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PubMed2004

Allograft diabetic nephropathy may progress to end-stage renal disease.

Mesangial expansion and glomerular basement membrane thickening characteristic of diabetic nephropathy recur in diabetic recipients of renal allografts from non-diabetic donors but progression to renal failure is minimally documented. Three female renal allograft recipients (aged 40, 62 and 73 yr), who developed end-stage renal disease (ESRD) due to recurrent diabetic nephropathy (two patients) and de novo diabetes (one patient) are reported. Onset of proteinuria, uncontrolled hypertension, azotemia, renal allograft pathologic findings and the need for hemodialysis were analyzed. None of the kidney donors (one cadaver, two living related) had known diabetes or perturbed glucose metabolism pre-transplantation. The three patients presented had different varieties of diabetes; type 1, type 2 and new onset diabetes after transplantation (NODAT). In each subject, proteinuria was detected by dipstick at a mean of 8.3 yr (range 8-9) post-transplantation and increased to the nephrotic range (3.7-4.8 g/day) inducing hypoalbuminemia and azotemia. A histopathologic diagnosis of allograft diabetic nephropathy was made in a mean of 11.7 yr (range 10-14), based on glomerular basement membrane thickening, nodular and diffuse intercapillary glomerulosclerosis, arteriolosclerosis, and tubular atrophy with marked tubular basement membrane thickening characteristic of advanced diabetic nephropathy. All three patients manifested uremia and resumed hemodialysis. Two patients died from sepsis within 2 months and one patient died 2.5 yr later after resumption of maintenance hemodialysis. We infer that recurrent or de novo diabetic nephropathy in renal allografts follows a clinical decade-long course irrespective of diabetes. Reports of ESRD due to allograft diabetic nephropathy (ADN) have been limited because of shorter survival of diabetic transplant recipients and few kidney biopsies performed in patients with chronic allograft dysfunction. The occurrence of allograft diabetic nephropathy in some, but not all patients, however, suggests that individual genetic variability modulates disease expression.

Adult↗

PubMed1978

Pathology of centenarians. II. Urogenital and digestive systems.

The urogenital and digestive systems in 23 centenarians (7 males and 16 females) were examined pathologically. In the urogenital system, macroscopic scar formation, chronic pyelonephritis and arterio- and arteriolosclerosis of the kidney usually were pronounced. Six instances of prostatic glandular hyperplasia were demonstrated, and three of these were associated with well-differentiated adenocarcinoma. The testis, ovary and uterus usually showed a strong tendency toward atrophic changes. In the digestive system, senile atrophy of the liver and formation of colonic diverticula were noted. In this series of aged subjects, malignant lesions of the gastrointestinal tract were rare. It is also noteworthy that the unsuspected lesion of massive gastrointestinal hemorrhage associated with the various observed disorders might have been the cause of death in some of these centenarians.

Aged↗

PubMed1998

Morphological studies of baseline needle biopsies from living donor kidneys: light microscopic, immunohistochemical and ultrastructural findings.

Fifty-seven consecutive living donors (31 women and 26 men aged 20.7-72.3 years, mean 50.6 years) were subjected to needle biopsy during nephrectomy, immediately before removal of the kidney. By light microscopy, semiquantitative scoring (0-3) was performed for arteriosclerosis, arteriolar hyalinosis (hyalin arteriolosclerosis), glomerulosclerosis, interstitial mononuclear cell infiltration, and interstitial fibrosis/tubular atrophy. Whereas vascular changes were striking in many biopsies (arteriosclerosis grades 2-3: 28/54 cases, arteriolar hyalinosis grades 2-3: 15/55 cases), glomerular and tubulointerstitial changes were mostly low grade. The morphological changes tended to be more pronounced in middle-aged and older individuals, but, in particular, vascular changes were seen also in the younger age group. Immunofluorescence microscopy revealed glomerular granular staining for IgM in 52.7% of the cases, IgA in 9.1%), IgG in 1.8%, and C3 in 12.7%. The main ultrastructural finding was glomerulosclerosis; one case with diffuse glomerular IgA showed distinct dense deposits, and one case showed similar dense deposits without IgA deposition. Arteriolar wall deposition of C3 was found in 58.2% of the cases, and IgM in 10.9%. Especially C3 occurred both with arteriolar hyalinosis and in arterioles without light microscopic alterations. The observation of significant vascular changes in baseline biopsies is relevant especially in the differential diagnosis of chronic rejection and cyclosporine nephropathy. The immunohistochemical findings strongly indicate the occurrence of immunoglobulins and complement factor C3 in both glomeruli and arterioles without clinical or morphological signs of renal disease. The possible pathophysiological significance of such deposits remains, however, uncertain.

Adult↗

PubMed2007

Distinguishing diabetic nephropathy from other causes of glomerulosclerosis: an update.

Diabetic nephropathy is a common cause of end-stage renal disease worldwide. It is characterised by diffuse or nodular glomerulosclerosis, afferent and efferent hyaline arteriolosclerosis, and tubulointerstitial fibrosis and atrophy. Diffuse and nodular diabetic glomerulosclerosis share similar histological features with other clinical conditions. Immunofluorescence and electron microscopy studies, and clinicopathological correlation are essential to differentiate diabetic nephropathy from other conditions that result in diffuse and nodular glomerulosclerosis.

Diabetic Nephropathies↗

PubMed2006

Parathyroid hormone stimulates endothelial expression of atherosclerotic parameters through protein kinase pathways.

Parathyroid hormone (PTH), the major systemic calcium-regulating hormone, has been linked to uremic vascular changes. Considering the possible deleterious action of PTH on vascular structures, it seemed logical to evaluate the impact of PTH on the receptor of advanced glycation end products (RAGE) and interleukin 6 (IL-6) mRNA and protein expression, taking into account that such parameters might be involved in the pathogenesis of vascular calcification, atherosclerosis, and/or arteriolosclerosis. Human umbilical vein cord endothelial cells (HUVEC) were stimulated for 24 h with 10(-12)-10(-10) mol/l PTH. The mRNA expression of RAGE and IL-6 was established by reverse transcriptase/PCR techniques. RAGE protein levels were determined by Western blot and IL-6 secretion was measured by ELISA. The pathways by which PTH may have an effect on HUVEC functions were evaluated. PTH (10(-11)-10(-10)mol/l) significantly increased RAGE mRNA and protein expression. PTH also significantly increased IL-6 mRNA expression without changes at protein levels. The addition of protein kinase (PKC or PKA) inhibitors or nitric oxide (NO) synthase inhibitors significantly reduced the RAGE and IL-6 mRNA expression and the RAGE protein expression. PTH stimulates the mRNA expressions of RAGE and IL-6 and the protein expression of RAGE. These stimulatory effects are probably through PKC and PKA pathways and are also NO dependent. Such data may explain the possible impact of PTH on the atherosclerotic and arteriosclerotic progression.

Atherosclerosis↗

PubMedDate not supplied

Vascular risk factors linked to multiple lacunar infarcts.

BACKGROUND: The pathogenesis of lacunar infarcts is still incompletely established. Data from the literature suggest that vascular risk factors differ among patients with multiple (MLI) and single lacunar infarcts (SLI). We reexamined this hypothesis using stricter inclusion criteria and a less selected study population. METHODS: We evaluated 136 patients consecutively admitted for first-ever minor stroke to a general hospital with the characteristics of a community hospital. Vascular risk factors were studied by univariate and multivariate statistical analyses among the following subgroups of patients, classified according to CT findings: (a) with lacunar infarct; (b) with nonlacunar infarct (NLI); (c) with SLI; (d) with MLI; (e) with single, either lacunar or nonlacunar, infarct. RESULTS: No significant difference was observed between patients with lacunar infarcts and patients with NLI. Compared to patients with SLI or NLI, patients with MLI had significantly more often a family history of hypertension, cardiomegaly on the chest radiograph and CT leukoaraiosis as well as a higher systolic and diastolic blood pressure on admission. Logistic regression analysis selected CT leukoaraiosis, Rx cardiomegaly and admission diastolic blood pressure as independent, significant predictors of MLI. CONCLUSION: In patients with first-ever minor stroke, the risk factor profile differs according to the evidence of SLI or MLI on the CT scan. In terms of risk factors, patients with SLI seem more similar to those with NLI than those with MLI. Based on the predicting effect of variables linked with type and severity of arterial hypertension, the CT appearance of MLI might express a more univocal and specific cerebrovascular pathology (hypertensive arteriolosclerosis).

Aged↗

PubMed2002

Pathophysiology of age-related cerebral white matter changes.

The pathogenesis of age-related cerebral white matter changes (WMC) is still a matter of investigation. Alterations of deep small vessels, such as arteriolosclerosis, are considered to play a central role in the development of WMC. Stenosis or occlusion of small vessels may cause sudden or more chronic ischemia resulting in small areas of necrosis (lacunar infarction) or diffuse alterations consistent with the definition of white matter incomplete infarct. Moreover, the arteriolosclerotic changes may cause loss of autoregulation in the deep white matter and consequent cerebral blood flow fluctuations in response to changes of systemic blood pressure. Both these types of mechanisms may be particularly harmful because the blood supply of the white matter is of the terminal type with scarce anastomoses. Other pathophysiological hypotheses on the origin of WMC have been raised, and they can probably be considered as complementary to the ischemic one. The small vessel alterations could lead to damage of the blood-brain barrier and chronic leakage of fluid and macromolecules in the white matter. The increased interstitial fluid concentration in abnormal white matter may be also a consequence of arterial hypertensive bouts. Genetically determined factors could play an important role in the development of WMC, and at least one disease (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy - CADASIL) characterized by severe leukoencephalopathy exists with a determined genetic origin. It is possible that other genetic factors contribute, by interaction with conventional risk factors, to the development of white matter injury in nonfamilial cases.

Aged↗

PubMedDate not supplied

Association between the G protein beta3 subunit 825t allele and radial artery hypertrophy.

The GNB3 C825T gene polymorphism has recently been identified and associated with hypertension, obesity and left ventricular hypertrophy. The aim of the study was to determine the relationship between the C825T polymorphism of the gene encoding for the G protein beta3 subunit (GNB3 C825T) and vascular hypertrophy. We studied a cohort of 306 subjects (age 49 +/- 12 years) without evidence of cardiovascular disease and never treated with cardiovascular drugs. Vascular phenotypes were evaluated for the common carotid and radial arteries using high-resolution echo-tracking devices. Genotype frequencies were in agreement with the Hardy-Weinberg equilibrium. For the radial artery, mean wall thickness was significantly higher in subjects carrying the 825T allele than in CC genotype subjects (240 +/- 54 microm for CT genotype and 241 +/- 53 microm for TT genotype vs. 222 +/- 52 microm for CC genotype, p = 0.01). The frequency of the 825T allele was significantly different in subjects with (52%) and without (35%) radial artery hypertrophy (chi(2) = 10.88, p < 0.001). The relative risk of radial artery hypertrophy in subjects carrying the 825T allele compared with those with the CC genotype was 3.02 (95% CI 1.53- 5.95). A logistic regression analysis indicated that the positive and significant association between the 825T allele and radial artery hypertrophy was independent of age, blood pressure, gender and BMI. In contrast, no association between genotypes and carotid artery wall thickening was observed. These results suggest that some genetic characteristics determine in part the patterns of radial artery geometrical changes. As the 825T allele is associated with vascular hypertrophy of a muscular artery but not with structural changes of an elastic artery, we hypothesize that the 825T allele may be a genetic marker of arteriolosclerosis.

Adult↗

PubMed1991

Leuko-araiosis.

Leuko-araiosis is an unspecific radiologic sign, seen with CT scan or with MRI. It can be found as well in normal elderly persons as in pathological conditions. For the sake of clarity, CT scan and MRI images have to be distinguished. CT leuko-araiosis is linked with vascular risk factors and with age. The situation is more complex for MRI leuko-araiosis (likely on account of the higher sensitivity of MRI). Some images (caps and rims), frequently seen in normal, even young, individuals, are more frequent in aging. On the contrary, abnormal images at a distance from the ventricle are more difficult to interpret. Some of them are due to pathological well defined conditions (small infarcts, Binswanger's disease, cysts, plaques). Others may be secondary to remote pathologies (such as infarcts). Others are due to little specific conditions, such as perivascular dilatations ('état criblé' due to brain vasogenic edema, or to brain atrophy whatever its cause, and more frequently seen in the elderly). Other changes, such as incomplete infarction or myelin pallor with gliosis, have been described. At last, in some cases, no clearcut pathological lesion could be found. Leuko-araiosis may be present in primary degenerative dementia of the Alzheimer type, but it is neither necessary nor sufficient to establish the diagnosis of Alzheimer's disease, and it does not seem more frequent than in elderly controls. The mechanism of leuko-araiosis in Alzheimer's disease is likely multifactorial (for example, cerebral atrophy, amyloid angiopathy, associated hypertensive arteriolosclerosis could be involved). The relationship between leuko-araiosis, myelin pallor and white matter atrophy is poorly understood, and remains to be studied.

Adult↗

PubMed1989

Significance of tubulointerstitial lesions in biopsy specimens of glomerulonephritic patients.

To evaluate the significance of tubulointerstitial lesions in the cortical area of renal biopsy specimens, clinicopathological studies were performed on 101 cases of IgA nephropathy, 31 cases of IgA-negative (non-IgA) proliferative glomerulonephritis and 75 cases of idiopathic membranous glomerulonephritis. The degree of tubulointerstitial lesions was assessed semiquantitatively by light microscopic observation and was correlated with the several histopathological and clinical parameters at biopsy, as well as with status at final follow-up (average follow-up period: 72 months). In these three types of glomerulonephritis, the degree of tubulointerstitial lesions in the cortical area was clearly correlated with the severity of glomerular injury, the prevalence of segmental sclerosis, global sclerosis, arteriolosclerosis, decreased renal function (GFR less than 70 ml/min) and hypertension (greater than 150/90 mm Hg) at the time of biopsy. The prevalence of stable renal function at final follow-up was statistically higher in the cases without tubulointerstitial lesions or with those whose lesions included less than 20% of the cortical area. From the above data, it was concluded that a semiquantitative evaluation of tubulointerstitial lesions in the cortex would reflect the severity of glomerular injury and also contribute to the assessment of prognosis in such primary glomerulonephritic patients.

Adult↗

PubMed1983

Posterior ischemic optic neuropathy. II. Histopathology of the idiopathic form.

The optic nerve and chiasm, obtained at autopsy, from 53 cases with clinical histories of cerebrovascular disturbances were histopathologically investigated, and ischemic changes in the posterior portion of the optic nerve were revealed in 12 cases. The progress of posterior ischemic optic neuropathy might be divided into necrotic, liquefactive and scar stages. The lesions were located in the transverse, peripheral, altitudinal and axial areas of the optic nerve. Occlusive changes of the vascular lumina due to atherosclerosis, arteriolosclerosis, capillosclerosis and emboli were demonstrated in association with the ischemic changes in the optic nerve parenchyma.

Adult↗

PubMed2005

Agonistic autoantibodies to the AT1 receptor in a transgenic rat model of preeclampsia.

We used rats transgenic for the human angiotensinogen (hAogen) gene and the human renin (hRen) gene and crossed the strains to produce a model of preeclampsia in the dams. The female (n=9) hAogen x male hRen cross had severe (telemetry-measured) hypertension and albuminuria, which developed during the last trimester of pregnancy and subsided after delivery. The converse cross (n=9) and control (n=9) SD rats did not. We demonstrated that the female hAogen x male hRen cross had agonistic antibodies capable of activating the angiotensin (Ang) II AT1 receptor (AT1R-AA) and defined the epitope on the receptor's second extracellular loop. The phenomenon also occurs in humans with preeclampsia. The rats displayed renal histology reminiscent of preeclampsia, including fibrin deposition confined to the glomeruli. The complement system was activated in glomeruli and IgG deposits were present that may represent AT1R-AA. Finally, we observed an atherosis-like lesion in the spiral arteries of the placental bed, which we called placental-bed arteriolosclerosis. Our model may be relevant to preeclampsia in humans.

Angiotensinogen↗

PubMed2002

Two types of lacunar infarcts: further arguments from a study on prognosis.

BACKGROUND AND PURPOSE: Earlier, we found that lacunar stroke patients with > or =1 asymptomatic lacunar infarcts on CT had leukoaraiosis and hypertension significantly more often than patients without such lesions, and we hypothesized that 2 types of small-vessel disease could be distinguished during life: arteriolosclerosis and microatheromatosis, respectively. Differences in prognosis might sustain this hypothesis of 2 lacunar stroke entities. Therefore, we performed a follow-up in 333 patients with first lacunar stroke, distinguishing those with > or =1 asymptomatic lacunar lesions (LACI+) from those without such lesions (LACI-). METHODS: Cross-sectional follow-up was performed after 785+/-479 days (mean+/-SD) in 104 LACI+ patients and 865+/-545 days in 229 LACI- patients. RESULTS: Mortality at the end of follow-up was 33% in LACI+ and 21% in LACI- patients [odds ratio (OR), 1.74; 95% confidence interval (CI), 1.01 to 3.01]. Stroke recurrence rate was 21% in LACI+ and 11% in LACI- (OR, 2.09; 95% CI, 1.08 to 4.06). Forty percent of LACI+ and 26% of LACI- patients had unfavorable outcome at the end of follow-up (OR, 1.95; 95% CI, 1.17 to 3.26). Kaplan-Meier curves showed less favorable survival in LACI+ (log-rank test, P=0.0218) and survival free of stroke (log-rank test, P=0.0121) than in LACI-. When we restricted the analysis to patients with both silent lesions and leukoaraiosis (n=63) compared with those without (n=196), differences were even more pronounced. CONCLUSIONS: Prognosis for mortality, recurrent stroke, and overall functional outcome in lacunar stroke patients with > or =1 silent lacunar lesions is more unfavorable than in patients without such lesions. These findings sustain the idea of 2 lacunar stroke entities.

Arteriosclerosis↗

PubMed1991

An autopsy study of the incidence of lacunes in relation to age, hypertension, and arteriosclerosis.

We investigated selected features of lacunes in 1,086 necropsy cases. Lacunes were found in brains from patients above the age of 40 years and were most common in brains from persons in their sixties but decreased in number in brains from older persons. The most common site of lacunes was the frontal lobe white matter, followed by the putamen, pons, parietal lobe white matter, thalamus, and caudate nucleus in descending order of frequency. By dividing the 1,086 cases into three groups according to blood pressure, we found more lacunes in the hypertensive and borderline hypertensive groups than in the normotensive group; the average number of lacunes per brain in each group was 3.61, 2.77, and 1.15, respectively. Diastolic hypertension was more closely related to the number of lacunes than was systolic hypertension. The extent of arteriolosclerosis of the medullary arteries in the frontal lobe white matter was measured and compared with the number of lacunes. There was a close correlation between lacunes and arterioloslerosis in all age groups.

Adult↗

PubMed1993

Associations of serum total cholesterol, different types of stroke, and stenosis distribution of cerebral arteries. The Akita Pathology Study.

BACKGROUND AND PURPOSE: The relation between serum total cholesterol levels and stroke is controversial. The Akita Pathology Study provides data on the association of serum total cholesterol, different types of stroke, and distribution of stenosis in cerebral arteries. METHODS: The data are based on 750 autopsied men aged 30 years and older who were admitted to a local hospital in northeast Japan between 1966 and 1984. The overall autopsy rate was 88%. The grade of stenosis in the cerebral arteries was determined blindly by one pathologist using Baker's method for basal cerebral arteries (atherosclerosis scores) and using microscopic examination of a single basal ganglion slide for the intracerebral penetrating arteries (arteriolosclerosis scores). RESULTS: The age-adjusted mean value of serum total cholesterol concentration was 164 mg/dL for cerebral hemorrhage, 177 mg/dL for infarction in penetrating artery regions, and 200 mg/dL for infarction in cortical artery regions. Mean serum cholesterol was lower in deaths caused by cerebral hemorrhage than in those caused by myocardial infarction and other cardiovascular disease. Mean atherosclerosis score of basal cerebral arteries was low for cerebral hemorrhage, intermediate for penetrating artery infarction, and high for cortical artery infarction. Stenosis of both basal and penetrating arteries was minimum or absent in cases of cerebral hemorrhage. Only the basal arteries were stenotic in cases of cortical artery infarction, whereas both basal and penetrating arteries were stenosed in cases of penetrating artery infarction. There were positive associations of serum cholesterol with stenosis of basal and penetrating arteries. Among cases of cerebral hemorrhage, serum total cholesterol levels were even lower in men with no significant stenosis in either basal or penetrating arteries than in men with stenosis in either type of artery. CONCLUSIONS: The association of serum cholesterol with pathogenesis varies among stroke types. Elevated serum cholesterol levels were associated with the presence of cortical artery infarction, while low serum cholesterol levels were associated with cerebral hemorrhage.

Adult↗

PubMed1995

Can transcranial Doppler really detect reduced cerebral perfusion states?

BACKGROUND AND PURPOSE: This study was designed to determine whether transcranial Doppler ultrasonography (TCD) may detect reduced perfusion states of the brain in patients with hypertension or diabetes mellitus with suspected cerebral atherosclerosis and arteriolosclerosis. METHODS: We determined blood flow velocity with TCD in the middle cerebral artery and cerebrovascular vasodilator responses to carbon dioxide in 22 patients with or without carotid artery occlusive disease and minor stroke; we compared the results with the measurements of cerebral blood flow and oxygen metabolism by positron emission tomography (PET). RESULTS: Blood flow velocity measured by TCD correlated with ipsilateral cerebral blood flow measured by PET in frontal, temporal, and striatal regions and throughout the entire hemisphere (P < .05 to P < .005). Relative changes in blood flow velocity and calculated cerebrovascular resistance tested by carbon dioxide inhalation both correlated closely with regional mean transit time (calculated as the ratio of cerebral blood volume divided by cerebral blood flow) in frontal, striatal, temporal, parietal, and occipital regions and also in the entire hemisphere (P < .05 to P < .0001). TCD variables did not correlate with hemispheric measurements of oxygen metabolism by PET. CONCLUSIONS: Although TCD is not useful in assessing impairments of cerebral metabolism, it is useful for detecting abnormalities of cerebral hemodynamics among patients with risk factors for cerebrovascular disease.

Adult↗

PubMed1996

Contribution of arterial blood pressure to the clinical expression of lacunar infarction.

BACKGROUND AND PURPOSE: The relation between symptomatic lacunar infarction, silent stroke, and arterial hypertension is controversial. METHODS: From 500 patients with ischemic or hemorrhagic stroke admitted to the Downtown Barcelona Stroke Registry between July 1992 and December 1994, we evaluated prospectively the prevalence of silent infarction in 249 patients who had a brain MRI. The association of risk factors with silent infarction was investigated with the use of logistic regression analysis. In a selected group of 43 patients with symptomatic lacunes, we performed at stroke follow-up transcranial Doppler sonography and 24-hour continuous blood pressure monitoring to evaluate whether blood pressure, cerebrovascular tone, and cerebral blood flow at rest and after the administration of 1 g acetazolamide correlated with silent infarction. RESULTS: A total of 147 silent infarctions were observed in 83 patients (33%). Most silent infarctions corresponded to small deep lesions in the territory of the lenticulostriate arteries. Patients with silent infarctions had higher systolic and diastolic blood pressure at stroke onset. However, on multivariate analysis, age greater than 60 years was the only risk factor associated with silent infarction. In a subgroup of 43 patients with symptomatic lacunes and patent extracranial vessels, systolic and diastolic pressure at stroke onset and diastolic pressure and vascular resistance at stroke follow-up were higher when silent infarctions co-existed. However, cerebral blood flow at rest and after acetazolamide injection were unrelated to silent infarction. CONCLUSIONS: Silent ischemia in patients with symptomatic lacunar and nonlacunar stroke was only associated with aging. However, a history of arterial hypertension was perhaps unrecognized, since hemodynamic testing and continuous blood pressure monitoring in patients with lacunar stroke suggested that the coexistence of silent lesions indicated a more generalized cerebral arteriolosclerosis.

Acetazolamide↗

PubMed1999

Impaired cerebrovascular reactivity as a risk marker for first-ever lacunar infarction: A case-control study.

BACKGROUND AND PURPOSE: Functional assessment of small arteries and arterioles could provide valuable information regarding the extent of diffuse arteriolosclerosis in patients with small-vessel disease. Therefore we attempted to clarify the role of cerebrovascular reactivity (CVR) as a risk marker for first-ever symptomatic lacunar infarction. METHODS: Forty-six patients with lacunar infarction and 46 sex- and age-matched control subjects were prospectively evaluated. Cerebral hemodynamics were studied with transcranial Doppler ultrasonography. CVR was examined by calculating the percent increase in mean flow velocity occurring after 15 mg/kg acetazolamide administration (Diamox test). RESULTS: CVR was significantly (P<0.0001, Student's t test) lower in cases (50.0+/-12. 7%) as compared with control subjects (65.2+/-12.4%). A multiple logistic regression analysis identified male sex (odds ratio [OR] 2. 3, P=0.02), age (OR 3.6, P<0.005), and the presence of lacunar infarction on magnetic resonance imaging (OR 5.3, P<0.001) as significant and independent factors associated with a reduction of CVR. Moreover, a cut-point of 55.6% (sensitivity 67%, specificity 82%) was established as the threshold value for distinguishing between pathological and normal CVR. CVR was significantly (P=0.02) lower in patients with multiple (46.38+/-12.6%) than with single (54. 83+/-11.58%) lacunar infarction. In addition, a trend of negative correlation was found between CVR and the number of lacunar infarctions (r=-0.26, P=0.08). In the multiple logistic model, history of hypertension (OR 7.24; 95% confidence interval 2.95 to 17. 79) and CVR (OR 0.8; 95% confidence interval 0.81 to 0.93) emerge as significant and independent predictors of first-ever lacunar infarction. CONCLUSIONS: These data suggest that impaired CVR is a risk marker for first-ever lacunar infarction.

Acetazolamide↗