Reduction In Arterial Compliance Research Articles

Spontaneous Bursts of Muscle Sympathetic Nerve Activity Reduce Femoral Arterial Compliance in Humans

Previous studies in rodents have demonstrated tonic sympathetic restraint of arterial compliance. To date, studies in humans have examined sympathetic restraint of compliance via either reflexively or pharmacologically manipulating sympathetic vasoconstriction and measuring resultant changes in compliance. The extent to which spontaneous bursts of muscle sympathetic nerve activity (MSNA) dynamically regulate arterial compliance in humans on a beat-by-beat basis remains unknown. Herein, we hypothesized that femoral arterial compliance would be transiently reduced following spontaneous bursts of MSNA. Further, we hypothesized that the magnitude of reduction in arterial compliance would be graded to the MSNA burst amplitude (index of net neural outflow). Beat-to-beat blood pressure (BP; Finometer), heart rate (ECG), MSNA (peroneal microneurography), and femoral artery blood flow (duplex Doppler ultrasound) were continuously measured over 10-20 minutes of quiet supine rest in 27 young, healthy men (age: 22 ± 1 years, resting MSNA burst frequency: 11 ± 5 bursts/minute). Customized labview programs were used to time-align neural cardiovascular variables with ultrasound data sampled at 30Hz, enabling the quantification of arterial compliance on a beat-by-beat basis defined as the change in arterial cross-sectional area divided by the change in blood pressure over the cardiac cycle. Bursts of MSNA were tracked for 10 cardiac cycles and changes in arterial compliance were quantified using signal-averaging for all bursts, and subsequently, for bursts of MSNA when sub-classified based on amplitude into quartiles (Q1= smallest 25% of bursts, Q4= largest 25% of bursts). Reductions in arterial compliance were significantly greater following cardiac cycles with bursts of MSNA compared to cardiac cycles without bursts of MSNA (bursts: -5.1 ± 0.6% vs. non-bursts: -0.8 ± 0.2%, p<0.001). Further, reductions in compliance appeared to be graded to MSNA burst amplitude (Q1: -6.5 ± 0.8%; Q4: -9.1 ± 1.3%, P=0.051). The latency (i.e., number of heartbeats) to nadir arterial compliance following bursts of MSNA was 4.2 ± 0.6 cardiac cycles. Collectively, these findings suggest that the sympathetic nervous system dynamically regulates femoral arterial compliance on a beat-to-beat basis. College of Nursing and Health Innovation, University of Texas at Arlington. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Cerebrovascular adaptations to habitual resistance exercise with aging.

Resistance training (RT) is associated with improved metabolism, bone density, muscular strength, and lower risk of osteoporosis, sarcopenia, and cardiovascular disease. Although RT imparts many physiological benefits, cerebrovascular adaptations to chronic RT are not well defined. Participation in RT is associated with greater resting peripheral arterial diameters, improved endothelial function, and general cardiovascular health, whereas simultaneously linked to reductions in central arterial compliance. Rapid blood pressure fluctuations during resistance exercise, combined with reduced arterial compliance, could lead to cerebral microvasculature damage and subsequent cerebral hypoperfusion. Reductions in cerebral blood flow (CBF) accompany normal aging, where chronic reductions in CBF are associated with changes in brain structure and function, and increased risk of neurodegeneration. It remains unclear whether reductions in arterial compliance with RT relate to subclinical cerebrovascular pathology, or if such adaptations require interpretation in the context of RT specifically. The purpose of this narrative review is to synthesize literature pertaining to cerebrovascular adaptations to RT at different stages of the life span. This review also aims to identify gaps in the current understanding of the long-term impacts of RT on cerebral hemodynamics and provide a mechanistic rationale for these adaptations as they relate to aging, cerebral vasculature, and overall brain health.

Influence of coupled hemodynamics-arterial wall interaction on compliance in a realistic pulmonary artery with variable intravascular wall properties.

Pulmonary hypertension is characterized by elevation of pulmonary artery (PA) pressure (p) and structural remodeling of the PA wall, leading to reduction in arterial compliance (c). As a step towards improving diagnosis of pulmonary disease, we use the PA branch geometry (main pulmonary artery (MPA) branching into left (LPA) and right (RPA) pulmonary arteries) obtained from MRI in conjunction with an inverse algorithm to obtain the pre-stress level in the artery walls. Next, a coupled blood-wall interaction (BWI) calculation provides hemodynamic information as well as compliance of the PA walls. We show that the computed load-free geometry from the inverse algorithm exhibits a 27.8% lower inner diameter (d) and 18.5% lower outer d compared to the in vivo geometry from MRI. Further, the mean p computed from the BWI computation in the main PA (pMPA-n) is within 4% of the mean pMPA-e (n-numerical; e-experimental). Also, the mean Q computed in the left PA (QLPA-n) is within 10% of the mean QLPA-e. Finally, the compliance cMPA-n is computed to be 27% lower than cMPA-e, while the cLPA-n is computed to be 20.4% lower than cLPA-e. Importantly, the PA shows significant intra-vascular variation in compliance, with the MPA showing higher overall compliance compared to the LPA (3.5-4 times).

Hybrid polymer microfluidic platform to mimic varying vascular compliance and topology.

Several cardiovascular pathologies and aging have been associated with alterations in the mechanical and structural properties of the vascular wall, leading to a reduction in arterial compliance and the development of constriction. In the past, rare efforts have been directed to understand the endothelial cell response to combined mechanical stimuli from fluid flow and substrate rigidity. Recent approaches using microfluidic platforms have limitations in precisely mimicking healthy and diseased vasculature conditions from altered topological and substrate compliance perspectives. To address this, we demonstrated an effective fabrication process to realize a hybrid polymer platform to test these mechanistic features of blood vessels. The salient features of the platform include circular microchannels of varying diameters, variation in substrate rigidity along the channel length, and the coexistence of microchannels with different cross sections on a single platform. The platform demonstrates the combined effects of flow-induced shear forces and substrate rigidity on the endothelial cell layer inside the circular microchannels. The experimental results indicate a pronounced cell response to flow induced shear stress via its interplay with the underlying substrate mechanics.

Morphometric changes of the left ventricle and characteristics of peripheral hemodynamics in patients with drug resistant hypertension

Aim. To study morphometric changes of the left ventricle (LV) and characteristics of peripheral hemodynamics in patients with drug resistant hypertension (HT). Material and methods. In total, 120 patients with unmanageable HT of 2-3 degrees, that considered by physicians as drug resistant HT, were included into the study. Patients with HT resistant to full-dose triple antihypertensive therapy (n=43) were included into Group 1. Patients with HT controlled by combination therapy (n=83) were included into Group 2. All the patients underwent echocardiography, volumetric compression oscillometry (to study hemodynamic parameters). Stiffness index (SI, m/s) and reflection index (RI,%) of the pulse wave were also analyzed. Results. The increase in linear and volumetric LV sizes, severe LV hypertrophy were found in Group 1. LV mass index (LVMI) in patients in Group 1 was 134.0±6,5g/m² vs 98.4±3.3 g/m² in Group 2 (p<0.001). LVMI in men in Group 1 was 150.02±10.7 g/m² vs 99.2±4.5 g/m² in Group 2 (p<0.001). LVMI in women in Group 1 was 126±7.8 g/m vs 102.5±3.4 g/m² in Group 2 (p<0.05). The relative left ventricular wall thickness in Group 1 was 0.60, vs 0.50 in Group 2 (p<0.05). In patients of group 1 compared with group 2 there were also found a reduction in arterial compliance (0.84±0.06 vs 1.0±005, respectively; p<0.05), increased pulse wave velocity (820.14±16 vs 741.11±19 cm/sec, respectively; p<0.05), and increase in specific peripheral vascular resistance. Conclusion. Most of patients with drug resistant HT have concentric LV hypertrophy and concentric LV remodeling. The microvasculature remodeling takes place much earlier and is accompanied by possible rarefaction. Increased vascular stiffness is more pronounced in patients with drug resistant HT. It was confirmed by decrease in arterial compliance, and increase in outer diameter of the artery, that led to increase in pulse wave velocity

Influence of Cardiac Function and Loading Conditions on the Myocardial Performance Index – Theoretical Analysis Based on a Mathematical Model –

The myocardial performance index (MPI) has emerged as a Doppler-derived index for global ventricular function capable of estimating combined systolic and diastolic performance. While several studies have reported its load-dependency, responses of the MPI to various hemodynamic changes have not been fully characterized. The response characteristics of the MPI were examined and compared with ejection fractions (EF) by changing hemodynamic parameters within the physiological range in a lumped parameter model of the cardiovascular system. At baseline, the MPI was 0.42 and the EF was 0.68. Heart rate increase resulted in a decrease in EF and an increase in the MPI. Reduction in end-systolic elastance decreased EF and increased the MPI. Volume overload and ventricular stiffening did not affect EF but paradoxically reduced the MPI. Increased afterload due to higher systemic resistance resulted in a decrease in EF and increase in the MPI, but afterload increase caused by reduced arterial compliance led to a decrease in both EF and MPI. These MPI characteristics caused paradoxical improvement of the MPI during disease progression of chronic heart failure in a simulation of mitral regurgitation. The MPI is affected by a wider variety of hemodynamic parameters than EF. In addition, it is predicted to decrease paradoxically with volume overload, reduction in arterial compliance, or ventricular diastolic stiffening. These MPI characteristics should be considered when assessing cardiovascular dynamics using this index.

The major cerebral arteries proximal to the Circle of Willis contribute to cerebrovascular resistance in humans

Cerebral autoregulation ensures constant cerebral blood flow during periods of increased blood pressure by increasing cerebrovascular resistance. However, whether this increase in resistance occurs at the level of major cerebral arteries as well as at the level of smaller pial arterioles is still unknown in humans. Here, we measure cerebral arterial compliance, a measure that is inversely related to cerebrovascular resistance, with our novel non-invasive magnetic resonance imaging-based measurement, which employs short inversion time pulsed arterial spin labelling to map arterial blood volume at different phases of the cardiac cycle. We investigate the differential response of the cerebrovasculature during post exercise ischemia (a stimulus which leads to increased cerebrovascular resistance because of increases in blood pressure and sympathetic outflow). During post exercise ischemia in eight normotensive men (30.4 ± 6.4 years), cerebral arterial compliance decreased in the major cerebral arteries at the level of and below the Circle of Willis, while no changes were measured in arteries above the Circle of Willis. The reduction in arterial compliance manifested as a reduction in the arterial blood volume during systole. This study provides the first evidence that in humans the major cerebral arteries may play an important role in increasing cerebrovascular resistance.

Mapping Micro-Mechanical and Micro-Structural Changes in the Ageing Aorta

In healthy individuals, arterial function is critically dependent on the biomechanical properties of stiff fibrillar collagens, resilient elastic fibre proteins and contractile smooth muscle cells. Although age-related reductions in arterial compliance (arteriosclerosis) are associated with chronic hypertension and hence with the development of aortic aneurysms, heart failure and stroke, the differential role played by each of these vascular components in the progression of disease remains unclear.The scanning acoustic microscope (SAM), when operated at frequencies close to 1GHz, is capable of measuring acoustic wave speeds (which are related to tissue stiffness) with a spatial resolution of ∼1 micrometer. Using unfixed tissue cryo-sections, we mapped variations in wavespeed from the intimal surface of young (less than 1.75years) and old (more than 8.00years) sheep aortas. Whilst there was a significant age-related increase in mean wavespeed, across the tissue (young: 1.847km/s, SEM 0.004km/s; old: 1.882km/s, SEM 0.003km/s; Mann Whitney U test, p<0.001) the increase was most pronounced in the inter-lamellar (IL) regions located between large elastic lamellae (EL) (wavespeed increase; IL: 0.047km/s, EL: 0.021km/s). Atomic force microscopy of ovine aorta cryo-sections identified both fine elastic fibres and collagen fibril bundles within this IL space. Collagen and elastin contents of young and old aortas were determined (as a percentage of tissue section area) using light microscopy of picrosirious red and Miller's stained sections respectively. Although collagen content increased significantly in old compared with young sheep (young: 30.97%, SD 2.63%; old: 44.86%, SEM 5.00%; Student's t-test p<0.05) there was no significant change in elastin content (young: 49.75%, SD 4.86%; old: 49.98%, SEM 4.27%; Student's t-test p=0.97).These observations suggest, therefore, that gross mechanical stiffening of the ageing aorta, may occur primarily as a result of localised collagen remodelling in the space between elastic lamellae.

Arterial Compliance in Multiple Sclerosis: A Pilot Study

A reduction in arterial compliance in patients with autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus has been previously reported. It is caused by the effect that systemic inflammation has on the cardiovascular system. Multiple sclerosis (MS), an immune-mediated disease that exclusively affects the central nervous system (CNS), has a significant inflammatory component that is limited to that compartment. The potential effects of its inflammatory mediators in the cardiovascular system are largely unknown. To examine large (C1) and small arterial compliance (C2) in patients with MS and compare them with healthy age-matched controls. To also determine whether any differences in C1 and C2 indices between participants diagnosed with relapsing remitting MS (RR-MS), secondary progressive MS (SP-MS), and controls exist. A total of 26 men and women between the ages of 18 and 64 diagnosed with MS and 25 healthy controls volunteered for this study. Arterial compliance was measured by using pulse contour analysis (PCA), which records and analyzes the blood pressure waveform data from the Arterial Pulse Wave Sensors. Significant differences in C1 and C2 were found between young RR-MS and healthy young controls (P < .05), with the MS group showing lower arterial C1 and C2 compliance. No significant differences (P > .05) were seen for C1 or C2 values between older RR-MS, SP-MS, and healthy controls. Arterial compliance is significantly compromised in young individuals with MS, compared with age-matched controls, but not for older individuals, suggesting a systemic effect of an inflammatory process that predominantly affects the CNS.

Allometric Hemodynamic Analysis of Isolated Systolic Hypertension and Aging

Isolated systolic hypertension (ISH) is prevalent in the elderly and the contributing factors are predominantly vascular in origin. We previously showed that the hemodynamic manifestation of ISH is the result of a concurrently mild increase in peripheral resistance with a large reduction in arterial compliance or greatly increased vascular stiffness. Such elastic mismatching can lead to increased wave reflections. Therefore, we hypothesize that significantly increased pulse wave reflections associated with a drastically reduced arterial compliance beyond normal aging is a principle contributing factor to the production of ISH. To investigate this, we developed a new allometric hemodynamic model that can account for the arterial compliance and peripheral resistance changes during the progression of aging. This model also affords the time domain analysis of forward and reflected waves during aging and ISH. Results show that a further and much greater reduction in arterial compliance beyond normal aging is necessary to produce ISH. Comparison of ISH with normal aging at 60-year old showed that in ISH the amount of wave reflections is much more pronounced, with a greater amplitude and earlier arrival in systole. The increased wave reflections in ISH further amplify the cyclic stress on the already stiffened blood vessels. Therefore, therapies to treat ISH patients need to focus on reducing pulse wave reflections as well as on improving large vessel compliance.

Efeitos hemodinâmicos e vasculares do treinamento resistido: implicações na doença cardiovascular

Resistance training has been proposed as a possible strategy for cardiovascular prevention and rehabilitation, and in this context, this review describes the cardiovascular effects mediated by this type of intervention. Increments in both muscular strength and capacity to perform daily tasks are well-characterized benefits of this type of training. More recently, studies using hemodynamic evaluation have shown cardiovascular stability in patients with coronary disease or heart failure during the performance of resistance exercise, with no apparent detriment to ventricular function or exacerbated increase in exercise blood pressure. Additionally, resting blood pressure also seems to be influenced by chronic resistance training, with a slight reduction in both systolic blood pressure (SBP) and diastolic blood pressure (DBP). The measurement of pressure levels after a single resistance exercise session shows the occurrence of post-exercise hypotension in normal and hypertensive individuals; however, there is controversy as to the intensity of the effort necessary to induce this effect. Recently, intervention studies have investigated resistance exercise effects on vascular variables as arterial compliance and endothelial function. Despite the small number of experiments available, evidence has shown a potential influence of resistance training on the reduction of arterial compliance. On the other hand, peripheral blood flow is increased after resistance training, whereas the endothelial function seems to be improved especially after combined aerobic and resistance training. Additional research is necessary for an analysis of the efficacy of this intervention on validated outcomes, and for a greater understanding of the physiological mechanisms responsible for vascular adaptations.

An experimental study of the flow temperature and velocity field in a heated stenosis

The degree of left ventricular hypertrophy is generally thought to reflect the severity of aortic stenosis. However, the compounded influence of arterial system load is poorly understood. We developed a computer model to investigate the effects of aortic valve stenosis in combination with various systemic arterial parameters in the development of left ventricular hypertrophy. Data show that an increased peripheral resistance and/or aortic valve resistance, results in an increase in left ventricular wall thickness and mass, while peak systolic wall stress remains constant. Changing arterial compliance to above normal level would not induce significant changes in wall thickness, while reduction in arterial compliance below normal would cause an increase in ventricular wall thickness. When a double load is imposed on the left ventricle by way of a stenotic valve and an increased arterial afterload, a greater and an aggregated increase in wall thickness results, hastening the hypertrophic process.

Vascular calcification and cardiovascular function in chronic kidney disease

Vascular calcification and arterial stiffening are independent predictors of all causes and cardiovascular mortality in chronic kidney disease (CKD). Few data are currently available comparing vascular calcification and its attendant functional cardiovascular consequences between CKD stage 4 patients and both peritoneal dialysis (PD) and haemodialysis (HD) (CKD stage 5) patients. We studied 134 subjects (60 HD, 28 PD and 46 CKD 4). Vascular calcification was quantified using multi-slice spiral CT scanning of a 5 cm standardized segment of superficial femoral artery. Pulse wave analysis and pulse wave velocity were assessed using applanation tonometry, to determine arterial compliance. Further digital arterial pulse wave analysis was used to measure systemic haemodynamic variables. All medications were recorded and biochemical variables were time averaged for the 6 months prior to entering the study. Forty-seven percent of CKD 4 patients demonstrated vascular calcification as compared with CKD 5 (71% PD and 73% HD, P = 0.02). HD patients had higher calcification scores (median 121) than either PD (median 21) or CKD 4 (median 0) (P = 0.008). There were no significant differences in baseline characteristics between the groups. Comparing tertiles of patients (based on calcification score), increased calcification score was associated with a reduction in arterial compliance (mean PWV 8.9 +/- 1.1, 11 +/- 3.6, 11.3 +/- 3.7 m/s, P = 0.005). The degree of calcification did not influence systolic blood pressure (BP), diastolic BP or heart rate. However, more heavily calcified patients demonstrated significantly higher mean pulse pressures (58 +/- 19, 74 +/- 22 and 72 +/- 25 mmHg, P = 0.001), lower total peripheral resistance (1.5 +/- 1, 1.3 +/- 0.8, 0.9 +/- 0.4, P = 0.01) and higher stroke volume (84 +/- 25, 95 +/- 29, 106 +/- 39 ml, P = 0.01). More heavily calcified patients were significantly older and predominantly male. This study has successfully utilized a novel technique for the quantification of calcification. We have demonstrated vascular calcification and associated cardiovascular dysfunction in CKD 4, PD and HD with significant differences between the groups. Thirty percent of individuals show no calcification, even those established on renal replacement therapy for a prolonged period of time. Further work is required to identify factors which promote progression of arterial calcification in those who are susceptible.

Extending the hydrodynamic hypothesis in chronic hydrocephalus

Dear Editor: I greatly enjoyed reading the review article and the theories put forward by Dr. Greitz [6] regarding the pathophysiology of hydrocephalus as well as the subsequent editorials and follow-up letter from Dr. Greitz [7]. Essentially, Dr. Greitz proposes a hydrodynamic theory for the pathophysiology of chronic hydrocephalus. This involves a reduction in the compliance of the arterial tree with, as a consequence, the subsequent failure of arterial pulse pressure dampening. This would cause an elevation in arteriolar and capillary pulse pressure and induce a hyperdynamic brain parenchymal pulsation, which in turn would compress the ventricular system, leading to hyperdynamic aqueduct flow and water-hammer dilatation of the ventricular system. I fully agree with this portion of the hypothesis but note, as the editorials did, that it does not go far enough in that it fails to answer the problems of the failure of bulk flow of CSF. I believe that the answer lies in what causes the reduction in arterial compliance and what other effects this reduction in compliance would have on the venous system and the CSF outflow through the arachnoid granulations. Dr. Greitz does not fully address where the reduction in compliance resides. If it were an intrinsic problem with the walls of the arterial tree (say, atherosclerosis or atheroma), then it is difficult to see why normal pressure hydrocephalus would not be a much more wide spread disease than it is. If, as I have argued, the reduction in compliance is in the walls delimiting the subarachnoid space [1] (the so-called walls of the container) then the result on the arterial tree would be the same as if the artery walls themselves were stiffer. This is because the arteries can only expand into the space made available by the shifting of CSF (water is incompressible), if the walls of the container are stiff and there is nowhere for the CSF to shift to, then the arteries also fail to expand. The benefit of moving the reduction in the compliance from the walls of the arteries to the walls of the container is that we can also begin to explain the other manifestations of chronic hydrocephalus. It has long been known that the compliance of the walls of the container has a direct effect on the apparent resistance to CSF resorption across the arachnoid granulations with, for example, experimentation on cats showing a significant reduction in CSF pressure from craniectomy [9]. In humans, craniectomy is performed for raised intracranial pressure and even in those with an obvious CSF resorption abnormality a percentage will go on to develop the “syndrome of the trephined”, which is a physiological state of reduced CSF pressure and low-pressure symptoms [5]. How can compliance affect the resistance to CSF flow across the arachnoid granulations? The answer is that it cannot affect resistance but can interact with impedance. I have argued that if the resistance to non-pulsatile flow across the arachnoid granulations were low but the walls of the granulations were rigid (a high percentage of collagen) then their impedance to pulsatile flow would be high [3]. A reduction in the CSF pulse pressure as occurs in craniectomy would reduce the overall “apparent” resistance to CSF outflow by minimising the effect of the high impedance and as a corollary an increase in CSF pulse pressure as is noted in hydrocephalus [4] (secondary to the reduction in dampening afforded by the walls of the container) would increase the apparent resistance to CSF flow by making the intrinsic high impedance of the granulations interact with a more pulsatile flow. It remains to be explained why CSF preferentially appears to be resorbed through the walls of the ventricular system into the deep brain parenchyma and not into the much larger capillary bed afforded by the cortex. The effect of a reduction in compliance does not just affect the arterial tree. The venous system also passes through the subarachG. A. Bateman (*) Department of Medical Imaging, John Hunter Hospital, Locked Bag 1, Newcastle Region Mail Centre, Newcastle 2310, Australia e-mail: grant.bateman@hnehealth.nsw.gov.au Tel.: +61-2-49213414 Fax: +61-2-49213428

Unfavorable Effects of Resistance Training on Central Arterial Compliance

0379 PURPOSE: A reduction in arterial compliance is an emerging risk factor for cardiovascular disease mortality and morbidity. We determined the effects of resistance (weight) training on carotid arterial compliance using the randomized intervention study design. METHODS: Twenty-eight healthy men aged 20–38 yrs were random1y assigned to exercise intervention (n = 14) or control (n = 14) group. The intervention group underwent supervised whole-body resistance training 3 days/wk for 4 months and detraining for the subsequent 4 months. The control group was instructed not to alter their normal activity levels during the entire study period. RESULTS: There were no significant differences in baseline carotid arterial compliance and betastiffness index (simultaneous carotid ultrasound and applanation tonometry) between the intervention and control groups. In the intervention group, resistance training increased maximal bench press (19%), dead lift (32%), and squat (55%) strength (all p < 0.001). Carotid arterial compliance decreased 19% (0.21 ± 0.02 mm2/mm Hg vs. 0.17 ± 0.01 mm2/mm Hg, mean ± SE) and beta-stiffness index increased 21% (2.12 ± 0.18 U vs. 2.50 ± 0.14 U) after resistance training (all p < 0.05). These changes returned to the baseline levels (0.20 ± 0.01 mm2/mm Hg and 2.24 ± 0.15 U) during the subsequent detraining period, confirming that the changes in arterial compliance was due to the effect of resistance training per se. There were no significant changes in any of the variables in the control group. Femoral arterial compliance (measure of peripheral artery compliance), brachial and carotid blood pressure, and carotid intima-media thickness did not change significantly in both groups. CONCLUSIONS: In marked contrast to the beneficial effect of regular aerobic exercise, resistance training reduces central arterial compliance in healthy men. Considering the recent guidelines that resistance training be incorporated into a preventive and rehabilitative program of overall physical activity, the present findings may have an important implication for exercise prescription.

Comparison of nicotine effects on hemodynamics and arterial stiffness between smokers and non-smokers

P-277 Key Words: Nicotine, Arterial Compliance,:ABS>

A new model of isolated systolic hypertension induced by chronic warfarin and vitamin K 1 treatment

Background Isolated systolic hypertension is the predominant form of hypertension in the elderly population. Reduction of arterial compliance appears to contribute to the elevation of pulse pressure (PP) and among potential mechanisms, gradual vascular calcification, fragmentation of elastic lamellae, and augmentation of rigid component like collagen could contribute to increase aortic stiffening. Few experimental models of the disease are currently available. Methods To induce large artery calcification, rats were treated with warfarin and vitamin K 1 (WK) for 4 and 8 weeks, to inhibit the maturation of matrix Gla protein. The impact of chronic PP elevation was determined on large artery and cardiac remodeling and on aortic endothelial function. Results The WK treatment led to aortic medial calcification and a proportional elevation of PP, attributable mainly to a selective elevation of systolic blood pressure. The chronic treatment also increased collagen, whereas elastin decreased in the aorta. Pulse wave velocity, an index of aortic stiffening, increased in rats treated with WK. However, indices of left ventricular and aortic hypertrophy and remodeling remained normal. In addition, the WK treatment did not modify the vasoconstriction to norepinephrine and endothelin-1, and the vasodilatory response to acetylcholine and sodium nitroprusside. Conclusions Chronic treatment with WK represents a new model of isolated systolic hypertension with several characteristics of the human disease. The relative ease to induce calcification in this model may help to foster more fundamental research, which is lacking in this type of hypertension.

Pulse pressure—a review of mechanisms and clinical relevance

The goal of this study was to review the origin, clinical relevance and treatment of pulse pressure (PP). Elevated PP is increasingly being recognized as a risk factor for cardiovascular, particularly coronary, disease. Pulse pressure is discussed in terms of both Windkessel and distributive models of the arterial circulation. Pulse pressure arises from the interaction of cardiac ejection (stroke volume) and the properties of the arterial circulation. An increased stiffness of the aorta and large arteries leads to an increase in PP through a reduction in arterial compliance and effects on wave reflection. A number of factors are known to influence arterial wall behavior and, therefore, PP. In addition to the effects of aging and blood pressure on arterial wall elasticity, there is some evidence that atherosclerosis, per se, amplifies these effects. Thus, the relationship between PP and coronary disease may be bidirectional. A number of dietary and lifestyle interventions have been shown to modify large artery behavior. These include aerobic exercise training and consumption of n-3 fatty acids. Conversely, strength training is associated with an increase in arterial stiffness and a higher PP. The effects of antihypertensive medication have been extensively studied, but many studies are difficult to interpret because of concomitant change in blood pressure, and to a lesser degree, heart rate. However a number of studies do suggest direct arterial wall effects, particularly for angiotensin-converting enzyme inhibitors. A distributed compliance model of the arterial circulation provides a framework for understanding the causes, effects and potential treatment of elevations in PP.

Large and Small Artery Compliance Changes During Hemodialysis

P116 Heart disease is a major cause of morbidity/mortality in hemodialysis (HD) patients. Studies show changes in arterial compliance, independent of BP, predict mortality in HD. Changes in calcium which occur during the HD treatment may contribute to a reduction in arterial compliance during HD. Pulse wave analysis (PWA) via tonometry provides measures of large and small artery compliance. We used PWA to measure changes in compliance during HD treatment. PWA was recorded immediately prior to a HD treatment (Baseline) and midway through the treatment (Mid-dialysis). Large (C1) and small artery compliance (C2), systemic vascular resistance (SVR), systolic blood pressure (SBP), and diastolic blood pressure (DBP) were measured. Serum calcium was measured before and during the HD treatment. RESULTS: Six HD patients (3M/3F) whose mean age was 39 ± 17 years, weighing 151.0 ± 29 lbs and the mean height was 68 ± 4 inches were studied. The hemodynamic data is shown in table: all values are expressed as mean ± SD. The results showed a downward trend (C1), and a statisitcally sgnificant reduction (C2) in large and small artery compliance, respectively, with modest statistically insignificant changes in SBP and DBP. The SVR increase was of marginal significance. The calcium level rose significantly. We conclude that PWA detects changes in hemodynamics during HD not evident using conventional BP which may increase cardiac workload and contribute to the high cardiovascular morbidity and mortality in HD patients.

Large and Small Artery Compliance Changes During Hemodialysis

P116 Heart disease is a major cause of morbidity/mortality in hemodialysis (HD) patients. Studies show changes in arterial compliance, independent of BP, predict mortality in HD. Changes in calcium which occur during the HD treatment may contribute to a reduction in arterial compliance during HD. Pulse wave analysis (PWA) via tonometry provides measures of large and small artery compliance. We used PWA to measure changes in compliance during HD treatment. PWA was recorded immediately prior to a HD treatment (Baseline) and midway through the treatment (Mid-dialysis). Large (C1) and small artery compliance (C2), systemic vascular resistance (SVR), systolic blood pressure (SBP), and diastolic blood pressure (DBP) were measured. Serum calcium was measured before and during the HD treatment. RESULTS: Six HD patients (3M/3F) whose mean age was 39 ± 17 years, weighing 151.0 ± 29 lbs and the mean height was 68 ± 4 inches were studied. The hemodynamic data is shown in table: all values are expressed as mean ± SD. The results showed a downward trend (C1), and a statisitcally sgnificant reduction (C2) in large and small artery compliance, respectively, with modest statistically insignificant changes in SBP and DBP. The SVR increase was of marginal significance. The calcium level rose significantly. We conclude that PWA detects changes in hemodynamics during HD not evident using conventional BP which may increase cardiac workload and contribute to the high cardiovascular morbidity and mortality in HD patients.