Aortic Pulse Research Articles

Effect of aortic pulse and fractional pulse pressures on early patency of sapheneous vein grafts

Coronary artery bypass grafting has a mortality benefit compared to medical therapy in some patient groups, such as those with left main or left anterior descending coronary artery disease, and those with left ventricular dysfunction. Therefore, patency of grafts, especially sapheneous grafts, is an important issue. Aortic pulse and fractional pulse pressures are strong and independent indicators of the risk of atherosclerosis. We studied whether there was any negative effect of increased aortic pulse and fractional pulse pressures on saphenous vein graft (SVG) patency in the short term. We evaluated aortic pulse and fractional pulse pressures of patients with occluded and patent SVGs, and investigated the relation between the two groups. One hundred and twenty-six patients with occluded SVGs with a mean age of 65.9+/-8.9 years and 114 patients with patent SVGs with a mean age of 66.9+/-8.6 years were studied consecutively. Aortic systolic and diastolic pressures were measured, and mean, pulse, and fractional pulse pressures (aortic pulse pressure/mean pressure) were calculated. Aortic pulse and fractional pulse pressures were significantly higher in the occluded SVG group than in the patent SVG group (58+/-19 and 48+/-13 mmHg, P=0.001; 0.59+/-0.16 and 0.50+/-0.10, P<0.001, respectively). In addition, a cut-off value of 50 mmHg and 0.52 for aortic pulse and fractional pulse pressures were determined, respectively. Increased aortic pulse (>50 mmHg) and fractional pulse (>0.52) pressures were present in 54.0 and 58.7% of patients in group 1 and 28.1 and 33.3% of patients in group 2, respectively (P=0.004 and P=0.005, respectively). Having increased aortic pulse and fractional pulse pressures increased the risk of SVG occlusion by 3.00 and 2.85-folds, respectively. The multiple-adjusted odds ratio of the risk of SVG occlusion was 6.86 (95% confidence interval 2.14-21.96) and 4.76 (95% confidence interval 1.58-14.30) for the higher aortic pulse and fractional pulse pressure levels compared with lower levels, respectively. Increased ascending aorta pulse and fractional pulse pressures have a significant and independent negative effect on the fate of SVGs.

Abstract 1196: Endogenous Nitric Oxide Synthase Inhibitors, Arterial Hemodynamics And Subclinical Vascular Disease: A Population-based Study

Background: Asymmetric dimethylarginine (ADMA) and NG-monomethyl-L-arginine (NMMA), endogenous nitric oxide-synthase inhibitors (End-NOSI), have been associated with cardiovascular risk factors (CVRF) and atherosclerosis. In addition, acute administration of NOSI cause hypertension through hemodynamic effects, but whether circulating End-NOSI are associated with these abnormalities is unknown. Methods: We studied 922 adults in a population-based study (PREVENCION study). We examined the correlation between End-NOSI/L-arginine and CVRF, as well as the relationship between these biomarkers and arterial hemodynamics, carotid-femoral pulse wave velocity (cf-PWV) and carotid intima-media thickness (c-IMT). We used general linear modeling for statistical analyses. Estimates (β) are standardized. Results: In multivariate analyses, LDL-cholesterol and C-reactive protein (CRP) were independent predictors of ADMA, whereas LDL-cholesterol and gender independently predicted NMMA. Age, gender, HDL-cholesterol and CRP were independent predictors of L-arginine. ADMA (β=0.09;p=0.008) and NMMA (β=0.11; p=0.001), but not L-arginine, were strong predictors of c-IMT, even after adjustment for CVRF, CRP and renal function. In contrast, ADMA and NMMA were not predictors of cf-PWV, blood pressure or hemodynamic abnormalities. Higher L-arginine independently predicted higher central (aortic) pulse pressure (β=0.09; p=0.002), incident wave amplitude (β=0.11; p&lt;0.001) and late systolic augmented pressure from wave reflections (β=0.07; p=0.003), but not systemic vascular resistance or cardiac output. Conclusions: ADMA and NMMA are differentially associated with CVRF, but both End-NOSI are independently predictors of carotid atherosclerosis. In contrast, they are not associated with large artery stiffness, hypertension or hemodynamic abnormalities. Our findings are consistent with a role for End-NOSI in atherosclerosis, but not in large artery stiffnening, hypertension or long-term hemodynamic regulation. L-arginine is independently associated with abnormal pulsatile hemodynamics, which may reflect abnormal L-arginine transport, leading to decreased intracellular bioavailability for NO synthesis.

The effects of central arterial pressure and autonomic dysfunction on elevations in N-terminal pro-B-type natriuretic peptide (NT-proBNP) in men with diabetes

Summary Background In diabetes, left ventricular dysfunction independent of coronary disease is common and is associated with elevations in NT-proBNP. Our aims were to determine the relative importance of central aortic pressure, cardiovascular autonomic function and arterial stiffness as predictors of elevated NT-proBNP. Methods Fifty males with diabetes mellitus and 21 males with IGT were studied. Arterial stiffness and wave reflections were assessed by measuring aortic and brachial pulse wave velocity (PWV) and augmentation index (AIX). Cardiovascular autonomic function was assessed by measurements of heart rate variability following standard manoeuvres. Results Comparing diabetes versus IGT subjects (mean±SD), both aortic PWV (9.7±2.4 versus 8.2±1.4m/s, p p r =0.74, p r =0.66, p r =0.43, p r =0.55, p r =0.37, p Conclusions Elevated central arterial pressure is a strong predictor of NT-proBNP concentrations in diabetic men without clinically apparent left ventricular dysfunction. This is indicative of the key influence of unfavourable large artery haemodynamics on the development of left ventricular dysfunction in diabetes.

Hemodynamic effects of methadone and dihydrocodeine in overdose

Background. Opioid overdose is an increasing health problem worldwide. The cardiovascular toxicity of opioids contributes to morbidity and mortality in overdose but the hemodynamic effects of opioids reported in animal and human studies are contradictory. Methods. We performed a prospective observational study of patients admitted to hospital following an overdose of methadone, dihydrocodeine, or low dose paracetamol (10 each). Basic cardiovascular indices including peripheral blood pressure, pulse rate, radial augmentation index and derived measures of aortic systolic, diastolic, pulse, and mean and end systolic pressures were measured every six hours for up to 18–23 hours after exposure or until hospital discharge. Results. Dihydrocodeine and methadone significantly reduced peripheral and aortic systolic, mean and end systolic pressures. Both opioids significantly decreased peripheral pulse pressure, but only methadone decreased aortic blood pressure. Dihydrocodeine reduced systemic and aortic diastolic blood pressure, an effect not induced by methadone. Methadone significantly reduced peripheral pulse pressure. Augmentation index and heart rate, however, did not change. Both opioids decreased arterial oxygen saturation. Conclusion. These results suggest that dihydrocodeine and methadone in overdose both have a significant effect on central and peripheral hemodynamics. These effects might be expected to reduce cardiac afterload, providing a pharmacological explanation for the apparent benefit of opioids in cardiovascular diseases.

Increased aortic pulse and fractional pulse pressures in patients with cardiac syndrome X

Background. Angina with normal coronary arteries, cardiac syndrome X, is a diagnosis of exclusion. The exact mechanism of this clinical syndrome remains unclear. Although the prognosis is as good as equal to that of the normal population, symptoms related to the syndrome largely impair quality of life. Aortic pulse and fractional pulse pressures are strong and independent indicators of the risk of coronary heart disease. An increase in these hemodynamic parameters is significantly associated with the presence of coronary artery disease in men and women. Methods and results. We evaluated aortic pulse and fractional pulse pressures of patients with cardiac syndrome X and control subjects, and investigated the relation between the two groups. One hundred and twenty‐six patients with cardiac syndrome X with a mean age of 53.1±9.5 years and 76 patients without the syndrome with a mean age of 53.1±11.2 years were studied consecutively from May 2004 to May 2005. Aortic systolic, diastolic, mean and pulse pressures were measured and the fractional pulse pressure was calculated (aortic pulse pressure/mean pressure). Aortic pulse and fractional pulse pressures were significantly higher in the cardiac syndrome X group than in the control group (51±13 mmHg and 43±9 mmHg, p<0.001; 0.54±0.11 and 0.47±0.08, p<0.001, respectively). All patients were classified into tertiles of aortic pulse pressure level to evaluate whether aortic pulse pressure was associated with the presence of cardiac syndrome X in the study. The multiple‐adjusted odds ratio of the risk of cardiac syndrome X was 6.72 (95% CI 2.76–16.37) for tertile 2 and 29.94 (95% CI 5.59–160.44) for tertile 3 of aortic pulse pressure level compared with tertile 1. In addition, all patients were divided into two groups as lower and higher levels of aortic fractional pulse pressure. The multiple‐adjusted OR of the risk of cardiac syndrome X was 4.09 (95% CI 2.05–8.15) for the higher group compared with the lower group of aortic fractional pulse pressure level. Conclusion. Ascending aorta pulse and fractional pulse pressures are significantly associated with the presence of cardiac syndrome X and these associations are independent of age and other cardiovascular risk factors.

Effect of cold, isometric exercise, and combination of both on aortic pulse in healthy subjects

The aortic pulse-wave velocity (PWV) and augmentation index were measured in 24 healthy adults at baseline, during a cold pressor test (CPT), during hand-grip isometric exercise test (HIE), and during a combination of CPT plus HIE. The PWV and augmentation index increased significantly during CPT and HIE compared with baseline (p <0.01). The combined effect of CPT and HIE on PWV and augmentation index was greater compared with the effect of each intervention alone.

An absent carotid pulse may indicate critical aortic stenosis

In severe valvular aortic stenosis, obstruction to ventricular contraction results in prolonged ventricular systole and diminished peak flow velocity. This may translate into weak or impalpable peripheral arterial pulses. We report a case of severe aortic stenosis associated with an impalpable carotid pulse (in the absence of local carotid artery disease) that became easily detectable following aortic valve replacement. In the presence of an aortic stenosis murmur, a weak or impalpable carotid pulse is indicative of critical aortic stenosis and warrants urgent investigation.

Comparative analysis of aortic impedance and wave reflection in ferrets and dogs

Our modified version of the T-tube arterial model (consisting of two parallel, loss-free transmission paths terminating in lumped loads of complex and frequency-dependent nature) was applied to experimental measurements of ascending aortic pressure and of ascending and descending aortic flows taken from dogs and ferrets. Our aim was to provide quantitative evaluation of the aortic pressure and flow pulse wave components as they relate to the distribution of arterial properties and relate to wave travel and reflection in mammalians of consistently different size and shape. Estimated effective lengths (distances to effective reflection sites) of the head-end (d(h)) and body-end (d(b)) transmission paths were approximately 12 and 30 cm, respectively, in the dog and 6.5 and 13 cm, respectively, in the ferret. These lengths and distributions of estimated arterial properties were consistent with the difference in the body size and with the more central location of the heart in the ferret's body than it is in the dog's body. In both animal species the ascending aortic pressure and flow waves could be interpreted in terms of forward and reflected components arising from the two distinct effective reflection sites, although the higher d(h)/d(b) ratio in the ferret determined the presence of one broad, indistinct minimum in the modulus of ascending aortic impedance in the frequency range from 0 to 10 Hz, rather than two distinct minima as observed in the dog.

Vasodilators, Aortic Elasticity, and Ventricular End-Systolic Stress in Nonanesthetized, Unrestrained Rats

We evaluated the effect of different vasodilators on ventricular end-systolic stress by investigating the impact of sodium nitroprusside, nifedipine, and hydralazine on blood pressure, aortic stiffness, and wave reflection during drug-induced hypotension (to 80 mm Hg mean blood pressure) in normotensive (central aortic mean blood pressure, 116 to 119 mm Hg; systolic pressure, 133 to 137 mm Hg), nonanesthetized, unrestrained rats. Aortic stiffness was evaluated from the slope of the linear regression relating pulse wave velocity (PWV) to central aortic mean or pulse pressure. The fall in central aortic systolic blood pressure was less than the fall in mean pressure, especially after hydralazine (122+/-4 mm Hg; sodium nitroprusside, 107+/-2; and nifedipine, 112+/-3 mm Hg; P<.05). The PWV/mean pressure slope was linear, positive, and similar in all three groups (hydralazine, 3.3+/-0.2; sodium nitroprusside, 3.8+/-0.3; and nifedipine, 3.9+/-0.3 cm x s[-1]x mm Hg[-1]; P>.05). The PWV/pulse pressure slope was linear, negative, and less steep in the case of hydralazine (-4.9+/-0.6; sodium nitroprusside, -15.5+/-3.7; and nifedipine, -13.5+/-2.9 cm x s[-1] x mm Hg[-1]; P<.05). The travel time and augmentation index of the reflected wave were similar in all groups. In conclusion, sodium nitroprusside and nifedipine had a more beneficial effect on end-systolic stress than did hydralazine. This does not appear to be related to any specific effect on wave reflection or the "static" relationship between PWV and aortic mean blood pressure; it may be related to the effects of these drugs on the "dynamic" relationship between PWV and pulse pressure.

Effects of sodium nitroprusside on blood circulation and acid–base and ionic balance in rainbow trout: indications for nitric oxide induced vasodilation

The effects of the nitric oxide (NO) releasing antihypertensive agent sodium nitroprusside (SNP) on rainbow trout (Oncorhynchus mykiss) were investigated using either waterborne exposures of up to 1.3 mM SNP over 60 and 90 min or injections via the dorsal aorta, and cardiovascular responses were compared. Doses of up to 40 μg∙kg−1into the blood stream resulted within 5 min in significantly reduced blood pressure and pulse pressure with tachycardia. Waterborne SNP below 0.53 mM had no effect, but concentrations above this level (to 1.3 mM) after 30–60 min produced significant tachycardia and vasodilation, resulting in dose- and time-dependent reductions in dorsal aorta pulse pressure, with maximum decreases of 50–57%. At and above 0.4 mM SNP waterborne exposure, blood [Formula: see text] was significantly increased, plasma Na+, K+, and Cl−values were unchanged, and there was a mild alkalosis. The cardiovascular effects of waterborne isosorbide dinitrate at 40 μM were similar to those of SNP. Exposure of fish to waterborne potassium ferricyanide (0.67 mM), which is structurally similar to SNP but does not release NO, produced only minor cardiovascular effects compared with those of SNP. Pretreatment of fish with propranolol (1.9 mg∙kg−1via the dorsal aorta) followed by exposure to 1 mM waterborne SNP showed that adrenergic responses were unlikely to be involved in the vasodilation. The results of pretreatment with methylene blue (1.5 mg∙kg−1via the dorsal aorta) followed by 1 mM waterborne SNP suggested that the vasodilation was induced by NO activation of soluble guanylyl cyclase. This study demonstrates that NO-releasing compounds cause vasodilation in rainbow trout in vivo and provides a novel way of studying the effects of altered vascular resistance in fish.

A new technique for study of impact of arterial elasticity on left ventricular mass in rats.

We investigated possible links between left ventricular mass and central arterial elasticity in the adult spontaneously hypertensive rat (SHR) and in a subgroup of SHR in which blood pressure was normalized by chronic antihypertensive drug treatment; results were compared with those of age-matched normotensive Wistar-Kyoto rats. Two indexes of arterial elasticity, based on the measurement of aortic pressure pulse wave velocity, were used. First, the slope relating carotidofemoral pulse wave velocity to blood pressure in the phenylephrine-infused pithed preparation was used as a pressure-independent index of wall elasticity. Second, to account for hypertension- and treatment-induced aortic remodeling, elastic modulus was determined from the pulse wave velocity recorded when blood pressure reached that measured in awake animals before anesthesia and pithing, together with values for wall thickness and lumen diameter evaluated by histomorphometric analysis after in situ fixation at the same pressure. In control SHR, regression analysis of variance revealed significant correlations between left ventricular mass and both wave velocity/pressure slope and elastic modulus. Chronic antihypertensive treatment normalized all three parameters. In conclusion, this new technique provides experimental evidence of a link between left ventricular mass and central arterial elasticity.

Reflex responses to stimulation of mechanoreceptors in the left ventricle and coronary arteries in anaesthetized dogs.

1. Previous work has shown that physiological increases in mean aortic root pressure, which change the pressure in both the coronary circulation and the left ventricle, result in reflex vasodilatation. This study was undertaken to attempt to localize the reflexogenic area mainly responsible for the reflex. 2. In anaesthetized, artificially ventilated dogs, cannulae connected to perfusion systems were inserted in the ascending aorta, left ventricular apex and left atrium. This allowed us to change the pressures in: (a) the aortic root including both the coronary arteries and the left ventricle; (b) aortic root and coronary arteries, at constant ventricular pressure; and (c) in the ventricle, with mean (although not pulse) aortic pressure constant. Aortic and carotid baroreceptors were perfused at constant pressure and reflex responses were determined from changes in perfusion pressures (flows constant) to a vascularly isolated hindlimb and to the remainder of the systemic circulation. 3. Combined changes in mean aortic root (coronary arterial) and ventricular systolic pressures consistently resulted in decreases in perfusion pressures. A change in only mean aortic root (coronary arterial) pressure, with ventricular pressure constant, also resulted in decreases in perfusion pressures and these were only a little smaller than those to the combined stimulus. Changes in ventricular systolic pressure resulted in responses averaging only about 30% of those to the combined stimulus. 4. Setting mean aortic root or ventricular systolic pressures at different levels did not affect the responses to changes in pressures in the other region. 5. These results show that physiological increases in pressure in the aortic root and coronary arteries, in the absence of changes in pressure in the left ventricle, cause reflex vasodilatation. The relatively small response occurring when ventricular pressure was changed could be due either to a contribution from ventricular receptors or to a change in the stimulus to coronary receptors resulting from changes in the ventricular or aortic pulse. 6. We conclude that the reflex effects of increases in mean aortic root pressure are due mainly to stimulation of coronary arterial baroreceptors.

Noninvasive Estimation of End‐Systolic Aortic Pressure in Children

To simplify the estimation of end‐systolic aortic pressure (Pes) noninvasively, a regression equation was derived from intra‐arterial measurements. Peak‐systolic (Pps), Pes, and diastolic aortic pressure (Pd), pulse pressure (Pp), heart rate, hemoglobin, body weight, and height were measured. Cardiac index and body surface area were calculated in 66 patients (17 with aortic runoff lesions, group I; 49 without lesions, group II) with various heart diseases without aortic stenosis (35 males, 31 females, mean age 4.6 years) during the course of diagnostic catheterization. Using a stepwise regression analysis, the following relationship was determined from the combined groups: Pes= 0.422*Pps+ 0.617*Pd+ 1.377. The correlation between Pes measured directly and Pes calculated from our formula was quite strong(r= 0.957, P= 0.0001), as was the correlations between each subgroup (r= 0.948, group I; r= 0.959, group II). The correlation between Pes calculated and that estimated using an indirect carotid pulse tracing method was also strong (r= 0.912, P= 0.0001, n= 31). This regression equation appears applicable to infants or children with aortic runoff lesions in whom it is difficult to measure Pes by noninvasive methods using the carotid pulse. (ECHOCARDIOGRAPHY, Volume 8, September 1991)

Correlation of noninvasive arterial compliance with anatomic pathology of atherosclerotic nonhuman primates

Fifteen cynomolgus monkeys were fed a control ( n = 3) or cholesterol-containing diet ( n = 12) for 26 months. An impedance plethysmograph and a calibrated volume plethysmograph were used to determine femoral arterial volume change, ΔV, from femoral arteries. Abdominal aorta pulse pressure was measured directly. The ratio of ΔV to pulse pressure, Δ P, defined femoral artery compliance. At necropsy, sections of pressure fixed common iliac, external iliac, femoral and carotid arteries were obtained for measurements. The site of the largest atherosclerotic lesion was chosen for histologic measurement. The percentage intima in arterial tissue (PIAT) was determined at the site of the largest atherosclerotic lesions in iliac arteries and averaged. Peak compliance was inversely correlated with the PIAT (Pearson correlation −0.39, P < 0.10, n = 21) which improved to r = −0.52, P < 0.01 ( n = 27) when the PIAT also included the carotid atherosclerosis. The correlation coefficients were comparable to those obtained for total plasma cholesterol concentration, and direct systolic and diastolic blood pressure. Peak compliance and α-cholesterol concentrations provided the best multiple linear regression fit for the prediction of PIAT.

透析患者の大動脈石灰化および脈波速度

透析患者の大動脈石灰化および脈波速度

Application of statistical methods for the analysis or interval related cardiac performance variations during cardiac arrhythmia in man.

To study the influence of the sequence of stimulation intervals on cardiac performance indices the relationship between properties of succeeding arrhythmic aortic pressure pulses of patients with atrial fibrillation has been analysed by methods of correlation and regression analysis. There are high correlations between properties of succeeding pulses and it can be shown that the pressure amplitude of one pulse correlates to the properties (diastole, diastolic pressure, pressure amplitude) of up to five preceding pulses. Furthermore, the diastolic pressure is also highly correlated with properties of more than one preceding pulse whereas the duration of the diastole and the RR-interval is independent of preceding pulse properties. We, therefore, conclude that there is no beat to beat regulation of intervals during atrial fibrillation. The relations between properties of succeeding pressure pulses have been summarised in a transfer function model, which allows the description of pulse properties from preceding pulse properties without lack of it. The parameters of the transfer function models are estimated from a sequence of arrhythmic pressure pulses and a parameter selection procedure was developed which identifies the optimal number of input variables (= properties of preceding pulses) required to describe the time course of one pulse property. In order to obtain informations about the presence of possible interval dependent potentiation effects, the transfer function model was used to stimulate the behaviour of the aortic pressure for different stimulation sequences, which have been used in the literature to study potentiation effect experimentally. From typical sequences of potentiation phenomena in the stimulated pulse sequence we conclude that frequency potentiation effects exist in the human myocardium.

Effect of cardiac arrhythmia on left ventricular and aortic blood pressure parameters in the horse

Transaortic blood pressures were recorded in seven horses using catheter mounted transducers during various types of supraventricular arrhythmia. Changes in left ventricular (LV) and aortic (Ao) pulse contours were associated with variation in pulse interval (PI). When PI lengthened there was a rise in LV end diastolic pressure (LVEDP) associated with a prolonged filling time. In contrast, a long PI resulted in a reduced end diastolic Ao pressure (AoEDP) due to a prolonged arterial 'run off'. LVdP/dt max representing the peak rate of rise of pressure during the isovolumic contraction period was not consistently affected by changes in PI. Stepwise linear regression was used to examine the simultaneous relationships of a number of variables derived from the LV and Ao contours. Peak LV pressure (LVPp) was directly related to AoEDP (seven of seven horses) and LVEDP (four of seven). Ao systolic pulse pressure (SPP) was directly related to LVEDP (four of seven) and inversely related to AoEDP (three of seven). Neither LVPp nor SPP were consistently related to LVdP/dt max. The peak positive gradient between LV and Ao pressures was inversely related to AoEDP (six of seven) and directly related to LVEDP and LVdP/dt max (three of seven). The peak rate of rise of the Ao pressure contour during ejection (AodP/dt max) was inversely related to AoEDP (seven of seven) and directly related to LVEDP (four of seven). It was also directly related to LVdP/dt max in four horses but was inversely related in one. The peak rate of fall of the LV pressure contour during relaxation (-LVdP/dt max) was directly related to LVPp (five of seven).

Direct measurement of left ventricular ejection time from echocardiographic posterior wall excursion time: validation of technique.

Echocardiography has proven useful in determining systolic time intervals. Left ventricular mean velocity of circumferential fiber shortening has been calculated utilizing the left ventricular ejection time measured in several manners, usually from the echocardiographic aortic valve opening time or indirect carotid pulse tracing. Left ventricular ejection time is related to the time of posterior wall excursion in patients without conduction defects or segmental wall motion abnormalities. Thus, a single echocardiographic view can measure ventricular diameters and approximate ejection time simultaneously without other echocardiographic or phonocardiographic measurements which may be cumbersome to obtain, particularly during dynamic echocardiographic studies.

Aortic and brachial pulse wave contour and timing in aortic valve disease.

The arrival time (QKd) and contour (ΔP/Δt) of the brachial arterial pressure wave was recorded noninvasively by Sphygmo-Recording, and was correlated with clinical and catheterization data

Optimal regulation of left ventricular ejection pattern

The optimal left ventricular ejection pattern which minimizes the total power required for a given level of cardiac output is derived. Theoretical predictions were based on a three element model of left ventricular load. The trajectory of the optimal aortic root flow pulse was found to be highly sensitive to changes in cardiac output and vascular parameter values. Results are consistent with physiological observations except for the initial portion of systole.