Ignite Creation Date:
2024-05-05 @ 11:56 AM
Last Modification Date:
2024-10-26 @ 9:17 AM
Study NCT ID:
NCT00189618
Status:
COMPLETED
Last Update Posted:
2008-10-06
First Post:
2005-09-12
Brief Title:
The Effects of Physical Training ASA Aspirin and Clopidogrel on the Walking Capacity of Patients With Stage II Peripheral Arterial Disease PAD
Sponsor:
Arteriogenesis Competence Network
Organization:
Arteriogenesis Competence Network
Study Overview
Official Title:
The Effects of Physical Training Aspirin and Clopidogrel on the Walking Capacity of Patients With Stage II Peripheral Arterial Disease
Status:
COMPLETED
Status Verified Date:
2008-10
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
To evaluate the change in walking capacity after a well organized and structured intensive physical training program with supportive pharmacotherapy with Clopidogrel or ASA It is hypothesized that statistically superior results will emerge from a structured training supported by Clopidogrel as compared to a structured training supported by ASA
Detailed Description:
Peripheral arterial disease PAD can not be seen in isolation but represents the peripheral manifestation of a generalized atherosclerosis The co-morbidity with coronary heart disease andor a cerebral atherosclerosis ranges between 20 and 90 depending on the degree of severity of PAD from 1-5 The relative risk of a predominantly cardiac death is increased by a factor of 2 already in asymptomatic PAD patients the risk will increase furthermore by another factor of 2 to 4 when patients become symptomatic PAD is not a rare disease but has a prevalence of 15 to 20 in an elderly western population 50 years of age While the clinical presentation of PAD is relatively benign in the majority of cases the disease carries a high risk potential with high directly and indirectly related costs Thus from a medical but also from a socio-economic point of view there is the need to control the PAD complication rate and related treatment costs as effectively as possible
The most physiological treatment approach which is internationally accepted is physical training There is agreement that physical training does improve the collateralisation of vascular lesions does improve the rheologic properties of blood but does also lead to a shift from glycolytic type 2 to oxidative type 1 muscle fibers in the working musculature This shift is associated with an increase in capillary density a fact which subsequently favors an optimal oxygen extraction and oxygen utilisation Another effect of physical training which may be of utmost importance relates to its potential to modify the patients risk factor profile It was shown in epidemiological clinical and experimental studies that even a moderate physical training does increase the insulin receptor sensitivity and hence positively influences one of the major factors for atherosclerosis does increase the fibrinolytic activity following prothrombotic stimulation does decrease the diastolic blood pressure in hypertensive patients does decrease the LDLHDL ratio and does decrease the overall cardiac mortality
The aim of any treatment of intermittent claudication is a clinically relevant improvement in the patients mobility and quality-of-life In a previous study it was shown that a 3 months structured supervised PAD rehabilitation program will satisfy this demand and will lead to an improvement of the initial painfree claudication distance of approximately 190 One third of the patients of this study were started on Clopidogrel as a supportive pharmacotherapy at the beginning of the trial It was interesting to note that optimal training results defined as an improvement of the ICD by 200 were only seen in patients who were treated with Clopidogrel but were not reported from patients who received ASA aspirin on top of training
Non-published data from the ArtNet preclinical group Dr I Höfer Dr I Buschmann Freiburg which were presented at an ArtNet meeting on March 24 2003 showed that using a rabbit hind leg model the magnitude of GM-CSF and MCP-1 induced arteriogenesis was reduced by approximately 40 when ASA was co-administered in contrast Clopidogrel when used in the same model was neutral
There is broad international agreement that patients with a generalized atherosclerosis and particularly patients suffering from PAD who are at high risk for ischemic coronary andor cerebral complications should be treated with an antiaggregant For pharmacoeconomic reasons the drug of choice normally is ASA
However following Höfers results ASA although effectively preventing thrombotic complications may hinder the arteriogenetic process required to normalize the physical capacity and QoL of PAD patients a negative ASA effect which is not found with Clopidogrel
Preliminary data in humans seem to support the hypothesis that in symptomatic stage II PAD patients Clopidogrel may be superior to ASA a hypothesis which in order to become conclusive must be confirmed by the results of an evidence level 1 clinical trial
Literature at the Centre
The most physiological treatment approach which is internationally accepted is physical training There is agreement that physical training does improve the collateralisation of vascular lesions does improve the rheologic properties of blood but does also lead to a shift from glycolytic type 2 to oxidative type 1 muscle fibers in the working musculature This shift is associated with an increase in capillary density a fact which subsequently favors an optimal oxygen extraction and oxygen utilisation Another effect of physical training which may be of utmost importance relates to its potential to modify the patients risk factor profile It was shown in epidemiological clinical and experimental studies that even a moderate physical training does increase the insulin receptor sensitivity and hence positively influences one of the major factors for atherosclerosis does increase the fibrinolytic activity following prothrombotic stimulation does decrease the diastolic blood pressure in hypertensive patients does decrease the LDLHDL ratio and does decrease the overall cardiac mortality
The aim of any treatment of intermittent claudication is a clinically relevant improvement in the patients mobility and quality-of-life In a previous study it was shown that a 3 months structured supervised PAD rehabilitation program will satisfy this demand and will lead to an improvement of the initial painfree claudication distance of approximately 190 One third of the patients of this study were started on Clopidogrel as a supportive pharmacotherapy at the beginning of the trial It was interesting to note that optimal training results defined as an improvement of the ICD by 200 were only seen in patients who were treated with Clopidogrel but were not reported from patients who received ASA aspirin on top of training
Non-published data from the ArtNet preclinical group Dr I Höfer Dr I Buschmann Freiburg which were presented at an ArtNet meeting on March 24 2003 showed that using a rabbit hind leg model the magnitude of GM-CSF and MCP-1 induced arteriogenesis was reduced by approximately 40 when ASA was co-administered in contrast Clopidogrel when used in the same model was neutral
There is broad international agreement that patients with a generalized atherosclerosis and particularly patients suffering from PAD who are at high risk for ischemic coronary andor cerebral complications should be treated with an antiaggregant For pharmacoeconomic reasons the drug of choice normally is ASA
However following Höfers results ASA although effectively preventing thrombotic complications may hinder the arteriogenetic process required to normalize the physical capacity and QoL of PAD patients a negative ASA effect which is not found with Clopidogrel
Preliminary data in humans seem to support the hypothesis that in symptomatic stage II PAD patients Clopidogrel may be superior to ASA a hypothesis which in order to become conclusive must be confirmed by the results of an evidence level 1 clinical trial
Literature at the Centre
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