Arterial HypertensionPhase 3ARTSNCT01318395
Aliskiren on Retinal Vasculature Treatment Study
A Phase 3 study testing Aliskiren in people with Arterial Hypertension, run by University of Erlangen-Nürnberg Medical School at 2 sites in Germany.
Trial summary
Hypertension affects approximately one fourth of the world population and therefore contributes substantially to the worldwide burden of cardiovascular (CV) disease and end-organ damage. Read more about this study
- Who is it for?
- Ages 18 to 75 years, men only
- Conditions the study is for
- Arterial Hypertension
- What is being tested?
- Aliskiren
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 56 participants
- Where
- 2 sitesGermany
- Study dates
- May 2010to Jun 2013
- Phase
- Phase 3
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 75 years
- Men only
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Male or female aged 18 to 75 years (females of child bearing potential must be using adequate contraceptive precautions)
- Females of childbearing potential or within two years of the menopause must have a negative urine pregnancy test at enrolment visit
- Patients with mild to moderate uncomplicated essential hypertension with a trough mean sitting DBP ≥ 90 mmHg and/or SBP ≥ 140 mmHg or pretreated arterial hypertension
- Written informed consent
- Agreement to attend all study visits as planned in the protocol
- Agreement to perform routinely self home blood pressure measurements as well as keep a blood pressure diary throughout the study and to inform the investigator if BP exceeds cutt off criteria given in the ICF
Who cannot join
- In the investigator's opinion the patient can not be withdrawn from their current antihypertensive medication
- Secondary hypertension (e.g. patients with hyperaldosteronism, pheochromocytoma, renal artery stenosis, renal parenchymal disease, coarctation of the aorta, Cushing's disease syndrome)
- Severe essential hypertension (systolic blood pressure ≥ 180 mmHg and/or diastolic blood pressure ≥ 110 mmHg) or treatment resistant hypertension (3 antihypertensive drugs and still SBP ≥ 140mmHg and/or DBP ≥ 90mmHg)
- History of hypertensive encephalopathy or intracerebral hemorrhage
- Diabetes mellitus Type 1 or Type 2
- History of epilepsia (no retinal exam possible)
Show all 21Show fewer
- Eye cataract (no retinal exam possible)
- History of the following within the last six months: myocardial infarction, unstable angina pectoris, percutaneous coronary intervention, heart failure
- Presence of significant renal, respiratory, hepatic, gastrointestinal, endocrine or metabolic, immunological, haematological or oncological, neurological and psychiatric diseases or dysfunction
- Impaired renal function as shown by estimated GFR (abbreviated MDRD formula) < 45 ml/min/1.73 m2
- Impaired hepatic function as shown by transaminases higher than three times the upper normal limit
- Known allergy or a known intolerance to any ARB or Aliskiren
- Females who are pregnant or lactating or who are not on an adequate contraception (Pearl-Index ≥ 1 %)
- Use of any investigational drug within 28 days before study entry
- Patients previously enrolled into the study
- History of drug, medication abuse.
- Serious disorders which may limit the ability to evaluate the efficacy or safety of the test drug(s), including cerebrovascular, cardiovascular, renal, respiratory, hepatic, gastrointestinal, endocrine or metabolic, immunological, haematological or oncological, neurological and psychiatric diseases
- Subject is the investigator or any subinvestigator, research assistant, pharmacist, study coordinator, other staff or relative thereof directly involved in the conduct of the protocol
- Mental conditions rendering the subject unable to understand the nature, scope and possible consequences of the study
- Subject unlikely to comply with protocol, e.g. uncooperative attitude, inability to return for follow-up visits and unlikelihood of completing the study
- Subject who do not give written consent, that pseudonymous data will be transferred in line with the duty of documentation and the duty of notification according to § 12 and § 13 GCP-V
Trial locations and contacts
2 sites in 1 country.
Germany2 sites
Clinical Research Unit, Department of Nephrology and Hypertension, University of Erlangen-Nürnberg
Erlangen, 91054
Clinical Research Unit, Department of Nephrology and Hypertension, University of Erlangen-Nürnberg
Nuremberg, 90471
About this study
Official title: Randomized, Double Blind, Active-controlled, Parallel Study to Analyse Effects of the Combination of Aliskiren and Valsartan on the Vascular Structure and Function of Retinal Vessels
Hypertension affects approximately one fourth of the world population and therefore contributes substantially to the worldwide burden of cardiovascular (CV) disease and end-organ damage.
Changes in small artery structure characterized by an increased wall-to-lumen ratio (WLR) are characteristic feature of target organ damage in hypertension. Of clinical importance, structural arteries of small subcutaneous arteries have been shown to be of prognostic significance, with adverse prognosis in subjects with higher WLR. However, the assessment of arteriolar structure from biopsies of subcutaneous tissue is invasive and impractical in clinical practice. A new approach focuses on retinal arteriolar structural parameters by using scanning laser Doppler flowmetry (SLDF) with automatic full-field perfusion imaging analyses (9). This approach allows the non-invasive assessment of both the outer diameter (OD) and inner diameter (ID) of retinal arterioles in vivo and, thus, analyses vascular remodeling of retinal arterioles by calculating WLR = (OD - ID) / ID).
Read more
A crucial role in the efforts of prevention of end-organ damage plays the renin angiotensin system (RAS). The increased mechanical strain on the vasculature at a higher BP can cause injury to the endothelial wall. Activation of the RAS increases BP and stimulates a local inflammatory response to repair the injury. Long-term or repeated response to injury leads to endothelial dysfunction and microvascular damage, and hence end-organ damage.
Combining RAS inhibitors may provide greater end-organ protection than use of either class alone. However, ONTARGET has failed to show superiority of the dual RAS blockade (ACE-I and ARB) in patients at high cardiovascular risk. The combination of ARBs and direct renin inhibitors (DRIs) emerged as the only available, valid and innovative option for blocking the RAS at two different sites (sequential blockade). Indeed, AVOID study and ALLAY study demonstrated that the DRI aliskiren has additional and to some extent blood pressure independent effects on albuminuria and left ventricular hypertrophy, both signs of subclinical organ damage in hypertension, respectively.
However, no data are available with respect to the effects of ARBs and DRIs on vascular properties in the short and long term To close this gab we focus in this study on vascular structural and functional changes since vascular adaptation to high blood pressure occurs in the early phase of hypertensive disease.
Read the detailed description
Hypertension affects approximately one fourth of the world population and therefore contributes substantially to the worldwide burden of cardiovascular (CV) disease and end-organ damage (1). Therefore, the goal of antihypertensive therapy is to provide effective long-term lowering of elevated blood pressure (BP) and prevention of hypertensive end-organ-damage and mortality (2).
Changes in small artery structure characterized by an increased wall-to-lumen ratio (WLR) are characteristic feature of target organ damage in hypertension. (3; 4). A clinical study examining small arteries obtained from gluteal biopsies of patients with hypertension revealed that an increased WLR of subcutaneous small arteries is one of the first manifestations of target organ damage in hypertension that occur before proteinuria and cardiac hypertrophy (5). Of clinical importance, structural arteries of small subcutaneous arteries have been shown to be of prognostic significance, with adverse prognosis in subjects with higher WLR (6-8). However, the assessment of arteriolar structure from biopsies of subcutaneous tissue is invasive and impractical in clinical practice. A new approach focuses on retinal arteriolar structural parameters by using scanning laser Doppler flowmetry (SLDF) with automatic full-field perfusion imaging analyses (9). This approach allows the non-invasive assessment of both the outer diameter and inner diameter of retinal arterioles in vivo and, thus, analyses vascular remodeling of retinal arterioles by calculating WLR = (outer diameter - inner diameter) / inner diameter) (10).
In a previous study, we could demonstrate that treated hypertensive patients with poor BP control have a greater WLR of retinal arterioles than those with good blood pressure control. Interestingly, in this cohort we did not find a significant relation between BP and WLR of retinal arterioles using correlation analyses. We have concluded that this lack of a relation might well be the result of the effects of some antihypertensive drugs to beneficially influence vascular structure (9). Subsequently, we analyzed WLR of retinal arterioles in a cohort of never-treated patients with essential hypertension and normotensive controls. In this cohort, both systolic BP and diastolic BP were significantly related to WLR of retinal arterioles independent of traditional CV risk factors and other confounders, e.g. subclinical inflammation, endothelial dysfunction and dietary salt intake. Moreover, in this cohort, the WLR of retinal arterioles was greater in hypertensive than in normotensive subjects (11).
A crucial role in the efforts of prevention of end-organ damage plays the renin angiotensin system (RAS) due its dual role on salt and water homeostasis (blood pressure) and the vascular response to injury. The increased mechanical strain on the vasculature at a higher BP can cause injury to the endothelial wall. Activation of the RAS increases BP and stimulates a local inflammatory response to repair the injury. Long-term or repeated response to injury leads to endothelial dysfunction and microvascular damage (12), and hence end-organ damage. Therefore increasing evidence is not suppressing, that antihypertensive medications which inhibit the RAS may provide incremental end-organ protection.
Recently, we have shown that hypertensive patients have an impaired vasodilatory response of retinal arterioles to Flickerlight test - which improves after treatment with Angiotensin Receptor Blockers (ARBs) - and have a reduced nitric oxide (NO) activity in the retinal circulation, that is normalized after treatment with ARBs (13; 14). Likewise, in a previous study analyzing the arterial resistance vessels also in the systemic circulation we found that in contrast to diuretics and placebo, valsartan improved endothelial function and vascular properties (estimated by pulse wave anlalysis) (15; 16).
Combining RAS inhibitors may provide greater end-organ protection than use of either class alone. However, the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) has failed to show superiority of the dual RAS blockade (Angiotensin converting enzyme inhibitor and ARB) in patients at high cardiovascular risk (17). The combination of ARBs and direct renin inhibitors (DRIs) emerged as the only available, valid and innovative option for blocking the RAS at two different sites (sequential blockade). Indeed, the Aliskiren in the Evaluation of Proteinuria in Diabetes (AVOID) study (18) and the Aliskiren in Left Ventricular Hypertrophy (ALLAY) study (19) demonstrated that the DRI aliskiren has additional and to some extent blood pressure independent effects on albuminuria and left ventricular hypertrophy, both signs of subclinical organ damage in hypertension, respectively (20).
However, no data are available with respect to the effects of ARBs and DRIs on vascular properties in the short and long term To close this gab we focus in this study on vascular structural and functional changes since vascular adaptation to high blood pressure occurs in the early phase of hypertensive disease.
- Conditions
- Arterial Hypertension
- Being tested
- Aliskiren, Placebo
- Medical subject headings
- Hypertension
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
AliskirenDrug
Also called Rasilez
orally 150 mg/d for 1 week, then orally 300 mg/d for 7 weeks
PlaceboDrug
orally once per day
| Study group | Role | What they receive |
|---|---|---|
| Aliskiren | Active comparator | Not described Receives: Drug: Aliskiren |
| Placebo | Placebo comparator | Not described Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
To investigate the combined effect of aliskiren and valsartan on vascular structure, assessed by wall to lumen ratio of retinal arterioles, in hypertensive patients.
WLR = (outer diameter - inner diameter) / inner diameter) of retinal arterioles
Measured: After 8 weeks of treatment with aliskiren versus placebo
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted18 Mar 2011 (estimated)
- Study startMay 2010
- Primary completionJun 2013
- Study completionJun 2013
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (3)Papers the sponsor has linked to this study.
- Other trials for Arterial HypertensionStudies of the same condition, open and under way.
- More trials run by University of Erlangen-Nürnberg Medical SchoolThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 3
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 56 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Erlangen-Nürnberg Medical School
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Roland E. Schmieder, University of Erlangen-Nürnberg Medical School
- Investigators
- Roland E Schmieder, MD, Principal investigator, University of Erlangen-Nürnberg
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01318395
- Sponsor's protocol ID
- CSPP100ADE07T
- Acronym
- ARTS
- Status last verified
- Jan 2018
- First submitted
- 17 Mar 2011
- Last updated
- 12 Jan 2018
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Jumar A, Ott C, Kistner I, Friedrich S, Schmidt S, Harazny JM, Schmieder RE. Effect of aliskiren on vascular remodelling in small retinal circulation. J Hypertens. 2015 Dec;33(12):2491-9. doi: 10.1097/HJH.0000000000000735.
PubMed 26398851Bosch A, Schmid A, Ott C, Kannenkeril D, Karg MV, Ditting T, Veelken R, Uder M, Schmieder RE. Copeptin Levels in Patients With Treatment-Resistant Hypertension Before and 6 Months After Renal Denervation. Am J Hypertens. 2020 Feb 22;33(2):182-189. doi: 10.1093/ajh/hpz155.
PubMed 31555795Bosch AJ, Harazny JM, Kistner I, Friedrich S, Wojtkiewicz J, Schmieder RE. Retinal capillary rarefaction in patients with untreated mild-moderate hypertension. BMC Cardiovasc Disord. 2017 Dec 21;17(1):300. doi: 10.1186/s12872-017-0732-x.
PubMed 29268712
Study at a glance
From the registry record, last updated by the sponsor on 12 Jan 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Randomized, Double Blind, Active-controlled, Parallel Study to Analyse Effects of the Combination of Aliskiren and Valsartan on the Vascular Structure and Function of Retinal Vessels
- ClinicalTrials.gov ID
- NCT01318395
- Acronym / sponsor ID
- ARTS / CSPP100ADE07T
- Conditions
- Arterial Hypertension
- Phase
- Phase 3
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 56 participants (actual)
- Lead sponsor
- University of Erlangen-Nürnberg Medical SchoolUniversity, hospital or other
- Study start
- May 2010
- Primary completion
- Jun 2013 (actual)
- Study completion
- Jun 2013 (actual)
- First posted
- 18 Mar 2011 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Hypertension affects approximately one fourth of the world population and therefore contributes substantially to the worldwide burden of cardiovascular (CV) disease and end-organ damage.
Changes in small artery structure characterized by an increased wall-to-lumen ratio (WLR) are characteristic feature of target organ damage in hypertension. Of clinical importance, structural arteries of small subcutaneous arteries have been shown to be of prognostic significance, with adverse prognosis in subjects with higher WLR. However, the assessment of arteriolar structure from biopsies of subcutaneous tissue is invasive and impractical in clinical practice. A new approach focuses on retinal arteriolar structural parameters by using scanning laser Doppler flowmetry (SLDF) with automatic full-field perfusion imaging analyses (9). This approach allows the non-invasive assessment of both the outer diameter (OD) and inner diameter (ID) of retinal arterioles in vivo and, thus, analyses vascular remodeling of retinal arterioles by calculating WLR = (OD - ID) / ID).
A crucial role in the efforts of prevention of end-organ damage plays the renin angiotensin system (RAS). The increased mechanical strain on the vasculature at a higher BP can cause injury to the endothelial wall. Activation of the RAS increases BP and stimulates a local inflammatory response to repair the injury. Long-term or repeated response to injury leads to endothelial dysfunction and microvascular damage, and hence end-organ damage.
Combining RAS inhibitors may provide greater end-organ protection than use of either class alone. However, ONTARGET has failed to show superiority of the dual RAS blockade (ACE-I and ARB) in patients at high cardiovascular risk. The combination of ARBs and direct renin inhibitors (DRIs) emerged as the only available, valid and innovative option for blocking the RAS at two different sites (sequential blockade). Indeed, AVOID study and ALLAY study demonstrated that the DRI aliskiren has additional and to some extent blood pressure independent effects on albuminuria and left ventricular hypertrophy, both signs of subclinical organ damage in hypertension, respectively.
However, no data are available with respect to the effects of ARBs and DRIs on vascular properties in the short and long term To close this gab we focus in this study on vascular structural and functional changes since vascular adaptation to high blood pressure occurs in the early phase of hypertensive disease.
Detailed description
Hypertension affects approximately one fourth of the world population and therefore contributes substantially to the worldwide burden of cardiovascular (CV) disease and end-organ damage (1). Therefore, the goal of antihypertensive therapy is to provide effective long-term lowering of elevated blood pressure (BP) and prevention of hypertensive end-organ-damage and mortality (2).
Changes in small artery structure characterized by an increased wall-to-lumen ratio (WLR) are characteristic feature of target organ damage in hypertension. (3; 4). A clinical study examining small arteries obtained from gluteal biopsies of patients with hypertension revealed that an increased WLR of subcutaneous small arteries is one of the first manifestations of target organ damage in hypertension that occur before proteinuria and cardiac hypertrophy (5). Of clinical importance, structural arteries of small subcutaneous arteries have been shown to be of prognostic significance, with adverse prognosis in subjects with higher WLR (6-8). However, the assessment of arteriolar structure from biopsies of subcutaneous tissue is invasive and impractical in clinical practice. A new approach focuses on retinal arteriolar structural parameters by using scanning laser Doppler flowmetry (SLDF) with automatic full-field perfusion imaging analyses (9). This approach allows the non-invasive assessment of both the outer diameter and inner diameter of retinal arterioles in vivo and, thus, analyses vascular remodeling of retinal arterioles by calculating WLR = (outer diameter - inner diameter) / inner diameter) (10).
In a previous study, we could demonstrate that treated hypertensive patients with poor BP control have a greater WLR of retinal arterioles than those with good blood pressure control. Interestingly, in this cohort we did not find a significant relation between BP and WLR of retinal arterioles using correlation analyses. We have concluded that this lack of a relation might well be the result of the effects of some antihypertensive drugs to beneficially influence vascular structure (9). Subsequently, we analyzed WLR of retinal arterioles in a cohort of never-treated patients with essential hypertension and normotensive controls. In this cohort, both systolic BP and diastolic BP were significantly related to WLR of retinal arterioles independent of traditional CV risk factors and other confounders, e.g. subclinical inflammation, endothelial dysfunction and dietary salt intake. Moreover, in this cohort, the WLR of retinal arterioles was greater in hypertensive than in normotensive subjects (11).
A crucial role in the efforts of prevention of end-organ damage plays the renin angiotensin system (RAS) due its dual role on salt and water homeostasis (blood pressure) and the vascular response to injury. The increased mechanical strain on the vasculature at a higher BP can cause injury to the endothelial wall. Activation of the RAS increases BP and stimulates a local inflammatory response to repair the injury. Long-term or repeated response to injury leads to endothelial dysfunction and microvascular damage (12), and hence end-organ damage. Therefore increasing evidence is not suppressing, that antihypertensive medications which inhibit the RAS may provide incremental end-organ protection.
Recently, we have shown that hypertensive patients have an impaired vasodilatory response of retinal arterioles to Flickerlight test - which improves after treatment with Angiotensin Receptor Blockers (ARBs) - and have a reduced nitric oxide (NO) activity in the retinal circulation, that is normalized after treatment with ARBs (13; 14). Likewise, in a previous study analyzing the arterial resistance vessels also in the systemic circulation we found that in contrast to diuretics and placebo, valsartan improved endothelial function and vascular properties (estimated by pulse wave anlalysis) (15; 16).
Combining RAS inhibitors may provide greater end-organ protection than use of either class alone. However, the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) has failed to show superiority of the dual RAS blockade (Angiotensin converting enzyme inhibitor and ARB) in patients at high cardiovascular risk (17). The combination of ARBs and direct renin inhibitors (DRIs) emerged as the only available, valid and innovative option for blocking the RAS at two different sites (sequential blockade). Indeed, the Aliskiren in the Evaluation of Proteinuria in Diabetes (AVOID) study (18) and the Aliskiren in Left Ventricular Hypertrophy (ALLAY) study (19) demonstrated that the DRI aliskiren has additional and to some extent blood pressure independent effects on albuminuria and left ventricular hypertrophy, both signs of subclinical organ damage in hypertension, respectively (20).
However, no data are available with respect to the effects of ARBs and DRIs on vascular properties in the short and long term To close this gab we focus in this study on vascular structural and functional changes since vascular adaptation to high blood pressure occurs in the early phase of hypertensive disease.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind (participant, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Aliskiren | Active comparator | Drug: Aliskiren |
| Placebo | Placebo comparator | Drug: Placebo |
Who may qualify
- Ages
- 18 to 75 years
- Sex
- Male only
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (6 listed)
- Male or female aged 18 to 75 years (females of child bearing potential must be using adequate contraceptive precautions)
- Females of childbearing potential or within two years of the menopause must have a negative urine pregnancy test at enrolment visit
- Patients with mild to moderate uncomplicated essential hypertension with a trough mean sitting DBP ≥ 90 mmHg and/or SBP ≥ 140 mmHg or pretreated arterial hypertension
- Written informed consent
- Agreement to attend all study visits as planned in the protocol
Key exclusion criteria (21 listed)
- In the investigator's opinion the patient can not be withdrawn from their current antihypertensive medication
- Secondary hypertension (e.g. patients with hyperaldosteronism, pheochromocytoma, renal artery stenosis, renal parenchymal disease, coarctation of the aorta, Cushing's disease syndrome)
- Severe essential hypertension (systolic blood pressure ≥ 180 mmHg and/or diastolic blood pressure ≥ 110 mmHg) or treatment resistant hypertension (3 antihypertensive drugs and still SBP ≥ 140mmHg and/or DBP ≥ 90mmHg)
- History of hypertensive encephalopathy or intracerebral hemorrhage
- Diabetes mellitus Type 1 or Type 2
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| AliskirenAlso: Rasilezorally 150 mg/d for 1 week, then orally 300 mg/d for 7 weeks | Drug | Aliskiren |
| Placeboorally once per day | Drug | Placebo |
Primary outcome
To investigate the combined effect of aliskiren and valsartan on vascular structure, assessed by wall to lumen ratio of retinal arterioles, in hypertensive patients.
Time frame: After 8 weeks of treatment with aliskiren versus placebo
WLR = (outer diameter - inner diameter) / inner diameter) of retinal arterioles
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Jan 2018.
- Results publication: PubMed 26398851Jumar A, Ott C, Kistner I, Friedrich S, Schmidt S, Harazny JM, Schmieder RE. Effect of aliskiren on vascular remodelling in small retinal circulation. J Hypertens. 2015 Dec;33(12):2491-9. doi: 10.1097/HJH.0000000000000735.
- Derived from this study: PubMed 31555795Bosch A, Schmid A, Ott C, Kannenkeril D, Karg MV, Ditting T, Veelken R, Uder M, Schmieder RE. Copeptin Levels in Patients With Treatment-Resistant Hypertension Before and 6 Months After Renal Denervation. Am J Hypertens. 2020 Feb 22;33(2):182-189. doi: 10.1093/ajh/hpz155.
- Derived from this study: PubMed 29268712Bosch AJ, Harazny JM, Kistner I, Friedrich S, Wojtkiewicz J, Schmieder RE. Retinal capillary rarefaction in patients with untreated mild-moderate hypertension. BMC Cardiovasc Disord. 2017 Dec 21;17(1):300. doi: 10.1186/s12872-017-0732-x.
Related trials for Arterial Hypertension
Active, not recruiting
Digital Reinforcement of Motivational Interviewing Micro-Skills Among Primary Care Healthcare Professionals
Hypertension (Without Type 2 Diabetes Mellitus)
Recruiting
Investigating Vascular Properties of HEMI and SPG Signals in Individuals With or at Risk for Chronic Kidney Disease
Chronic Kidney Disease, Hypertension (HTN)
Recruiting
Trial Phase: Syndemic Adapted Medly Uganda
Mental Health
Not yet recruitingPhase 2/3
An Open-Label Extension Study to Evaluate Inhaled Treprostinil SMI in Participants With Pulmonary Hypertension Associated With Chronic Obstructive Pulmonary Disease (PH-COPD)
Pulmonary Hypertension Associated With Chronic Obstructive Pulmonary Disease
Enrolling by invitation
Testing Implementation Strategies to Support Clinic Fidelity to an Outpatient Hypertension Bundle
Pregnancy Related, Hypertension
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Roland E Schmieder, MD principal investigator
University of Erlangen-Nürnberg
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 3 study testing Aliskiren in people with Arterial Hypertension, run by University of Erlangen-Nürnberg Medical School at 2 sites in Germany.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 6 inclusion and 21 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 12 Jan 2018. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites in Germany. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 3 studies compare the treatment with the current standard treatment or a placebo in a large group, to confirm how well it works and watch for side effects.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
To investigate the combined effect of aliskiren and valsartan on vascular structure, assessed by wall to lumen ratio of retinal arterioles, in hypertensive patients. (time frame: After 8 weeks of treatment with aliskiren versus placebo). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT01318395, which also lists 3 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 12 Jan 2018.