Changes In Central Aortic Pressure Research Articles

Determinants of central aortic pressure and pulse pressure amplification changes in patients with aortic aneurysm: the role of aortic diameter and aortic aneurysm location level

Abstract Background The presence of aortic aneurysm can alters pulse wave propagation and reflection, causing changes in central aortic pressure and pulse pressure amplification (PPA) between the aorta and the brachial artery that might be associated with unfavorable hemodynamic effects for the central arteries and the heart. However, the impact of the location of the aneurysm and increase of the aortic diameter on central blood pressure (CBP) is not fully understood. Objective To investigate central aortic pressure and PPA regarding to association with arterial stiffness and aortic diameter in patients with ascending aortic aneurysm (AA), descending thoracic and abdominal aortic aneurysm (TAA and AAA). Methods 122 patients (96 males, 65±11 years) with aortic aneurysm were enrolled before aortic repair. The parameters of the aorta were evaluated by MSCT angiography: 44 patients (30 males, 55±13 years) had AA (the maximum diameter: 59.9±14.2 mm), 13 patients (11 males, 62±11 years) had TAA (the maximum diameter: 62.8±8.0 mm) and 65 patients (54 males, 69±8 years) had AAA (the maximum diameter: 52.3±17.2 mm). Brachial blood pressure (BBP) was measured by OMRON. CBP, augmentation index (AIx), carotid-femoral pulse wave velocity (PWV) were assessed by SphygmoCor. PPA was calculated as a difference between the values of central and brachial pulse pressure (CPP and BPP). Results Patients of the three groups did not differ in BPP (AA: 59.2±17.6; TAA 56.8±12.8; AAA: 59.3±11.4 mm Hg; P=0.5). Intergroup comparison revealed a difference in CPP between the three patients groups: CPP was higher in patients with AA and AAA, lower in patients with TAA (AA: 50.3±16.2; TAA 43.8±10.8; AAA: 50.0±11.2 mm Hg; P=0.05). PPA was lower in patients with AA and AAA than in patients with TAA (9.6±6.7 and 9.3±4.2 vs. 13.0±6.5 mm Hg; P=0.05 and P=0.04, respectively). IAx was higher in patients with AA and AAA than in patients with TAA (25.2±8.1 and 27.6±8.2 vs. 17.2±8.2 mm Hg; P=0.008 and P=0.001, respectively). A decrease of PPA across all patients correlated with an increase of IAx (r = - 0.268; P=0.003). CPP decreased with an increase of the aortic diameter for each level of the aneurysm (AA: r = - 0.460, P=0.016; TAA: r = - 0.833, P=0.003; AAA: r = - 0.275, P=0.05). PWV decreased with the expansion of the maximum aortic diameter at the level of the AA, TAA and AAA: (r = - 0.389, P=0.03; r = - 0.827, P=0.02 and r = - 0.350, P=0.01, respectively). Conclusion In patients with aortic aneurysm measurements of lower central pulse pressure and reduced PWV indicate an association with increased diameter of the aneurysm. An increase in augmentation index, early return of reflected waves, thus smaller PP amplification and higher CPP were identified in patients with ascending and abdominal aortic aneurysm compared by patients with descending thoracic aortic aneurysm. Funding Acknowledgement Type of funding source: None

Effect of Short-Term Cold Exposure on Central Aortic Blood Pressure in Patients with CKD

Objectives: Study determined effects of arterial hypertension and impaired kidney function on acute cold exposure induced changes in peripheral and central aortic blood pressure (BP). Methods: Five-six subjects were divided into 3 groups including 20 hypertensive patients with normal kidney function (AH-non-CKD), 20 patients with hypertension and CKD (AH-CKD) stage 3b–4 and 16 healthy normotensive subjects (C). Baseline BP, central BP, and central pulse pressure, unadjusted augmentation index (AI) and central augmented pressure were assessed by applanation tonometry (SphygmoCor) before entering the room with constant temperature −10°C (°C), after 10 min in the cold room and in same conditions in room temperature. Results: Cold exposure led to significant increase of central aortic, systolic, and diastolic BP in both AH-non-CKD (p < 0.01) and AH-CKD (p < 0.001). The central aortic BP did not change in healthy subjects. The increase of central aortic systolic blood pressure was significantly larger in AH-CKD compared to AH-non-CKD group (p = 0.0002). Increase of aortic central and brachial systolic and diastolic BP was significantly larger in AH-CKD and AH-non-CKD patients than in controls. AI increased and subendocardial viability ratio and heart rate decreased after cold exposure in all groups. Central aortic and brachial rate pressure product increased by approximately 2,300 bpm × mm Hg (p < 0.001) and 1,600 bpm × mm Hg (p < 0.001), respectively, in the AH-CKD group and by 1,000 bpm × mm Hg (p = 0.007) and 500 bpm × mm Hg (p = 0.19) in AH-non-CKD group after cold exposure. Conclusion: Short-term cold exposure induces larger increase of brachial and central aortic BP in patients with arterial hypertension than in healthy subjects. The changes in central aortic pressure are augmented in hypertensive patients with impaired kidney function.

Organoprotective properties of therapy by fixed combination of perindoprile and amlodipine in patients with arterial hypertension and diabetes mellitus type 2

Actuality: the contribution of changes in central aortic pressure (CAP) to target organ damage and the effect of a fixed combination of perindopril with arnolate with amlodipine besylate on these parameters in patients with arterial hypertension (AH) and type 2 diabetes (DM) has not been studied. Objective: to reveal the relationship between the main indicators of CAP and the damage of target organs (vessels, kidneys and heart) in patients with AH and type 2 diabetes; assess the organoprotective properties of a 12-week therapy with a fixed combination of perindopril arginate with amlodipine besylate in this category of patients. Materials and methods: 30 patients with AH stage III and DM at the age of 45 to 65 years were examined. The indicators of CAP were determined by Vasotens 24 software (“Petr Telegin” LLC, Russia). The structural and functional state of the myocardium was assessed echocardiographically with a Doppler sensor. The pulse wave velocity (PWV) was measured with Polyspectr 8/E apparatus (Neurosoft, Russia). To evaluate the kidney function, the glomerular filtration rate (GFR) was calculated, and albumin excretion in the urine was determined. A fixed combination of perindopril arginine / amlodipine besylate was administered for 12 weeks. Results: 12-week therapy was accompanied by the achievement of target values of blood pressure in 100% of patients, a decrease in office systolic and diastolic blood pressure. There was a significant improvement in indicators of CAP, which was accompanied by a statistically significant decrease in PWV in vessels of the elastic and muscular type, an improvement in the functional state of the kidneys: a decrease in the level of the albumin/creatinine ratio of urine, an increase in rGFR, by a significant decrease in the left ventricular myocardium index. Conclusion: admission of a fixed combination of perindopril and amlodipine in patients with AH in combination with type 2 diabetes for 12 weeks is accompanied by reliable cardio, nephroprotective and endotheliotropic effects, statistically significantly reduces systolic and diastolic CAP, augmentation index in daytime and night hours, leads to a significant reduction of rigidity of the main arteries.

Acute effects of haemodialysis on central venous and arterial pressure characteristics.

Haemodynamic stability of patients during haemodialysis (HD) sessions is of pivotal importance and accurate determination of dry weight remains a challenge. Little information is available about central venous and aortic pressure during dialysis. In this pilot study we used a non-invasive technique to describe the changes in central venous pressure (CVP) during dialysis. An ultrasound-assisted pressure-manometer was used at the cephalic vein during haemodialysis to quantify CVP. Central aortic pressure changes were assessed as aortic augmentation index and subendocardial viability ratio. Bioimpedance was applied to measure total body water, as well as extracellular and intracellular water before and after HD. Measurements were performed prior during and after 1 and 2 h on HD. Ten patients were included with a median age of 72 years (23-82). Haemodialysis reduced the weight by 2.0 kg, corresponding to a measured decrease in total body water of 1.9 L. The mean CVP showed a significant decrease (9.0-0.8 cmH₂O; P = 0.0005) during dialysis. The significant drop in CVP was found during the first hour (9-2.8 cmH₂O). Starting and stopping dialysis was reflected by a reduction of 2.6 cmH₂O and a rise of 2.8 cmH₂O (n.s.). Aortic augmentation index decreased from 26.1% to 21.0% (n.s.). Subendocardial viability ratio increased from 126% to 156% (P < 0.05) during HD, and decreased to 139% direct after HD (n.s.). This is the first study that illustrates a prominent reduction of CVP during the first hour of haemodialysis. Non-invasive CVP measurement is feasible during haemodialysis and adds another piece in the puzzle of factors involved in haemodynamic stability.

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Changes in Central Aortic Pressure, Endothelial Function and Biomarkers in Hypertensive African-Americans with the Cardiometabolic Syndrome: Comparison of Amlodipine/Olmesartan versus Hydrochlorothiazide/Losartan

Sixty-six self-identified African-American subjects with stage 1 and 2 hypertension and characteristics of the cardiometabolic syndrome were treated with amlodipine/olmesartan (A/O) versus losartan/hydrochlorothiazide (L/H) for 20 weeks in an open-label, active comparator fashion. Subjects not meeting a blood pressure (BP) value of <125/75 mm Hg on either regimen at week 14 were placed on additional or alternative therapy. After 20 weeks of therapy, systolic BP was reduced by 34.6 ± 4.2 mm Hg in the A/O group and by 27.0 ± 4.1 mm Hg in the L/H group (p = 0.012 A/O vs. L/H). Diastolic BP was reduced by 16.9 ± 2.0 mm Hg in the A/O group and by 12.3 ± 2.0 mm Hg in the L/H group (p = 0.022 A/O vs. L/H). There was a substantial increase in endothelial function of 44 and 103% in the L/H and A/O groups, respectively (p < 0.005 A/O vs. L/H). Central aorta augmentation pressure was significantly reduced by 42% with the A/O treatment, and a smaller, significant reduction of 28% was observed with the L/H treatment (p = 0.034 A/O vs. L/H). There was a reduction in sIL-6 levels of 20 and 33%, a reduction in serum leptin levels of 22 and 40%, and an increase in serum adiponectin of 19 and 46% in the L/H and A/O groups, respectively (p < 0.005 A/O vs. L/H for each biomarker). Treatment with A/O after 14 weeks reduced pulse wave velocity by 22% (p = 0.011 time comparison), whereas L/H treatment had no significant effect. Our findings suggest that, in addition to effective BP reduction, A/O differentially regulates markers of inflammation and obesity, thereby potentially providing greater vascular protection.

A cohort evaluation on arterial stiffness and hypertensive disorders in pregnancy.

BackgroundHypertensive disorders in pregnancy are associated with systemic endothelial dysfunction leading to impaired physiological vasodilation. Recent evidence has shown central aortic pressures obtained through pulse wave analysis, at less than 14 weeks of gestation, to be predictive of pre-eclampsia. In light of this, we aimed to evaluate the role of central aortic stiffness in the prediction and discrimination of hypertensive disorders in pregnancy.MethodsA cohort study of women with viable, singleton pregnancies at less than 14 weeks of amenorrhoea, and without multiple pregnancies, autoimmune or renal disease, diagnosed with aneuploidy or fetal anomaly will be recruited from a single maternity hospital and followed up till delivery and puerperium. A targeted sample size of 1000 eligible pregnant women will be enrolled into the study from antenatal clinics. Main exposure under study is central aortic pulse pressure using radial pulse wave recording, and the outcomes under follow-up are gestational hypertension and pre-eclampsia. Other measures include lifestyle factors such as smoking, physical exercise, psychometric evaluations, vasoactive factors, uterine artery pulsatility index, height and weight measurements. These measures will be repeated over 4 antenatal visits at 11-14, 18-22, 28-32 and above 34 weeks of gestation. Double data entry will be performed on Microsoft Access, and analysis of data will include the use of random effect models and receiver operating characteristic curves on Stata 11.2.DiscussionThe proposed study design will enable a longitudinal evaluation of the central aortic pressure changes as a marker for vascular compliance during pregnancy. As measures are repeated over time, the timing and severity of changes are detectable, and findings may yield important information on how aberrant vascular responses occur and its role in the early detection and prediction of hypertensive disorders.

Validation of a novel method to determine non-invasively the rate of central aortic pressure changes

Introduction: One of the most sensitive indices of myocardial contractility is represented by the rate of increase of intraventricular pressure during isovolumetric contraction (dP/dt) and (dP/dtejc), which represents the rate of change of pressure during ejection. Today these parameters can be obtained only by invasive catheterization methods. We developed a novel technique that leads to the non-invasive reconstruction of the central aortic pressure. The technique is based on the concept of applying multiple successive occlusive pressures on the brachial artery from peak systole to diastole using an inflatable cuff and plotting the values against time intervals. The hypothesis is that the time intervals required for the aortic pressure wave to overcome a given occlusive brachial pressure applied by a sphyngomanometer on the arm are equal to time needed to reach the same pressure in the central aorta plus the propagation time to the brachial point, which is constant in the same patient throughout the measurements.Methods and results: We tested the hypothesis using an animal experiment. The new non-invasive device was mounted on the left forelimb of the animal. A Millar pressure transducer catheter was inserted to the aorta and the aorta pressure was recorded at time intervals of 1 ms. A second catheter was inserted into the coronary arteries and used to create controlled occlusion of the arteries using a balloon inflated to 10 atm. Measurements were obtained before the intervention was started, and throughout the sequence of repeated occlusions and deflations. At the end of the sequence, IV dobutamine was administered and results were monitored for 10 min while the heart rate and blood pressure were rising. Non-invasive dP/dtejc was reduced typically by 20% in response to balloon inflation. In long occlusion periods, stabilization and sometimes recovery of dP/dtejc is observed. By plotting dP/dtejc measured by the new non-invasive device versus catheter measurements a correlation factor of 0.843 was found.Conclusion: A newly developed method of non-invasive measurement of central dP/dt has been found to correlate to invasive measurements in an animal model.

Relationship between Radial and Central Arterial Pulse Wave and Evaluation of Central Aortic Pressure Using the Radial Arterial Pulse Wave

Since a decrease of central aortic pressure contributes to the prevention of cardiovascular events, simple measurement of not only brachial blood pressure but also central aortic pressure may be useful in the prevention and treatment of cardiovascular diseases. In this study, we simultaneously measured radial artery pulse waves non-invasively and ascending aortic pressure invasively, before and after the administration of nicorandil. We then compared changes in central aortic pressure and radial arterial blood pressure calibrated with brachial blood pressure in addition to calculating the augmentation index (AI) at the aorta and radial artery. After nicorandil administration, the reduction in maximal systolic blood pressure in the aorta (Deltaa-SBP) was -14+/-15 mmHg, significantly larger than that in early systolic pressure in the radial artery (Deltar-SBP) (-9+/-12 mmHg). The reduction in late systolic blood pressure in the radial artery (Deltar-SBP2) was -15+/-14 mmHg, significantly larger than Deltar-SBP, but not significantly different from Deltaa-SBP. There were significant relationships between Deltaa-SBP and Deltar-SBP (r=0.81, p<0.001), and between Deltaa-SBP and Deltar-SBP2 (r=0.91, p<0.001). The slope of the correlation regression line with Deltar-SBP2 (0.83) was larger and closer to 1 than that with Deltar-SBP (0.63), showing that the relationship was close to 1:1. Significant correlations were obtained between aortic AI (a-AI) and radial AI (r-AI) (before nicorandil administration: r=0.91, p<0.001; after administration: r=0.70, p<0.001). These data suggest that the measurement of radial artery pulse wave and observation of changes in the late systolic blood pressure in the radial artery (r-SBP2) in addition to the ordinary measurement of brachial blood pressure may enable a more accurate evaluation of changes in maximal systolic blood pressure in the aorta (a-SBP).

A Novel Noninvasive Myocardial Performance Index For Ruling Out Acute Coronary Syndrome In The Emergency Department

Definitive diagnosis in patients presenting to the emergency department (ED) with chest pain is difficult due to limitations of the electrocardiogram (ECG) as the primary assessment tool. Most patients presenting with chest discomfort have a nonischemic ECG and biomarkers of myocardial necrosis within normal limits. Because of the limitation of initial risk stratification tools, many patients who do not actually have acute coronary syndrome (ACS) are admitted to hospital. The current study describes a new, noninvasive apparatus that quantifies central aortic pressure changes (dP/dt), an established indicator of myocardial contractility. We hypothesize that a higher dP/dt occurs in non ischemic chest pain than during ischemic chest pain. This appears to be a result of reduced myocardial contractility during ischemia, whereas chest pain of non cardiac origin increases dP/dt by the stress of the pain itself. The study follows 102 patients presenting at the ED with acute chest pain. In 55 patients, the device indicated chest pain to be of non cardiac origin (dP/dt index above threshold value of ≥150). Of these 55, negative ECG and myocardial enzyme dynamics ruled out coronary origin during the first twenty-four hours after admission (sensitivity 93%, negative predictive value 98% specificity 61%, positive predictive value 28%, accuracy 66%). Initial findings indicate that adding noninvasive dP/dt measurements to the classical triage of chest pain in the ED could help prevent unnecessary hospitalization in a substantial number of patients with low probability for ACS.

Detection of chest pain of non-cardiac origin at the emergency room by a new non-invasive device avoiding unnecessary admission to hospital

Recent advances in the treatment of acute coronary syndromes has raised awareness that prompt presentation for chest pain may be life saving. Most patients presenting with chest discomfort have a...

The effect of blood pressure variations on muscle fatigue with chronic arterial occlusion

Summary o 1. Dogs with chronic arterial occlusion had quadriceps muscle fatigue patterns studied with rhythmic stimulation with varying levels of aortic blood pressure. 2. The femoral artery pressures distal on an occlusion directly reflected changes in central aortic pressure. 3. Elevated femoral artery pressure due to intravenous infusion of levarterenol and phenylephrine significantly improved the muscle fatigue pattern while histamine infusion lowered femoral pressure and worsened the fatigue pattern. 4. This mechanism is suggested as a possible explanation for spontaneous improvement in some patients with intermittent claudication who develop hypertension.

RELATION OF RETROGRADE PRESSURE IN THE SINUS NODE ARTERY TO SINUS TACHYCARDIA FROM STELLATE STIMULATION.

Abstract During sinus tachycardia following stimulation of the stellate ganglion, retrograde pressure in the sinus node artery decreased below control level. This decrease occurred independently of changes in central aortic pressure and was, furthermore, not observed in other atrial or ventricular coronary arteries. Procedures which abolished the cardiac accelerator response from adrenergic stimuli also eliminated the period of decreased retrograde pressure. These observations are considered compatible with the hypothesis of an inverse relationship between the caliber of the intranodal artery and the rate of pacemaking discharge by the sinus node.