View clinical trials related to Microvascular Angina.
Filter by:Microvascular angina (MVA) is caused by abnormalities of the small vessels in the heart. Endothelin is a small chemical that circulates and accumulates in the blood vessel walls, causing them to narrow or go into spasm and thicken in the longer term especially as levels of endothelin increase. As a result, patients experience pain, psychological burden and an inability to carry out daily activities. Originally developed by AstraZeneca for cancer treatment, prior research has confirmed that Zibotentan relaxes the small blood vessels of patients with MVA which lends support to the idea that Zibotentan may bring some benefits to patients with MVA. This trial therefore proposes to look into re-purposing zibotentan as a new treatment for patients with MVA. The primary objective is to assess the effect of add-on treatment with Zibotentan to treadmill exercise times in adult patients with MVA and impaired exercise intolerance. Zibotentan could provide a new treatment pathway for patients, as well as be made available to the NHS at substantially lower cost than the currently used medications. The trial aims to initially invite approx. 356 participants for genetic testing. A minimum of 100 participants will go forward into the main study, receiving either 10mg zibotentan or a dummy matched tablet (placebo) daily over two 12 weeks periods of each, completing their final visit at week 34. The study assessments will involve a health check at each visit, including information on the patient's wellbeing, blood tests, some quality of life questionnaires, and an exercise test. Participants will also have the option to consent to additional sub-study cardiovascular MRI scanning. Finally, participants will be invited to provide consent for long-term follow-up (maximum 20 years) of their electronic medical records (no additional patient contact).
In medical practice, a combination of clinical exam, electrocardiograms, circulating biomarkers, and imaging is used to gain insights on the prognosis after myocardial infarction. Novel molecular non-invasive tools are needed that help clinicians overcome the adverse events of post-myocardial infarction remodelling and thereby achieve improved therapy for its prevention. Coagulation factor XIII (FXIII) decay has been linked to major adverse cardiac events (MACE) in patients with acute coronary syndromes. Given the correlation between both intramyocardial haemorrhage and microvascular damage with acute phase complications in ST-elevation myocardial infarction, we hypothesise that excessive FXIII decay within the first week may predict acute phase outcomes in these patients. If this holds true, FXIII determination could be used as diagnostic and prognostic tool.
Angina is form of chest pain that is due to a lack of blood to the heart muscle. Angina is commonly triggered by stress and exertion, and is a common health problem worldwide. The diagnosis and treatment of angina is usually focused on detection of blockages in heart arteries, and relief of this problem with drugs, stents or bypass surgery. However, about one third of all invasive angiograms that are performed in patients with angina do not reveal any blockages. Many of such patients may have symptoms due to narrowings in the very small micro vessels (too small to be seen on an angiogram). The purpose of this research is to undertake a 'proof-of-concept' clinical trial to gather information as to whether routine tests of small vessel function in the heart might help identify patients with a stable coronary syndrome due to a disorder of coronary function (vasospastic or microvascular angina), and appropriately rule out this problem in patients with normal test results. The diagnostic strategy enables stratification of patient sub-groups to optimized therapy (personalised medicine). Evidence of patient benefits in this study would support the plan for a larger study that would be designed to impact on healthcare costs and patient reported outcome measures (PROMS).
Angina is the most common symptom of coronary heart disease among women but unlike men most women do not have stenosis of the coronary arteries. In a large proportion of these women, coronary microvascular dysfunction (CMD) is thought to be the cause of angina. However, CMD is also demonstrable in the asymptomatic population, and may merely be an innocent bystander related to the presence of cardiovascular risk factors rather than a cause of angina symptoms. The aim of this study is to determine whether comprehensive intervention is feasible and results in improvement in both angina and microvascular function in these patients.
The Tako-Tsubo Cardiomyopathy (TTC) and the Cardiac Syndrome X (CSX) are respectively acute and chronic heart diseases, which mimic myocardial infarction and stable angina pectoris without alterations of large coronary vessels. The causes and the most appropriate and best treatment for these diseases have not been yet clarified, but there are indications, that mental and psychosocial aspects may also contribute to these two diseases. So far, there is no study, which has comprehensively evaluated the interactions between mind and heart in these two conditions. The purpose of this study is to search for possible differences in mental activity, response to stressful events and function of specific areas of the brain deeply involved in relation between mind and heart. 45 subjects will be recruited and divided equally into: patients with CSX, patients with TTC (at least 6 months ago) and patients with previous acute myocardial infarction (at least 6 months ago). All participants will undergo a clinical interview and several questionnaires that assess various mental functions, the stress response and the quality of life. In addition, in a separate visit the participants will undergo a Magnetic Resonance Imaging without contrast medium that helps to assess function of specific areas of the brain.
The aim of the present study is to evaluate the effect of treatment with Liraglutide on the coronary microvasculature and angina symptoms, in overweight patients with microvascular dysfunction and angina pectoris but no coronary artery stenosis.
The aim of this study is to explore effects of long term treatment with ACE-inhibitor on the small vessel function assessed by coronary flow reserve (CFR) by transthoracic echocardiography and flow mediated dilation in normotensive patients with small vessel disease (CFR<2.2) and Angina Pectoris but no obstructive coronary artery disease.
Serial assessment of angina status and ischemia on stress echo over one year among patients with moderate ischemia on stress imaging and non-obstructive CAD on coronary CT angiography.
The purpose of this study is to look at the effects of the drug Ranolazine compared to Placebo on symptoms of chest pain or chest tightness (known as angina), exercise endurance and ability, and changes in blood flow to the very small arteries of the heart (known as coronary microvascular function) in patients who do not have significant blockages in their major heart arteries. Ranolazine is a drug that is already approved by the FDA for angina, but it may be particularly effective in people with disease in their tiny heart vessels (known as coronary microvascular disease). This trial aims to enroll 50 patients with angina who undergo baseline bicycle exercise testing with monitoring of the heart's electrical activity and oxygen consumption (known as cardiopulmonary exercise test) and coronary angiogram (taking pictures of the heart arteries through small hollow tubes placed through the wrist or groin). If severe blockages in the main arteries are not found then testing for coronary microvascular function will be performed. Subsequently, participants will then be randomized 50/50 to either Ranolazine or Placebo. After taking the study drug for 12 weeks, they will then repeat the cardiopulmonary exercise test and the coronary angiogram with testing for microvascular function.
High density lipoprotein cholesterol (HDL-C) is in the centrum of the process of reverse cholesterol transport from peripheral cells to the liver[10]. HDL-C promotes endothelial generation of nitric oxide (NO) and improves endothelial function and arterial vasoreactivity[11]. In several studies, lower HDL-C level was reported to be associated with increased coronary artery disease (CAD) risk[12-14]. HDL-C also has anti- inflammatory and anti-oxidant activities[15,16]. Concerning anti-inflammatory activity, HDL-C inhibits the activation of monocytes/macrophages and neutrophils[17,18] and inhibits the expression of endothelial adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) and E-selectin[15]. In this study we aimed to investigate the relation of HDL-C level with systemic inflammatory markers in patients with cardiac syndrome X (CSX).