelet membrane and thus to modulate its hyperactivity.
Seventy rats were separated into five groups: one group of 12 was used as a control and received a purified diet, and four groups of streptozotocin-induced diabetic rats, totalling 58, were fed the same diet without or with selenium (Se) supplementation. Of the noncontrol rats, 14 were without supplementation (Group D), 14 were fed a Se-rich yeast diet (i.e., selenion) (Group DSel), 14 received selenomethionine (Group DSm), and 16 received selenomethionine + tocopherol acetate (Group DSmE). Supplementation with Se in all groups was 0.99 micromole/100g of diet and with tocopherol acetate was 0.145 micromole/100 g. All diabetic rats were mildly balanced by insulin. After 24 weeks of diet, plasma glucose tended to decrease in diabetic Se-supplemented groups DSmE > DSm > DSel versus Group D. In DSm and DSmE groups, plasma lipid peroxides also decreased compared with Group D, but this decrease reached significance only for DSmE (P < 0.01 for both TBARS and conjugated dienes). Plasma triglycerides also decreased in DSm and DSmE groups versus Group D (P < 0.01; P < 0.05, respectively). At the same time, Se increased significantly in kidneys of Groups DSel and DSm versus D and more weakly in Group DSmE, but in this case was associated with a large increase of vitamin E. These beneficial effects of selenium supplement and more so of selenium combined with vitamin E were associated with a protection of kidneys in diabetic rats which found expression in a significant correction of renal hyperfiltration (P < 0.05) and in a diminution of the number and severity of glomerular lesions (P < 0.0005).
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Twenty-eight male Sprague Dawley rats were divided into two groups: a control group (C) of 15 animals and a streptozotocin-induced diabetes group mildly balanced by insulin (D) of 13 animals. After 15 weeks, plasma and high-density lipoprotein (HDL) lipids were determined in each group. Apoprotein A-I concentration was evaluated in HDL fractions. The capacity of the HDL fraction to inhibit thrombin and ADP-induced aggregation of normal platelets was determined for each rat, and in an additional experiment the relation dose-effect of HDL was established. The effect of HDL of the two groups on the stabilization of prostacyclin was compared by aggregation bioassay. After 15 weeks, HDL cholesterol (free + esterified). After 15 weeks, HDL cholesterol (free + esterified) tended to increase in group D compared with group C (P < 0.08). By contrast, apoprotein A-I was very significantly decreased in HDL-D compared with HDL-C (P < 0.001). These alterations were accompanied by a significantly decreased capacity of HDL (60 micrograms/ml platelet suspension) to inhibit ADP-induced aggregation (P< 0.0001) in group D compared with group C. Furthermore, HDL-D incubated 45 or 90 min with prostacyclin showed a significantly decreased capacity to stabilize prostacyclin compared with HDL-C (P<0.04; P <0.03, respectively). These alterations in HDL could be involved in thrombosis and atheromatous complications associated with this disease.
The aim of our work was to determine whether fatty acid modifications in smooth muscle cell phospholipids affect cholesterol efflux and desorption. [3H]Cholesterol was used to label cholesterol pools in the whole cell or selectively in the plasma membrane. Cells were incubated for 12 h in order to increase oleate, linoleate, arachidonate, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) in phospholipids. Cholesterol efflux was monitored using native or tetranitromethane modified high-density lipoprotein3 (HDL3). When all cholesterol pools were labeled, the efflux from cells treated with different fatty acids were not different. Plasma membrane cholesterol efflux remained unchanged after oleate, linoleate or arachidonate treatments, but was markedly increased after EPA and DHA enrichment, both with native HDL3 and with tetranitromethane-high-density lipoprotein. These results suggest that the positive effects of n-3 fatty acid consumption on the atherosclerotic process could be linked in part to an increase in plasma membrane cholesterol efflux from vascular smooth muscle cells.
PURPOSE: Patients undergoing major vascular surgery are at relatively high risk of cardiac events, and pharmacological stress echocardiography is increasingly used for peri-operative risk stratification. PATIENTS AND METHODS: One hundred and twenty-one patients undergoing vascular surgery (age 65 +/- 7 years) were studied by dipyridamole echocardiography testing in six different centres. Of the total 136 patients, 15 were subsequently excluded because surgery was either cancelled (n = 8) or postponed pending cardiac revascularization (n = 7) because of the presence of a 'high-risk' stress echo response (identified 'a priori' as a positive dipyridamole echocardiography testing with a dipyridamole-time < 5 min and/or a peak wall motion score index > 2, upon scoring each segment from 1 = normal to 4 = dyskinetic in an 11-segment model). RESULTS: No major complications occurred during dipyridamole echocardiography testing. Technically adequate images were obtained in all patients; however, in one patient only the low dipyridamole dose (56 mg.kg-1 over 4 min) was given to limit side effects. Of the 121 patients undergoing surgery 28 (23%) had a positive test. Peri-operative events occurred in nine patients (8%): two deaths, two myocardial infarctions, five cases of unstable angina. Sensitivity and specificity of dipyridamole echocardiography testing for predicting cardiac events were 78% and 81%, respectively, with a positive predictive value of 25% and a negative predictive value of 98%. Dipyridamole echocardiography testing effectively singled out patients with, from those without, events, but neither clinical parameters, such as Detsky score, nor baseline echo parameters, such as resting wall motion score index or ejection fraction were able to distinguish between such patients. CONCLUSION: In conclusion, dipyridamole echocardiography testing is safe and well tolerated in patients undergoing major vascular surgery, and provides an effective pre-operative screening test for risk stratification of these patients mainly due to the extremely high negative predictive value. Stress echocardiography is a better discriminator than clinical and rest echocardiographic variables.
This study was performed to assess the prevalence of spontaneous improvement of regional left ventricular function in patients after acute myocardial infarction, and to evaluate the role of low-dose dobutamine stress echocardiography for its prediction. In 57 patients with a first acute myocardial infarction (thrombolysis, n = 27; Q-wave, n = 49), regional wall motion was evaluated with 2-dimensional echocardiography at rest, during a low-dose dobutamine stress test performed within 1 week after hospital admission, and at 3-month follow-up. Myocardial viability was considered if there was an improvement of > or = 1 grade in dyssynergic segments from rest to low-dose dobutamine infusion; recovery of regional function was defined as an improvement of > or = 1 grade between rest and follow-up echocardiograms. Wall motion score index decreased from rest to low-dose dobutamine echocardiography (1.46 +/- 0.29 to 1.39 +/- 0.30, p < 0.0001), and this change persisted at follow-up study (1.37 +/- 0.30). No differences were found between patients who did and did not undergo thrombolyis, or between those who had Q-wave and non-Q-wave infarction. At baseline echocardiography, 189 of 627 segments were dyssynergic (85 hypokinetic, 104 akinetic). Viability at low-dose dobutamine stress echocardiography was more frequent in hypokinetic than in akinetic segments (30 of 85 vs 12 of 104, odds ratio 4.18, 95% confidence interval [CI] 1.87 to 9.48).(ABSTRACT TRUNCATED AT 250 WORDS)
In the present study, we investigated the in vitro effects of D-myo-inositol 1,2,6-trisphosphate (PP-56) on platelets from normal and streptozotocin-induced diabetic rats. PP-56 markedly inhibited aggregation, in a dose-related manner, when added in vitro, more efficiently with thrombin- than with ADP-induced aggregation and, after 90 min incubation, more in diabetic than in normal platelets. The PP-56 platelet inhibitory effect seems to be related to its phosphate content. PP-56 blocked the release of malondialdehyde from erythrocytes, but to the same extent in normal and diabetic rats. PP-56, after 20 min incubation, restored the platelet phosphoinositide turnover, which was significantly modified in diabetic rats. This last observation could explain at least part of the specificity of PP-56 for normalizing platelet aggregation in diabetic animals after long-term administration in vivo.
This study was performed to determine whether vitamin E supplementation in streptozotocin-induced diabetic rats treated by insulin could reduce serum oxidation markers (malondialdehyde: MDA, Schiff bases, anti-protein-MDA adduct antibodies) and modulate lipid changes. After 10 weeks, diabetes induced in rats a significant increase in Schiff bases (P < 0.006) and anti-protein-MDA adduct antibodies (P < 0.01). These alterations were accompanied by a significant rise in serum free fatty acids (225%), triglycerides (35%), and phospholipids (30%) and changes in fatty acid distribution in these fractions and in cholesterol esters. Vitamin E supplementation in diabetic rats reduced Schiff bases and anti-protein-MDA adduct antibodies and tended to restore the fatty acid profile close to control rats without decreasing quantitatively serum lipids enhanced by diabetes. Concerning fatty acids, vitamin E chiefly reduced stearic acid (C18:0) in free fatty acids, cholesterol esters, and phospholipids and cancelled the decrease in low molecular triglycerides observed in diabetic rats. Furthermore, vitamin E maintained the ratio of monounsaturated and polyunsaturated fatty acids, particularly with respect to oleic acid (C18:1), dihomo-gamma-linolenic acid (C20:3 n-6), eicosapentaenoic (C20:5 n-3), and docosapentaenoic acid (C22:5 n-3), in serum phospholipids. These changes observed in vitamin E supplemented rats, compared to vitamin E-untreated diabetic rats, could favor prevention of accelerated atherogenesis. Particularly, the decrease of serum peroxides and enhancement in phospholipid fatty acids (C20:3 n-6, C20:5 n-3, and C22:5 n-3) could induce the preferential formation of prostaglandins (PGE1, PGI2, PGI3) which are protective in cardiovascular diseases.
During the atherogenic process in vivo, arterial smooth muscle cells (SMC) undergo changes in their phenotype. In the present study, rat SMC from primary cultures and from subcultures before 10 and after 200 passages, showing contractile-like, synthetic and transformed phenotypes, respectively, were compared in regard to their lipid content and biosynthesis. The rationale for comparing these phenotypes rests in the similar changes in phenotype of SMC that occur in the formation and progression of atherosclerotic lesions. Phenotype changes were shown to be associated with changes in the phospholipid content of SMC. Phospholipid levels increased, but not as significantly as did cholesterol levels when passing from contractile to synthetic and transformed cells (1.23 +/- 0.18, 2.28 +/- 0.26 and 3.25 +/- 0.23 micrograms/10(6) cells, respectively). Cholesterol normalized in respect to cell protein was increased to the same extent. Lipid synthesis as judged by [14C]acetate incorporation was increased 3- to 12-fold in the synthetic and transformed cells, respectively, compared to contractile cells. After thin-layer chromatography, radioactivity was shown to be markedly increased in most of the lipid fractions, but label in the cholesterol fraction of synthetic and transformed cells was increased by 7- and 21-fold, respectively. Thus, SMC in vitro were shown to drastically increase cholesterol biosynthesis associated with phenotype changes. Such changes are known to occur in vivo and might represent a critical step in the deposition of excess cholesterol within foam cells.
Diabetes is known to be associated with an increase in aldose reductase activity, platelet hyperaggregability, lipid peroxidation, and cataract formation. A molecule, D-myo-inositol 1,2,6-trisphosphate (PP-56), derived from phytic acid, could in principle, by supplying myoinositol to tissues and acting as an antioxidant, counteract some of the manifestations of diabetes. Thus, the effects of PP-56 on platelet aggregation, fatty acids, and polyols were investigated in uncontrolled streptozotocin-induced diabetes in rat in relation to cataract and lipid peroxidation. A decrease in the response of platelet aggregation to thrombin and ADP (P less than 0.05, P less than 0.001) and in the level of sorbitol and the ratio sorbitol/myo-inositol (P less than 0.01) in platelets was observed in the rats treated by PP-56 for 7-8 weeks. These beneficial effects were associated with an incidence of cataract reduced by 26 to 44% (P less than 0.05 to P less than 0.001) depending on the duration of treatment. They were also accompanied by a significant lower plasma level of malondialdehyde (P less than 0.05), and, more markedly, of conjugated dienes (P less than 0.001) as well as an increase in platelet lipids of the 20:4(n-6)/20:3(n-6) ratio, an index of delta 5 desaturase activity. PP-56 appears to modulate fatty acid desaturases and aldose reductase in platelets and delay by a few weeks the development of cataract in this acute model of diabetes.