Vascular hypertrophy and insulin resistance have been associated with abnormal left ventricular (LV) geometry in population studies. We wanted to investigate the influence of vascular hypertrophy and insulin resistance on LV hypertrophy and its function in patients with hypertension. In 89 patients with essential hypertension and electrocardiographic LV hypertrophy, we measured blood pressure; insulin sensitivity by hyperinsulinaemic euglucaemic clamp; minimal forearm vascular resistance (MFVR) by plethysmography; intima-media cross-sectional area of the common carotid arteries (IMA) by ultrasound; and LV mass, relative wall thickness (RWT), systolic function and diastolic filling by echocardiography after two weeks of placebo treatment. LV mass index correlated to IMA/height (r=0.36, P=0.001), serum insulin (r=-0.25, P
This study was designed to evaluate whether plasma asymmetric dimethylarginine (ADMA) has any role in predicting hemodynamic responses in clinically healthy young subjects. ADMA, as an endogenous nitric oxide (NO) synthase inhibitor, has been demonstrated to associate with hypertension and vascular reactivity in experimental but not undoubtedly in physiological settings.
A total of 199 subjects aged 31.4 years (range 24-39 years) were studied. Plasma ADMA and symmetric dimethylarginine (SDMA) were assessed by isocratic high-pressure liquid chromatography using precolumn derivatization with o-phtaldialdehyde at baseline. Blood pressure (BP) was measured by casual measurements in the beginning of the study and after a follow-up period of 2.45 +/- 0.42 years (range, 1.86-3.19 years). Hemodynamic regulation was assessed by noninvasive methods after a follow-up.
Plasma ADMA had a negative association with resting systemic vascular resistance index (SVRI) (r = -0.23, P
The central hemodynamic state in 111 patients has been studied, 78 (70.27%) of them underwent surgical operation. The depression of central homodynamic indices which correlated with the severity of patients' state, cardiovascular system reserves, was revealed by means of current diagnostic procedures. Among the main reliable characteristics of central hemodynamic by which we can forecast consequences of disease are an ejection fraction of the left ventricle, stroke volume, and minute volume. In the process of preoperative preparation it is necessary to consider common peripheral vascular resistance fluctuation. An increase in this peripheral vascular resistance can lead to myocardial infarction, acute disorder of coronal blood flow, hypertension stroke. The optimal tactics of treatment of such patients with heart insufficiency is the correction of coronal blood flow after an operation and assessment the risk of carrying out an surgical operation.
PURPOSE: To compare local ophthalmic blood flow changes with flow changes in carotid and vertebral arteries in diabetic patients with retinopathy of different grades. MATERIAL AND METHODS: Ten patients with proliferative or preproliferative retinopathy, 10 with mild retinopathy, and 10 matched controls were prospectively studied with ultrasound. Color and duplex Doppler imaging was used to quantitate blood flow in the central retinal arteries (CRA), ophthalmic arteries (OA), common carotid (CCA) and vertebral arteries (VA). Peak systolic velocity (PSV), mean velocity (MV), and resistance index (RI) in CRA, OA, CCA and VA, and volume flow (VF) were measured in CCA and VA. RESULTS: There was a non-significant increase in the CRA and OA velocities in mild retinopathies, a decrease of about 30% in MV, and a slightly increased RI in proliferative or preproliferative retinopathies. There was a decrease of about 15% in the carotid MV and a 20% decrease in the vertebral MV and a decrease of about 30% in VF in the CCA and VA in severe retinopathies. The MV ratio of CRA/CCA was lower in the severe retinopathy group than in the controls. CONCLUSION: The study showed a non-significant increase of ocular blood flow velocities in mild diabetic retinopathy and a significant decrease of flow velocities in severe diabetic retinopathy. This decrease in flow primarily seems to reflect the general decrease of blood flow in the cervical arteries.
We investigated whether hypoxemia without acidemia affects ductus venosus (DV) blood velocity waveform pattern in sheep fetuses with intact placenta and whether worsening acidemia and impending fetal death are related to changes in DV velocimetry in fetuses with increased placental vascular resistance. A total of 34 fetuses were instrumented at 115-136/145 days of gestation. Placental embolization was performed in 22 fetuses on the fourth postoperative day, 24 h before the experiment. The control group was comprised of 12 fetuses with intact placenta. The experimental protocol consisted of fetal hypoxemia that was induced by replacing maternal inhaled oxygen with medical air. To further deteriorate fetal oxygenation and blood-gas status, uterine artery volume blood flow was reduced by maternal hypotension. Fetuses that underwent placental embolization were divided into two groups according to fetal outcome. Group 1 consisted of 12 fetuses that completed the experiment, and group 2 comprised 10 fetuses that died during the experiment. DV pulsatility index for veins (PIV) and fetal cardiac outputs (COs) were calculated. Placental volume blood flow, fetal blood pressures, and acid base and lactate values were monitored invasively. On the experimental day, the mean gestational age did not differ significantly between the groups. In groups 1 and 2, the baseline mean DV PIV and fetal COs were not statistically significantly different from the control group. In the control group, the DV PIV values increased significantly with hypoxemia. In groups 1 and 2, the DV PIV values did not change significantly, even with worsening acidemia and imminent fetal death in group 2. During the experiment, the fetal COs remained unchanged. We conclude that fetal hypoxemia increases the pulsatility of DV blood velocity waveform pattern. In fetuses with elevated placental vascular resistance, DV pulsatility does not increase further in the presence of severe and worsening fetal acidemia and impending fetal death.
We aimed to investigate age and gender differences in arterial stiffness, and whether this cardiovascular risk factor was detectable in healthy Caucasians before established disease was manifest.
A growing number of risk factors including diabetes, obesity, hypertension, hyperlipidaemia, smoking and age have been linked to the adverse cardiovascular end-points of myocardial infarction, stroke and heart failure. These risk factors lead to an increase in arterial stiffness. Measuring this stiffness at an early age may identify candidates for primary preventative intervention strategies by nurses.
Caucasian Canadians (n = 176) were recruited. Peripheral and central blood pressure, pulse pressure, augmentation pressure, arterial compliance (augmentation index and pulse wave velocity) and sub-endocardial viability ratio (SEVR), were assessed using applanation tonometry (SphygmoCor system). Blood was drawn for fasting lipid and glucose profiling.
Women participants had significantly stiffer arteries than men (augmentation index: 28 SEM = 1% vs. 18 SEM = 2% respectively; p
Preeclampsia is a long-term cardiovascular risk factor for the mother and possibly the offspring. Preeclampsia and cardiovascular diseases share common pathophysiological features, including endothelial dysfunction. We explored whether endothelial function, measured noninvasively, as well as circulating biomarkers reflecting lipid metabolism, angiogenesis, and inflammation, differed in paired mothers and offspring 5 to 8 years after delivery. Twenty-six mother and child pairs after pregnancies complicated by preeclampsia were compared with 17 mother and child pairs after uncomplicated pregnancies. In addition, we assessed whether concentrations of maternal circulating biomarkers at delivery predicted findings 5 to 8 years postpartum. We also included an assessment of early onset preeclampsia and specifically addressed the effects of small for gestational age. Endothelial function was significantly reduced in both mothers and children after preeclampsia when combined with a small-for-gestational-age infant compared with mothers and children after pregnancies without a small-for-gestational-age infant (mothers: P
Impaired endothelial function has been implicated as a cause of cardiovascular disease. Little is known of the relations of measures of endothelial function in resistance and conduit arteries to incident cardiovascular disease in the general population, and available techniques have not been compared.
In 1016 participants (70 years of age) of the population-based Prospective Study of the Vasculature in Uppsala Seniors (PIVUS) study (52% women), we measured endothelium-dependent vasodilation using the invasive forearm technique with acetylcholine given in the brachial artery, the brachial artery ultrasound technique with measurement of flow-mediated dilatation, and the pulse-wave analysis-based method with ß-2-agonist terbutaline provocation. During 5 years of follow-up, 101 participants experienced a composite end point of myocardial infarction, stroke, or death, excluding the 85 persons with a history of myocardial infarction or stroke at baseline. In logistic regression models adjusted for several established and novel cardiovascular disease risk factors and medications, endothelium-dependent vasodilation by the invasive forearm technique with acetylcholine was associated with risk of the end point (odds ratio, 0.72 per SD; 95% confidence interval, 0.56 to 0.93; P=0.01). Endothelial function by the other 2 methods was not related to risk of the end point. Addition of endothelium-dependent vasodilation to the Framingham risk score improved discrimination of risk of the end point.
Endothelium-dependent vasodilation in resistance arteries, but not in the brachial conduit artery (flow-mediated dilatation), was associated with 5-year risk of a composite end point of death, myocardial infarction, or stroke independently of major cardiovascular disease risk factors. This vascular measurement improved risk discrimination when added to an established risk score in an elderly population.
OBJECTIVE: We hypothesized that a decrease in fetal oxygenation without acidemia in a near-term fetal sheep leads to cardiovascular hemodynamic changes that are detectable by Doppler ultrasonography. STUDY DESIGN: Twelve ewes and fetuses were instrumented at 112 to 127 days of gestation. After a 5-day recovery period, experiments were performed with general anesthesia. Uterine and placental volume blood flows and fetal arterial and venous blood pressures were measured. Fetal cardiovascular hemodynamics was assessed by Doppler ultrasonography. All the measurements were performed at baseline, during fetal hypo-oxygenation, and at recovery phase. RESULTS: A drop in fetal Po2 was related to increased (P
Limitation of coronary perfusion of different degree induces inhomogeneous changes in resistance of vessels in the hypoperfusing zone: an adequate dilatory regulatory reaction may be followed by an increase in resistance of the coronary vessels. An active component of diastolic coronary resistance used to analyze vascular reactions, rate and character of changes in resistance under conditions of coronary perfusion as well as histological and electron-microscopic estimation of the vascular wall state testify to reversibility and active character of the observed changes in coronary resistance including its increase. This increase is pathogenetically significant as it may induce further development of the coronary perfusion disorder.