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Biomedical subjects

M C Roncaglioni

Publications and source records attributed to M C Roncaglioni.

11 recordsLinked to original sources
PubMed1992

Von Willebrand factor, plasminogen activator inhibitor-1 and C-reactive protein are markers of thrombolytic efficacy in acute myocardial infarction.

Plasma von Willebrand factor, plasminogen activator inhibitor activity and C-reactive protein were assessed as markers of coronary recanalisation in 30 patients with acute myocardial infarction receiving tissue-type plasminogen activator (t-PA). Blood samples were taken before t-PA (time 0), 4-hourly for 24 h and daily up to 72 h. A continuous electrocardiogram was recorded in the first 24 h. Coronary arteriography was performed 90 min and 24 h after the start of t-PA. Patients with a patent infarct artery (n = 17), compared to those with occluded artery (n = 13), showed a fall in von Willebrand factor from 0 to 24 h (p = 0.001), a greater fall in plasminogen activator inhibitor from 24 to 48 h (p = 0.04) and a fall in C-reactive protein from 48 to 72 h (p = 0.002). The accuracy of these indices compared favourably with time to peak plasma MB creatine kinase and > or = 50% resolution of maximal ST-deviation on the electrocardiogram. Thus, changes in plasma von Willebrand factor, plasminogen activator inhibitor and C-reactive protein during the first 3 days of myocardial infarction are indicative of thrombolytic efficacy. Their concordant behaviour may reflect a common regulatory mechanism.

Adult↗
PubMed1992

Role of family history in patients with myocardial infarction. An Italian case-control study. GISSI-EFRIM Investigators.

BACKGROUND: A family history of heart disease has been reported to increase the risk of coronary heart disease. We examined the relation between family history of myocardial infarction (MI) and risk of acute MI to establish the independency of this association, the degree of risk in relation to the number and age of relatives affected, and the possible interaction between family history and other major risk factors for MI. METHODS AND RESULTS: In a case-control study conducted in Italy within the framework of the GISSI-2 Trial, 916 cases of newly diagnosed MI and 1,106 hospital controls were identified. Using a structured questionnaire, data were collected on the history of MI in first-degree relatives and the age at which the event occurred. Compared with subjects without family history of MI in first-degree relatives, the relative risk (RR) of MI was 2.0 (95% confidence interval, CI, 1.6-2.5) in those with one and 3.0 (95% CI, 2.0-4.4) in those with two or more relatives affected (chi 2(1) test for trend, 54.1; p less than 0.001). Such an increase was not substantially affected by allowance for recognized risk factors. The risk related to family history involving at least two relatives was higher for early MI (less than 55 years) (RR, 20.0; 95% CI, 3.3-121.2) compared with later MI (less than or equal to 65 years) (RR, 3.5; 95% CI, 1.8-6.6). When known risk factors were considered for their interaction with family history, the effect on RR was approximately multiplicative for several variables, including smoking, serum cholesterol, hypertension, and hyperlipidemia but not for diabetes and body mass index. Thus, the presence of both family history and smoking and cholesterol levels greater than or equal to 226 mg/dl led to an RR of 14 (95% CI, 3.7-50.0) and 8.3 (95% CI, 1.8-38.7), respectively. CONCLUSIONS: This study indicates that a family history of MI is an independent risk factor for MI, and that the number of relatives and the age at which they were affected is related to the strength of the association. There is a multiplicative effect on RR between family history and several major risk factors for MI.

Case-Control Studies↗
PubMed1977

Bleeding in renal failure: is von Willebrand factor implicated?

Normal or increased concentrations of factor VIII procoagulant activity (VIIIC), factor VIII-related antigen (VIIIRA), and factor VIII-von Willebrand activity (VIIIVWF) were found in the predialysis plasma of 10 out of 11 patients with chronic renal failure (CRF). All patients had a bleeding time longer than 15 minutes and platelet retention to glass beads lower than 40%. The only patient who had reduced concentrations of all three factor VIII complex components was subsequently shown to have von Willebrand's disease. In four patients with CRF, very low platelet retention, and slightly prolonged bleeding time none of the three factor VIII COMPLEX COMPONENTS WERE SELECTIVely modified in predialysis samples. These findings suggest that the bleeding tendency common in CRF is not necessarily linked to defective plasma factor VIII-related activities.

Adult↗
PubMed1977

Ditazole and platelets. I. Effect of ditazole on human platelet function in vitro.

Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) has been shown to be a strong in vitro inhibitor of human platelet aggregation brought about by release reaction inducers; in contrast, it did not significantly affect primary ADP-induced aggregation. Ditazole strongly inhibited the release of platelet-bound 14C-serotonin under the influence of Thrombofax, whereas it did not interfere with the transport and storage of serotonin in nonstimulated platelets. The effect of ditazole was not potentiated by acetylsalicylic acid. Ditazole also inhibited ADP-reptilase clot retraction and modified thrombin-induced clot formation. The inhibition of platelet aggregation exerted by ditazole in plasma could be removed following gel filtration of platelets on Sepharose 2-B gel. This would indicate that ditazole does not act on platelets by a 'hit and run' mechanism.

Adenosine Diphosphate↗
PubMed1977

Interference by fenfluramine with the storage of 14C-5-hydroxytryptamine in rat platelets.

(+)Fenfluramine decreases the 14C-5HT stored in rat platelets both in in vitro and in in vivo systems, indicating a release of the amine. The effect of (+) fenfluramine in vitro increases by increasing the concentration of the drug, the time of incubation with platelets and the temperature. It is not accompanied by loss of lactate dehydrogenase thus excluding an unspecific damage to the platelet membrane induced by the drug. In addition it is not inhibited either by inhibitors of the uptake of 5HT (chlorimipramine, Lilly 110140) or by inhibitors of the platelet 'release reaction' (acetylsalicylic acid) or by an excess of cold 5HT in the incubation medium. The effect of (+) fenfluramine in vivo is dose-dependent and increases gradually up at least 18 hr after i.p. drug's administration. It is significantly inhibited in rats pretreated by either chlorimipramine or Lilly 110140, but not by acetylsalicyclic acid. In analogy with the effect of (+) fenfluramine on rat brain 5HT, it is suggested that this drug could enter platelets by utilizing the 5HT uptake mechanism, at least in vivo.

Animals↗
PubMedDate not supplied

[Thrombosis].

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Anticoagulants↗