Microvascular angina | |
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Other names | cardiac syndrome X, coronary microvascular dysfunction (CMD), microvascular coronary disease |
Specialty | Cardiology |
Microvascular angina (MVA), previously known as cardiac syndrome X, [1] also known as coronary microvascular dysfunction(CMD) or microvascular coronary disease is a type of angina (chest pain) with signs associated with decreased blood flow to heart tissue but with normal coronary arteries. [2] [3]
The use of the term cardiac syndrome X (CSX) can lead to the lack of appreciation of how microvascular angina is a debilitating heart related pain condition with the increased risk of heart attack and other heart problems. Women may have difficulty accessing the specialist care of a cardiologist for this reason.[ citation needed ]
Some studies have found an increased risk of other vasospastic disorders in cardiac microvascular angina patients, such as migraine and Raynaud's phenomenon. Treatment typically involves beta-blockers, such as metoprolol, however beta blockers can make coronary spasms worse. [4]
Microvascular angina is a separate condition from variant angina.
Patients often experience myocardial ischemia symptoms, such as heaviness, tightness, pressure or squeezing in the chest area, which can also include sweating, nausea, shortness of breath (dyspnea), fatigue. [5]
While there is no formal definition of microvascular angina, the general consensus is that it entails all of the following:
There is no specific known cause for microvascular angina but rather a multitude of risk factors that act together. It is believed that the lack of blood flow caused by a microvascular disease and enhanced pain perception are two of the factors that may cause it. [6] The microvascular dysfunctions refer to the abnormalities in the very small blood vessels of the heart. The narrowing of these vessels may lead to lack of oxygen in specific areas of the cardiac muscle causing chest pain. Several studies have shown that patients living with microvascular angina may have an enhanced pain perception, and usually feel more intense chest pain than individuals without microvascular angina.
The risk factors include abdominal obesity, meaning excessive visceral fat tissue in and around the abdomen, atherogenic dyslipidemia which is a blood fat disorder, and elevated blood pressure. [7] Other risk factors are insulin resistance or intolerance to glucose, prothrombotic state or proinflammatory state. Older people are more at risk to develop this condition, and there is some evidence that suggests that there are genetic mutations that predispose to the syndrome. [8] Women are more prone to this condition than men, as well as those who have a history of heart disease in the family. [9]
This condition is typically characterized by a series of structural and functional changes within the heart's microcirculation, such as endothelial dysfunction (which affects the inner lining of blood vessels), microvascular arteriolar remodeling (changes in the vessel structure) such as intimal thickening, smooth muscle cell proliferation, perivascular fibrosis, and increased microvascular resistance (which impedes blood flow). There are also differences in coronary blood flow reserve (the capacity to increase blood flow during increased demand) and IMR (index of microcirculatory resistance). [10]
In a large percentage of patients, there is a finding of systemic microvascular abnormalities, causing reduced blood flow in the microvasculature of the cardiac muscles. When the blood vessels constrict and fail to dilate there is decreased oxygen levels to the cardiac muscles resulting in hypoxia which lead to chest pain. [11]
While numerous physiological mechanisms have been proposed, none have been proven.
Patients with the structural coronary microvascular dysfunction endotype (inability to dilate) tend to have a high vascular tone at rest and high vascular tone at stress. Patients with this endotype typically show normal CBF (coronary blood flow) at rest, lower stress CBF, lower coronary flow reserve (CFR) and elevated hyperemic index of microcirculatory resistance (hMR). Their microvascular resistance and endothelial dysfunction is elevated. [10]
It is characterized by luminal obstruction, vascular-wall infiltration, vascular remodeling, perivascular fibrosis and capillary rarefaction. [10]
In this type individuals may have impaired vasodilatory capacity and endothelial function, leading to reduced coronary blood flow and compromised myocardial perfusion, especially during stress or increased demand. [10]
Functional coronary microvascular dysfunction endotype (exhausted dilatory capacity) presents a low vascular tone at rest and low vascular tone at stress. Individuals often display elevated rest CBF, normal stress CBF, lower CFR and normal hMR, normal microvascular resistance and higher nitric oxide synthase (NOS) activity. [10] It is characterized by endothelial dysfunction, smooth-muscle dysfunction and autonomic dysfunction. [10] Endothelial function and vasodilatory capacity is relatively preserved resulting in adequate myocardial perfusion under resting conditions. [10]
Microvascular angina is a diagnosis of exclusion. Typically this will necessitate both a clinical diagnosis, appropriate stress testing, and a coronary angiogram that meet the above criteria. Cardiac MRI can be used to diagnose microvascular angina. Studies are ongoing to validate this approach.
There is growing evidence that microvascular angina is caused by a functional disorder of the microvessels, coronary microvascular dysfunction (CMD). Blood vessels either fail to dilate or constrict in response to various stressors such as exercise, the cold or emotional stress.
An angiogram with acetylcholine can demonstrate microvascular dysfunction which can affect the microvessels and larger coronary arteries leading to either microvascular angina or coronary artery spasms (Prinzmetal's angina). These are considered discrete conditions though some individuals can be affected by both.
Microvascular angina can be diagnosed using different tests and exams, but it is mainly a diagnosis of exclusion. However, sedentary and overweight individuals with a family history of type 2 diabetes should be tested regularly to determine whether they have irregular levels of glucose or lipids, or blood pressure abnormalities, [12] factors which are usually associated with microvascular angina. A first test to be taken is an exercise stress test which shows if the heart is not getting blood during exertion.
Angiograms may be useful and conclusive when microvascular angina they offer a detailed image of the heart. However, they cannot detect potential abnormalities in the small arteries, and the doctor may ask for more tests in order to rule out other heart conditions, such as Prinzmetal's angina (variant/vasospastic angina, coronary artery spasm) which has similar symptoms.
Chest pain caused by microvascular angina is most of the time unpredictable and it can occur when at rest and/or during exercise. The pain associated with microvascular angina is normally more intense and it lasts for longer periods of time compared to pain caused by other conditions.
Many gastric conditions can cause chest pains (sub-sternal pain), while this is usually associated with consumption of food this is not always the case, and is a very common differential diagnosis. [13]
For example, a stable angina causes chest pain that goes away when at rest. Another difference is that while chest pain caused by any type of stable angina is relieved with nitroglycerin, this drug is not effective in most patients with microvascular angina.
Microvascular angina is a chronic long term condition which increases the risk of heart attack and other cardiac events such as heart failure and frequent hospital admissions. The treatment consists of drugs, mainly to relieve chest pain, but a very important part of the treatment is regularly visiting the doctor and repeating the tests to make sure the condition was taken care of in full.
The first step in managing Microvascular angina is the administration of nitrates which may relieve the chest pain. They are used because of their ability to relax the muscles of the heart and blood vessels. However, they prove to be inefficient in as many as half of patients. Alternative treatments may consist of calcium channel blockers or beta blockers which reduce chest pain by relaxing the muscle cells lining the artery and improving blood flow to the heart while lowering blood pressure. Aminophylline may also work, while estrogen can be effective in women.
There is at present no known cure however a change in lifestyle is important. Patients should start following healthier diets which are low in saturated fats, and should participate in regular physical activities. However, any patient with a heart disease condition should first seek for a medical opinion before starting exercising. Quitting smoking is also highly recommended.
The reasons why women are more prone than men to develop a Microvascular angina are still not clear. However, it is believed[ by whom? ] that hormones along with other risk factors unique to women play a very important role.[ vague ] The constant changing of the estrogen levels may be one of the reasons along with the changes brought by birth.
Microvascular angina was first described by H. G. Kemp in 1973 as angina-like chest pain in the absence of angiographic evidence of coronary obstruction. [16]
An antianginal is a drug used in the treatment of angina pectoris, a symptom of ischaemic heart disease.
Coronary artery disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), myocardial ischemia, or simply heart disease, involves the reduction of blood flow to the cardiac muscle due to build-up of atherosclerotic plaque in the arteries of the heart. It is the most common of the cardiovascular diseases. Types include stable angina, unstable angina, and myocardial infarction.
Angina, also known as angina pectoris, is chest pain or pressure, usually caused by insufficient blood flow to the heart muscle (myocardium). It is most commonly a symptom of coronary artery disease.
Coronary artery bypass surgery, also known as coronary artery bypass graft, is a surgical procedure to treat coronary artery disease (CAD), the buildup of plaques in the arteries of the heart. It can relieve chest pain caused by CAD, slow the progression of CAD, and increase life expectancy. It aims to bypass narrowings in heart arteries by using arteries or veins harvested from other parts of the body, thus restoring adequate blood supply to the previously ischemic heart.
Microangiopathy is a disease of the microvessels, small blood vessels in the microcirculation. It can be contrasted to macroangiopathies such as atherosclerosis, where large and medium-sized arteries are primarily affected.
Vasospasm refers to a condition in which an arterial spasm leads to vasoconstriction. This can lead to tissue ischemia and tissue death (necrosis). Cerebral vasospasm may arise in the context of subarachnoid hemorrhage. Symptomatic vasospasm or delayed cerebral ischemia is a major contributor to post-operative stroke and death especially after aneurysmal subarachnoid hemorrhage. Vasospasm typically appears 4 to 10 days after subarachnoid hemorrhage.
Variant angina, also known as Prinzmetal angina,vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina. Variant angina differs from stable angina in that it commonly occurs in individuals who are at rest or even asleep, whereas stable angina is generally triggered by exertion or intense exercise. Variant angina is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the heart's smooth muscle tissue in the vessel walls. In comparison, stable angina is caused by the permanent occlusion of these vessels by atherosclerosis, which is the buildup of fatty plaque and hardening of the arteries.
A vascular bypass is a surgical procedure performed to redirect blood flow from one area to another by reconnecting blood vessels. Often, this is done to bypass around a diseased artery, from an area of normal blood flow to another relatively normal area. It is commonly performed due to inadequate blood flow (ischemia) caused by atherosclerosis, as a part of organ transplantation, or for vascular access in hemodialysis. In general, someone's own vein (autograft) is the preferred graft material for a vascular bypass, but other types of grafts such as polytetrafluoroethylene (Teflon), polyethylene terephthalate (Dacron), or a different person's vein (allograft) are also commonly used. Arteries can also serve as vascular grafts. A surgeon sews the graft to the source and target vessels by hand using surgical suture, creating a surgical anastomosis.
In medicine, collateralization, also vessel collateralization and blood vessel collateralization, is the growth of a blood vessel or several blood vessels that serve the same end organ or vascular bed as another blood vessel that cannot adequately supply that end organ or vascular bed sufficiently.
Coronary vasospasm refers to when a coronary artery suddenly undergoes either complete or sub-total temporary occlusion.
Coronary artery anomalies are variations of the coronary circulation, affecting <1% of the general population. Symptoms include chest pain, shortness of breath and syncope, although cardiac arrest may be the first clinical presentation. Several varieties are identified, with a different potential to cause sudden cardiac death.
Takotsubo cardiomyopathy or takotsubo syndrome (TTS), also known as stress cardiomyopathy, is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the muscular portion of the heart. It usually appears after a significant stressor, either physical or emotional; when caused by the latter, the condition is sometimes called broken heart syndrome.
Coronary ischemia, myocardial ischemia, or cardiac ischemia, is a medical term for a reduced blood flow in the coronary circulation through the coronary arteries. Coronary ischemia is linked to heart disease, and heart attacks. Coronary arteries deliver oxygen-rich blood to the heart muscle. Reduced blood flow to the heart associated with coronary ischemia can result in inadequate oxygen supply to the heart muscle. When oxygen supply to the heart is unable to keep up with oxygen demand from the muscle, the result is the characteristic symptoms of coronary ischemia, the most common of which is chest pain. Chest pain due to coronary ischemia commonly radiates to the arm or neck. Certain individuals such as women, diabetics, and the elderly may present with more varied symptoms. If blood flow through the coronary arteries is stopped completely, cardiac muscle cells may die, known as a myocardial infarction, or heart attack.
A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing infarction to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck or jaw. Often such pain occurs in the center or left side of the chest and lasts for more than a few minutes. The discomfort may occasionally feel like heartburn.
Coronary steal is a phenomenon where an alteration of circulation patterns leads to a reduction in the blood flow directed to the coronary circulation. It is caused when there is narrowing of the coronary arteries and a coronary vasodilator is used – "stealing" blood away from those parts of the heart.
A myocardial bridge (MB) is a congenital heart defect in which one of the coronary arteries tunnels through the heart muscle itself (myocardium). In normal patients, the coronary arteries rest on top of the heart muscle and feed blood down into smaller vessels which then take blood into the heart muscle itself. However, if a band of muscle forms around one of the coronary arteries during the fetal stage of development, then a myocardial bridge is formed – a "bridge" of heart muscle over the artery. Each time the heart squeezes to pump blood, the band of muscle exerts pressure and constricts the artery, reducing blood flow to the heart. This defect is present from birth. MBs can range from a few mm in length to 10 cm or more. The overall prevalence of myocardial bridge is 19%, although its prevalence found by autopsy is much higher (42%).
Spontaneous coronary artery dissection (SCAD) is an uncommon but potentially lethal condition in which one of the coronary arteries that supply the heart, spontaneously develops a blood collection, or hematoma, within the artery wall due to a tear in the wall. SCAD is one of the arterial dissections that can occur.
Management of acute coronary syndrome is targeted against the effects of reduced blood flow to the affected area of the heart muscle, usually because of a blood clot in one of the coronary arteries, the vessels that supply oxygenated blood to the myocardium. This is achieved with urgent hospitalization and medical therapy, including drugs that relieve chest pain and reduce the size of the infarct, and drugs that inhibit clot formation; for a subset of patients invasive measures are also employed. Basic principles of management are the same for all types of acute coronary syndrome. However, some important aspects of treatment depend on the presence or absence of elevation of the ST segment on the electrocardiogram, which classifies cases upon presentation to either ST segment elevation myocardial infarction (STEMI) or non-ST elevation acute coronary syndrome (NST-ACS); the latter includes unstable angina and non-ST elevation myocardial infarction (NSTEMI). Treatment is generally more aggressive for STEMI patients, and reperfusion therapy is more often reserved for them. Long-term therapy is necessary for prevention of recurrent events and complications.
Kounis syndrome is defined as acute coronary syndrome caused by an allergic reaction or a strong immune reaction to a drug or other substance. It is a rare syndrome with authentic cases reported in 130 males and 45 females, as reviewed in 2017; however, the disorder is suspected of being commonly overlooked and therefore much more prevalent. Mast cell activation and release of inflammatory cytokines as well as other inflammatory agents from the reaction leads to spasm of the arteries leading to the heart muscle or a plaque breaking free and blocking one or more of those arteries.
Attilio Maseri OMRI KSG was an Italian academic and physician specialized in cardiology, considered a leading researcher in the field of ischemic heart disease. His patients included Queen Elizabeth II and Pope John Paul II.