Pharmacoutilization of statin therapy after acute myocardial infarction. A real practice analysis based on administrative data.

BACKGROUND: Despite randomized and controlled trials indicating continuous treatment with statin therapy as a factor in reducing morbidity and mortality after acute myocardial infarction, records reveal a high percentage of patients at risk who are either not receiving treatment or being treated inadequately. METHODS: An administrative database kept by the Local Health Unit of Ravenna and listing patient baseline characteristics, drug prescriptions and hospital admissions was used to perform: 1) an analysis of patients discharged alive from hospital each year between 1996 and 2000 with a diagnosis of acute myocardial infarction, and 2) a retrospective cohort study of drug utilization, and particularly the use of statins, year by year. All prescriptions for statins filled in the 6 months after hospital discharge were considered and used to classify patients in terms of their exposure to statin therapy and of their pharmacoutilization. RESULTS: A total of 2265 subjects were enrolled (446 in 1996, 440 in 1997, 443 in 1998, 443 in 1999, and 493 in 2000). The percentage of patients treated with statins increased each year (from 22.6% in 1996 to 43.8% in 2000) as did the percentage of adequately dosed patients (from 4.3% in 1996 to 23.9% in 2000). The overall cost of dispensed statins amounted to 10,610 euros in 1996 and 45,102 euros in 2000. The proportion of cost for statins accountable to adequately dosed patients ranged from 36.4% in 1996 to 77.4% in 2000. The average cost per adequately dosed patient ranged from 203.40 euros in 1996 to 296.00 euros in 2000 and increased year by year. CONCLUSIONS: Pharmacoutilization of statin therapy was found to be unsatisfactory in each study year. Interestingly, however, the trend indicated by the study suggests increasing percentages of patients being exposed to the treatment, and of adequately dosed patients. These results may be attributed to a greater awareness of the need for proper treatment, and may be considered as reflecting a significant improvement in drug management.

Morphometry of age pigment (lipofuscin) and of ceroid pigment deposits associated with vitamin E deficiency.

Consistent amounts of lipofuscin and of ceroid pigment associated with vitamin E deficiency are reported to represent morphological correlates of aging and increased oxidative stress. A reliable quantification of these yellow autofluorescent deposits is of critical biological significance, thus we carried out a computer-assisted morphometric study on the accumulation of lipofuscin in physiological aging and of ceroid pigment in vitamin E deficiency, respectively. The total area and the size distribution of lipofuscin or ceroid pigment deposits were measured in CA3 hippocampal pyramidal neurons of 6-, 12-, 18- and 25-month-old rats, as well as in vitamin E deficient animals of 18 months of age. An increase in the mean total area of lipofuscin and ceroid pigment was found in aging and in vitamin E deficiency. In both conditions, the proportion of large discrete deposits also increased. The similarity of changes observed in old and adult vitamin E deficient animals suggests that the underlying processes initiated by the absence of alpha-tocopherol from the diet of adult rats and in physiological aging may share some common mechanisms.

Morphometric investigations of the mitochondrial damage in ceroid lipopigment accumulation due to vitamin E deficiency.

Numeric (Nv) and volume (Vv) densities, as well as the average size (skeleton: Sk) of synaptic mitochondria from adult, normally fed and adult, vitamin E deficient animals (11 months of age) were semiautomatically measured by computer-assisted morphometry in the cerebellar granular layer. Nv, Vv and the average mitochondrial volume (V) were measured on perikaryal Purkinje cell organelles preferentially stained for succinic dehydrogenase (SDH) activity. Adult vitamin E deficient animals showed a significant decrease of Nv, a significant increase of Sk and an unchanged value of Vv. While in adult normally fed animals the mitochondria of increased size (Sk>5 microm) were 5.3%, in the adult vitamin E deficient rats this fraction accounted for 25.5%. In Purkinje cell perikarya, vitamin E deficiency resulted in a significant decrease of Vv, Nv and V, as well as a steeper reduction of the percentage of SDH-positive mitochondria of larger size. Taken together, these findings document that vitamin E deficiency is responsible of mitochondrial morphometric alterations in adult rats. Structurally deteriorated mitochondria are reported to play a role in producing increased amounts of free radicals, which can facilitate the accumulation of ceroid pigment.