Coronary vasospasm

Coronary vasospasm refers to when a coronary artery suddenly undergoes either complete or sub-total temporary occlusion. ^[1]

Contents

• Signs and symptoms
• Complications
• Risk factors
• Pathophysiology
• Diagnosis
• EKG findings
• History
• See also
• References
• Further reading
• External links

In 1959, Prinzmetal et al. described a type of chest pain resulting from coronary vasospasm, referring to it as a variant form of classical angina pectoris. ^[2] Consequently, this angina has come to be reported and referred to in the literature as Prinzmetal angina. ^[3] A subsequent study distinguished this type of angina from classical angina pectoris further by showing normal coronary arteries on cardiac catheterization. This finding is unlike the typical findings in classical angina pectoris, which usually shows atherosclerotic plaques on cardiac catheterization. ^[3]

When coronary vasospasm occurs, the occlusion temporarily produces ischemia. A wide array of symptoms or presentations can follow: ranging from asymptomatic myocardial ischemia, sometimes referred to as silent ischemia, to myocardial infarction and even sudden cardiac death. ^{[4] [1]}

Signs and symptoms

Coronary vasospasm classically produces chest pain at rest, also known as variant angina (vasospastic angina or Prinzmetal's angina). ^[5] Chest pain is more common at certain times of the day, usually from late night to early morning. ^[6] These episodes can be accompanied by nausea, vomiting, cold sweating, and even syncope. ^{[7] [8]} Coronary vasospasm is also associated with symptoms of fatigue and tiredness, dyspnea, and palpitations. ^[5] These can sometimes be the primary presenting symptoms, but they can also occur in conjunction with chest pain. ^[5]

There are cases of coronary vasospasm that occur without any symptoms at all, leading to episodes of silent or asymptomatic myocardial ischemia. ^{[7] [8]}

Risk factors

Unlike classical angina pectoris, traditional cardiovascular risk factors are not thought to be significantly associated with coronary vasospasm. ^[9] The exception to this is with smoking, which is known to be a modifiable risk factor for vasospastic angina. ^{[9] [10]}

There are several risk factors that are thought to precipitate, or trigger, episodes of coronary vasospasm. Many of these factors work by exerting effects on the autonomic nervous system. One of the mechanisms through which this occurs is via increasing sympathetic nervous system activity. The resulting increased sympathetic outflow leads to vasoconstrictive effects on blood vessels. ^[9] For example, cocaine use can trigger vasospasm in coronary arteries through its actions on adrenergic receptors causing vasoconstriction. ^[11] Exercise, cold weather, physical activity or exertion, mental stress, hyperventilation are additional precipitating factors. ^{[9] [7]}

Pathophysiology

The exact pathophysiology behind coronary vasospasm has not been elucidated. Instead, a combination of different factors has been proposed to contribute to coronary vasospasm. ^[12] In general, it is thought that an abnormality within a coronary artery causes it to become hyperreactive to vasoconstrictor stimuli. This abnormality can be located in one segment of the coronary artery, or it may be diffuse and present throughout the entire artery. If and when vasoconstrictor stimuli act upon the hyperreactive segment of the artery, then vasospasm can result. ^[9] Ultimately, when large coronary arteries undergo vasospasm, this can lead to either complete or transient occlusion of blood flow within the artery. As a result, ischemia to the tissues served by the artery can occur. Symptoms due to ischemia can follow. ^[13]

Some of the factors that have been proposed to contribute to coronary vasospasm include the following: ^{[1] [12]}

• Endothelial dysfunction
  • Certain vasodilatory agents exert their effects by working via the endothelium, the cells that make up the lining of blood vessels. Specifically, these agents work by enhancing the production of nitric oxide from endothelial nitric oxide synthase. Normally, nitric oxide then works to promote vasodilation in a blood vessel through its own mechanisms such as inhibiting the release of agents that cause vasoconstriction. ^[12]
  • Endothelial dysfunction wherein there is a deficiency in the production of nitric oxide has been found to be associated with coronary vasospasm in some but not all cases. ^[12] Vasodilatory agents with mechanisms dependent on a functional endothelial nitric oxide synthase can cause vasoconstriction instead in the setting of endothelial dysfunction, leading to coronary vasospasm. ^[12]
• Chronic inflammation
  • Various markers of low-grade chronic inflammation have been found in cases of coronary vasospasm. ^{[14] [15]}
  • In addition to this, one of the risk factors for coronary vasospasm is smoking. ^{[9] [10]} Chronic inflammation due to smoking has been shown to be damaging to endothelial cell function. ^[16]
• Oxidative Stress
  • Oxygen free radicals contribute to the pathogenesis of coronary vasospasm through their damaging effects on vascular endothelial cells and degrading nitric oxide, an important vasodilatory agent. ^{[1] [12] [17]}
• Smooth Muscle Hypercontractility
  • At a cellular level, pathways that lead to enhanced myosin light chain phosphorylation promote vasoconstriction. Increased activity of Rho-kinase leading to enhanced myosin light chain phosphorylation has been implicated in the pathogenesis of coronary vasospasm. ^{[1] [18]}

Diagnosis

There are no set criteria to diagnose coronary vasospasm. Thorough history taking by a clinician can assist in the diagnosis of coronary vasospasm. In cases where symptoms of chest pain are present, identifying features that distinguish episodes of vasospastic angina from traditional angina can aid in the diagnosis. ^[6] Features such as chest pain at rest, a diurnal variation in tolerance for exercise with a reduction in tolerance for exercise in the morning, and responsiveness of chest pain to calcium channel blockers as opposed to beta blockers can be important clues. ^[6]

EKG can occasionally be used to diagnose episodes of coronary vasospasm. However, relying on EKG is not always possible due to the transient nature of coronary vasospasm episodes. ^{[6] [19]} Due to the challenge of capturing episodes of coronary vasospasm spontaneously, provocative testing to induce coronary vasospasm during coronary catheterization can be used to make the diagnosis. ^[19] Provocative testing relies upon the use of pharmacological agents that promote or trigger episodes of vasospasm. Agents commonly administered include ergonovine and acetylcholine. Both pharmacological agents have vasoconstrictive effects on coronary arteries. ^[19] However, in the clinical setting, provocative testing is not routinely performed. ^[20] The reason for this is due to the adverse effects of these pharmacological agents. ^[20]

History

Chest pain due to coronary vasospasm was described in the medical literature by Prinzmetal et al. in 1959. ^[2] This discovery led to this type of angina being referred to in the literature as Prinzmetal angina. ^{[3] [20]} A following study further distinguished this angina from classical angina pectoris due to the fact that the results showed that the patients with chest pain due to coronary vasospasm lacked evidence of atherosclerosis on cardiac catheterization. ^{[3] [20]} Angina due to coronary vasospasm is also known as variant angina. ^[20]

During the 70’s and 80’s, intense research ^[21] headed by Dr. Robert A. Chahine resulted in the delineation of Spasm's role in Prinzmetal's angina, allowing for easy identification and effective treatment. ^[22]

See also

• Myocardial bridge, a common congenital heart anomaly in which one of the coronary arteries tunnels through the heart muscle (myocardium) itself.

Related Research Articles

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.

Microvascular angina (MVA), previously known as cardiac syndrome X, 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.

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.

Acute coronary syndrome (ACS) is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is centrally located pressure-like chest pain, often radiating to the left shoulder or angle of the jaw, and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly women, older people, and people with diabetes mellitus.

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.

Unstable angina is a type of angina pectoris that is irregular or more easily provoked. It is classified as a type of acute coronary syndrome.

Nitroglycerin, also known as glyceryl trinitrate (GTN), is a vasodilator used for heart failure, high blood pressure (hypertension), anal fissures, painful periods, and to treat and prevent chest pain caused by decreased blood flow to the heart (angina) or due to the recreational use of cocaine. This includes chest pain from a heart attack. It is taken by mouth, under the tongue, applied to the skin, or by injection into a vein.

Nicorandil is a vasodilator drug used to treat angina.

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.

Myocardial stunning or transient post-ischemic myocardial dysfunction is a state of mechanical cardiac dysfunction that can occur in a portion of myocardium without necrosis after a brief interruption in perfusion, despite the timely restoration of normal coronary blood flow. In this situation, even after ischemia has been relieved and myocardial blood flow (MBF) returns to normal, myocardial function is still depressed for a variable period of time, usually days to weeks. This reversible reduction of function of heart contraction after reperfusion is not accounted for by tissue damage or reduced blood flow, but rather, its thought to represent a perfusion-contraction "mismatch". Myocardial stunning was first described in laboratory canine experiments in the 1970s where LV wall abnormalities were observed following coronary artery occlusion and subsequent reperfusion.

Abdominal angina is abdominal pain after eating that occurs in individuals with ongoing poor blood supply to their small intestines known as chronic mesenteric ischemia. Although the term angina alone usually denotes angina pectoris, angina by itself can also mean "any spasmodic, choking, or suffocative pain", with an anatomic adjective defining its focus; so, in this case, spasmodic pain in the abdomen. Stedman's Medical Dictionary Online defines abdominal angina as "intermittent abdominal pain, frequently occurring at a fixed time after eating, caused by inadequacy of the mesenteric circulation resulting from arteriosclerosis or other arterial disease. Synonym: intestinal angina."

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.

A nitrovasodilator is a pharmaceutical agent that causes vasodilation by donation of nitric oxide (NO), and is mostly used for the treatment and prevention of angina pectoris.

Coronary ischemia, myocardial ischemia, or cardiac ischemia, is a medical term for abnormally 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 bridge (MB) is a common congenital heart anomaly in which one of the coronary arteries tunnels through the heart muscle (myocardium) itself.

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.

Arterial occlusion is a condition involving partial or complete blockage of blood flow through an artery. Arteries are blood vessels that carry oxygenated blood to body tissues. An occlusion of arteries disrupts oxygen and blood supply to tissues, leading to ischemia. Depending on the extent of ischemia, symptoms of arterial occlusion range from simple soreness and pain that can be relieved with rest, to a lack of sensation or paralysis that could require amputation.

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