PubMed Health⌕ Search

Biomedical subjects

J Kuusisto

Publications and source records attributed to J Kuusisto.

At least 55 records · Page 3Linked to original sources
PubMed1996

Epidemiological evidence for the association of hyperglycaemia and atherosclerotic vascular disease in non-insulin-dependent diabetes mellitus.

Non-insulin-dependent diabetes mellitus (NIDDM) increases the risk for all manifestations of atherosclerotic vascular disease, coronary heart disease (CHD), cerebrovascular disease and peripheral vascular disease. Only a small proportion of this excess risk can be explained by the effects of conventional cardiovascular risk factors, which implies that the diabetic state or factors related to it have to play a significant role in the pathogenesis of macrovascular disease in NIDDM. Six recent prospective population-based studies including a large number of NIDDM patients have indicated that poor glycaemic control evaluated by fasting hyperglycaemia or glycosylated haemoglobin levels increases the risk for CHD, stroke and amputation independently of other risk factors. A dose-response relationship between markers of glycaemic control and the incidence of cardiovascular mortality and morbidity has been demonstrated in all these studies. However, there is so far no direct proof that strict glycaemic control would delay or prevent atherosclerotic complications.

Adult↗
PubMed1996

Retroperitoneal fibrosis with antineutrophil cytoplasmic antibodies.

A middle aged man showed retroperitoneal fibrosis with signs of vasculitis verified by biopsy of the retroperitoneal mass. Antineutrophil cytoplasmic antibodies (ANCA) with cytoplasmic staining pattern (cANCA) were strongly positive, although there were no clinical or histological signs of Wegener's granulomatosis. No cases of cANCA associated retroperitoneal fibrosis have been described except in connection with Wegener's granulomatosis. ANCA have been found to associate with any inflammatory disorders. This observation may broaden the clinical spectrum of cANCA positive vasculitides.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1995

Osteopontin is expressed in human aortic valvular lesions.

BACKGROUND: Nonrheumatic stenosis of trileaflet aortic valves, in which calcification is a prominent feature, has been termed a "degenerative" condition, but it has been demonstrated recently that chronic inflammation is a characteristic feature of the developing lesion of aortic stenosis. This observation raised the possibility that calcification in the aortic valve might be actively regulated. Thus, the present study investigated whether osteopontin, a protein implicated in the regulation of both normal and dystrophic calcification, could be detected in lesions of valvular aortic stenosis. METHODS AND RESULTS: Morphological and immunohistochemical studies were performed on 14 human aortic valves, representing a range of pathology from normal to clinically stenotic. The extent of calcification and macrophage accumulation and their relation to the presence of osteopontin protein were characterized. Highly statistically significant associations were found between the degree of osteopontin expression and the degrees of both calcification and macrophage accumulation in early through late lesions of aortic stenosis. Further, in situ hybridization localized osteopontin mRNA to a subset of lesion macrophages. CONCLUSIONS: These results suggest that, rather than representing a degenerative and unmodifiable process, calcification in aortic stenosis may be, in part, an actively regulated process with the potential for control either through modification of inflammation or synthesis of proteins such as osteopontin, which may modulate calcification in this tissue.

Aortic Valve↗
PubMed1995

Prospective study of small LDLs as a risk factor for non-insulin dependent diabetes mellitus in elderly men and women.

BACKGROUND: The excess risk of atherosclerosis among patients with non-insulin dependent diabetes mellitus (NIDDM) is well documented. However, the presence of conventional risk factors cannot fully account for this excess risk, and the underlying mechanism remains to be elucidated. The present study prospectively evaluated the role of small LDL, a known risk factor for coronary heart disease, as a risk factor for the development of NIDDM. METHODS AND RESULTS: The study was based on a nested case-control sample of 204 elderly men and women from Kuopio, Finland. LDL subclasses were characterized by size with 2% to 14% polyacrylamide gels produced by recently developed methods. Logistic regression analysis showed that subjects with a predominance of small LDL (LDL subclass phenotype B) had a greater than two fold increased risk for developing NIDDM over the 3.5-year follow-up period. This association was independent of age, sex, glucose intolerance, and body mass index but was not independent of fasting triglyceride or insulin levels. Further, an increase of 5A in LDL diameter was associated with a 16% decrease in risk of NIDDM, and a composite variable of LDL diameter and triglyceride and HDL cholesterol concentrations, identified by principal-components analysis, was also associated with NIDDM. These associations may be attributable to the role of small LDL as a marker for insulin resistance. CONCLUSIONS: This study is the first to demonstrate that a predominance of small LDL particles is a risk factor for the future development of NIDDM, and it implies that small LDL contributes to risk of coronary heart disease in prediabetics.

Aged↗
PubMed1995

The association of apolipoprotein E polymorphism with memory: a population based study.

Several studies have shown an association between the apolipoprotein epsilon 4 allele and Alzheimer's disease (AD). The allele epsilon 2 has been associated with survival and longevity. We wanted to examine whether the relationship between cognitive efficiency and apolipoprotein E polymorphism (APOE) exists in a random sample of 916 non-demented elderly subjects. Episodic memory was examined with the list learning test, and with immediate and delayed recall of the figures. Semantic memory was examined with the Category and Verbal Fluency Tests. Constructional abilities were examined by copying the figures. Attention functions were examined with Trail Making A and B tests. We found that subjects with APOE E2/2 and 2/3 phenotypes showed better learning ability than those subjects with the APOE E2/4, 3/4 or 4/4 phenotypes. Impaired memory was not related to the excess of cardiovascular diseases in the subjects with APOE E2/4, 3/4, 4/4 phenotypes. Thus they may be associated, at least partly, with genetic factors.

Aged↗
PubMed1995

Hyperinsulinemic microalbuminuria. A new risk indicator for coronary heart disease.

BACKGROUND: Both hyperinsulinemia and microalbuminuria have been shown to increase coronary heart disease (CHD) risk, but the interaction among hyperinsulinemia, microalbuminuria, and the risk for CHD has not been investigated in previous studies. METHODS AND RESULTS: The risk of CHD in relation to hyperinsulinemia and microalbuminuria was examined in a cohort of 1069 elderly nondiabetic subjects from Kuopio, east Finland, during 3.5 years of follow-up. The overall incidence of CHD death was 2.8%, and 6.9% of study subjects died of CHD or had a nonfatal myocardial infarction (later referred to as all CHD events). In the highest fasting-insulin quintile (fasting insulin > or = 114.0 pmol/L), there was a slightly but insignificantly higher incidence rate of both CHD mortality and all CHD events compared with lower quintiles. The incidence rates of CHD mortality and all CHD events were significantly higher in the highest urinary albumin/creatinine ratio (ACR) quintile (ACR > or = 3.22 mg/mmol) compared with lower quintiles (P < .05 and P < .01, respectively). Hyperinsulinemic microalbuminuria (simultaneous presence of fasting insulin > or = 114.0 pmol/L and ACR > or = 3.22 mg/mmol) markedly increased the risk of CHD mortality (12.5%, P < .001) and all CHD events (18.8%, P < .001) compared with normoinsulinemic subjects without microalbuminuria (2.2% and 5.8%, respectively). In univariate logistic regression analyses, hyperinsulinemic microalbuminuria was a strong predictor of both CHD death (odds ratio [OR], 5.93; P < .001) and all CHD events (OR, 3.39; P = .002). Multivariate logistic regression analyses were also performed, including sex, current smoking, waist-hip ratio, systolic blood pressure, and HDL cholesterol, with insulin, ACR, or both as independent variables. Even after adjustment for these variables, hyperinsulinemic microalbuminuria remained a strong predictor of CHD death (OR, 7.91; P < .001) and all CHD events (OR, 2.95; P = .014). The group with hyperinsulinemic microalbuminuria was characterized by the most adversely affected risk factor pattern (high triglycerides > or = 2.3 mmol/L, low HDL cholesterol < or = 0.9 mmol/L in men and < or = 1.20 mmol/L in women, and hypertension). CONCLUSIONS: Simultaneous occurrence of hyperinsulinemia and microalbuminuria identifies a group of subjects with a highly increased risk for CHD in elderly nondiabetic subjects.

Aged↗
PubMed1995

Polymorphisms of the human hexokinase II gene: lack of association with NIDDM and insulin resistance.

Skeletal muscle and adipose tissue hexokinase II is a promising candidate gene for non-insulin-dependent diabetes mellitus (NIDDM) and insulin resistance. Therefore, we investigated the association of alleles at four polymorphic loci in this gene with NIDDM and insulin resistance in 110 Finnish diabetic patients with NIDDM and in 97 Finnish control subjects with normal glucose tolerance and a negative family history of diabetes. The four polymorphic nucleotide substitutions (silent) in the coding region of the hexokinase II gene were: GAC 251 GAT (exon 7), AAC 692 AAT and CCG 736 CCC (exon 15), and CTG 766 CTA (exon 16). Allele frequencies of each of these polymorphisms did not differ between patients with NIDDM and control subjects. In addition, subjects who were homozygous for the less frequent allele of each of the four polymorphisms had a similar degree of insulin resistance, as determined by the euglycaemic clamp technique, as did the subjects who were homozygous for the common allele in both control subjects and in patients with NIDDM. In conclusion, polymorphisms in the hexokinase II gene are not associated with the risk of NIDDM or insulin resistance in the Finnish population.

Adipose Tissue↗
PubMed1995

Serum proinsulin levels are disproportionately increased in elderly prediabetic subjects.

Insulin resistance and impaired insulin secretion are thought to be the primary defects in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM). Disproportionately increased proinsulin relative to insulin levels are suggested to be an early indicator of a failing pancreas. We examined the relationship of fasting specific insulin, proinsulin, and 32, 33 split proinsulin concentrations, and the proinsulin: insulin ration to the risk of developing NIDDM 3.5 years later in 65-74-year-old non-diabetic Finnish subjects participating in a population-based study (n=892) on diabetes and heart disease. Altogether 69 subjects developed NIDDM over a 3.5-year follow-up (cases). The cases were compared to randomly-selected gender-matched control subjects (n=69) and control subjects matched for gender, glucose tolerance status (normal or impaired), and body mass index (n=69). There were no differences in insulin concentrations between cases and random or matched control subjects [median and interquartile range: 123 (77-154), 108 (74-143), 118 (83-145) pmol/l, p=0.271]. Random control subjects had lower proinsulin and 32, 33 split proinsulin concentrations and split proinsulin: insulin ratios compared to cases [5.7 (3.8-9.0) vs 7.3 (4.8-10.0) pmol/l, p=0.005; 7.3 (4.5-13.0 vs 10.4 (7.1-18.0) pmol/l, p=0.002; 0.073 (0.057-0.110) vs 0.097 (0.060- 0.135), p=0.003]. Matched control subjects had lower proinsulin concentrations and proinsulin: insulin ratios compared to cases [5.9 (4.0-7.7) vs 7.3 (4.8-10.0) pmol/l, p=0.019; 0.048 (0.035-0.071) vs 0.064 (0.045-0.100), p=0.008]. When cases were compared to matched control subjects a 1 SD increase in baseline proinsulin: insulin ratio was associated with a 1.37-fold risk (p=0.020) of developing diabetes. Moreover, this association was independent of fasting glucose concentration at baseline. Thus, in elderly prediabetic subjects disproportionately increased proinsulin concentration, an indicator of defective insulin secretion, is associated with conversion to diabetes over a short time period.

Aged↗
PubMed1995

Apolipoprotein E4 phenotype is not an important risk factor for coronary heart disease or stroke in elderly subjects.

The allele e4 (apo e4) of apolipoprotein E (apo E) has been associated with an increased risk for coronary heart disease (CHD) in cross-sectional studies in middle-aged subjects. We investigated the risk of CHD and stroke with respect to the number of apo e4 alleles in a prospective study of a Finnish nondiabetic cohort including 1067 subjects 65 to 74 years old at baseline. During the 3.5-year follow-up, CHD mortality was 2.8%, total CHD incidence 6.9%, and the cumulative occurrence of CHD (prevalence at baseline and the 3.5-year incidence combined) 17.0%. The incidence of stroke was 3.4%, and the cumulative occurrence of stroke was 6.0%. The CHD mortality was 3.4% in subjects with no apo e4 allele (n = 734), 1.7% in those with one apo e4 allele (n = 296), and 0% in subjects with two apo e4 alleles (n = 37) (P = NS between the three groups). The incidence of CHD according to the number of apo e4 alleles was 6.9% (no apo e4 alleles), 7.4% (one apo e4 allele), and 2.7% (two apo e4 alleles), and the cumulative occurrence of CHD was 16.5%, 18.6%, and 13.5%, respectively (P = NS). The incidence of stroke was 3.8% in subjects with no apo e4 allele, 2.7% in those with one apo e4 allele, and 0% in those with two apo e4 alleles (P = NS). The cumulative occurrence of stroke was 6.0%, 6.4%, and 2.7%, respectively (P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Glucokinase gene variants in subjects with late-onset NIDDM and impaired glucose tolerance.

OBJECTIVE: To investigate the frequency of variants of the glucokinase (GCK) gene in subjects with late-onset non-insulin-dependent diabetes mellitus (NIDDM) and in subjects with late-onset impaired glucose tolerance (IGT). RESEARCH DESIGN AND METHODS: The study population included 36 Finnish patients with late-onset NIDDM who were treated with diet for > 8 years or who were newly diagnosed and 40 subjects with late-onset IGT who had low or normal insulin levels when tested by an oral glucose tolerance test. All exons, exon-intron junctions, and islet and liver promotor regions of the GCK gene were amplified with the polymerase chain reaction and screened for mutations using single-strand conformation polymorphism analysis. RESULTS: A silent third-base substitution (TAC: >TAT) in codon 215 of exon 6 was found in 2.8% of NIDDM patients and in 5.0% of IGT subjects. Polymorphisms were found in islet exon 1 at nucleotide 403 (C-->G) in 16.7% of NIDDM patients and in 17.5% of IGT subjects and in the noncoding region of the islet promotor at nucleotide -30 (G-->A) in 13.9% of NIDDM patients and in 25.0% of IGT subjects. Furthermore, in liver intron 1 a variant (C-->T), 12 base pairs upstream from the splice acceptor site, was found in 5.6% of NIDDM patients and in 7.5% of IGT subjects. CONCLUSIONS: These results indicate that the mutations in the coding region of the GCK gene are not likely to play a major role the pathogenesis of late-onset NIDDM or IGT in the Finnish population.

Diabetes Mellitus, Type 2↗
PubMed1994

Association of apolipoprotein E phenotypes with late onset Alzheimer's disease: population based study.

OBJECTIVE: To determine the association between the e4 allele of apolipoprotein E and Alzheimer's disease in a randomly selected population sample. DESIGN: Cross sectional population based study. SUBJECTS: 980 people aged 69 to 78 (349 men, 631 women). SETTING: Population of Kuopio, eastern Finland. MAIN OUTCOME MEASURES: Presence of e4 allele and diagnosis of Alzheimer's disease by detailed neurological and neurophysiological evaluation. RESULTS: 46 (4.7%) subjects were classified as having probable or possible Alzheimer's disease. The frequency of the apolipoprotein E e4 allele was 0.359 in patients with Alzheimer's disease and 0.165 subjects without dementia (P < 0.0001). The prevalence of Alzheimer's disease was 2.9% in subjects with no e4 alleles, 7.6% in subjects with one e4 allele, and 21.4% in subjects with two e4 alleles of apolipoprotein E. CONCLUSIONS: Allele e4 of apolipoprotein is associated with Alzheimer's disease in a dose-response fashion in a randomly selected elderly population.

Aged↗
PubMed1994

Hyperinsulinemia predicts multiple atherogenic changes in lipoproteins in elderly subjects.

Several studies have shown that hyperinsulinemia and insulin resistance are associated with high triglyceride and low high-density lipoprotein (HDL) cholesterol levels. However, previous studies have been cross-sectional, and thus the presence of hyperinsulinemia or insulin resistance could be a consequence of the underlying lipid disorder instead of its cause. Therefore, we examined the relation of fasting insulin level measured in a cross-sectional study in nondiabetic subjects 65 to 74 years old (n = 881) to the risk of developing lipid disorders 3.5 years later. The incidence of the following lipid abnormalities was calculated: hypertriglyceridemia (n = 49/732, incident cases/subjects free of the particular disorder at baseline), high low-density lipoprotein (LDL) cholesterol level (n = 43/696), low HDL cholesterol level (n = 33/708), high apolipoprotein (apo) B level (n = 72/699), low apoAI level (n = 47/711), low serum LDL cholesterol/serum apoB ratio (n = 55/685), and low serum HDL cholesterol/serum apoAI ratio (n = 48/707). Baseline insulin level was not significantly associated with the development of high LDL cholesterol or low HDL cholesterol levels. Baseline insulin was associated with the development of hypertriglyceridemia (odds ratio [OR], 1.64; 95% confidence interval [CI], 1.12 to 2.40; P = .011), high apoB (OR, 1.54; 95% CI, 1.13 to 2.10; P = .006), low apoAI (OR, 1.72; 95% CI, 1.22 to 2.42; P = .002), low LDL cholesterol/apoB ratio (OR, 1.99; 95% CI, 1.36 to 2.90; P < .001), and low HDL cholesterol/apoAI ratio (OR, 1.93; 95% CI, 1.34 to 2.79; P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Characterization of the early lesion of 'degenerative' valvular aortic stenosis. Histological and immunohistochemical studies.

BACKGROUND: Nonrheumatic stenosis of trileaflet aortic valves, often termed senile or calcific valvular aortic stenosis, is considered a "degenerative" process, but little is known about the cellular or molecular factors that mediate its development. METHODS AND RESULTS: To characterize the developing aortic valvular lesion, we performed histological and immunohistochemical studies on Formalin-fixed and methanol-Carnoy's-fixed paraffin-embedded aortic valve leaflets or on frozen sections obtained at autopsy from 27 adults (age, 46 to 82 years) with normal leaflets (n = 6), mild macroscopic leaflet thickening (n = 15), or clinical aortic stenosis (n = 6). Focal areas of thickening ("early lesions") were characterized by (1) subendothelial thickening on the aortic side of the leaflet, between the basement membrane (PAS-positive) and elastic lamina (Verhoeff-van Gieson), (2) the presence of large amounts of intracellular and extracellular neutral lipids (oil red O) and fine, stippled mineralization (von Kossa), and (3) disruption of the basement membrane overlying the lesion. Regions of the fibrosa adjacent to these lesions were characterized by thickening and by protein, lipid, and calcium accumulation. Control valves showed none of these abnormalities. Immunohistochemical studies were performed using monoclonal antibodies directed against macrophages (anti-CD68 or HAM-56), and contractile proteins of smooth muscle cells or myofibroblasts (anti-alpha-actin and HHF-35) or rabbit polyclonal antiserum against T lymphocytes (anti-CD3). In normal valves, scattered macrophages were present in the fibrosa and ventricularis, and occasional muscle actin-positive cells were detected in the proximal portion of the ventricularis near the leaflet base, but no T lymphocytes were found. In contrast, early lesions were characterized by the presence of an inflammatory infiltrate composed of non-foam cell and foam cell macrophages, occasional T cells, and rare alpha-actin-positive cells. In stenotic aortic valves, a similar but more advanced lesion was seen. CONCLUSIONS: The early lesion of "degenerative" aortic stenosis is an active inflammatory process with some similarities (lipid deposition, macrophage and T-cell infiltration, and basement membrane disruption) and some dissimilarities (presence of prominent mineralization and small numbers of smooth muscle cells) to atherosclerosis.

Aged↗
PubMed1994

Non-insulin-dependent diabetes and its metabolic control are important predictors of stroke in elderly subjects.

BACKGROUND AND PURPOSE: Non-insulin-dependent diabetes mellitus (NIDDM) is a major risk factor for stroke in the middle-aged population, but few prospective population-based studies are available in the elderly. Moreover, the importance of metabolic control and the duration of diabetes in diabetic subjects has remained controversial. There are no previous studies on association of insulin with the risk of stroke. The present study examined whether NIDDM, its metabolic control and duration, and insulin level predict stroke. METHODS: We measured cardiovascular risk factors including glucose tolerance, plasma insulin, and glycosylated hemoglobin A1c in a Finnish cohort of 1298 subjects aged 65 to 74 years and investigated the impact of these risk factors on the incidence of both fatal and nonfatal stroke during 3.5 years of follow-up. RESULTS: Of 1298 subjects participating in the baseline study, 1069 did not have diabetes and 229 had NIDDM. During the 3.5-year follow-up, 3.4% (n = 36) of nondiabetic subjects and 6.1% (n = 14) of NIDDM subjects had a nonfatal or fatal stroke. The incidence of stroke was significantly higher in diabetic women compared with nondiabetic women (odds ratio [OR], 2.25; 95% confidence interval [CI], 1.65 to 3.06). In contrast, the risk of stroke was not significantly higher in diabetic men than in nondiabetic men (OR, 1.36; 95% CI, 0.44 to 4.18). In multivariate logistic regression analyses including all study subjects, fasting and 2-hour glucose (P < .01 and P < .05, respectively), glycosylated hemoglobin A1c (P < .01), atrial fibrillation (P < .05), hypertension (P < .05), and previous stroke (P < .01) predicted stroke events. In diabetic subjects, fasting and 2-hour glucose (P < .01 and P < .05, respectively), glycosylated hemoglobin A1c (P < .05), the duration of diabetes (P < .05), and atrial fibrillation (P < .05) were the baseline variables predicting stroke events. Finally, fasting insulin (P < .05), hypertension (P < .05), and previous stroke (P < .01) were associated with stroke incidence in nondiabetic subjects. CONCLUSIONS: Our 3.5-year follow-up study provides evidence that NIDDM, its metabolic control, and the duration of diabetes are important predictors of stroke in elderly subjects, particularly in women. Moreover, fasting insulin level appears to be a risk factor for stroke in elderly nondiabetic subjects.

Aged↗
PubMed1994

Insulin receptor substrate-1 variants in non-insulin-dependent diabetes.

Insulin receptor substrate-1 (IRS-1) plays an important role in insulin-stimulated signaling mechanisms. Therefore, we investigated the frequency and clinical significance of variants in the coding region of this gene in patients with non-insulin-dependent diabetes (NIDDM). Initial screening included a population-based sample of 40 Finnish patients with typical NIDDM. Applying single strand conformation polymorphism analysis the following amino acid substitutions were found among the 40 NIDDM patients: Gly818-Arg, Ser892Gly, and Gly971Arg. The first two variants have not been previously reported. Additional samples of 72 patients with NIDDM and 104 healthy control subjects with completely normal oral glucose tolerance test and a negative family history of diabetes were screened. The most common polymorphism was the Gly971Arg substitution which was found in 11 (9.8%) of 112 NIDDM patients and in 9 (8.7%) of 104 control subjects. The Gly818Arg substitution was found in 2 (1.8%) of NIDDM patients and in 2 (1.9%) of control subjects, and the Ser892Gly substitution was found in 3 (2.7%) NIDDM patients and in 1 (1.0%) control subject. The Gly971Arg substitution was not associated with an impairment in insulin secretion capacity (estimated by insulin responses in an oral glucose tolerance test or by the hyperglycemic clamp) or insulin action (estimated by the euglycemic clamp). Of the three amino acid substitutions observed Ser892Gly is the most interesting one since it abolishes one of the potential serine phosphorylation sites (SPGE) which is located immediately NH2-terminal to the only SH2 binding site of growth factor receptor-bound protein (GRB2), and thus could potentially influence some aspects of signal transduction and metabolic response to insulin.

Aged↗
PubMed1994

Microalbuminuria precedes the development of NIDDM.

Several studies have indicated that insulin resistance, elevated blood pressure (BP), and dyslipidemia precede the onset of non-insulin-dependent diabetes mellitus (NIDDM). Little data, however, exist on the presence of renal disease in prediabetic subjects. We measured albumin excretion in a cross-sectional population study in subjects 65-74 years of age living in eastern Finland in relation to the risk of developing diabetes 3.5 years later. The prevalence of microalbuminuria (urinary albumin-to-urinary creatinine ratio > or = 2 mg/mmol) was 1.3-, 1.8-, and 2.0-fold higher among subjects with impaired glucose tolerance (n = 242), newly diagnosed NIDDM subjects (n = 92), and previously diagnosed NIDDM subjects (n = 136), respectively, compared with subjects with normal glucose tolerance (n = 826). Nondiabetic subjects with microalbuminuria had multiple abnormalities in cardiovascular risk factors including elevated BP, high triglyceride concentration, high insulin concentration, and a low high-density lipoprotein cholesterol concentration, a cluster of risk factors typical for prediabetic individuals. The relationship between microalbuminuria and the incidence of NIDDM over the 3.5-year follow-up was studied in 891 subjects who were free of diabetes at baseline. Converters to diabetes (n = 69) had a higher prevalence of hypertension (68.1 vs. 54.4%, P < 0.05) and a higher prevalence of microalbuminuria (43.5 vs. 30.4%, P < 0.05) than nonconverters (n = 822). In logistic regression analysis, microalbuminuria predicted the development of NIDDM independently of BP level.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1994

NIDDM and its metabolic control predict coronary heart disease in elderly subjects.

The aim of this study was to evaluate whether noninsulin-dependent diabetes (NIDDM) and its metabolic control and duration predict coronary heart disease (CHD) events during a 3.5-year follow-up in a randomly selected Finnish population sample 65-74 years of age at baseline. Of 1,298 subjects participating in the baseline study, 1,069 were nondiabetic and 229 had NIDDM. During the follow-up, 3.4% of nondiabetic and 14.8% of NIDDM subjects died from CHD or had a nonfatal myocardial infarction (MI). The impact of NIDDM on CHD mortality and morbidity was more marked in women than in men. Odds ratios (ORs) and their 95% confidence intervals for CHD death and nonfatal MI in women with NIDDM compared with women with normal glucose tolerance were 11.7 (3.8-36.4) and 4.7 (3.6-6.1). In men, the corresponding ORs were 0.43 (0.1-1.9) and 1.4 (0.6-3.2). In multiple logistic regression analyses including all study subjects, NIDDM (P < 0.01), male sex (P < 0.05), and previous MI (P < 0.01) predicted CHD death (n = 45). NIDDM (P < 0.01), male sex (P < 0.05), previous MI (P < 0.05), current smoking (P < 0.001), systolic blood pressure (P < 0.001), and low high-density lipoprotein cholesterol (P < 0.01) predicted all CHD events (CHD death or nonfatal MI) (n = 107). In NIDDM subjects, only glycated hemoglobin A1c (GHbA1c) at baseline (P < 0.01) and duration of diabetes (P < 0.05) predicted CHD death (n = 15) and all CHD events (n = 33). There was a significant increase in the risk of CHD death and all CHD events in NIDDM subjects with GHbA1c levels higher than 7.0% compared with diabetic subjects with lower GHbA1c (ORs 4.3 [1.1-16.7] and 2.2 [1.0-5.1]). In conclusion, NIDDM and its metabolic control and the duration of diabetes are important predictors of CHD in elderly subjects, particularly in women.

Aged↗