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Clinical Trial
. 1991 Dec;36(12 Suppl 1):33-48.

[Modern trends in the therapy of arteriosclerosis in the light of new physiopathological findings]

[Article in Italian]
Affiliations
  • PMID: 1841788
Clinical Trial

[Modern trends in the therapy of arteriosclerosis in the light of new physiopathological findings]

[Article in Italian]
A Barsotti. Cardiologia. 1991 Dec.

Abstract

In the last years, a plasmatic fibrinogen increase, a fibrinolytic system activity reduction and platelet activation, seemed to play a significant role on the genesis and progression of atheromatous plaques, especially when combined to a plasmatic lipoprotein increase. The results obtained in normolipidaemic patients (2000 asymptomatic subjects, 364 non-insulin diabetic patients randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 69 nifedipine-30 mg/daily-treated subjects, and 38 patients submitted to nifedipine-30 mg/daily-combined to indobufen-400 mg/daily-therapy), are reported. The results obtained in hyperlipidaemics (blood cholesterol level > 240 mg/dl; 356 patients, randomly divided into 2 groups, treated and not treated with bezafibrate 400 mg/daily, 56 patients with simvastatin 40 mg/daily and 85 with low saturated fat and low cholesterol diet), are also reported. Follow-up of all the patients was 4 years, but the simvastatin group followed-up only 1 year. An ultrasound examination of carotid and femoral arteries was performed in all the patients by means of a Duplex Scanner ATL Ultramark 5, with a high resolution probe (10 MHz). Subjects were graded into I-VI classes, according to the vessel progressive atherosclerotic impairment. In normolipidaemics, wall atheromatous changes were seen with increasing frequency with age, and a significant relationship among plaque progression rate and developed cerebrovascular symptoms, developed symptomatic peripheral symptoms, increased cardiovascular events and mortality rate, was evidenced. Non-insulin dependent diabetes, combined to normal levels of blood lipoproteins, appears an independent risk factor, superimposable to hyperlipidaemia. In this group of patients, bezafibrate therapy significantly reduced plaque progression, acting on blood coagulation factors and similar results were obtained in nifedipine and nifedipine plus indobufen groups. Also in hyperlipidaemics treated with diet, simvastatin and bezafibrate, the plaque progression was significantly reduced with respect to control group, especially when blood lipoproteins and coagulation were normalized. In conclusion, hyperlipidaemia, Ca++ and blood coagulation disorders, appear to be the main factors affecting the plaque progression, and the prevalence of each factor in the atheroma development must be well evaluated in the single patients to establish an adequate therapeutic strategies.

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