Therefore, this study aimed to detect the effects of RDN on arterial stiffness as measured with aortic pulse wave velocity PWV and distensibility in addition to cardiac function and T1 mapping at baseline and at 6-month follow-up.
Methods: RDN was performed in a total of 16 patients with treatment-resistant hypertension, and the procedures were conducted at two university hospitals using two different RDN devices. All patients and age-matched controls underwent a comprehensive clinical examination and cardiac magnetic resonance protocols both at baseline and at a 6-month follow-up. This improvement was independent of the reduction in SBP. Keywords: renal denervation, cardiovascular MR, arterial stiffness. Arterial hypertension affects more than one-quarter of the adult population worldwide.
This condition is defined as treatment-resistant hypertension TRH. Renal sympathetic denervation RDN has been introduced as a new treatment for TRH, and several studies have indicated a profound antihypertensive effect. However, recent randomized studies have failed to demonstrate antihypertensive effects of RDN. Arterial stiffness and its hemodynamic consequences are established predictors of adverse cardiovascular outcomes.
Arterial stiffness is positively associated with systolic hypertension, coronary artery disease, stroke, and heart failure, which all are among the leading causes of mortality in developed countries.
International Journal of Vascular Medicine
However, body habitus and age-related changes affect the calculation when the length of the pulse wave is projected over the body surface. Long-standing hypertension is known to induce cardiac failure often by means of fibrotic cardiac remodeling. Several antihypertensive medications have been demonstrated to reduce or slow down the development of cardiac fibrosis; therefore, the detection of fibrosis at an early stage is important.
When the fibrotic changes are diffuse, a different approach is needed. Therefore, we included the novel method of myocardial T1 mapping in this study. This method directly measured the T1 relaxation time of the entire myocardium in a voxel-by-voxel manner. These measurements can then be used to build myocardial T1 maps that highlight tissue pathologies.
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In , Mortensen et al published data from a pilot study 19 that indicated that RDN improved the central hemodynamics and arterial stiffness, and these results were primarily based on PWV measurements performed with ultrasound and tonometry. However, the influence of RDN on arterial stiffness remains uncertain.
Additionally, we were interested in the possible influences of RDN on cardiac function, myocardial mass, and myocardial T1 values, both at baseline and at 6-month follow-up. Trial Id NCT study, patients who were referred specifically for therapy from hospitals and specialist practices in eastern and central Norway were thoroughly examined by experienced physicians in the nephrology outpatient clinic of the Oslo University Hospital in Ullevaal, Norway, during the time period August through June and at the St.
Patients with documented intolerance of medications could be included in the study even if they had not used a diuretic and even if they had used fewer than three medications. Patients in this study used at the time of inclusion 5. A total of 88 patients were referred, 30 patients were accepted for therapy, and among these, 16 patients were found to be eligible for RDN and CMR. Nine healthy volunteers constituted the normotensive control group, and this group was age-matched with the RDN group Table 1. This study was approved by the respective Regional Committees for Research Ethics in Norway and by the institutional research committees at Oslo University Hospital and St.
All patients provided written informed consent for participation in the study and the publication of the results. CMR was performed at baseline and at 6 months in both groups, using a 1. No meals, caffeine, or smoking was allowed for at least 3 hours beforehand. The images were analyzed quantitatively using dedicated software cmr 42 v 5. A retrospective electrocardiography-gated gradient-echo pulse sequence with velocity encoding was applied to measure the through-plane flow at two predefined positions in the ascending and abdominal aorta.
The imaging parameters on the 1. We calculated 50 phases to obtain a temporal resolution of approximately 25 ms depending on the heart rate. Notes: This figure demonstrates where the phase contrast velocity maps were obtained at the two levels of the aorta.
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A standardized approach was used to measure the path lengths following the midline courses of the aortas. The distensibility of the aorta as derived from the flow measurements at the mid-ascending aorta was calculated using the following formula:. The entire heart was imaged in the short axis orientation using electrocardiography-gated breath-hold multishot echo-planar imaging.
The acquisition of T1 data was successfully conducted in nine controls and eight patients in the RDN group. All examinations were performed using a 1. The data were collected from three planes of the left ventricule LV orthogonal to the two-chamber view, ie, the basal, mid, and apical levels.
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Each categorical variable is expressed as the number and the percentage of patients. The demographic and clinical data are expressed as the mean values with standard deviations or proportions. The baseline characteristics were compared between groups using independent-sample t -tests. In addition, we built a multiple linear regression model and assessed the influence of relevant variables upon PWV and distensibility.
The statistical analyses were performed using SPSS statistics version Table 2 Blood pressure, aortic and left ventricular measurements illustrating the differences between the groups and effect of renal denervation in the RDN group. None of these changes were significant. There were also no significant differences between the control group and the RDN group. All the above-mentioned variables were also used in a multiple linear regression model with both PWV and distensibility as dependent variables.
The model showed that none of the independent variables significantly predict neither PWV nor distensibility. All variables were also used in a multiple regression model with both PWV and distensibility as dependent variables. Additionally, there was an age-matched control group. The main findings were that RDN improved hemodynamics as demonstrated by significantly increased distensibility and a borderline significantly decreased PWV at 6 months after RDN.
These changes occurred independently of the BP-lowering effect. RDN uses a radiofrequency pulse to disrupt the sympathetic nerve fibers going both to and from the kidneys and is known to have several effects.
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Research has demonstrated that the sympathetic drive plays an important role in the regulation of BP, the strength of cardiac muscle contraction, and vessel wall tonus. Our work has potentially demonstrated the beneficial and independent effect of RDNs on the cardiovascular hemodynamics. The same conclusion was also reached in a large study in ten European centers. The insignificant reduction in ambulatory hour SBP accords with the results of recent studies. This study demonstrated that aortic stiffening as characterized by PWV and distensibility was improved in the treatment group.
We also demonstrated that this improvement was independent of reductions in BP. The mechanism of the observed BP independent improvement of PWV and distensibility remains unclear, but it seems reasonable to suggest that the changes done to the sympathetic drive are of importance. It is possible that central hemodynamics is more affected by changes in sympathetic drive than peripheral hemodynamics.
If this is the case, it could explain why the improved aortic distensibility is independent of changes in BP. An important advantage of our study is that CMR provided precise and direct measurements of the pulse wavelengths of the aorta even in very sinuous conditions and thereby provided accurate PWV values. Furthermore, CMR is capable of locally assessing the pulse waves in the aorta and thus minimizes the influences of peripheral arteries on the aortic PWV. For noninvasive assessments of PWV, estimations of the pulse wave travel distance are critical.
The PWV serves as an excellent and well-accepted predictor of cardiovascular mortality, 27 and it has been stated that arterial stiffness serves as a better predictor of cardiovascular risk and end-organ damage than peripheral brachial pressures.
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This finding indicates that this group of patients had a greatly increased risk of a major cardiovascular event. We did not observe any significant changes in the left ventricular measurements in the treatment group. There were no changes in the T1 values in the RDN-treated patients between baseline and follow-up. Because hypertensive disease is known to induce cardiac fibrosis, 16 our study of hypertensive patients who were treated with RDN aimed to identify differences in the T1 values between hypertensive patients and controls.
We also hypothesized that RDN would lead to a reduction in cardiac fibrosis and a subsequent reduction in native T1 values. We were unable to observe any changes, most likely because the hypertensive patients did not in fact have any cardiac fibrosis. The data in our study were generated from a modest number of patients, and all associated limitations apply.
Moreover, there was no blinding regarding the RDN treatment, and it is possible that this influenced the behaviors of the patients. Nevertheless, the size of our study is comparable to those of other publications that have investigated RDN, and the results were consistent even though we applied more thorough methods regarding patient selection than in the Symplicity HTN-1 and -2 studies.
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