Coronary vasospasm

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

Contents

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]

Complications

Depending on how long the occlusion lasts, a spectrum of different myocardial ischemic syndromes can occur. Shorter episodes of occlusion can lead to what is referred to as silent myocardial ischemia due to its asymptomatic nature. [1] These episodes can also be accompanied by arrhythmias. [1] Longer episodes of occlusion can lead to stable or unstable angina, myocardial infarction, and sudden cardiac death. [1]

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]

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]

EKG findings

When coronary vasospasm causes an artery to undergo complete occlusion, an EKG might show evidence of ST-segment elevation in the leads indicative of that artery's territory. Transient ST-segment depression can also occur, usually in the setting of sub-total occlusion of an artery. [7]

Additional EKG findings in coronary vasospasm include evidence of arrhythmias that might be induced by ischemia: ventricular premature contractions, ventricular tachycardia, ventricular fibrillation, and more. [7]

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]

Related Research Articles

An antianginal is a drug used in the treatment of angina pectoris, a symptom of ischaemic heart disease.

<span class="mw-page-title-main">Angina</span> Chest discomfort due to not enough blood flow to heart muscle

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.

<span class="mw-page-title-main">Chest pain</span> Discomfort or pain in the chest as a medical symptom

Chest pain is pain or discomfort in the chest, typically the front of the chest. It may be described as sharp, dull, pressure, heaviness or squeezing. Associated symptoms may include pain in the shoulder, arm, upper abdomen, or jaw, along with nausea, sweating, or shortness of breath. It can be divided into heart-related and non-heart-related pain. Pain due to insufficient blood flow to the heart is also called angina pectoris. Those with diabetes or the elderly may have less clear symptoms.

Microvascular angina, previously known as cardiac syndrome X, is angina 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.

<span class="mw-page-title-main">Acute coronary syndrome</span> Medical condition

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.

<span class="mw-page-title-main">Variant angina</span> Medical condition

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.

<span class="mw-page-title-main">Unstable angina</span> Medical condition

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.

<span class="mw-page-title-main">Nitroglycerin (medication)</span> Medication

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.

<span class="mw-page-title-main">Nicorandil</span> Chemical compound

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.

<span class="mw-page-title-main">Takotsubo cardiomyopathy</span> Sudden temporary weakening of the heart muscle

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. Examples of physical stressors that can cause TTS are sepsis, shock, subarachnoid hemorrhage, and pheochromocytoma. Emotional stressors include bereavement, divorce, or the loss of a job. Reviews suggest that of patients diagnosed with the condition, about 70–80% recently experienced a major stressor, including 41–50% with a physical stressor and 26–30% with an emotional stressor. TTS can also appear in patients who have not experienced major stressors.

<span class="mw-page-title-main">Wellens' syndrome</span> Medical condition

Wellens' syndrome is an electrocardiographic manifestation of critical proximal left anterior descending (LAD) coronary artery stenosis in people with unstable angina. Originally thought of as two separate types, A and B, it is now considered an evolving wave form, initially of biphasic T wave inversions and later becoming symmetrical, often deep, T wave inversions in the anterior precordial leads.

<span class="mw-page-title-main">Nitrovasodilator</span> Drug that causes vasodilation by releasing nitric oxide

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.

<span class="mw-page-title-main">Coronary ischemia</span> Medical condition

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.

<span class="mw-page-title-main">Myocardial bridge</span> Medical condition

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. It is important to note that even a very thin ex. <1 mm and/or short ex. 20 mm MB can cause significant symptoms. 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%).

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.

References

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  2. 1 2 Prinzmetal, Myron; Kennamer, Rexford; Merliss, Reuben; Wada, Takashi; Bor, Naci (September 1959). "Angina pectoris I. A variant form of angina pectoris". The American Journal of Medicine. 27 (3): 375–388. doi:10.1016/0002-9343(59)90003-8. ISSN   0002-9343. PMID   14434946.
  3. 1 2 3 4 Cheng, Tsung O. (1972-05-01). "Variant Angina of Printzmetal with Normal Coronary Arteriograms: A Variant of the Variant". Annals of Internal Medicine. 76 (5): 862. doi:10.7326/0003-4819-76-5-862_2. ISSN   0003-4819.
  4. ↑ Robert, Chahine (1984). "Coronary Artery Spasm". JAMA: The Journal of the American Medical Association. 251 (8): 1097. doi:10.1001/JAMA.1984.03340320073040. S2CID   72379696.
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  11. ↑ Talarico GP, Crosta ML, Giannico MB, Summaria F, Calò L, Patrizi R (May 2017). "Cocaine and coronary artery diseases: a systematic review of the literature". Journal of Cardiovascular Medicine. 18 (5): 291–294. doi:10.2459/JCM.0000000000000511. PMID   28306693. S2CID   13605509.
  12. 1 2 3 4 5 6 Matta A, Bouisset F, Lhermusier T, Campelo-Parada F, Elbaz M, Carrié D, Roncalli J (2020-05-15). "Coronary Artery Spasm: New Insights". Journal of Interventional Cardiology. 2020: 5894586. doi: 10.1155/2020/5894586 . PMC   7245659 . PMID   32508542.
  13. ↑ Jcs Joint Working Group (August 2010). "Guidelines for diagnosis and treatment of patients with vasospastic angina (coronary spastic angina) (JCS 2008): digest version". Circulation Journal. 74 (8): 1745–62. doi: 10.1253/circj.CJ-10-74-0802 . PMID   20671373.
  14. ↑ Matta, Anthony; Bouisset, Frederic; Lhermusier, Thibault; Campelo-Parada, Fran; Elbaz, Meyer; Carrié, Didier; Roncalli, Jerome (2020-05-15). "Coronary Artery Spasm: New Insights". Journal of Interventional Cardiology. 2020: 1–10. doi: 10.1155/2020/5894586 . PMC   7245659 . PMID   32508542.
  15. ↑ Itoh, Teruhiko; Mizuno, Yuji; Harada, Eisaku; Yoshimura, Michihiro; Ogawa, Hisao; Yasue, Hirofumi (2007). "Coronary Spasm is Associated With Chronic Low-Grade Inflammation". Circulation Journal. 71 (7): 1074–1078. doi: 10.1253/circj.71.1074 . ISSN   1346-9843. PMID   17587713.
  16. ↑ Messner Barbara; Bernhard David (2014-03-01). "Smoking and Cardiovascular Disease". Arteriosclerosis, Thrombosis, and Vascular Biology. 34 (3): 509–515. doi: 10.1161/ATVBAHA.113.300156 . PMID   24554606.
  17. ↑ Kusama, Yoshiki; Kodani, Eitaro; Nakagomi, Akihiro; Otsuka, Toshiaki; Atarashi, Hirotsugu; Kishida, Hiroshi; Mizuno, Kyoichi (2011). "Variant Angina and Coronary Artery Spasm: The Clinical Spectrum, Pathophysiology, and Management". Journal of Nippon Medical School. 78 (1): 4–12. doi: 10.1272/jnms.78.4 . ISSN   1347-3409. PMID   21389642.
  18. ↑ Shimokawa, Hiroaki (2000). "Cellular and Molecular Mechanisms of Coronary Artery Spasm". Japanese Circulation Journal. 64 (1): 1–12. doi: 10.1253/jcj.64.1 . ISSN   0047-1828. PMID   10651199.
  19. 1 2 3 Specchia, G.; de Servi, S. (1984), "Provocative Testing for Coronary Spasm", Breakdown in Human Adaptation to ‘Stress’, Dordrecht: Springer Netherlands, pp. 916–922, doi:10.1007/978-94-011-8064-1_70, ISBN   978-94-011-8066-5 , retrieved 2020-11-22
  20. 1 2 3 4 5 Slavich, Massimo; Patel, Riyaz Suleman (March 2016). "Coronary artery spasm: Current knowledge and residual uncertainties". IJC Heart & Vasculature. 10: 47–53. doi: 10.1016/j.ijcha.2016.01.003 . ISSN   2352-9067. PMC   5462634 . PMID   28616515.
  21. ↑ Robert, Chahine (1986). "Coronary Artery Spasm". Postgraduate Medicine. 79 (4): 78–91. doi:10.1080/00325481.1986.11699314.
  22. ↑ Robert A., Chahine (1983). Corronary Artery Spasm. Futura Publishing Company. ISBN   9780879931926.

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