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PubMed2002

C-reactive protein and soluble vascular cell adhesion molecule-1 are associated with elevated urinary albumin excretion but do not explain its link with cardiovascular risk.

An elevated urinary albumin excretion rate (UAER) is associated with an increased risk of cardiovascular mortality, but the pathophysiological mechanism underlying this association is poorly understood. To investigate the role of endothelial dysfunction, leukocyte adhesion, and low-grade inflammation (1) in the development of elevated UAER (study I) and (2) in linking elevated UAER with risk of cardiovascular mortality (study II), we performed a prospective study in an age-, sex-, and glucose tolerance- stratified sample of a population-based cohort aged 50 to 75 years. High levels of von Willebrand factor, soluble vascular cell adhesion molecule-1 (sVCAM-1), and C-reactive protein (CRP) were used as markers of endothelial dysfunction, leukocyte adhesion, and low-grade inflammation, respectively. For study I, subjects who had normal UAER at baseline (n=316 subjects, 66 with type 2 diabetes) were reexamined after a mean follow-up of 6.1 years. The development of elevated UAER was defined as a mean albumin-to-creatinine ratio >2.0 mg/mmol at follow-up. Age-, sex-, and glucose tolerance- adjusted logistic regression analyses showed the development of elevated UAER to be significantly associated with levels of sVCAM-1 and CRP (odds ratio 1.14 [95% CI 1.02 to 1.27] per 10% increase of sVCAM-1 and odds ratio 1.17 [95% CI 1.04 to 1.32] per 50% increase of CRP). The results were not materially different after additional adjustment for hypertension, body mass index, cardiovascular disease, and creatinine clearance or stratification by the presence of diabetes. For study II, the vital status of all subjects (n= 575) was determined after a mean follow-up of 6.6 years. Eighty-one of 575 subjects died (30 died of cardiovascular disease). The presence of elevated UAER at baseline was associated with a 4.1-fold (1.94 to 8.73) increased risk of cardiovascular death after adjustment for age, sex, and glucose tolerance status. Adjustment for levels of von Willebrand factor, sVCAM-1, or CRP did not materially affect the results, nor did additional adjustment for the presence of hypertension, retinopathy, and cardiovascular disease and for levels of homocysteine, triglycerides, and high density lipoprotein cholesterol. Leukocyte adhesion (sVCAM-1) and low-grade inflammation (CRP) are determinants of the development of elevated UAER. However, these determinants do not explain the association between elevated UAER and cardiovascular mortality.

Aged↗

PubMed1995

Ten LDL receptor mutants explain one third of familial hypercholesterolemia in a German sample.

Mutational defects in the LDL receptor are responsible for familial hypercholesterolemia (FH); thus far more than 150 mutations have been described. Nevertheless, systematic searches among the Germans have not been conducted. We used single-strand conformational polymorphism and polymerase chain reaction to find mutations in 10 index patients and in 40 other individuals with heterozygous FH. Our screen in the 10 index patients revealed 7 hitherto undescribed mutations. A screen of the 40 additional FH patients disclosed 20 defective of 54 total alleles and allowed specific diagnoses in 88 family members. We also found two families in which the children were markedly affected by FH, but the expected parental expression of the trait was not manifest. This observation suggests a role for additional environmental and genetic influences. Our report represents the first comprehensive effort to identify FH mutations in Germany. We found 10 mutations and these mutations explain 37% of FH cases. Our data may have relevance to expected FH patterns in central Europe.

Adult↗

PubMedDate not supplied

Small liver fenestrae may explain the susceptibility of rabbits to atherosclerosis.

Rabbits fed cholesterol rapidly develop high serum cholesterol levels which lead to the development of atherosclerosis. This is related to the retention of cholesterol-rich chylomicron remnants in the circulation. In most animals, such as rats, chylomicron remnants are rapidly removed from the circulation by the liver. The first barrier to this removal is the fenestrated endothelium of liver sinusoids. Measurements made of a large number of sinusoidal fenestrae by scanning electron microscopy have shown the average diameters to be 89 nm in rats and 49 nm in rabbits. We postulate that the small size of endothelial fenestrae in the liver sinusoids of rabbits hinders the egress of chylomicron remnants from the sinusoidal blood, explaining the subsequent development of hypercholesterolemia and atherosclerosis.

Animals↗

PubMedDate not supplied

Body mass, blood pressure, glucose, and lipids. Does plasma insulin explain their relationships?

Obesity, hypertension, a high plasma level of glucose, and some lipid abnormalities (high plasma levels of cholesterol and triglycerides) often occur in the same individuals. Some authors have postulated that the elevated levels of plasma insulin in obese individuals may explain this association. To explore this hypothesis further, the relationships between body mass index, fasting plasma glucose and insulin, blood pressure, serum lipids, and apoproteins were investigated in a group of 2144 healthy middle-aged men. Analysis of the data show that the associations between body mass index and blood pressure or lipid variables are largely independent of plasma glucose and insulin. Plasma glucose is strongly related to blood pressure in nonobese subjects. Plasma insulin is not associated with blood pressure independently of body mass index and plasma glucose; however, the simultaneous elevation of body mass index, plasma glucose, and insulin is strongly associated with blood pressure. The results also confirm that plasma insulin is positively related to triglycerides and negatively related to high density lipoprotein cholesterol independently of plasma glucose and body mass index.

Age Factors↗

PubMed2003

Impaired renal clearance explains elevated troponin T fragments in hemodialysis patients.

BACKGROUND: Patients with severe renal dysfunction often have unexplained elevated serum concentrations of cardiac troponin T (cTnT). We investigated whether in vivo fragmentation of cTnT could explain these increases. METHODS AND RESULTS: cTnT, creatine kinase isoenzyme MB, and myoglobin serum concentrations were measured in all 63 dialysis patients of our in-hospital dialysis department. A highly sensitive immunoprecipitation assay, followed by electrophoresis and Western blotting, was used to extract and concentrate cTnT and its possible fragments from serum of these 63 hemodialysis patients. Although creatine kinase isoenzyme MB values excluded recent ischemic myocardial events in 55 of the 63 cases, cTnT fragments ranging in size from 8 to 25 kDa were present in the serum samples of all dialysis patients. CONCLUSIONS: cTnT is fragmented into molecules small enough to be cleared by the kidneys of healthy subjects. Impaired renal function causes accumulation of these cTnT fragments and is very likely the cause of the unexplained elevations of serum cTnT found in patients with severe renal failure.

Aged↗

PubMed2004

Explaining the increase in coronary heart disease mortality in Beijing between 1984 and 1999.

BACKGROUND: Coronary heart disease (CHD) mortality is rising in many developing countries. We examined how much of the increase in CHD mortality in Beijing, China, between 1984 and 1999 could be attributed to changes in major cardiovascular risk factors and assessed the impact of medical and surgical treatments. METHODS AND RESULTS: A validated, cell-based mortality model synthesized data on (1) patient numbers, (2) uptake of specific medical and surgical treatments, (3) treatment effectiveness, and (4) population trends in major cardiovascular risk factors (smoking, total cholesterol, blood pressure, obesity, and diabetes). Main data sources were the WHO MONICA and Sino-MONICA studies, the Chinese Multi-provincial Cohort Study, routine hospital statistics, and published meta-analyses. Age-adjusted CHD mortality rates increased by approximately 50% in men and 27% in women (1608 more deaths in 1999 than expected by application of 1984 rates). Most of this increase ( approximately 77%, or 1397 additional deaths) was attributable to substantial rises in total cholesterol levels (more than 1 mmol/L), plus increases in diabetes and obesity. Blood pressure decreased slightly, whereas smoking prevalence increased in men but decreased substantially in women. In 1999, medical and surgical treatments in patients together prevented or postponed approximately 642 deaths, mainly from initial treatments for acute myocardial infarction ( approximately 41%), hypertension (24%), angina (15%), secondary prevention (11%), and heart failure (10%). Multiway sensitivity analyses did not greatly influence the results. CONCLUSIONS: Much of the dramatic CHD mortality increases in Beijing can be explained by rises in total cholesterol, reflecting an increasingly "Western" diet. Without cardiological treatments, increases would have been even greater.

Adult↗

PubMed1993

Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland. A paradox.

BACKGROUND: For decades, the coronary heart disease (CHD) mortality rate has been four or more times higher in Finland than in France despite comparable intakes of dietary cholesterol and saturated fat. A potential answer to this paradox is provided by this study of 40 countries and the analyses of other nutrients in the diets besides cholesterol and saturated fat. METHODS AND RESULTS: CHD death rates for men aged 55 to 64 years were derived from the World Health Organization annual vital statistics. Dietary intakes were gathered from the Food and Agriculture Organization of the United Nations database. Forty countries at various levels of economic development and 40 dietary variables were investigated, including a lipid score that combined the intakes of cholesterol and saturated fat (Cholesterol-Saturated Fat Index [CSI]). The CSI was significantly and positively related to CHD mortality in the 40 countries. The countries with low CSIs had low CHD death rates. Countries with high CSIs had a wide range of CHD death rates. France, Finland, and other Western industrialized countries had similar CSIs. After adjusting for cholesterol and saturated fat, milk and many components of milk (butterfat, milk protein, calcium from milk, and riboflavin) and total calcium remained positively related to CHD mortality for all 40 countries. There were differences in the consumption of these foods and nutrients in France and Finland. Milk and butterfat (fat from milk, cream, cheese, and butter) consumption was higher in Finland than in France. The consumption of plant foods, recently shown to be protective against CHD (vegetables and vegetable oils containing monounsaturated and polyunsaturated fatty acids), was greater in France than in Finland. CONCLUSIONS: Over the years, France and Finland, with similar intakes of cholesterol and saturated fat, consistently have had very different CHD mortality rates. This paradox may be explained as follows. Given a high intake of cholesterol and saturated fat, the country in which people also consume more plant foods, including small amounts of liquid vegetable oils, and more vegetables (more antioxidants) had lower rates of CHD mortality. On the other hand, milk and butterfat were associated with increased CHD mortality, possibly through their effects on thrombosis as well as on atherosclerosis.

Cholesterol, Dietary↗

PubMed1996

Remodeling rather than neointimal formation explains luminal narrowing after deep vessel wall injury: insights from a porcine coronary (re)stenosis model.

BACKGROUND: Oversized balloon dilatation of normal porcine coronary arteries usually heals without stenosis formation. METHODS AND RESULTS: With the purpose of developing a stenotic model and examining the mechanisms of luminal narrowing after angioplasty, we produced a circumferential deep vessel wall injury by inflating and withdrawing an oversized chain-encircled angioplasty balloon in the left anterior descending coronary artery (LAD) of 20 pigs. Three pigs died and did not complete the study. In 8 pigs (group 1), serial coronary arteriography was performed. The lumen diameter (mean+/-SD) before dilation was 3.4 +/- .4 mm; after dilation, 4.2 +/- 0.6 mm; and at follow-ups 2 and 4 weeks later, 1.6 +/- 0.4 mm (P<.0001). In 9 pigs (group 2) examined postmortem 3 weeks after dilatation, histology revealed that the injury was deep (out to adventitia) in all arteries and completely circumferential (360 degrees) in all but two arteries. Adventitia was markedly thickened as a result of neoadventitial formation. Injury correlated strongly with neointimal formation (middle LAD, r=.71, P=.00001, but neither injury nor neointima correlated with lumen size (r=.14, P=.46 and r=.34, P=.07, respectively); ie, neointimal formation did not explain late luminal narrowing. Lumen size, however, did correlate strongly with vessel size (r=.74, P=000005). The late loss in lumen diameter observed angiographically in group 1 substantially exceeded that caused by neointimal formation seen by histology in group 2. CONCLUSIONS: The chain-encircled angioplasty balloon produced a circumferential deep vessel wall injury that healed by luminal narrowing. In this porcine model, arterial remodeling was more important than neointimal formation in late luminal narrowing.

Angioplasty, Balloon↗

PubMed2000

Evidence for genetic factors explaining the birth weight-blood pressure relation. Analysis in twins.

Epidemiological studies have consistently shown an inverse association between birth weight and systolic blood pressure in later life after adjustment for current size. To examine whether this association is explained by intrauterine or genetic factors, we investigated birth weight and blood pressure data in 53 dizygotic and 61 monozygotic adolescent twin pairs. Birth weight was obtained from the mothers. Blood pressure measurements were performed 6 times at rest and during mental stress. The dizygotic but not the monozygotic twins with the lowest birth weight from each pair had a systolic blood pressure measured at rest and during the reaction time experiment that was higher compared with their cotwins with the highest birth weight (dizygotic twins: blood pressure at rest, 119. 4+/-9.7 mm Hg versus 117.3+/-8.5 mm Hg, P=0.07, and during a reaction time task, 126.2+/-10.8 versus 123.6+/-9.5, P=0.09; monozygotic twins: blood pressure at rest, 117.4+/-6.4 versus 118. 4+/-9.0, P=0.4, and during a reaction time task, 122.9+/-8.4 versus 124.2+/-10.8, P=0.2). The differences in blood pressure between the cotwins with the lowest and the cotwins with the highest birth weight were different in dizygotic compared with monozygotic twin pairs (for blood pressure at rest, P=0.05; for blood pressure during reaction time, P=0.03). After adjustment for differences in current weight, intrapair differences in birth weight were negatively and significantly associated with differences in systolic blood pressure at rest and during the reaction time task in dizygotic twins (regression coefficient, -5.7 mm Hg/kg [95% confidence interval, -10.4 to -1.0] and -6.3 [-12.7 to 0], respectively) but not in monozygotic twins (-0.1 [-5.4 to 5.2] and +3.5 [-1.8 to 8.8], respectively). Interaction analysis indicated that the associations were different between dizygotic twins and monozygotic twins (P=0.1 and P<0.05, respectively). These data suggest that genetic factors may play an important role in the association between birth weight and blood pressure.

Adolescent↗

PubMed2005

Explaining the phenomenon of nitrate tolerance.

During the last century, nitroglycerin has been the most commonly used antiischemic and antianginal agent. Unfortunately, after continuous application, its therapeutic efficacy rapidly vanishes. Neurohormonal activation of vasoconstrictor signals and intravascular volume expansion constitute early counter-regulatory responses (pseudotolerance), whereas long-term treatment induces intrinsic vascular changes, eg, a loss of nitrovasodilator-responsiveness (vascular tolerance). This is caused by increased vascular superoxide production and a supersensitivity to vasoconstrictors secondary to a tonic activation of protein kinase C. NADPH oxidase(s) and uncoupled endothelial nitric oxide synthase have been proposed as superoxide sources. Superoxide and vascular NO rapidly form peroxynitrite, which aggravates tolerance by promoting NO synthase uncoupling and inhibition of soluble guanylyl cyclase and prostacyclin synthase. This oxidative stress concept may explain why radical scavengers and substances, which reduce oxidative stress indirectly, are able to relieve tolerance and endothelial dysfunction. Recent work has defined a new tolerance mechanism, ie, an inhibition of mitochondrial aldehyde dehydrogenase, the enzyme that accomplishes bioactivation of nitroglycerin, and has identified mitochondria as an additional source of reactive oxygen species. Nitroglycerin-induced reactive oxygen species inhibit the bioactivation of nitroglycerin by thiol oxidation of aldehyde dehydrogenase. Both mechanisms, increased oxidative stress and impaired bioactivation of nitroglycerin, can be joined to provide a new concept for nitroglycerin tolerance and cross-tolerance. The consequences of these processes for the nitroglycerin downstream targets soluble guanylyl cyclase, cGMP-dependent protein kinase, cGMP-degrading phosphodiesterases, and toxic side effects contributing to endothelial dysfunction, such as inhibition of prostacyclin synthase, are discussed in this review.

Aldehyde Dehydrogenase↗

PubMed1982

Pulse wave reflection: can it explain the differences between systemic and pulmonary pressure and flow waves? A study in dogs.

We have studied the effect of changes in pulse wave reflection on the configurations of pressure and flow in systemic and pulmonary circulation. Electromagnetic flow transducers, atrial catheters, and pacing leads were implanted in 10 dogs. In four animals, the flow transducer was placed on the pulmonary artery, in another four on the ascending aorta, and in two additional dogs on both vessels. One week later, ascending aortic and/or pulmonary artery flow and pressure (catheter tip manometer) were measured under general anesthesia (Nembutal, 30 mg/kg, iv). When the pulmonary circulation was studied (six dogs), measurements were made before and during serotonin infusion (0.5-0.75 mg/min). When the systemic circulation was studied (six dogs), measurements were made before and during nitroprusside infusion (50-200 micrograms/min). To quantify the arterial load, we calculated pulmonary and systemic input impedances. To estimate the amount of reflection, we used a reflection index which we defined as the amplitude ratio of reflected and forward wave. Nitroprusside decreased total peripheral resistance, increased total arterial compliance, and decreased the reflection index; similarity between aortic pressure and flow wave shapes increased, and they looked more like their pulmonary counterparts. Serotonin increased pulmonary vascular resistance, decreased pulmonary arterial compliance, and increased the reflection index. Resemblance of pressure and flow waves decreased. The differences in wave shapes can thus be explained by the amount of reflection: the less reflection the more pressure and flow resemble each other.

Animals↗

PubMed1985

Coronary diastolic pressure-flow relation and zero flow pressure explained on the basis of intramyocardial compliance.

In the controversy about the mechanisms determining the high zero flow pressures and the further interpretation of coronary diastolic pressure flow relations, this paper takes a stand in favor of intramyocardial compliance as the primary cause of the high zero flow pressures. An attempt has been made to estimate the compliance distribution within the coronary circulation and to show the specific effect of intramyocardial compliance on arterial and venous pressure-flow relations. Since no data are available on the distensibility of coronary arterioles and capillaries, these data were taken from studies on mesenteric vessels. Based on these data, it is shown that, depending on the transmural pressure, smooth muscle tone may either increase or decrease arteriolar compliance. A compliance distribution has been proposed based on assumed pressure, volume, and distensibility distributions. For all but the venous division of the circulation, experimental data on volume could be found in the literature. Based on this compartmental analysis, it is predicted that overall intramyocardial compliance may exceed epicardial arterial compliance by a factor 45. The literature presenting functional evidence for intramyocardial compliance effects has been reviewed. Experimental results on venous outflow during long diastoles have been analyzed. Pf = 0 coronary pressure at zero flow, is higher when measured later in diastole. It is shown that this may be explained by charging of intramyocardial compliance in the period before flow ceases. The discrepancy between results on pressure-flow relations in the fully dilated bed and autoregulated bed are related to the differences in pressure, resistance, and compliance distributions.

Animals↗

PubMed1996

Heart failure in rats causes changes in skeletal muscle morphology and gene expression that are not explained by reduced activity.

In patients with congestive heart failure, skeletal muscle is characterized by a smaller proportion of slow-twitch oxidative fibers and reduced oxidative enzyme activity. However, whether these changes result from disuse or occur as a direct consequence of heart failure is unresolved. To address this issue, 18 rats with heart failure 8 weeks after left coronary artery ligation and 13 sham-operated control rats underwent quantification of locomotor activity by a photocell activation technique, measurements of hemodynamics and infarct size, histochemical and morphological analyses of the soleus and plantaris muscles, and Northern analyses of muscle contractile protein and oxidative enzyme mRNA expression. Although the rats with heart failure had elevated left ventricular end-diastolic pressures (24.1 +/- 2.6 mm Hg) and a mean infarct size of 35.1 +/- 4.1%, activity levels were similar to those found in the sham-operated rats (3849 +/- 304 versus 3526 +/- 130 counts per hour). With heart failure, there was a significant reduction of type I fibers in the soleus muscle and type IIa fibers in the plantaris muscle, with corresponding increases in intermediate staining of type IIab fibers in both muscles. This was associated with a 17% decrease in citrate synthase activity in both the soleus and plantaris muscles (26.2 +/- 1.6 versus 30.7 +/- 3.4 and 29.1 +/- 2.4 versus 35.7 +/- 3.4 mumol/L per minute per gram, respectively [P < .05]). In the soleus muscle, mRNA for both beta-myosin heavy chains and cytochrome C oxidase III (normalized to 18S RNA) was reduced (0.27 +/- 0.02 versus 0.65 +/- 0.02 and 0.23 +/- 0.04 versus 0.64 +/- 0.02 U), whereas the messages for IIx and IIb myosin heavy chains were increased. A similar decrease in messages for cytochrome oxidase and the primary myosin isoform was observed in the plantaris muscle. Both soleus beta-myosin heavy chain and cytochrome C oxidase expression show significant inverse relationships to left ventricular end-diastolic pressure and infarct size. In contrast, there was no relationship between either beta-myosin heavy chain or cytochrome C oxidase expression and locomotor activity. These results indicate that in rats heart failure produces changes in skeletal muscle gene expression at the pretranslational level that cannot be explained by inactivity.

Animals↗

PubMed2000

Decreased severity of brain infarct can in part explain the decreasing case fatality rate of stroke.

BACKGROUND AND PURPOSE: Case fatality rates for stroke has declined in most Western industrialized countries during recent decades. One possible explanation for this is a decrease in the severity of stroke symptoms. We therefore sought evidence for a change in stroke severity and its relationship with case fatality rates. METHODS: We compared the severity of symptoms among first-ever stroke patients in 2 population-based prospective stroke registers maintained during 1972 to 1973 and 1989 to 1991 in Finland. Patients who were evaluated by study assistants or the investigator during the first week after the onset of symptoms were included in the study, and their severity of symptoms was assessed with the use of comparable scales modified from the Scandinavian Stroke Scale. RESULTS: A total of 244 and 594 patients were registered, and a portion of them (155 [63.5%] and 360 [60.6%]) were included in the analyses in the registers for Espoo-Kauniainen from 1972 to 1973 and for 4 separate districts in Finland from 1989 to 1991, respectively. The death rates during the first week among those who were not included did not differ between the registers. The severity of symptoms decreased significantly between the registers in both patients with brain infarct or intracerebral hemorrhage but not in those with subarachnoid hemorrhage. The severity of symptoms was an independent factor of case fatality at 1 month. CONCLUSIONS: The severity of symptoms of brain infarcts has decreased and can in part explain the decreased case fatality rate of stroke in Finland. However, the change in patients with intracerebral hemorrhage may be overestimated due to undiagnosed intracerebral hemorrhages in the first register resulting from the lack of brain CT.

Aged↗

PubMed2005

Levels of hematopoiesis inhibitor N-acetyl-seryl-aspartyl-lysyl-proline partially explain the occurrence of anemia in heart failure.

BACKGROUND: Anemia is common in patients with chronic heart failure (CHF) and is associated with a poor prognosis. However, only a minority of patients with CHF have impaired renal function or underlying hematinic deficiencies. It has been shown that inhibition of the renin-angiotensin system is associated with the development of anemia. The aim of the present study was to determine possible mechanisms linking anemia to renin-angiotensin system activity in CHF patients. METHODS AND RESULTS: We initially evaluated 98 patients with advanced stable CHF who were treated with ACE inhibitors (left ventricular ejection fraction, 28+/-1%; age, 69+/-1 years; 80% male), 10 of whom had an unexplained anemia (normal hematinics and no renal failure). These 10 anemic patients were matched with 10 nonanemic patients in terms of age and left ventricular ejection fraction. Serum ACE activity was 73% lower in anemic CHF patients compared with nonanemic CHF patients (P=0.018). Moreover, serum of these patients inhibited in vitro the proliferation of bone marrow-derived erythropoietic progenitor cells of healthy donors by 17% (P=0.003). Levels of the hematopoiesis inhibitor N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is almost exclusively degraded by ACE, were significantly higher in anemic CHF patients and were clearly correlated to erythroid progenitor cell proliferation (r=-0.64, P=0.001). CONCLUSIONS: Serum ACE activity is markedly lower in anemic CHF patients, and serum of these patients inhibits hematopoiesis. The clear correlation between Ac-SDKP and proliferation of erythroid progenitor cells suggests an inhibitory role of Ac-SDKP on hematopoiesis in CHF patients, which may explain the observed anemia in patients treated with ACE inhibitors.

Aged↗

PubMed2001

Pressure amplification explains why pulse pressure is unrelated to risk in young subjects.

Pulse pressure rather than diastolic pressure is the best predictor of coronary heart disease risk in older subjects, but the converse is true in younger subjects. We hypothesized that this disparity results from an age-related difference in pressure amplification from the aorta to brachial artery. Data from 212 subjects age < 50 years and 230 subjects age > or =50 years were abstracted from a community database. All subjects were free from cardiovascular disease, diabetes, and medication. Peripheral blood pressure was assessed by sphygmomanometry. Radial artery waveforms recorded noninvasively by applanation tonometry were used to derive central blood pressure. Pressure amplification (peripheral/central pulse pressure ratio) was linearly related to age (r=0.7; P<0.001). There was an inverse, linear relationship between amplification and diastolic pressure in the younger group (r=0.3; P<0.001) but not in older subjects (r=0.1; P=0.2). There was no relationship in either group when the amplification ratio was calculated with nonaugmented central pressure. Amplification is reduced in older subjects because of enhanced wave reflection. In younger, but not older, subjects, amplification declines as diastolic pressure rises. Therefore, peripheral pulse pressure underestimates the effect that diastolic pressure has on central pulse pressure in younger subjects. This may explain why diastolic pressure is a better predictor of risk in this age group and suggests that assessment of central pressure may improve risk stratification further.

Adult↗

PubMedDate not supplied

Size contrast and assimilation explained by the statistics of natural scene geometry.

The term "size contrast and assimilation" refers to a large class of geometrical illusions in which the apparent sizes of identical visual targets in various contexts are different. Here we have examined whether these intriguing discrepancies between physical and perceived size can be explained by a visual process in which percepts are determined by the probability distribution of the possible real-world sources of retinal stimuli. To test this idea, we acquired a range image database of natural scenes that specified the location of every image point in 3-D space. By sampling the possible physical sources of various size contrast or assimilation stimuli in the database, we determined the probability distributions of the size of the target in the images generated by these sources. For each of the various stimuli tested, these probability distributions of target size in different contexts accurately predicted the perceptual effects reported in psychophysical studies. We conclude that size contrast and assimilation effects are a further manifestation of a fundamentally probabilistic process of visual perception.

Bayes Theorem↗

PubMed2003

Local interactions in neural networks explain global effects in Gestalt processing and masking.

One of the fundamental and puzzling questions in vision research is how objects are segmented from their backgrounds and how object formation evolves in time. The recently discovered shine-through effect allows one to study object segmentation and object formation of a masked target depending on the spatiotemporal Gestalt of the masking stimulus (Herzog & Koch, 2001). In the shine-through effect, a vernier (two abutting lines) precedes a grating for a very short time. For small gratings, the vernier remains invisible while it regains visibility as a shine-through element for extended and homogeneous gratings. However, even subtle deviations from the homogeneity of the grating diminish or even abolish shine-through. At first glance, these results suggest that explanations of these effects have to rely on high-level Gestalt terminology such as homogeneity rather than on low-level properties such as luminance (Herzog, Fahle, & Koch, 2001). Here, we show that a simple neural network model of the Wilson-Cowan type qualitatively and quantitatively explains the basic effects in the shine-through paradigm, although the model does not contain any explicit, global Gestalt processing. Visibility of the target vernier corresponds to transient activation of neural populations resulting from the dynamics of local lateral interactions of excitatory and inhibitory layers of neural populations.

Calibration↗