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Biomedical subjects

D Geroldi

Publications and source records attributed to D Geroldi.

At least 19 recordsLinked to original sources
PubMed2003

Silent myocardial ischemia in diabetic and nondiabetic patients with coronary artery disease.

BACKGROUND: Patients with diabetes mellitus are at increased risk for CAD; silent ischemia is reported to be frequent in diabetic populations. The aim of the present study was to evaluate the prevalence of silent ischemia in diabetic and nondiabetic patients with assessed CAD. METHODS AND RESULTS: We recruited a total of 618 patients with CAD: 309 were consecutive diabetic patients and 309 were age- and gender-matched nondiabetic patients. Myocardial ischemia was evaluated both during daily life and during exercise testing. Angina pectoris during daily life was more frequent in diabetic than in nondiabetic patients (80% vs. 74%, P<0.05). The anginal pain intensity either during daily life or acute myocardial infarction (MI), the prevalence of a previous MI, the extent of CAD and ergometric parameters were similar in diabetics and nondiabetics. Silent ischemia during exercise was documented in 179 (58%) diabetics and in 197 (64%) nondiabetics (nonsignificant, ns). Both diabetics and nondiabetics with silent exertional myocardial ischemia differed from symptomatic subjects in higher heart rate values (P<0.01), systolic blood pressure (P<0.01), rate-pressure product (P<0.001), work load (P<0.01) and maximum ST-segment depression at peak exercise (P<0.05). CONCLUSIONS: The incidence of silent myocardial ischemia during exercise was similar in diabetic and nondiabetic CAD patients. Surprisingly, diabetics showed a higher prevalence of angina pectoris during daily activity than nondiabetics. A significant association between the presence of symptoms during daily life and exercise was observed in both groups. Our results may contribute to the planning of the clinical management of diabetic CAD patients and confirm the individual attitude to pain of CAD patients independent of the presence of diabetes.

Analysis of Variance↗
PubMed2001

Association of lipoprotein(a) levels and apolipoprotein(a) phenotypes with coronary artery disease in Type 2 diabetic patients and in non-diabetic subjects.

AIMS: We investigated whether in Type 2 diabetic patients lipoprotein(a) (Lp(a)) levels and apolipoprotein(a) (apo(a)) polymorphism are associated with angiographically documented coronary artery disease (CAD). We also examined whether there are differences in the distributions of Lp(a) levels and apo(a) phenotypes between CAD patients with and without diabetes. METHODS: A hundred and seven diabetic patients with CAD, 274 diabetic patients without CAD, 201 non-diabetic patients with CAD, and 358 controls were enrolled. RESULTS: Diabetic patients with CAD showed Lp(a) levels (21.2 +/- 17.7 vs. 15.1 +/- 17.8 mg/dl; P = 0.0018) and a percentage of subjects with at least one apo(a) isoform of low molecular weight (MW) (67.2% vs. 27.7%; P = 0.0000) significantly greater than diabetic patients without CAD. Multivariate analysis showed that in diabetic patients Lp(a) levels and apo(a) phenotypes were significantly associated with CAD; odds ratios (ORs) of high Lp(a) levels for CAD were 2.17 (1.28-3.66), while ORs of the presence of at least one apo(a) isoform of low MW were 5.35 (3.30-8.60). Lp(a) levels (30.2 +/- 23.7 vs. 21.2 +/- 17.7 mg/dl; P = 0.0005) and the percentage of subjects with at least one apo(a) isoform of low MW (87.0% vs. 67.2%; P = 0.0001) were significantly higher in CAD patients without than in those with diabetes. CONCLUSIONS: Our data suggest that Lp(a) levels and apo(a) phenotypes are independently associated with CAD in Type 2 diabetic patients; thus both these parameters may be helpful in selecting diabetic subjects at high genetic cardiovascular risk. However, Lp(a) levels and apo(a) polymorphism seem to be cardiovascular risk factors less important in diabetic than in non-diabetic subjects. Diabet. Med. 18, 589-594 (2001)

Apolipoproteins↗
PubMed2000

Severe hypercalcemia and systemic lupus erythematosus.

A rare case of severe hypercalcemia strongly associated with Systemic Lupus Erythematosus (SLE) is reported. On admission, a young woman showed severe hypercalcemia and photosensitivity. Criteria for diagnosis of SLE were not sufficient. All causes, common and uncommon, of hypercalcemia were excluded. Radiographs of the skeleton were normal. One year later diagnosis of SLE was evident. In addition, diffuse and severe osteopenia and chest deformities had occurred. The treatment of SLE normalized persistently calcemia. Mild elevation of calcium levels occurred during flares of SLE. It has been hypothesized that hypercalcemia in patients with SLE could be caused by the presence of stimulatory anti-PTH receptor antibodies. This case report suggests that in patients with severe hypercalcemia associated with SLE early diagnosis and treatment of SLE may prevent bone loss. In these patients the prevention of severe bone damage is very important. Indeed, severe osteopenia may favour skeletal deformities and fractures; in addition it may represent a serious obstacle in using adequate doses of glucocorticoids for treatment of SLE.

Adult↗
PubMed1999

Genetics and cardiovascular risk: a role for apolipoprotein(a) polymorphism.

Apolipoprotein(a) [apo(a)] is the specific apolipoprotein of lipoprotein(a) [Lp(a)], a recognized cardiovascular risk factor. Apo(a) is characterized by a high genetic polymorphism with at least 34 isoforms in plasma. Recent studies have shown that in atherothrombosis apo(a) polymorphism could play a role independent of Lp(a) levels. In particular, apo(a) phenotypes seem to have their highest predictive value for coronary heart disease, when apo(a) isoforms are detected by high resolution phenotyping methods and when an adequate operative cut-off of apo(a) polymorphism is used. A strong association between apo(a) phenotypes and coronary heart disease has been also found in hypertensive, diabetic, and uremic patients. Moreover, apo(a) phenotypes seem to correlate well with the severity of coronary atherosclerosis and the age of clinical onset of coronary heart disease. These studies suggest that apo(a) polymorphism may have a great clinical usefulness in a primary prevention setting, since apo(a) phenotypes could be used together with Lp(a) levels as strong genetic predictors of atherothrombosis. The analysis of apo(a) polymorphism appears to be particularly useful in healthy subjects with a family history of atherothrombotic diseases, in patients with diseases at high cardiovascular risk (diabetes, hypertension, hypercholesterolemia) and in subjects with conditions modifying Lp(a) levels.

Apolipoproteins A↗
PubMed1999

Association between apolipoprotein(a) phenotypes and coronary heart disease at a young age.

OBJECTIVES: The purpose of this study was to investigate lipoprotein(a) [Lp(a)] levels and apolipoprotein(a) [apo(a)] phenotypes in relation to age of onset of coronary heart disease (CHD). BACKGROUND: Although Lp(a) levels have been extensively analyzed in relation to age of CHD, apo(a) phenotypes have not. METHODS: Three hundred and thirty-five consecutive CHD patients were enrolled and grouped according to their age of CHD onset (<45 years; 45 to 54 years; > or = 55 years). RESULTS: In each patient group Lp(a) levels were higher than in an age-matched control group, but among the patient groups no differences in Lp(a) levels were observed. Apolipoprotein(a) phenotype distributions showed significant differences between patients and age-matched control subjects. Among the patient groups the difference in percentage of subjects with two apo(a) isoforms of low molecular weight (MW) was highly significant (p < 0.001). Multivariate analysis showed that apo(a) phenotypes were the best predictors of early CHD (p < 0.000001). The age-specific odds ratios (ORs) of the presence of at least one apo(a) isoform of low MW for CHD declined with age; in particular apo(a) phenotypes had their highest predictive value in younger persons (OR: 14.62). The OR for the presence of two isoforms of low MW/presence of only isoforms of high MW was 40.88 in the younger age group, 27.17 in age group of 45 to 54 years and 15.83 in the older age group. CONCLUSIONS: The present article reports the first evidence of a strong independent association of apo(a) phenotypes with the age of onset of CHD. Thus, if our data are confirmed by larger studies, apo(a) phenotypes might be used together with Lp(a) levels as powerful genetic markers in assessing the actual risk of developing CHD at a young age.

Adult↗
PubMed1998

Apolipoprotein(a) phenotypes as genetic markers of coronary atherosclerosis severity.

We investigated Lp(a) levels and apo(a) polymorphism in relation to the severity of coronary artery disease, expressed both by the number of coronary arteries stenosed and three different coronary scoring systems. In a sample of 267 patients with coronary artery disease, a Mono-, Bi- or Multi-vessel coronary stenosis was documented by angiography. Twenty-five apo(a) isoforms were detected by a high resolution phenotyping method. Lp(a) levels did not show any differences among subgroups of patients. Both the percentage of apo(a) isoforms of low molecular weight (<655 kDa) (P=0.00015) and the percentage of subjects with at least one apo(a) isoform of low molecular weight (P=0.00027) were significantly correlated with increasing number of coronary vessels stenosed. In multivariate analysis, only apo(a) isoforms of low molecular weight were predictors of coronary atherosclerosis severity, when we used as the dependent variable both the '1-2-multi-vessels' categorization (P=0.000067) and the Gensini (P=0.008767), or Green Lane (P= 0.000001) or Dahlen (P=0.000102) coronary scoring system. Our data show that apo(a) isoforms of low molecular weight are associated with a greater severity of coronary atherosclerosis. If these data are confirmed by prospective studies, apo(a) phenotypes might be used as genetic markers of a greater severity of coronary atherosclerotic lesions.

Analysis of Variance↗
PubMed1998

Lipoprotein(a) levels and apolipoprotein(a) polymorphism in type 1 diabetes mellitus: relationships to microvascular and neurological complications.

To investigate plasma concentrations of lipoprotein(a) [Lp(a)] and apolipoprotein(a) [apo(a)] polymorphism in relation to the presence of microvascular and neurological complications in type 1 diabetes mellitus, 118 young diabetic patients and 127 age-matched controls were recruited. Lp(a) levels were higher in patients than in controls, but the apo(a) isoforms distribution did not differ between the two groups [higher prevalence of isoforms of high relative molecular mass (RMM) in both groups]. Microalbuminuric patients had Lp(a) levels significantly greater than normoalbuminuric patients, and normoalbuminuric patients showed higher Lp(a) levels than controls. Patients with retinopathy or neuropathy showed similar Lp(a) levels to those without retinopathy or neuropathy. No differences in apo(a) isoforms frequencies were observed between subgroups with and without complications (higher prevalence of isoforms of high RMM in every subgroup). However, among patients with retinopathy, those with proliferative retinopathy had higher Lp(a) levels and a different apo(a) isoforms distribution (higher prevalence of isoforms of low RMM) than those with non-proliferative and background retinopathy (higher prevalence of isoforms of high RMM). Our data suggest that young type 1 diabetic patients without microalbuminuria have Lp(a) levels higher than healthy subjects of the same age. Lp(a) levels are further increased in microalbuminuric patients. High Lp(a) levels and apo(a) isoforms of low RMM seem to be associated with the presence of proliferative retinopathy, but have no relation to neuropathy.

Adult↗
PubMed1998

Apolipoprotein(a) phenotypes and their predictive value for coronary heart disease: identification of an operative cut-off of apolipoprotein(a) polymorphism.

BACKGROUND: Apolipoprotein(a) isoforms of low-molecular weight are associated with coronary heart disease. However, because of the high number of apolipoprotein(a) isoforms, it is difficult to assess the cardiovascular risk linked to the apolipoprotein(a) gene of a subject; indeed a cut-off of apolipoprotein(a) polymorphism has not been established. The aim of this investigation was to identify an 'operative' cut-off that discriminates apolipoprotein(a) isoforms associated with high genetic risk for coronary heart disease. METHODS: Two hundred and fifty-one patients with coronary heart disease and 284 controls were recruited. Apolipoprotein(a) isoforms were detected using a high-resolution phenotyping method. RESULTS: Twenty-seven apolipoprotein(a) isoforms with apparent molecular weight varying from 280 to 820 kDa were identified. Several cut-offs of apolipoprotein(a) polymorphism were used in order to compare the frequencies of apolipoprotein(a) isoforms of low and high molecular weight between patients and controls: the cut-off between 640 and 655 kDa had the highest chi 2 (130.40). Even when possible differences in apolipoprotein(a) phenotypes (subjects with at least one isoform of low molecular weight and subjects with only isoforms of high molecular weight) were assessed, the same cut-off showed the highest chi 2 (122.47). Multivariate analysis showed that apolipoprotein (a) isoforms had the greatest predictive value for coronary heart disease (F value = 107.0720), when the cut-off between 640 and 655 kDa was used. CONCLUSIONS: The cut-off between 640 and 655 kDa appears to be the most efficient in identifying subjects at high cardiovascular risk linked to apolipoprotein(a) gene, since this cut-off discriminates apolipoprotein(a) isoforms expressing a greater risk for coronary heart disease.

Aged↗
PubMed1997

Association of lipoprotein(a) levels and apolipoprotein(a) phenotypes with coronary heart disease in patients with essential hypertension.

BACKGROUND: Besides hypertension, several cardiovascular risk factors can play a role in the development of coronary heart disease (CHD) in hypertensive patients. Lipoprotein(a) [Lp(a)] is an important and independent cardiovascular risk factor, but its role in the development of CHD in hypertensives has not been studied. OBJECTIVE: To investigate whether or not Lp(a) levels and isoforms of apolipoprotein(a) [apo(a)] are predictors of CHD in patients with essential hypertension. METHODS: Lp(a) levels and apo(a) polymorphism were evaluated in 249 patients with essential hypertension, in 142 non-hypertensive patients with CHD and in 264 healthy controls. RESULTS: Hypertensives with CHD (n = 61) had Lp(a) levels [19 (range 0.5-73.5) versus 7 mg/dl (range 0-83.5), P < 0.001] and a percentage of apo(a) isoforms of low (< 655 kDa) relative molecular mass (RMM, 59.2 versus 25.9%, P < 0.001) higher than did those without CHD (n = 188). Moreover, there were more subjects with at least one apo(a) isoform of low RMM in the subgroup of patients with CHD than there were in that of those without CHD (80.3 versus 30.8%, P< 0.001). Lp(a) levels and apo(a) polymorphism did not differ significantly between hypertensive and non-hypertensive patients with CHD. Stepwise regression analysis indicated that high Lp(a) levels (P= 0.002073) and particularly the presence of at least one apo(a) isoform of low RMM (P < 0.000001) are strong predictors of CHD in hypertensive patients. CONCLUSIONS: Our data show that high Lp(a) levels and the presence of at least one apo(a) isoform of low RMM are strong and independent genetic risk factors for CHD in hypertensive patients. These findings suggest that Lp(a) and apo(a) isoforms should be assessed together with other cardiovascular risk factors to establish the overall CHD risk status of each hypertensive patient

Aged↗
PubMed1996

Lipoprotein(a) plasma concentrations, apolipoprotein (a) polymorphism and family history of coronary heart disease in patients with essential hypertension.

AIM: The purpose of the study was to investigate lipoprotein (a) (Lp(a)) levels and apolipoprotein (a) (apo(a)) phenotypes, and their relationship with a family history of coronary heart disease (CHD) in patients with essential hypertension (EH). METHODS: One hundred and eight newly diagnosed patients with mild to moderate EH and 159 controls were studied. Lp(a) levels were determined with an ELISA method. Apo(a) isoforms were identified by a capillary immunoblotting technique. RESULTS: Lp(a) levels and frequency distribution of apo(a) isoforms did not show significant differences between patients and controls. Lp(a) levels in hypertensives with a family history of CHD were significantly higher than in those without a family history of CHD (P < 0.01). Hypertensives with a family history of CHD showed significantly different frequencies of apo(a) isoforms to those without a family history of CHD (P < 0.05). In EH patients with a family history of CHD, apo(a) isoforms of low molecular weight (MW) had a higher prevalence (62.6%), while in hypertensives without a family history of CHD, apo(a) isoforms of high MW were prevalent (81.6%); the difference between the two subgroups was significant (P < 0.001). Multivariate analysis showed that both Lp(a) levels and apo(a) isoforms of low MW are significant variables in distinguishing between the subgroups. CONCLUSIONS: Lp(a) levels and apo(a) phenotypes do not differ between hypertensives and controls. High Lp(a) levels and apo(a) isoforms of low MW are strongly associated with a family history of CHD in hypertensives. The quantification of Lp(a) levels and the characterization of apo(a) phenotypes may be used for assessment of familial predisposition to CHD in hypertensives.

Apolipoproteins↗
PubMed1993

Characterization of apo(a) polymorphism by a modified immunoblotting technique in an Italian population sample.

Apo(a), the specific lipoprotein(a) (Lp(a)) apolipoprotein, is characterized by different isoforms (from 6 to 11 on SDS-PAGE) encoded by a system of autosomal codominant alleles. Electrophoresis on agarose gel displays a better resolving power than SDS-PAGE (a larger number of apo(a) isoforms is detected). The aim of this work was to set up a simple technique that uses a capillary blotting apparatus and a polyvinylidene difluoride membrane for protein transfer. We tested an Italian population sample of 202 healthy subjects (123 men and 79 women) and we detected 22 apo(a) isoforms varying from 280 to 775 kDa. In our sample, 135 subjects (66.5%) had a single-band phenotype, 64 (31.7%) had a double-band phenotype and 3 subjects (1.5%) had no detectable bands ('null' phenotype). This simple and reproducible technique could be applied in the genetic screening of apo(a) polymorphisms and for clinical investigations of the risk of developing cardiovascular diseases.

Adult↗
PubMed1991

Factors involved in drug interference on enzyme activities of three mitochondrial populations from rat hippocampus.

The maximal rate (Vmax) of some mitochondrial enzyme activities related to energy transduction (citrate synthase, alpha-ketoglutarate dehydrogenase, malate dehydrogenase, succinate dehydrogenase, NADH-cytochrome c reductase, cytochrome oxidase) and amino acid metabolism (glutamate dehydrogenase, glutamate-pyruvate transaminase and glutamate-oxaloacetate transaminase) are evaluated in non synaptic ("free") and intrasynaptic mitochondria from brain hippocampus. The different mitochondrial populations were isolated from rat subjected to single i.p. treatment with saline solution, almitrine (30 mg/kg) and delta-yohimbine (10 mg/kg). In control rats, the mitochondrial populations exhibit different enzymatic patterns. Acute treatment with almitrine decreases cytochrome oxidase activity in intra-synaptic mitochondria, while acute treatment with delta-yohimbine decreases succinate dehydrogenase activity in both types of free and intra-synaptic mitochondria. NADH-cytochrome c reductase activity is also decreased by acute treatment with almitrine ("free" and "synaptic" mitochondria) and delta-yohimbine (synaptic mitochondria only).

Adaptation, Physiological↗
PubMed1989

Enzyme activities in perikaryal and synaptic mitochondrial fractions from rat hippocampus during development.

When pharmacological or basic neurochemical systematic characterization of mitochondrial enzymatic systems correlated to energy transduction processes is attempted, studies must be based on subcellular fractions with a high degree of purity from specific brain areas and from individual animals. Distinct populations of mitochondria heterogenous with respect to biochemical enzyme characteristics from rat brain hippocampus are described. Two mitochondrial populations were derived from synaptosomes by lysis and a third consists of free non-synaptic mitochondria. The maximum rate of some cerebral enzyme activities which are part of energy transduction (citrate synthase, malate dehydrogenase; total NADH-cytochrome c reductase, cytochrome oxidase) and amino acid metabolism (glutamate dehydrogenase) were tested on these mitochondrial populations of 8- and 16-week-old rats. A comprehensive analysis of the data suggests that extensive but highly diversified catalytic expressions of the enzymes studied occur in the hippocampus. This is true even when a short period of the rat life span is studied. Hence the varying pattern of evolution of the differing cerebral mitochondria, probably a consequence of different metabolic functions, should be taken into account in any pharmacological study on these systems.

Age Factors↗
PubMed1989

Action of piracetam and clonidine on different mitochondrial populations from hippocampus.

The maximum rate (Vmax) of some mitochondrial enzymatic activities related to energy transduction (citrate synthase, malate dehydrogenase, NADH-cytochrome c reductase (as total activity), cytochrome oxidase) and amino acid metabolism (glutamate dehydrogenase) were evaluated in non-synaptic (free) and synaptic mitochondria from rat brain hippocampus. Three types of mitochondria were isolated from rats subjected to single i.p. treatments with piracetam (300 mg.kg-1) or with clonidine (750 micrograms.kg-1). With respect to the enzymatic pattern of three types of non-synaptic and synaptic mitochondria, in hippocampus a different maximum rate of both NADH-cytochrome c reductase and cytochrome oxidase was observed, these activities in particular being lowest in the "synaptic heavy" mitochondrial subfraction than in the "synaptic light" one; in addition, other enzyme activities are different in the "free" as compared to both the "light" and "heavy" mitochondria. This confirms that in various types of brain mitochondria a different metabolic machinery exists. Acute treatment with piracetam decreased citrate synthase, glutamate dehydrogenase, NADH-cytochrome c reductase and cytochrome oxidase activities only in the "heavy" mitochondria obtained from synaptosomes. Acute treatment with clonidine decreased the citrate synthase, NADH-cytochrome c reductase and cytochrome oxidase activities only in the same type of mitochondria, i.e. synaptic "heavy" mitochondria. However, this drug increased the same enzymatic activities in "free" mitochondria, some of them being increased or decreased in "light" intrasynaptic ones. Therefore in vivo administration of piracetam mainly affects some specific enzyme activities (suggesting a specific molecular trigger mode of action) of the intrasynaptic mitochondria (suggesting a specific subcellular trigger site of action), the effect on enzyme activities by clonidine being more complex.

Animals↗