Nitroglycerin reduces augmentation index and central blood pressure independent of effects on cardiac preload

Objective To determine whether reduction in central pressure augmentation and central systolic blood pressure by nitroglycerine (NTG) results from effects on pre-load or is due to arterial dilation. Methods We compared effects of NTG with those of lower body negative pressure (LBNP). Hemodynamic measurements were made at rest,during LBNP (10,20 and 30 mmHg,each for 15 min) and after NTG (10,30 and 100 μg/min,each dose for 15 min) in ten healthy volunteers. Cardiac pre-load,stroke volume and cardiac output were assessed by echocardiography. Central pressure augmentation and central systolic pressure were obtained by radial tonometry using a transfer function. Results LBNP (20 mmHg) and NTG (30 μg/min) reduced pre-load (as measured by the peak velocity of the S wave in the superior vena cava) to a similar degree [by (26.8±3.8)% and (23.9±3.4)%,respectively]. Compared to LBNP,NTG reduced systemic vascular resistance [by (32.9±7.5)%,P<0.01],decreased peripheral and central pressure augmentation [by (20.8±3.4)% units and (12.9±2.9)% units,respectively,each P<0.01]. Conclusion These results suggest that a reduction in pre-load does not explain reduction in pressure augmentation and central systolic blood pressure by NTG and that these effects are mediated through arterial dilation.

Changes in Brachial and Central Blood Pressure after Short Term Continuous Positive Airway Pressure Treatment of Patients with Moderate-to-Severe Obstructive Sleep Apnoea and Impaired Renal Function

Background: Previous studies of continuous positive airway pressure (CPAP) treatment for obstructive sleep apnoea (OSA) have shown conflicting results on the effect on blood pressure (BP), and patients with chronic kidney disease (CKD) have not been included in these studies. As OSA is a frequent comorbidity in patients with CKD, it is of relevance to evaluate the effect of CPAP treatment on BP in this population. Aim: In this prospective follow-up study, we measured the effect of short term CPAP treatment of moderate-to-severe OSA on brachial and central BP, plasma level of syndecan-1 and vasoactive hormones, renal handling of sodium, subjective sleepiness, and quality of life in patients with impaired renal function. Methods: From December 2015 until March 2017, 25 patients were invited to participate in the study at the University Clinic in Nephrology and Hypertension, Aarhus University and Holstebro Hospital. At baseline and at follow-up after three to four months of CPAP treatment, we performed 24 h brachial and central ambulatory BP measurement, blood sampling measurements of plasma concentrations of syndecan-1, renin, angiotensin II, aldosterone, vasopressin, creatinine, haemoglobin A1c, and cholesterol, cardio respiratory monitoring, 24 h urine collection for measurement of urinary excretion of albumin, aquaporin-2, and epithelial sodium channel, Epworth Sleepiness Scale (ESS), and SF-36 (quality of life). Results: At follow-up, the 17 included patients with mean baseline estimated glomerular filtration rate 66 mL/min/1.73 m2 had a significant decrease in systolic office-, 24 h- and daytime-BP (13, 7, and 8 mmHg, respectively, p Conclusion: Short-term CPAP treatment of patients with moderate-to-severe OSA and reduced renal function decreased 24 h- and daytime-BP significantly and reduced urinary albumin excretion. Our results underline the importance of treatment of OSA in hypertensive patients with impaired renal function.

Benidipine has effects similar to losartan on the central blood pressure and arterial stiffness in mild to moderate essential hypertension

Background Central blood pressure （BP） is pathophysiologically more important than peripheral BP for the pathogenesis of cardiovascular disease. Arterial stiffness is also a good predictor of cardiovascular morbidity and mortality. The effects of benidipine, a unique dual L-IT-type calcium channel blocker, on central BP have not been reported. This study aimed to compare the effect of benidipine and Iosartan on the central BP and arterial stiffness in mild to moderate essential hypertensives. Methods This 24 weeks, multi-center, open label, randomized, active drug comparative, parallel group study was designed as a non-inferiority study. The eligible patients （n=200） were randomly assigned to receive benidipine （n=101） or Iosartan （n=99）. Radial artery applanation tonometry and pulse wave analysis were used to measure the central BP, pulse wave velocity （PWV） and augmentation index （AIx）. We also measured the metabolic and inflammatory markers. Results After 24 weeks, the central BP decreased significantly from baseline by （16.8±14.0/10.5±9.2） mmHg （1 mmHg =0.133 kPa） （systolic/diastolic BP; P 〈0.001） in benidipine group and （18.9±14.7/12.1±10.2） mmHg （P 〈0.001） in Iosartan group respectively. Both benidipine and Iosartan groups significantly lowered peripheral BP （P 〈0.001） and AIx （P 〈0.05）, but there were no significant differences between the two groups. The mean aortic, brachial and femoral PWV did not change in both groups after 24-week treatment. There were no significant changes of the blood metabolic and inflammatory biomarkers in each group. Conclusion Benidipine is as effective as Iosartan in lowering the central and peripheral BP, and improving arterial stiffness.

The effect of acute aerobic exercise on central arterial stiffness,wave reflections,and hemodynamics in adults with diabetes:A randomized cross-over design

Background:Individuals with diabetes have greater central arterial stiffness,wave reflections,and hemodynamics,all of which promote the accelerated cardiovascular pathology seen in this population.Acute aerobic exercise has been shown to be an effective strategy for reducing central arterial stiffness,wave reflections,and hemodynamics in healthy individuals;however,the effects of acute aerobic exercise in reducing these outcomes is not well established in people with diabetes.Recently,implementation of high-intensity interval exercise(HIIE)has shown superior improvements in cardiovascular health outcomes when compared to traditional aerobic exercise.Yet,the effect of HIIE on the aforementioned outcomes in people with diabetes is not known.The purpose of this study was to(i)describe the central arterial stiffness,wave reflections,and hemodynamic responses to a bout of HIIE and moderate-intensity continuous exercise(MICE)in adults with diabetes;and(ii)compare the effects of HIIE and MICE on the aforementioned outcomes.Methods:A total of 24 adult men and women(aged 29-59 years old)with type 1(n=12)and type 2(n=12)diabetes participated in a randomized cross-over study.All participants completed the following protocols:(i)HIIE:cycling for 4×4 min at 85%-95%of heart rate peak(HR_(peak)),interspersed with 3 min of active recovery at 60%-70%HR_(peak);(ii)MICE:33 min of continuous cycling at 60%-70%HR_(peak);and(iii)control(CON):lying quietly in a supine position for 30 min.Results:A significant group￡time effect was found for changes in central systolic blood pressure(F=3.20,p=0.01)with a transient reduction for the HIIE group but not for the MICE or CON groups.There was a significant group￡time effect for changes in augmentation index at a heart rate of 75 beats/min(F=2.32,p=0.04)with a decrease following for HIIE and MICE but not for CON.For all other measures of central arterial stiffness and hemodynamics,no significant changes were observed(p>0.05).Conclusion:A bout of HIIE appears to lead to a greater transient reduction in central systolic blood pressure than the reduction observed following MICE;however,both HIIE and MICE improved augmentation index at a heart rate of 75 beats/min in people with diabetes.There was no significant difference in response to HIIE and MICE in all outcomes.This provides preliminary evidence on the role of HIIE on such outcomes in people with diabetes.

Central aortic systolic blood pressure can better predict prolonged QRS duration than brachial artery systolic blood pressure in rural community residents

Background Central aortic systolic blood pressure（CASP） has been shown to be a stronger predictor of target-organ damage and cardiovascular events than brachial systolic blood pressure（BSBP）, but there was no data about whether CASP can predict prolonged QRS duration more than BSBP. We examined the association of CASP and BSBP with QRS duration in rural community residents. Methods We retrospectively analyzed 490 rural community residents. Standard resting 12-lead ECG and central aortic blood pressure（CABP） were measured noninvasively in all subjects at baseline. The QRS duration was equal to or more than 120 ms being defined as prolonged QRS duration. Results The prolonged QRS duration group showed higher CASP（139.38 ± 11.67 vs. 135.36 ± 16.22, P = 0.031） and BSBP（136.03 ± 6.74 vs. 124.44 ± 13.01, P 〈 0.001） as compared with controls. Multivariate linear regression analysis showed that CASP, BSBP and heart rate were independently affecting QRS duration. Logistic regression analyses showed that CASP（OR 1.057, 95%CI： 1.027, 1.088, P 〈 0.001）and BSBP（OR 1.056, 95%CI： 1.027, 1.086, P = 0.032） were independent predictors of prolonged QRS duration after adjustment for age, sex, body mass index, heart rate. CASP had a better predictive value for prolonged QRS duration than（AUC： 0.793 vs. 0.601, P 〈 0.001） BSBP. Conclusions Our findings demonstrate that both CASP and BSBP are risks for prolonged QRS duration, but CASP can predict prolonged QRS duration better than BSBP.

Acute Effects of Tolvaptan on Renal Hemodynamics in Autosomal Dominant Polycystic Kidney Disease —A Randomized, Cross-Over, Double Blind, Placebo-Controlled Study of Renal Plasma Flow and Glomerular Filtration Rate

Background: Previous studies have shown that reduced renal plasma flow (RPF) may play a role in progression of renal disease in autosomal dominant polycystic kidney disease (ADPKD). Tolvaptan, a vasopressin 2 antagonist, reduces growth of total kidney volume and slows the decrease in estimated glomerular filtration rate (eGFR) in ADPKD. The purpose of this randomized, cross-over, double-blind, placebo-controlled study was to investigate if acute tolvaptan treatment increases RPF in ADPKD patients. Methods: Eighteen ADPKD patients (chronic kidney disease stages I-III) were investigated twice (min. 10 days apart) after acute treatment with either tolvaptan 60 mg or placebo. Two hours after treatment RPF and GFR were estimated by Technetium-99m diethylenetriamine penta-acetic acid (99-mTc-DTPA) renography. During the examination day, central and brachial blood pressures (BP) were measured using Mobil-O-Graph? PWA. We also measured plasma concentrations of vasopressin (p-AVP), renin (PRC), angiotensin II (p-AngII) and aldosterone (p-Aldo), urine excretion of aquaporin 2 (u-AQP2), urine output (OU), urine osmolality (u-Osm) and fractional excretion of sodium (FENa). Results: 99-mTc-DTPA renography showed a similar RPF (673 ± 262 ml/min after tolvaptan vs. 650 ± 209 ml/min after placebo, p = 0.571) and GFR (78 ± 26 ml/min after tolvaptan vs. 79 ± 21 ml/min after placebo p = 0.774) after tolvaptan and placebo treatment. P-AVP and UO increased and u-Osm decreased after tolvaptan and remained unchanged during placebo. Systolic BP tended to decrease during renography during tolvaptan. Very small or insignificant changes were seen in PRC, p-AngII and p-Aldo. Conclusions: Acute tolvaptan treatment did not change renal hemodynamics in ADPKD.