Clinical Trial Details
— Status: Completed
Administrative data
NCT number |
NCT02045459 |
Other study ID # |
16821 |
Secondary ID |
1K23HL119620-01 |
Status |
Completed |
Phase |
N/A
|
First received |
|
Last updated |
|
Start date |
May 2014 |
Est. completion date |
May 17, 2021 |
Study information
Verified date |
May 2021 |
Source |
University of Virginia |
Contact |
n/a |
Is FDA regulated |
No |
Health authority |
|
Study type |
Interventional
|
Clinical Trial Summary
For part of this study, we are collecting information from patients that have been
experiencing the symptoms mentioned above. We are taking this information and creating a
chest pain registry to follow trends and compare different patients having similar symptoms.
We hope to gain insight into the quality of life, symptoms, and cardiac events of those who
are having similar symptoms. The type of information we will collect includes: demographics,
quality of life, levels of anxiety related to angina pain and cardiac events occurring within
a 2 year period of time.
In addition, we are performing a cardiac stress MRI for research purposes to look at the
blood flow in the small vessels in your heart. During the stress cardiac MRI, we will give
you a medication called Regadenoson (Lexiscan) which "stresses" your heart by dilating the
blood vessels to your heart. This drug is approved by the U.S. Food and Drug Administration
(FDA) for this purpose. We will then be able to measure the myocardial perfusion reserve
(MPR) which is a measure of blood flow through the small blood vessels to see if an abnormal
MPR and small blood vessel disease is associated with an increased risk of cardiovascular
events, such as heart attack. At this point, there is no specific therapy for small vessel
disease. In addition we have phase II of this study which is to determine if exercise and
intensive medical therapy together compared to intensive medical therapy alone improves pain
from the heart and improves overall quality of life.
Description:
Cardiac angina is a major source of morbidity, affecting more than 5% of the U.S.
population.2 It leads to more than 1.5 million hospitalizations and $190 billion in costs
yearly.3 Obstructive coronary artery disease (CAD) is the most common cause of angina.
However, no obstructive CAD is found on elective coronary angiography in more than 50% of
cases.4, 5 These patients with angina but no obstructive CAD are a heterogeneous group. Some
have noncardiac explanations for their angina or nonobstructive epicardial abnormalities such
as coronary spasm. However, many patients with angina and no obstructive CAD have
microvascular dysfunction from endothelial dysfunction or microvascular obstructive disease
as the cause. These patients have microvascular angina.
The coronary microvasculature is responsible for more than 70% of coronary resistance and
thus plays a key role in regulating blood flow to match demand.6 Microvascular dysfunction
can occur in the setting of dilated, hypertrophic, and restrictive cardiomyopathies. However,
it is commonly seen in the setting of atherosclerotic risk factors or can be idiopathic.6, 7
Microvascular dysfunction is manifest as insufficient stress myocardial blood flow and/or
reduced myocardial perfusion reserve (MPR), the ratio of stress flow to rest flow, in
response to a stress such as vasodilator administration. Absolute myocardial blood flow and
MPR can be assessed noninvasively with high precision and accuracy by cardiac magnetic
resonance (CMR) imaging Reduced MPR in patients with angina is associated with significant
morbidity, including a high risk of cardiac events, high medical costs, and a decreased
quality of life.Despite the poor prognosis of this population, therapeutic options to reduce
angina and improve MPR have not been well studied. Preliminary analysis shows that statins
may improve endothelial function. ACE-inhibitors and beta-blockers improve symptoms in
Syndrome X, a related disorder in which patients have angina, no obstructive CAD, and
ischemic changes but a better prognosis. Therapeutic exercise has also been used in the
Syndrome X population, improving exercise tolerance and endothelial function and reducing
symptom severity.Improvements in MPR could be expected with exercise due to the reduced
resting flow and increased MPR seen in healthy volunteers and improved endothelial function
from increased nitric oxide bioactivity in patients with probable microvascular dysfunction.
However, no studies have examined the effect of these medications or their synergism with
exercise on MPR, aerobic capacity, anginal symptoms, or quality of life in patients with
angina and reduced MPR. Identification of an effective therapy that improved symptoms and
prognosis would have dramatic impact on this highly prevalent patient population.
The primary goal of this study is to characterize which patients with angina but no
obstructive CAD have reduced MPR and test the effectiveness of intensive medical therapy plus
a 12-week supervised exercise program versus intensive medical therapy alone to improve MPR,
aerobic capacity, and the patient-centered outcomes of cardiac events, angina severity, and
quality of life in this population with microvascular angina.