Segregation analysis of systolic and diastolic blood pressure in Middle Dalmatia Island population

A complex segregation analysis of systolic and diastolic blood pressure has been performed on pedigree data from rural populations inhabiting Middle Dalmatian islands of Brac, Hvar and Korcula and the Peljesac peninsula. The purpose of the performed analysis was to possibly elucidate a signal of a large-effect gene responsible for high prevalence of hypertension present in this population (the age-adjusted prevalence of developed hypertension being 31.82% in males and 28.23% in females). The analysis was performed on a sample of 389 two- and three-generation families consisting of 2 to 19 observed individuals (1126 examinees in total, 526 males and 600 females, aged 17 to 83). Since the examinees were randomly selected from census data encompassing 22.6% of the total population--the family relations having been established afterwards--the selected sample can be considered representative for the examined populations. By applying the usual transmission probability tests, the major gene model has been accepted for systolic as well as for diastolic blood pressure. The most parsimonious models showed that: (a) inheritance of blood pressure in the Middle Dalmatia population can be attributed to the effect of a major gene responsible for 34% (systolic) and 36% (diastolic) blood pressure variation; (b) alleles of that major gene act in co-dominant fashion; (c) allele frequency for high blood pressure (A2) is 18% (systolic) and 15% (diastolic blood pressure); and (d) the residual (non-major gene) familial correlation is negligible and can be constrained to zero. Since the results are also indicating heterogeneity within the sample in the genetic determination of the systolic blood pressure, the obtained results thus justify further search for the most promising subpopulation for incoming genetic epidemiological investigations of hypertension.     

Endogamy and variation in blood pressure levels in Croatian island isolates

Blood pressure variation was investigated among populations inhabiting islands and peninsula of Middle Dalmatia, Croatia. The number of previous anthropological studies pointed to isolation and different genetic population structure in this environmentally fairly homogeneous area. Variation in blood pressure (systolic and diastolic) among the populations of the islands of Brac, Hvar, Korcula, and the Peljesac peninsula was assessed at three levels involving village populations, regional (western and eastern) populations and the entire island populations. The blood pressure data were collected from 3834 adult individuals inhabiting 37 rural communities and were adjusted for age and body mass index. Variation in blood pressure levels existed among regions and villages. Due to the history of differential settlement, small village sizes and high levels of reproductive isolation, the observed blood pressure variation could be attributed to founder effect, genetic drift and inbreeding. The involvement of genetic factors was tested by relating blood pressure variation among villages to degree of isolation among them. Blood pressure means and proportions of hypertensives increased with endogamy levels in males. In females, this effect could not be observed. However, in both sexes the highest proportions of hypertensives (more than 40%) were found in villages that are most reproductively closed (endogamy greater than 80%). These populations are considered particularly promising for further genetic epidemiological research.     

Heritability of blood pressure increases during mental stress.

We studied the influence of mental stress on the contributions of genes and environment to individual variation in systolic (SBP) and diastolic (DBP) blood pressure by structural equation modelling in 320 adolescent male and female twins. Blood pressure data were collected during rest and during a reaction time and a mental arithmetic task. Univariate analyses of SBP and DBP showed familial aggregation for blood pressure. A genetic explanation for this resemblance was most likely, although during rest conditions a model that attributed familial resemblance to shared environmental factors, also fitted the data. There was no evidence for sex differences in heritabilities. Multivariate analyses showed significant heterogeneity between sexes for the intercorrelations of the blood pressure data measured under different rest and task conditions. Multivariate genetic analyses were therefore carried out separately in males and females. For SBP and DBP in females and for SBP in males an increase in heritabilities was seen for blood pressure measured during stress, as compared to rest measurements. The influence of shared environmental factors decreased during stress. For DBP in males no significant contributions of shared environment were found. The multivariate analyses indicated that the same genetic and environmental influences are expressed during rest and stress conditions.     

Family resemblance for anthropometric and blood pressure measurements in Black Caribs and Creoles from St. Vincent Island

This paper examines family resemblance for five anthropometric measurements (height, weight, triceps skinfold, upper arm circumference relaxed [UACR] and flexed [UACF] and for systolic and diastolic blood pressure in a group of adult Caribbean islanders of primarily African ancestry. Six hypotheses about family resemblance are tested by using path analysis and likelihood ratios. Significant intergenerational transmission is found only for height and UACR. For weight, UACF, and diastolic blood pressure, non-transmissible sibling resemblance is the primary component of family resemblance, although significant marital resemblance exists for diastolic blood pressure. Triceps skinfold and systolic blood pressure show no evidence of any family resemblance. Although results for highly heritable traits such as height are comparable to reports from other populations, measurements with a large contribution from common family environment or residual environmental effects, such as triceps skinfold or blood pressure, have much lower family resemblance in this population than in other populations. We hypothesize that this difference is due to the fact that adult children and their parents do not share a common household in this culture and to the presence of major nonfamilial environmental factors contributing to obesity and hypertension in this population.     

Cross-trait familial resemblance for body fat and blood pressure: familial correlations in the Québec Family Study.

Cross-trait resemblance between body fat and blood pressure (BP) was examined among families in the Québec Family Study by using a bivariate familial correlation model assessing both intraindividual (e.g., comparison of father's body fat with his own BP) and interindividual (e.g., comparison of father's body fat with son's BP) cross-trait correlations. Each of six body-fat measures-(i) percent body fat, (ii) body-mass index, (iii) the sum of six skinfolds, (iv) the ratio of the sum of six skinfolds to total fat mass, (v) the ratio of the trunk skinfold sum to the extremity skinfold sum, and (vi) the regression of the trunk-extremity skinfold ratio on the sum of six skinfolds--was analyzed separately with systolic BP and with diastolic BP. Results showed that (1) upper-body fat was the strongest interindividual correlate of BP (especially the correlation of trunk-extremity ratio with diastolic BP), suggesting shared pleiotropic genetic and/or common familial environmental effects; (2) summary body-fat measures either were inconsistent (in the case of both percent body fat and sum of six skinfolds) or gave no evidence of interindividual cross-trait resemblance with BP (in the case of body-mass index); and (3) intraindividual resemblance between the sum of six skinfolds and BP largely vanished once the skinfold sum was adjusted for fat mass, suggesting that the intraindividual association may be mediated largely by the absolute amount of subcutaneous fat rather than by the subcutaneous proportion. Finally, the magnitude of the spouse resemblance for the trunk-extremity ratio with diastolic BP suggests that a significant proportion of the resemblance may be due to environmental influences. In summary, our investigation confirms a heritable link between BP and truncal-abdominal fat as predicted by the metabolic-syndrome hypothesis. That this result is obtained in primarily normotensive, nonobese families, suggests the connection involves normal metabolic paths.     

Systolic and diastolic blood pressures as predictors of coronary heart disease in middle aged Norwegian men.

Systolic and diastolic blood pressures were compared as predictors of mortality from coronary heart disease in Norwegian men aged 35-49. A total of 39,207 men were followed up for an average of 8.9 years; 385 died of coronary heart disease. Diastolic blood pressure seemed to be the better predictor, the difference being most pronounced in the age group 35-39. At this age 26% more deaths from coronary heart disease were found in the upper quintile of diastolic blood pressure compared with the upper quintile of systolic blood pressure. At ages 45-49 there were almost the same numbers of deaths from coronary heart disease in the upper quintiles of systolic and diastolic pressures. These findings suggest that the relative predictive strength of systolic and diastolic blood pressure may be dependent on age. Furthermore, for very obese men the association between blood pressure and death from coronary heart disease is much weaker.     

Relative roles of heredity and physical activity in adolescence and adulthood on blood pressure.

Part of the association between physical activity and low blood pressure (BP) may be a consequence of genetic selection. We investigated the association of genetic factors and physical activity in adolescence and adulthood with BP. BP was measured with a Finapres device in 71 monozygotic and 104 dizygotic male twin pairs using no antihypertensive medication. Subjects' mean age was 50.4 yr (range 40-72 yr). Subjects were interviewed about their lifetime exercise and other health habits. Exercise was classified as aerobic, power, or other, and these were further divided into adolescence (12-20 yr of age), the previous year, and lifetime. Genetic modeling was conducted to estimate genetic and environmental components of variance of systolic and diastolic BP. Aerobic exercise in adolescence and high-intensity aerobic exercise throughout the lifetime were associated with low diastolic BP in adulthood. Of the variance in diastolic BP, genetic factors accounted for 35% and aerobic exercise in adolescence for 5%. For systolic BP, genetic factors accounted for 39% of the variance. In turn, genetic factors accounted for 44% of the variance in aerobic exercise in adolescence. The genetic factors in part accounting for the variance in diastolic BP and those in part accounting for variance in aerobic exercise in adolescence were correlated. The association between aerobic exercise in adolescence and low diastolic BP in adulthood is a new finding, as is the observation that the factors partly share the same genes.     

Familial aggregation of blood pressure in 558 adopted children.

Blood pressure was measured in each member of 398 French-Canadian families with at least one adopted child of the same ethnic origin. Measurements were made at home by a nurse, usually with the subject seated. One comparison per family between parents and randomly chosen index children was made, using age- and sex-adjusted scores. The correlation in blood pressure scores between parents and natural children was highly significant (P less than 0.001), at 10.2% for systolic and 13.7% for diastolic in 140 homes with at least one natural child, but the correlation between parents and adopted children was nonsignificant, at 0.81% and 1.0%, in 398 homes with at least one adopted child. The correlation between pairs of natural children was significant (P less than 0.05), at 7.84% for systolic and 8.41% for diastolic, in 80 homes with more than one natural child but nonsignificant, at 0.49% and 1.69%, respectively, for pairs of adopted children in 138 families with more than one adopted child. It is concluded that heredity explains most of the familial resemblance of blood pressure in children.     

Relationship between African admixture and blood pressure variation in the Caribbean

The genetic contribution to blood pressure variance is examined by studying a selected group of genes. Of 368 individuals, 48.1% received one-half or more of their genes from an African ancestor and of this group 18.1 and 17.0% exhibit systolic and diastolic hypertension, respectively. A chi-square test was used to examine the dependence of blood pressure on percentage African ancestry. The chi-square values were not significant for systolic or diastolic pressures. It is likely that other factors are strongly related to African admixture and these factors are the true modifiers of blood pressure.     

Heterogeneity of genetic control of blood pressure in ethnically different populations.

We review the literature on statistical genetic analyses of blood pressure in samples from various ethnic backgrounds using different statistical methods and packages. We then provide the results of a complex segregation analysis performed on familial data on systolic and diastolic blood pressure in 2 ethnically different populations, Chuvashans and Turkmenians. Two types of major gene models were tested in the segregation analysis: Model type 1 tests for a Mendelian mode of transmission and estimates genotype-specific averages regardless of age and sex effect, and model type 2 estimates age and sex effects on each of 3 genotypes within the putative major genotype. In both total samples, by both types of segregation analysis, familial aggregation of both systolic and diastolic blood pressure was inconsistent with the Mendelian mode of inheritance. In the next step of analysis the pedigrees in both samples were sorted into 2 groups on the basis of 2 likelihoods as obtained under Mendelian and nontransmission models for each entire sample. This procedure resulted in the appearance of 2 subsamples (large and small) in each ethnic sample. The segregation analysis that was carried out then on the larger subsample provided consistent evidence to support the major gene effect on systolic and diastolic blood pressure in 2 ethnic groups. Interestingly, model type 2 showed that in both ethnically different large subsamples, for each sex the genotype predisposing to a larger mean value of systolic (or diastolic) blood pressure also displayed the highest rate of blood pressure increase with age. We discuss in detail possible sources of heterogeneity in familial transmission of blood pressure observed in our 2 samples, and we suggest a method to improve the analysis of heterogeneity for trait inheritance.     

Prostaglandins modulate baroreflex-induced changes in blood pressure and myocardial function in anesthetized dogs

The purpose of our study was to investigate the role of prostaglandins in the changes in myocardial function and peripheral and coronary vascular resistance which accompany a generalized increase in sympathetic tone caused by carotid baroreflex unloading in the anesthetized dog. Bilateral carotid artery occlusion (BCO) with heart rate held constant by electrical pacing (150 beats/min) resulted in increases in systolic, (33%) diastolic (40%), and mean (35%) arterial pressures, LV systolic pressure (33%) and left ventricular (LV) dP/dt (37%). After blockade of prostaglandin synthesis with indomethacin (N = 11) or meclofenamate (N = 6) the increases in systolic (41%), diastolic (45%), and mean (41%) arterial pressures, LV systolic pressure (39%), LV dP/dt (52%), and cardiac work caused by BCO were significantly greater, in spite of the initially higher baseline values (11-18%) following the administration of the drugs. In contrast, the changes in circumflex coronary blood flow and coronary vascular resistance to BCO were essentially the same before and after inhibition of prostaglandin synthesis. Systemic prostaglandin synthesis may, therefore, play a significant role in the control of systemic arterial pressure and myocardial function, most probably by modulating the release of norepinephrine from adrenergic nerve terminals, without adversely affecting coronary blood flow regulation.     

The genetics of coronary heart disease: the contribution of twin studies.

Despite the decline in coronary heart disease in many European countries, the disease remains an enormous public health problem. Although we know a great deal about environmental risk factors for coronary heart disease, a heritable component was recognized a long time ago. The earliest and best known examples of how our genetic constitution may determine cardiovascular risk relate to lipoprotein(a), familial hypercholesterolaemia and apolipoprotein E. In the past 20 years a fair number of polymorphisms assessed singly have shown strong associations with the disease but most are subject to poor repeatability. Twins constitute a compelling natural experiment to establish the genetic contribution to coronary heart disease and its risk factors. GenomEUtwin, a recently funded Framework 5 Programme of the European Community, affords the opportunity of comparing the heritability of risk factors in different European Twin Registries. As an illustration we present the heritabilities of systolic and diastolic blood pressure, based on data from over 4000 twin pairs from six different European countries and Australia. Heritabilities for systolic blood pressure are between 52 and 66% and for diastolic blood pressure between 44 and 66%. There is no evidence of sex differences in heritability estimates and very little to no evidence for a significant contribution of shared family environment. A non-twin based prospective case/cohort study of coronary heart disease and stroke (MORGAM) will allow hypotheses relating to cardiovascular disease, generated in the twin cohorts, to be tested prospectively in adult populations. Twin studies have also contributed to our understanding of the life course hypothesis, and GenomEUtwin has the potential to add to this.     

Failure to realise growth potential in utero and adult obesity in relation to blood pressure in 50 year old Swedish men.

OBJECTIVES: To clarify the type of fetal growth impairment associated with increased blood pressure in adult life, and to establish whether this association is influenced by obesity and is mediated through impairment of insulin action. DESIGN: Cross sectional survey with retrospective ascertainment of size at birth from obstetric archives. SUBJECTS: 1333 men resident in Uppsala, Sweden, who took part in a 1970 study of coronary risk factors at age 50 and for whom birth weight was traced. MAIN OUTCOME MEASURES: Systolic and diastolic blood pressure at age 50. RESULTS: In the full study population for a 1000g increase in birth weight there was a small change in systolic blood pressure of -2.2mmHg (95% confidence interval -4.2 to - 0.3mmHg) and in diastolic blood pressure of -1.0mmHg (-2.2 to 0.1mmHg). Much stronger effects were observed among men who were born at term and were in the top third of body mass index at age 50, for whom a 1000g increase in birth weight was associated with a change of -9.1mmHg (-16.4 to-1.9mmHg) systolic and -4.2mmHg (-8.3 to -0.1mmHg) diastolic blood pressure. Men who were light at birth (<3250g) but were above median adult height had particularly high blood pressure. Adjustment for insulin concentrations reduced the associations of birth weight with systolic and diastolic blood pressure. CONCLUSIONS: A failure to realise growth potential in utero (as indicated by being light at birth but tall as an adult) is associated with raised adult blood pressure. Impaired fetal growth may lead to substantial increases in adult blood pressure among only those who become obese. Metabolic disturbances, possibly related to insulin resistance, may provide a pathway through which fetal growth affects blood pressure.     

Heritability of Longitudinal Changes in Coronary-Heart-Disease Risk Factors in Women Twins

Numerous studies have demonstrated genetic influences on levels of coronary heart disease (CHD) risk factors, but there also may be genetic effects on the intraindividual variation in these risk factors over time. Changes in risk factors are likely to reflect genetic-environmental interactions and may have important implications for understanding CHD risk. The present study examines the heritability of changes in CHD risk factors, using data from the two examinations by the Kaiser Permanente Women Twins Study, performed a decade apart. The sample consisted of 348 pairs of women twins who participated in both examinations, including 203 MZ pairs and 145 DZ pairs. Average ages at the two examinations were 41 and 51 years, respectively. By means of three different statistical analytic approaches, moderate heritability estimates were demonstrated for changes in LDL cholesterol (h2 = .25-.36) and in HDL cholesterol (h2 = .23-.58), some of which were statistically significant. Although small to moderate heritability estimates were found for systolic blood pressure (.18-.37; P < .05 for some estimates), no genetic influence on changes in diastolic blood pressure was detected. Based on longitudinal twin data in women, this study demonstrates a genetic influence on changes in both lipoprotein risk factors and systolic blood pressure over a decade. In addition to environmental factors, which clearly are operating, the effect of various "variability genes" may be acting independently of the genetic influences on the absolute levels of these risk factors. Both mapping the gene(s) underlying intraindividual variations in these CHD risk factors and understanding their function(s) could lead to targeted intervention strategies to reduce CHD risk among genetically susceptible individuals.     

Cardiovascular risk factors in a French-Canadian population: resolution of genetic and familial environmental effects on blood pressure by using extensive information on environmental correlates.

Genetic and environmental influences on systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial blood pressure (MBP) were examined in 371 French-Canadian families by using path analysis. Familial environment was estimated with environmental indices constructed from as many as 14 (of a pool of more than 100) correlates of blood pressure (BP). Approximately 20% of the variance in BP can be accounted for by the composite index, and the types of variables and the direction of their effects vary as a function of age and of the multivariate context. Path analysis of the family data suggests that genetic heritability is relatively high in children (from 0.49 for SBP to 0.56 for MBP) but much smaller in adults (from 0.08 for DBP to 0.18 for SBP). The proportion of variability explained by familial environment is estimated to be the same in children and adults and is much higher than reported to date (from 0.30 for SBP to 0.42 for DBP). In addition, sibships share significant nontransmitted environmental effects, and there is no evidence to suggest specific maternal effects in the aggregation of BP. Two unique findings emerge from this study. First, unlike in most earlier studies, we were able to arrive at the same parsimonious model for each of the BP variables. Second, the familial environment accounts for a substantial proportion of the variability in BP, which has been considerably underestimated in earlier studies.     

Low blood pressure and dementia in elderly people: the Kungsholmen project.

OBJECTIVE--To examine the relation between blood pressure and dementia in elderly people. DESIGN--Cross sectional, population based study. SETTING: Kungsholmen district of Stockholm, Sweden. SUBJECTS-- 1642 subjects aged 75-101 years. MAIN OUTCOME MEASURES--Prevalence and adjusted odds ratio of dementia by blood pressure. RESULTS--People with systolic pressure < or = 140 mm Hg were more often diagnosed as demented than those with systolic pressure >140 mm Hg: odds ratios (95% confidence interval) adjusted for age, sex, and education were 2.98 (2.17 to 4.08) for all dementias, 2.91 (1.93 to 4.38) for Alzheimer''s disease, 2.00 (1.09 to 3.65) for vascular dementia, and 5.07 (2.65 to 9.70) for other dementias. Similar results were seen in subjects with diastolic pressure < or = 75 mm Hg compared with those with higher diastolic pressure. When severity and duration of dementia were taken into account, only moderate and severe dementia were found to be significantly related to relatively low blood pressure, and the association was stronger in subjects with longer disease duration. Use of hypotensive drugs and comorbidity with cardiovascular disease did not modify the results for all dementias, Alzheimer''s disease, and other dementias but slightly reduced the association between vascular dementia and diastolic blood pressure. CONCLUSIONS--Both systolic and diastolic blood pressure were inversely related to prevalence of dementia in elderly people. We think that relatively low blood pressure is probably a complication of the dementia process, particularly Alzheimer''s disease, although it is possible that low blood pressure may predispose a subpopulation to developing dementia.     

Exercise reduces arterial pressure augmentation through vasodilation of muscular arteries in humans

Exercise markedly influences pulse wave morphology, but the mechanism is unknown. We investigated whether effects of exercise on the arterial pulse result from alterations in stroke volume or pulse wave velocity (PWV)/large artery stiffness or reduction of pressure wave reflection. Healthy subjects (n = 25) performed bicycle ergometry. with workload increasing from 25 to 150 W for 12 min. Digital arterial pressure waveforms were recorded using a servo-controlled finger cuff. Radial arterial pressure waveforms and carotid-femoral PWV were determined by applanation tonometry. Stroke volume was measured by echocardiography, and brachial and femoral artery blood flows and diameters were measured by ultrasound. Digital waveforms were recorded continuously. Other measurements were made before and after exercise. Exercise markedly reduced late systolic and diastolic augmentation of the peripheral pressure pulse. At 15 min into recovery, stroke volume and PWV were similar to baseline values, but changes in pulse wave morphology persisted. Late systolic augmentation index (radial pulse) was reduced from 54 +/- 3.9% at baseline to 42 +/- 3.7% (P < 0.01), and diastolic augmentation index (radial pulse) was reduced from 37 +/- 1.8% to 25 +/- 2.9% (P < 0.001). These changes were accompanied by an increase in femoral blood flow (from 409 +/- 44 to 773 +/- 48 ml/min, P < 0.05) and an increase in femoral artery diameter (from 8.2 +/- 0.4 to 8.6 +/- 0.4 mm, P < 0.05). In conclusion, exercise dilates muscular arteries and reduces arterial pressure augmentation, an effect that will enhance ventricular-vascular coupling and reduce load on the left ventricle.     

Community care compared with hospital outpatient care for hypertensive patients.

Three hundred and seventy-six patients with treated diastolic blood pressures of less than 105 mm Hg and no history of accelerated hypertension or renal failure were selected from among those attending the Hammersmith Hospital hypertension clinic. Their average lying treated blood pressure was 146 mm Hg systolic and 90 mm Hg diastolic and average age 56 years; 18% were black, 6% Asian, and 76% white. The patients were mostly having multiple treatment, 90% receiving a diuretic, 35% methyldopa, 33% propranolol, 18% atenolol, 9% hydrallazine, and 7% bethanidine. They were randomly allocated to either two years of further hospital outpatient care or referred back to their general practitioners. During the two years 19 (10%) of the 187 patients followed up in hospital defaulted and three had their treatment discontinued. Twelve (6%) of the 189 followed up by their general practitioners defaulted from follow-up and nine had their treatment discontinued. At the end of the trial the average lying blood pressure was 148 mm Hg systolic and 88 mm Hg diastolic in the hospital group and 149 mm Hg systolic and 90 mm Hg diastolic in the general practice group. The change in blood pressure was calculated for each individual and showed an average fall of 1.6 mm Hg in standing diastolic pressure in the hospital group and a rise of 1.4 mm Hg in the general practice group (p less than 0.05). The 90% confidence limits for a difference in standing diastolic pressure between the groups were 1 and 5 mm Hg with the pressure lower in the hospital group. General practice care was not quite as effective in controlling blood pressure as continued specialist supervision over two years in this selected group of treated outpatients with mild or moderate hypertension, but these results show that the discharge back to general practitioners of patients who are well controlled after hospital treatment is a sensible policy.     

The role of genetic and environmental factors in phenotypic variability of arterial pressure and body weight and their interconnection (a family study)

Contribution of genetic and environmental factors into phenotypic variability of blood pressure and body mass as well as into phenotypic correlation between these traits was defined. It was shown that additive genetic determinant is responsible for considerable level of blood pressure and body mass variability. Those common environmental factors are of importance which operate within the limits of one generation. Maternal effect of systolic and diastolic blood pressure variability is negligible. The correlation between systolic and diastolic blood pressure is determined both by environmental and genetic factors, whereas that between blood pressure and body mass is mediated by only environmental factors. The contribution of environmental factors into correlation between blood pressure and body mass lessens with age. The results obtained may be applied in development of population and individual programmes for preventing cardiovascular diseases.     

Afterload and blood pressure amplitude in dilated cardiomyopathy]

The beat-to-beat variability of the diastolic blood pressure induces small variations in the afterload of the left ventricle. These variations influence myocardial contractility, and thus blood pressure amplitude. We assessed the interdependence of blood pressure and changes in the afterload. We continuously recorded blood pressure (duration 200 s, at rest) in 20 patients with dilated cardiomyopathy (ejection fraction 32 +/- 13%, left ventricular diameter 67 +/- 8 mm) and in 20 healthy volunteers. Interbeat intervals, diastolic pressures, systolic pressure amplitudes and mean slopes of systolic pressure amplitudes were measured. Correlation coefficients (r) were calculated to assess the interdependence of blood pressure amplitudes/mean systolic slopes and the preceding diastolic pressures/interbeat intervals, respectively. In healthy volunteers we found a strong interdependence between blood pressure amplitude and the preceding diastolic pressures (r = 0.62 +/- 0.21 and 0.47 +/- 0.22). Higher diastolic pressures were followed by higher blood pressure amplitudes, and by steeper slopes of the systolic peaks. In patients with dilated cardiomyopathy, such interdependence was significantly lower (r = 0.33 +/- 22 and r = 0.28 +/- 0.35), and in patients with severely reduced left ventricular function (ejection fraction < 32%) was only marginal (r = 0.23 +/- 0.27 and 0.21 +/- 0.44, respectively). The forces of the isovolumetric contraction necessary to initiate the ejection phase of the left ventricle depend on the afterload, i.e. on the diastolic pressure. The responses of amplitude and slope of the systolic blood pressure to small changes in the afterload make it possible to assess left ventricular contractility. The latter is impaired in dilated cardiomyopathy.