[Guidelines for antithrombotic therapy in atrial fibrillation: what the Italian Hemostasis and Thrombosis Society thinks].
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Adult↗
Biomedical subjects
D Prisco
Publications and source records attributed to D Prisco.
[Low-molecular weight heparin: questions asked to the physician].
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Anticoagulants↗
Effect of temperature and incubation time on D-dimer serum levels in healthy subjects.
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Adult↗
Risk factors for cardiovascular disease in renal transplant recipients: new insights.
Long-term survival of renal transplant recipients appears to be influenced by the occurrence of thromboembolic complications and cardiovascular disease. In order to investigate the prevalence of new hemostasis-related risk factors for venous and arterial thrombosis, we investigated 63 renal transplant recipients and 66 age- and sex-matched control subjects. We assayed antiphospholipid antibodies [lupus anticoagulant (LA) and anticardiolipin antibodies (aCL)], lipoprotein (a) [Lp(a)], plasminogen activator inhibitor-1 (PAI-1), and total homocysteine (tHcy) levels. We found a significantly higher prevalence of positivity for LA (P < 0.001); no difference was detected in the prevalence of aCL between patients and controls. PAI-1 levels were significantly higher in renal transplant recipients than in controls [12.3 IU/ml (2-45.5) vs 7.9 IU/ml (4-18.0); P < 0.0001] with an odd ratio (OR) of 11.8 (4.9-28.5) in univariate analysis and of 5.8 (2.1-15.4) in multivariate analysis. Lp(a) levels were higher in patients then in controls [159 mg/l (1-992) vs 100.5 mg/l (10-412); P < 0.005] with an OR of 5.9 (1.9-18.4) in univariate analysis and of 3.5 (0.9-13.4) in multivariate analysis. Fasting levels of tHcy were significantly higher in renal transplant recipients [7.0 micromol/l (4.0-68) vs 8.1 micromol/l (2.0-24.0); P < 0.00001] with an OR of 40.4 (14.7-111) in univariate analysis and of 33.1 (11.1-115.5) in multivariate analysis. After methionine loading test, we documented levels of tHcy above the 90th percentile of controls in 60/63 patients (95%). Finally, we found a significant correlation between tHcy and PAI-1 plasma levels (r = 0.76; P < 0.000001). Our results show a high prevalence of hemostasis-related risk factors for arterial and venous thrombosis in renal transplant recipients, suggesting the need for the investigation of these patients for the presence of these risk factors in order to improve their long-term survival and to tailor therapy.
Autoantibodies↗
Videolaparoscopic cholecystectomy induces a hemostasis activation of lower grade than does open surgery.
BACKGROUND: Tissue injury after trauma and surgery may induce alterations in blood coagulation and fibrinolysis, and the hypercoagulable state observed after surgery can be associated with the risk of postoperative thromboembolic complications. Recently, videolaparoscopic (VLPS) cholecystectomy has been introduced, and its advantages over the open procedure seem related to the reduced surgical trauma. The aim of this study was to investigate hemostatic system alterations in patients who undergo open and VLPS cholecystectomy. METHODS: Fibrinogen, prothrombin fragment F1+2, D-dimer, and plasminogen activator inhibitor type-1 (PAI-1) activity was determined in 10 patients who underwent open (group A) and 10 patients who underwent VLPS cholecystectomy (group B), respectively. Blood samples were obtained the day of surgery in the morning (B1), after anesthesia (A1), 1 hour after the start of surgery (S1), then 30 min (E.05) and 24 h (E.24) after the surgery. RESULTS: No significant differences were observed in baseline values between groups A and B for the parameters investigated. At 24 h after surgery, fibrinogen increased significantly (p < 0.05) in group A and also was significantly higher than in group B (p < 0.05). In group A, a marked increase in F1+2 levels (p < 0.01) was observed in all the samples, with the maximum values on the first day after surgery (3.7 nmol/l; 1.2-6.0 nmol/l), whereas in group B, a slight but significant increase in F1+2 levels (2.1 nmol/l; 1.1-3.9 nmol/l; p < 0.01) was observed only 30 min after the end of surgery. In both groups A and B, D-dimer markedly increased after surgery, without statistical significant differences between the two groups at any time. The PAI-1 activity plasma levels remained in the normal range during and after surgery in both groups. CONCLUSIONS: These results indicate that VLPS surgery induces an activation of the clotting system that, although of low degree and short duration, can lead to a transient prothrombotic state.
Adult↗
Angiotensin converting enzyme DD genotype affects the changes of plasma plasminogen activator inhibitor-1 activity after primary percutaneous transluminal coronary angioplasty in acute myocardial infarction patients.
Angiotensin converting enzyme (ACE) DD genotype, and plasminogen activator inhibitor (PAI-1) 4G/4G genotype have been reported to affect PAI-1 activity in control subjects and atherosclerotic patients, but no data are available on the influence of angiotensin II type 1 receptor (AT1R) A1166C polymorphism on the inhibitor levels. The degree of fibrinolytic activation after percutaneous transluminal coronary angioplasty (PTCA) has been found to affect the risk of restenosis. The aim of this study was to investigate the possible influence of ACE I/D, AT1R A1166C, and PAI-1 4G/5G polymorphisms on the changes of PAI-1 activity after primary successful percutaneous transluminal angioplasty. In 29 consecutive acute myocardial infarction patients, undergoing primary successful angioplasty, genotyping of ACE I/D, AT1R A1166C, and PAI-1 4G/5G polymorphisms was performed by polymerase chain reaction and restriction fragment length polymorphism analysis, and PAI-1 plasma activity (chromogenic method) was assessed before and after angioplasty. Following angioplasty, PAI-1 activity increased in 10 of 29 patients and decreased or remained unchanged in 19 of 29. ACE DD genotype was significantly (P = 0.04) associated with an increase of PAI-1 activity post angioplasty (OR DD/ID+II = 6.5, CI 95% 4.83-8.22). Whereas no effect of PAI-1 4G/5G and AT1R A1166C polymorphisms on PAI-1 response to angioplasty was demonstrated, these data suggest that renin-angiotensin system genes are involved in the regulation of the fibrinolytic response to balloon injury, possibly affecting angiotensin converting enzyme activity. This interaction between the renin-angiotensin system and hemostasis may be a mechanism by which ACE DD genotype affects the risk of restenosis after percutaneous transluminal angioplasty.
Aged↗
Carbon fiber post adhesion to resin luting cement in the restoration of endodontically treated teeth.
Carbon fiber posts (CFP) are widely used in the restoration of endodontically treated teeth to enhance the mechanical behavior in spite of metallic posts and to prevent vertical fractures of the tooth under chewing loads. The post is cemented inside the canal lumen using polymer resins with Young's modulus lower than dentine. In this conditions the stress concentration is located at the post-cement interface and in the cement bulk itself, preserving radicular dentine from dangerous stress accumulation. The mechanical resistance of CFP posts cemented in human dentine was evaluated by the means of mechanical pull-out tests assisted by the finite element analysis. The average bond strength and the critical stress values of the CHP-cement interface were 25 MPa and 50 MPa respectively.
Journal Article↗
High prevalence of mild hyperhomocysteinemia in patients with abdominal aortic aneurysm.
PURPOSE: In vitro studies have recently demonstrated that homocysteine interacts with the aortic wall by inducing both elastolysis and endothelial perturbation. The aim of this study was to evaluate homocysteine plasma levels and their relationships with aortic diameter and endothelial damage in patients with abdominal aortic aneurysm. SUBJECTS AND METHODS: Fifty-eight consecutive male patients (mean age, 69.5 +/- 6.6 years; age range, 49-78 years) who underwent abdominal aortic aneurysm surgery were enrolled in the study. Twenty-two of 58 patients had no clinical or instrumental evidence of atherosclerosis. Sixty control subjects were age matched and sex matched with the patients. In all of the subjects, we evaluated total homocysteine and thrombomodulin plasma levels and the distribution of the C677T methylenetetrahydrofolate reductase gene mutation. RESULTS: Hyperhomocysteinemia was found in 26 (48%) of the 58 patients with abdominal aortic aneurysm, and homocysteine plasma levels were significantly higher in patients than in control subjects (15.7 +/- 6.5 micromol/L vs 9.6 +/- 3.9 micromol/L; P <. 0001). In addition, the subgroup of patients with abdominal aortic aneurysm who did not show evidence of atherosclerosis showed homocysteine plasma levels significantly higher than those in the controls (14.8 +/- 6.1 micromol/L vs 9.6 +/- 3.9 micromol/L; P <. 001). A larger aneurysmal size was detected in hyperhomocysteinemic patients than in those with normal homocysteine plasma levels (5.09 +/- 0.84 cm vs 5.79 +/- 1.5 cm; P <.05). The genotype distribution of the C677T methylenetetrahydrofolate reductase mutation was as follows: TT 21%, TC 55%, and CC 24% in the patients; TT 10%, TC 58%, and CC 32% in the controls. Moreover, in patients a significant correlation (P <.005) between homocysteine plasma level and 677TT methylenetetrahydrofolate reductase genotype was found. Thrombomodulin plasma levels were significantly higher (P <.00005) in patients (median, 30 ng/mL; range, 10-164 ng/mL) than in controls (median, 19 ng/mL; range, 13-44 ng/mL), and thrombomodulin levels were significantly higher (P <.005) in hyperhomocysteinemic patients (median, 39.5 ng/mL; range, 15-164 ng/mL) than in normohomocysteinemic patients (median, 27.5 ng/mL; range, 10-85 ng/mL). In addition, in patients with abdominal aortic aneurysm, a direct significant correlation (P <.005) was found between homocysteine and thrombomodulin. CONCLUSIONS: These data indicate an association between the presence of AAA in patients selected for surgical treatment of AAA and elevated homocysteine plasma levels and suggest that homocysteine may induce endothelial perturbation and stimulation in these patients.
Aged↗
Angiotensin-converting enzyme DD genotype, angiotensin type 1 receptor CC genotype, and hyperhomocysteinemia increase first-trimester fetal-loss susceptibility.
Complications of pregnancy have been found to be related with thrombophilic polymorphisms that explain about 30% of obstetric complications. We evaluated the angiotensin converting enzyme (ACE) and the angiotensin type 1 receptor (AT1R) gene polymorphisms in the renin-angiotensin system (RAS) as possible risk factors for fetal loss. Fifty-nine women with a history of three or more first-trimester fetal losses and 70 healthy women with a history of normal pregnancies were enrolled in this study. Thrombophilic factors, ACE insertion/deletion (I/D) and AT1R A1166C polymorphisms, prothrombin G20210A and factor V Leiden mutations were analyzed. At univariate and multivariate analysis, a significant association between ACE DD and AT1R CC genotype and fetal loss was observed. The effect of the ACE DD genotype on the risk of fetal loss was higher in AT1R C allele carriers. The prevalence of hyperhomocysteinemia (Hcy) (defined as baseline plasma levels higher than the 95% percentile; cut-off, 10.5 micromol/l per l) was significantly higher in women with fetal loss, and an association between Hcy and fetal loss was detected. All patients showed normal antithrombin, protein C, protein S, and plasminogen activator inhibitor-1 (PAI-1) values. The presence of one risk factor not associated with others was found in 33 out of 59 patients (56%); ACE DD genotype was the most prevalent risk factor. Our results identify new possible predictive markers for fetal loss in RAS polymorphisms and Hcy. Large-scale studies are warranted to attribute clinical relevance to these polymorphisms as risk factors for complicated pregnancies.
Adult↗
Tissue factor and homocysteine levels in ischemic heart disease are associated with angiographically documented clinical recurrences after coronary angioplasty.
BACKGROUND: In ischemic heart disease (IHD) patients high plasma levels of Tissue Factor (TF), the trigger of coagulation cascade, are present. Homocysteine (Hcy) is a risk factor for coronary artery disease, and several different pathophysiological mechanisms by which Hcy may play a role in thrombus formation have been postulated in "in vitro" studies. We investigated the "in vivo" role of Hcy in affecting plasma levels of TF, its inhibitor Tissue Factor Pathway Inhibitor (TFPI) and hypercoagulability. METHODS AND RESULTS: We investigated 119 IHD patients who underwent PTCA and compared them with 103 healthy subjects. TF, TFPI, Thrombin-Antithrombin complexes (TAT) and Hcy levels were significantly higher in the patients than in the controls. A positive correlation was found between Hcy and TF (r = 0.54; p < 0.0001), Hcy and TFPI (r = 0.26; p <0.05) as well as Hcy and TAT (r = 0.33; p <0.0001) levels. An inverse correlation existed between folate intake and Hcy levels (r = -0.28; p = 0.001). Hcy levels within the first quartile and in the highest quartile were associated with a lower (p < 0.001) and higher (p <0.0001) rate of clinical recurrences, respectively. Patients with TF values in the first quartile had a lower rate of angiographically documented clinical recurrences as compared to those in the fourth quartile (p <0.01); those in the highest quartile of TF showed a higher rate of recurrences (p = 0.001). Multivariate analysis confirmed these results (first quartile of Hcy: OR 0.02, C1 0.002-0.27; fourth quartile of Hcy: OR 36.5, C1 3.6-365/first quartile of TF: OR 0.006, C1 0.001-0.44; fourth quartile of TF: OR 16.4, C1 3.0 - 90.0), also after adjustment for risk factors and Hcy and TF respectively. CONCLUSIONS: In this study we show that TF, TFPI and TAT levels are correlated with Hcy plasma levels in IHD patients, providing evidence of an "in vivo" pathophysiological mechanism of hyperhomocysteinemia. The observed association between angiographically documented clinical recurrences and TF and Hcy values awaits confirmation in studies designated to evaluate this issue on a larger number of patients.
Adult↗
Microheterogeneity in the distribution of the 844ins68 in the cystathionine beta-synthase gene in Italy.
Cystathionine beta-synthase (CBS) is an important enzyme for methionine metabolism. A common 844ins68 insertion variant in the CBS gene has been described. This 68-bp duplication of the intron 7-exon 8 boundary within the CBS gene already has been reported to be associated in cis with the T833C mutation. Heterozygosity for CBS deficiency is considered an important cause of hyperhomocysteinemia that strongly relates to cardiovascular disease, as well as homozygosity for another common variant, the C677T mutation of 5,10-methylene tetrahydrofolate reductase. We analysed the prevalence of the 844ins68 variant in the CBS gene in 595 unrelated apparently healthy individuals from nine Italian regions and in 133 patients with coronary artery disease. Our data confirm that the T833C mutation cosegregates in cis with the 844ins68 in all carriers of the insertion. Furthermore, no statistical difference was found in the insertion variant allele frequency between controls and coronary artery disease patients. Our study indicates a microheterogeneity in the distribution of the 844ins68 in the Italian population.
Cystathionine beta-Synthase↗
World distribution of the T833C/844INS68 CBS in cis double mutation: a reliable anthropological marker.
Mild hyperhomocysteinemia is associated to mutations either in cystathionine beta-synthase (CBS) or in 5,10-methylenetetrahydrofolate reductase (MTHFR) genes. In 1995, Sebastio et al. characterized a 68 bp insertion in cis with the most common CBS mutation (T833C) detected in homocystinuric patients. Recently, this double mutation has been detected in Italian and North-American controls. Compared to a group of patients affected by coronary artery disease, North-American controls showed not statistically significant difference. Moreover, Italian controls displayed a microheterogeneity in the mutant allele frequency distribution depending on their geographical origin (North or South of Italy). Aim of our study was to evaluate the prevalence of the double in cis mutation in different populations. We studied 377 healthy subjects belonging to various human groups. Genomic DNA, extracted from peripheral blood samples, was amplified using specific primers; PCR fragments were digested with Bsr I restriction enzyme to detect the double mutation. Our data show a significant heterogeneity among the populations studied, therefore this mutation turned out to be a reliable anthropogenetic marker. The distribution of the double mutation will contribute, with other DNA polymorphisms, to evaluate the genetic admixture of mixed populations such as Afro-Americans.
Alleles↗
The pre-procedural platelet state predicts clinical recurrence after coronary angioplasty.
Percutaneous transluminal coronary angioplasty is an established therapy for coronary artery disease, but restenosis still occurs at a rate of 25%-40%. The aim of this study was to investigate the acute effect of percutaneous transluminal coronary angioplasty on platelet function and the relationship between platelet function and clinical recurrence. Spontaneous platelet aggregation was assessed before and after successful coronary angioplasty in 155 patients (120 men, 35 women). Patients were followed for a mean time of 20 months; follow-up angiography was performed only in patients with clinical recurrence. In 122 of 155 patients (79%) a significant increase in spontaneous platelet aggregation was observed immediately after coronary angioplasty. Baseline spontaneous platelet aggregation in platelet-rich plasma was significantly lower in patients with clinical recurrence than in those without (P<0.05). Kaplan-Meier event-free survival estimate showed a significant difference in clinical recurrence between patients with spontaneous platelet aggregation in platelet-rich plasma below and above the first quintile (P<0.05) with a relative risk of 2.5. In conclusion. these results indicate that percutaneous transluminal coronary angioplasty enhances spontaneous platelet aggregation and that the platelet state before coronary angioplasty affects the risk of clinical recurrence after the procedure.
Adult↗
The influence of smoking on von Willebrand factor is already manifest in healthy adolescent females: the Floren-teen (Florence Teenager) Study.
The early onset of atherosclerosis and the involvement of physiological biochemical, and environmental factors in its pathogenesis is well documented. Few data are available on the role of risk factors related to hemostasis in the pathogenesis of atherosclerosis in the young and, in particular, little information is available on adolescent populations. In the Study of Preventive Medicine and Education Program (Floren-teen Study), von Willebrand factor, a risk factor for cardiovascular disorder, was studied, together with classical cardiovascular risk factors, in apparently healthy students from two high schools in Florence. Familial and personal history, physical examination, and cardiovascular risk factors were evaluated in 144 students (aged 17-19 years). Blood was withdrawn to assess von Willebrand factor (ELISA) and lipid parameters. Levels of von Willebrand factor were significantly higher (P<0.044) in smokers than in nonsmokers and were correlated with the number of cigarettes per day in the whole group (P=0.01) and in females (P=0.006). In females a positive correlation was observed between von Willebrand factor and high-density lipoprotein cholesterol (P=0.0365). There was no significant correlation between von Willebrand factor and blood pressure or between von Willebrand factor and physical activity. In conclusion, this study shows an association between levels of von Willebrand factor and smoking habits and is the first show that even a brief period of smoking affects levels of von Willebrand factor in healthy adolescent females independently of other risk factors. These results stress the relevance of extending prevention programs to reduce smoking in high school students.
Adolescent↗
Electrophysiologic procedures and activation of the hemostatic system.
BACKGROUND: Thromboembolism occurs in 0.4% to 2% of the subjects undergoing radiofrequency ablation (RFA), but its mechanisms remain unclear. Our aim was to evaluate several parameters of the hemostatic system in relation to the electrophysiologic procedure. METHODS: Thirty consecutive patients were enrolled in the study. Fifteen underwent electrophysiologic study and 15 underwent radiofrequency ablation. Before the ablation procedure, all subjects were given an intravenous heparin bolus (2500 IU). Blood samples were drawn immediately before, at the end of, and 24 hours after the procedures. Spontaneous platelet aggregation in whole blood and in platelet-rich plasma, markers of clotting activation (prothrombin fragment 1+2 and the thrombin-antithrombin complex) and the fibrinolytic system (plasminogen activator inhibitor and D-dimer) levels were evaluated. RESULTS: At the end of the procedure, spontaneous platelet aggregation in whole blood, prothrombin fragment 1+2, thrombin-antithrombin complex, and D-dimer levels increased significantly in all patients. The hemostatic changes were more marked after RFA than after electrophysiology. Spontaneous aggregation in whole blood, prothrombin fragment 1+2, and thrombin-antithrombin complex levels at 24 hours after the procedure were similar to those observed before the procedure in both groups; D -dimer levels were still elevated with respect to preprocedure levels, with a trend toward higher levels in patients undergoing RFA rather than electrophysiology. A significantly more marked activation of coagulation (prothrombin fragment 1+2, P <.005) was found in patients in whom the mean duration of energy application was higher than 23.5 seconds. CONCLUSIONS: Our data suggest that antithrombotic prevention with a prolonged administration of heparin and/or the association of antiplatelet agents should be considered in patients undergoing RFA.
Adult↗
Acquired activated protein C resistance in postmenopausal women is dependent on factor VIII:c levels.
Activated protein C (APC) resistance is an established risk factor for venous thromboembolism. In 5% to 10% of patients with venous thromboembolism, the APC resistance phenotype is observed in the absence of factor V Leiden mutation. Moreover, some physiologic and pathologic conditions are associated with an "acquired" APC resistance, not caused by the Leiden mutation, such as inflammatory diseases, pregnancy, or oral contraceptive therapy. Several studies have demonstrated the effect of menopause on the hemostatic system, but no data are available about APC resistance. We found a high prevalence of APC resistance in postmenopausal women, not associated with factor V Leiden mutation. The mechanism that underlies this acquired APC resistance may be related to the higher levels of factor VIII, which showed a strong inverse correlation with APC resistance, whereas no correlation was found between the normalized APC ratio, factor V levels, and protein S values. Higher levels of factor VIII correlated with a marker of coagulation activation, such as prothrombin fragments 1 plus 2. Therefore, to identify women receiving hormone replacement therapy who have a greater risk for deep venous thrombosis, the APC resistance coagulation test should be used instead of the genetic study.
Activated Protein C Resistance↗
Usefulness of screening for congenital or acquired hemostatic abnormalities in women with previous complicated pregnancies.
Activated protein C resistance (APCR) is a common cause of familial thrombophilia and venous thrombosis. The aim of the study was to investigate the prevalence of APCR associated with factor V Leiden mutation and its relevance in comparison to other risk factors for thromboembolic disorders in women with a history of previous complicated pregnancies (history of fetal loss in the second and third trimester n = 34, preeclampsia n = 46). The frequency of APCR was significantly higher in women with a history of fetal loss and preeclampsia (23.5 and 26.1%, respectively) compared with a control group (3.8%). The prevalence of antithrombin, protein C and protein S deficiencies and the presence of antiphospholipid antibodies were also investigated: the prevalence of at least one disorder was 41.2% in the group with previous fetal loss, 37.0% in the group with previous preeclampsia and 7.5% in the control group.
Activated Protein C Resistance↗
High prevalence of anti-beta2 glycoprotein I antibodies in patients with ischemic heart disease.
Ischemic cardiac manifestations have been reported in a various percentage of patients with anti-phospholipid antibodies. As concerns the relationship between anti-beta2 glycoprotein I antibodies (anti-beta2-GPI) and ischemic heart disease (IHD), it was investigated in only one coronary primary prevention study. We investigated the prevalence of anti-beta2-GPI in a well characterized group of patients with different clinical manifestation of IHD. Sera from 37 patients (mean age 62.7 +/- 9.9) with IHD (20 with unstable angina-UA and 17 with effort angina-EA) and from 40 healthy subjects, matched for age and sex, were tested for the presence of IgG and IgM anti-beta2-GPI using an ELISA technique. Eleven/37 patients (29.7%) resulted positive for anti-beta2-GPI. A positivity for IgG anti-beta2-GPI was found in 10 patients, 1 patient was positive for IgM and 1 for both isotypes. The prevalence of anti-beta2-GPI in the control group resulted significantly lower (2.5%; p < 0.005) than in patients with IHD. Positivity for anti-beta2-GPI was found in 9/20 (45%) patients with UA and only in 2/17 patients (11.8%) with EA (p = 0.0365). IgG anti-beta2-GPI levels (median 7.7U/ml, range 2.6-24.1) were significantly higher in patients with UA compared to patients with EA (median 4.6 U/ml, range 2.3-11.5; p = 0.02) and controls (median 3.15 U/ml, range 2.3-9.0; p < 0.0001); also IgM levels resulted higher in patients with unstable angina. A positivity for anti-beta2-GPI was observed in 4/13 patients (30.8%) with a previous myocardial infarction (MI) and in 7/24 (29.2%) patients without a previous MI. Our findings suggest that anti-beta2-GPI could represent an expression of the T-cell activation detectable in patients with unstable angina. The lack of a significant difference in the prevalence of these antibodies in patients with or without a previous MI suggests that anti-beta2-GPI are not induced by tissue necrosis.
Aged↗