Ignite Creation Date:
2024-05-05 @ 5:18 PM
Last Modification Date:
2024-10-26 @ 9:30 AM
Study NCT ID:
NCT00424801
Status:
TERMINATED
Last Update Posted:
2009-05-06
First Post:
2007-01-19
Brief Title:
Effects of Intensive Long-Term Vasodilation in Hypertensive Patients With Microvascular Angina Pectoris
Sponsor:
University of Aarhus
Organization:
University of Aarhus
Study Overview
Official Title:
Intensive Non-Sympathetic Activating Vasodilatory Treatment in Hypertensive Patients With Microvascular Angina Pectoris
Status:
TERMINATED
Status Verified Date:
2009-05
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Due to recent findings relating MRI contrast to nephrogenic systemic fibrosis
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The purpose of this study is to determine if long-term vasodilatory treatment is more effective than the standard treatment in hypertensive patients with microvascular angina pectoris
Detailed Description:
Patients with hypertension frequently develop angina pectoris This can be caused by either epicardial stenotic disease or equally frequent by increased resistance in small resistance vessels - microvascular dysfunction This increased resistance is caused by a process called remodelling where the existing material in the vessel wall is rearranged around a smaller lumen whereas the sensitivity of the smooth muscle cells to agonist stimuli is unchanged Under resting conditions the resistance is determined by both the tone in the smooth muscle cells in the vessel walls and the structure of the vessels themselves RREST Under hyperemic conditions the muscles relax and the resistance is determined only by vessel structure RMIN
A literature survey of the various studies on this subject has shown that structural changes relates to tone rather than blood pressure This suggests that resistance vessel structure will be normalized only by an antihypertensive treatment which normalizes RREST ie rely on vasodilatation as a cause of the antihypertensive effect more than reduction of cardiac output
The main hypothesis is that it is possible to reverse the structural changes in the resistance vessels by vasodilatory treatment for eight months thereby achieving lower coronary and peripheral minimal resistance as determined by MRI and plethysmography respectively higher work capacity on exercise-ECG and less tendency to angina in these patients
We will include 80 patients with essential hypertension angina pectoris CCS class II-III and signs of ischemia on exercise-ECG or myocardial SPECT but without significant stenosis in angiography The patients are randomised in a parallel open-label design to either vasodilatory lercanidipine valsartan doxazosin and nicorandil or standard treatment metoprolol diltiazem and isosorbide mononitrate The aim of treatment in both arms is BP below 12080 and the protocol allows further add-on therapy to reach this goal The patients will be followed for eight months with a titration period of two months MRI plethysmography exercise-ECG and echocardiography will be performed before and after the study period The primary endpoint is minimal coronary resistance as determined by MRI secondary endpoints are peripheral vascular resistance as determined by plethysmography work capacity and ischemia threshold on exercise-ECG or myocardial SPECT
A literature survey of the various studies on this subject has shown that structural changes relates to tone rather than blood pressure This suggests that resistance vessel structure will be normalized only by an antihypertensive treatment which normalizes RREST ie rely on vasodilatation as a cause of the antihypertensive effect more than reduction of cardiac output
The main hypothesis is that it is possible to reverse the structural changes in the resistance vessels by vasodilatory treatment for eight months thereby achieving lower coronary and peripheral minimal resistance as determined by MRI and plethysmography respectively higher work capacity on exercise-ECG and less tendency to angina in these patients
We will include 80 patients with essential hypertension angina pectoris CCS class II-III and signs of ischemia on exercise-ECG or myocardial SPECT but without significant stenosis in angiography The patients are randomised in a parallel open-label design to either vasodilatory lercanidipine valsartan doxazosin and nicorandil or standard treatment metoprolol diltiazem and isosorbide mononitrate The aim of treatment in both arms is BP below 12080 and the protocol allows further add-on therapy to reach this goal The patients will be followed for eight months with a titration period of two months MRI plethysmography exercise-ECG and echocardiography will be performed before and after the study period The primary endpoint is minimal coronary resistance as determined by MRI secondary endpoints are peripheral vascular resistance as determined by plethysmography work capacity and ischemia threshold on exercise-ECG or myocardial SPECT
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None