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Biomedical subjects

I Catalano

Publications and source records attributed to I Catalano.

14 recordsLinked to original sources
PubMed1992

Effects of defibrotide on fibrinolytic activity in diabetic patients with stable angina pectoris.

18 type II diabetes mellitus patients with coronary artery disease (CAD) have been studied. Tissue plasminogen activator (t-PA) antigen and activity, plasminogen activator inhibitor (PAI) antigen and activity, thrombin-antithrombin III (TAT) complexes were determined in blood samples. Diabetic CAD patients showed higher TAT levels with clearly increased PAI levels whereas t-PA levels levels were similar in patients and controls. Long term defibrotide treatment induced marked changes in fibrinolytic parameters of these diabetic patients with CAD with increased t-PA activity, that could be related to an evident reduction of PAI antigen and activity. Drugs able to modulate PAI activity may be useful in clinical conditions at high risk of thrombotic vascular complications like diabetics with stable angina.

Aged↗
PubMed1992

Increased thromboxane biosynthesis in type IIa hypercholesterolemia.

BACKGROUND: Increased platelet thromboxane (TX)A2 production has been described in type IIa hypercholesterolemia. To verify the relevance of these capacity-related measurements to the actual rate of TXA2 biosynthesis in vivo, we studied the urinary excretion of its major enzymatic metabolites in 46 patients with type IIa hypercholesterolemia and 20 age-matched controls. METHODS AND RESULTS: Urinary 11-dehydro-TXB2 and 2,3-dinor-TXB2 were measured by previously validated radioimmunoassays. The excretion rate of 11-dehydro-TXB2 was significantly (p less than 0.001) higher in patients (68.7 +/- 35.1 ng/hr, mean +/- SD) than in controls (22.4 +/- 9.4 ng/hr), with metabolite excretion greater than 2 SD of the normal mean in 74% of the patients. Urinary 11-dehydro-TXB2 was significantly (p less than 0.01) correlated with the threshold aggregating concentration of collagen (r = -0.641) and arachidonate (r = -0.734) and with agonist-induced platelet TXB2 production in vitro (r = 0.647 and 0.748, respectively). Moreover, a statistically significant correlation (r = 0.673, p less than 0.001, n = 66) was found between 11-dehydro-TXB2 excretion and total plasma cholesterol. The enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor simvastatin (20 mg/day for 6 months) significantly reduced cholesterol levels by 22-28% and urinary 11-dehydro-TXB2 excretion by 32-42% in 10 patients. However, the reduction in the latter did not correlate with the reduction in the former and may have resulted from a nonspecific effect of simvastatin. Moreover, selective inhibition of platelet cyclooxygenase activity by low-dose aspirin (50 mg/day for 7 days) was associated with cumulative inhibition of 11-dehydro-TXB2 excretion by approximately 70% in six patients. CONCLUSIONS: TXA2 biosynthesis is enhanced in the majority of patients with type IIa hypercholesterolemia; this is, at least in part, a consequence of abnormal cholesterol levels, as suggested by the correlation between the two. Low-dose aspirin can largely suppress increased metabolite excretion, thus suggesting that it reflects TXA2-dependent platelet activation in vivo.

Adult↗
PubMed1991

Increased plasminogen activator inhibitor antigen levels in diabetic patients with stable angina.

PAI-1 antigen, tPA antigen and thrombin - antithrombin III complexes (TAT) levels were measured in 10 males with stable angina and type-II diabetes mellitus and in 16 males with stable angina without diabetes or other risk factors (hyperfibrinogenaemia, hyperlipidaemia, diabetes, hypertension, smoking and obesity) known to increase PAI levels. Ten healthy men of equivalent age served as controls. Because only diabetics with coronary artery disease (CAD) showed a decreased fibrinolytic capacity, a second study was performed on the 16 non-diabetic CAD patients to determine whether submaximal workload induces significant changes of tPA and PAI levels. TAT levels were increased in CAD, and significantly so in the diabetic group. tPA levels were increased only in the CAD patients without diabetes. PAI levels were significantly increased in diabetic CAD patients (5.26 +/- 1.96 ng/ml) but not in the stable angina patients without diabetes (2.97 +/- 1.44 ng/ml). Immunologically-reactive tPA released after exercise was higher in the 16 CAD patients without diabetes than in controls. Our data could indicate that in stable angina without diabetes there is no chronic latent activation of the clotting system, with no impairment of fibrinolytic activity. On the other hand, the presence of diabetes mellitus seems to influence the fibrinolytic capacity in CAD, particularly increasing PAI levels.

Adult↗
PubMed1990

Thromboxane biosynthesis and platelet function in type II diabetes mellitus.

It has been suggested that platelet hyperreactivity in patients with diabetes mellitus is associated with increased platelet production of thromboxane. We therefore compared the excretion of a thromboxane metabolite and platelet function in 50 patients with Type II diabetes mellitus who had normal renal function and clinical evidence of macrovascular disease and in 32 healthy controls. The mean (+/- SD) excretion rate of urinary 11-dehydro-thromboxane B2 was significantly higher in the patients than in the controls (5.94 +/- 3.68 vs. 1.50 +/- 0.79 nmol per day; P less than 0.001), irrespective of the type of macrovascular complication. Tight metabolic control achieved with insulin therapy reduced the levels of 11-dehydro-thromboxane B2 by approximately 50 percent. The fractional conversion of exogenous thromboxane B2 (infused at a rate of 4.5, 45.3, or 226.4 fmol per kilogram of body weight per second) to urinary 11-dehydro-thromboxane B2 was assessed in four patients, in whom it averaged 5.4 +/- 0.1 percent; this value did not differ from that measured in healthy subjects. Aspirin in low doses (50 mg per day for seven days) reduced urinary excretion of the metabolite by approximately 80 percent in four patients. The fact that thromboxane biosynthesis recovered over the following 10 days was consistent with a platelet origin of the urinary metabolite.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Platelet function in hypo- and hyperthyroidism.

Alterations in cardiovascular hemodynamics are found in patients with hypofunction of the thyroid. Frank hypothyroidism favours the development of coronary heart disease. Platelets are thought to be important in atherosclerotic lesions initiation and progression. We studied platelet sensitivity to several agonists and to a physiological antagonist, prostacyclin, and thromboxane production in patients with hyperthyroidism and hypothyroidism. No statistically significant differences were found between platelets activities in patients and control subjects. We conclude that increased platelet function is not a direct indicator of susceptibility to cardiovascular diseases in patients with hypothyroidism whereas the hyperdynamic state, cardinal manifestation of thyrotoxicosis, is not associated with platelet activation.

Adult↗
PubMed1989

Platelet function in patients with type 2 diabetes mellitus: the effect of glycaemic control.

In the present study the effects of a short term intensive glycaemic control obtained with subcutaneous insulin therapy on lipids and apoprotein levels, platelet aggregation, platelet sensitivity to prostacyclin and platelet thromboxane production were investigated in 20 patients with type 2 diabetes and vascular disease. In 11 out of the 20 patients there was a significant improvement of glycaemic control (fructosamine reduction). Only with tight improvement of glycaemic control there was significant change in the concentration of ADP and collagen required to produce 50% of the maximum aggregation wave response, in the responsiveness of platelet to PGI2 and in the TxB2 synthesis. Lower Apo B levels were also shown in the tight control group suggesting that Apo B changes may have influenced platelet aggregation and thromboxane synthesis.

Adult↗
PubMed1989

[Antiplatelet effects of combined therapy with ticlopidine and low doses of aspirin on patients with ischemic cardiopathy].

The aim of study was to evaluate the effects on platelet function, in 8 patients with ischemic heart disease, of the following treatments administered consecutively: ticlopidine in a daily dose of 500 mg (10 days); aspirin in a daily dose of 50 mg (10 days); ticlopidine plus ASA, at the same dosages, for the last 10 days. Only ticlopidine plus ASA significantly inhibited EC 50 of ADP, collagen and arachidonate. Platelet activation and platelet sensitivity to prostacyclin was affected by ticlopidine and ticlopidine plus ASA but not by ASA alone. We conclude that in our ischemic heart disease patients the association of ticlopidine and low dose aspirin seems superior to each drug alone in inhibiting platelet activity.

Aged↗
PubMed1988

In vitro effects of gallopamil on platelet aggregation and thromboxane generation.

The in vitro effects of gallopamil, a highly specific calcium-channel blocker, on platelet function were investigated. Gallopamil caused a dose-dependent inhibition of platelet aggregation. In fact, the drug in concentrations as low as 0.5 microgram/ml inhibited platelet activating factor and epinephrine-induced platelet aggregation. Similarly, the inhibition of adenosine diphosphate and epinephrine-induced thromboxane generation was demonstrated. Since platelet activation and thromboxane release may be related to myocardial ischemia, it is conceivable that some of the antianginal effects of gallopamil may in part be due to platelet inhibitory effects.

Blood Platelets↗
PubMedDate not supplied

Thrombin-antithrombin III complexes in type II diabetes mellitus.

Several studies suggest that diabetes is associated with a hypercoagulable state. Therefore determination of thrombin-antithrombin complex (TAT) could represent a sensitive parameter for specific detection of a latent activation of the clotting system. The present study documents increased plasma TAT in a heterogeneous group of non-insulin-dependent diabetic patients. The finding of increased TAT levels both in diabetic patients with vascular complications and in vascular disease patients without diabetes suggests a relationship between existing vascular disease and the hemostatic mechanism that produces augmented thrombin activity. In acute vascular occlusions the presence of diabetes seems to increase activation of the coagulative system.

Adult↗