Vasospastic angina: symptoms, causes and treatment

Author Ольга Кияница

2018-09-28

Among all the variants of angina, the most unfavorable course has vasospastic angina. It is characterized by sudden onset of attacks, moreover, it can quickly turn into a myocardial infarction or sudden death. Therefore, it is very important, if there is a risk of developing this disease, to know the symptoms, causes and its treatment.

Vasospastic angina (variant, Prinzmetal's angina) is a form of angina caused by spasm of the coronary artery due to a sudden occlusive vasoconstriction of the epicardial artery, which leads to a sharp reduction in coronary blood flow. This is usually followed by transmural myocardial ischemia, which is usually manifested by an increase in the ST segment on the electrocardiogram.

The classic form of vasospastic angina occurs at rest (variation of Prinzmetal stenocardia), but in some patients the spasm can be caused by physical exertion or stressful situations.

A spasm may occur on the background of significant or minor coronary stenosis, as well as in angiographically normal epicardial arteries. In some cases, the lesion may affect most of the coronary segments (multifocal spasm). Despite the availability of effective treatments for coronary artery spasm, the diagnosis of variant angina is rarely seen in patients with this disease.

Video: Vasospastic angina pectoris. Young disease

Historical information

angina pectoris stress, noting the relationship between the manifestation of an attack with tension and calm during rest.Later, the pathology was associated with fixed obstructive coronary atherosclerotic disease and dynamic depression of the ST segment on the ECG during pain.

In 1959, Prinzmetal et al. Described 32 cases of angina pectoris arising in a state of rest, while reporting that the clinical characteristics of these patients differed from the classical angina pectoris of Heberden, because:

  1. Angina does not occur when you are stressed, and performing exercises to perform a stress test was usually negative.
  2. During the onset of pain, an increase in the ST segment was noted, and not its depression, as in the classic version.
  3. Often episodes of angina pectoris recurred, while awakening the patient from sleep.
  4. The attacks may be associated with arrhythmias or progression of myocardial infarction.

Given these differences, Prinzmetal coined the term “variant angina,” and suggested that this condition is caused by “increased coronary tone” or vasospasm. Since then, significant progress has been made in understanding this condition. In particular, the main pathophysiological mechanism responsible for the manifestation of the syndrome, which is an occlusive spasm of the epicardial coronary artery, was studied. A provocative test for spasm was also developed, which helps in the diagnosis of the disease.

Causes and mechanism of development

Epidemiology

  • Vasospastic angina is about 2.0% of hospitalizations with a clinical picture of unstable angina.
  • Most often determined in adulthood (from 50 to 60 years). The ratio between men and women is 5: 1.
  • Smoking is the only recognized risk factor.
  • The use of certain substances (for example, alcohol, cocaine, 5-fluorouracil, sumatriptan) may contribute to the development of vasospastic angina.
  • In rare cases, variant angina is associated with systemic vasomotor disorders, such as migraine and Raynaud's syndrome, indicating the presence of a general vascular disorder.

Pathogenesis

The development of coronary spasm is due to the interaction of two components:

  1. The presence of local hyperreactivity to vasoconstrictor stimuli of the coronary segment.
  2. The continuing effects of vasoconstrictor stimuli that cause a spasm in the hyper-reactive segment.

Vascular smooth muscle hyperreactivity is probably due to a post-receptor cell abnormality in the regulation of myofibril contraction. A similar assumption was considered to induce spasm by several stimuli acting on various cellular receptors, as well as the malfunctioning of specific antagonist receptors (for example, alpha-blockers, serotonin antagonists, etc.).

Recent research results show that increased activity of the intracellular enzyme Rho-kinase and impaired function of K + -ATP-dependent channels may be part of cellular pathways potentially involved in coronary spasm. In addition, the increased activity of the membrane Na + -H + channel of metabolism, the main regulator of intracellular pH, is believed to be a possible stimulator of abnormal vasoreactivity.

Clinical features

Distinctive symptoms of vasospastic angina often include:

  • Periodic episodes of rest angina, often occurring in the early morning hours.
  • ST elevation on electrocardiogram.
  • The fast action of short-acting nitrates.

Vasospastic angina pectoris is characterized by the occurrence of “hot phases” with frequent repetition of attacks that alternate with “cold phases”, with remission of symptoms for weeks or months.

Angina attacks are usually short in duration (2-5 minutes, sometimes not more than 30 seconds) and can be repeated during one attack, which can last 20-30 minutes.

A high degree of suspicion of this disease is recurring short-term episodes of nocturnal angina pectoris, which are quickly removed by hypoglossal nitrates. Also, a similar diagnosis can be made with recurrent angina associated with syncope or even cardiac arrest, as patients with variant angina may experience malignant arrhythmias during ischemic attacks.

With the exception of tobacco smoking, the usual risk factors in the form of atherosclerosis most often do not contribute to the development of variant angina. Also, exercise usually does not provoke an attack of “angina pectoris”, whereas hyperventilation and exposure to cold can cause characteristic manifestations.

Variant angina may not manifest for a long time, and then disturb the patient with several severe attacks. During these “hot phases,” stimulating factors that usually do not provoke an episode of variant angina may contribute to the manifestation of the disease.

The circadian nature of this disorder is also well known and illustrated by Yasue H. et al. [1].
Yasue H, Omote S, Takizawa A, Nagao M, Miwa K, Tanaka S: Circulation 1979, 59: 938-948]. Accordingly, ST increases in patients with vasospastic angina most often occur in the early morning (5–8 hours), but in rare cases, these patients recur in the afternoon (3–4 evenings).

Diagnostics

The history of the disease and the registration of electrocardiography during a spontaneous attack are of paramount importance in the diagnosis of vasospastic angina. However, spontaneous episodes are rarely able to register with a standard ECG, so additional research methods are used.

  • An ambulatory ECG monitoring can be useful, especially during the active phase of the disease. Allows you to detect episodes of ST segment changes, as well as related arrhythmias.
  • The stress test with ECG recording usually does not give results, but during active spasm caused by exercise, characteristic changes in half of patients with variant angina can be determined.
  • Coronary angiography - variant angina today is considered only in patients with normal angiography; however, the original description of this condition, created by Prinzmetal, included patients with significant coronary artery disease, where the spasm reached uncritical stenosis, thereby creating a blockage of the transition vessel and, therefore, ischemia associated with an increase in ST, which was weakened by sublingual nitrates. Subsequent studies reported a “variant variant”, where variant angina was found in patients with normal angiography [2 - Variant angina of Prinzmetal with normal coronary arteriograms. Cheng TO, Bashour T, Kelser GA, Jr., Weiss L, Bacos J: A variant of the variant. Circulation 1973, 47: 476-485].
  • A provocative study of coronary spasm - originally conducted in bed with ECG monitoring. However, after several deaths using this approach, provocative tests were carried out primarily during coronary angiography, where the spasm can be quickly identified and treated with intracoronary nitrates, if necessary. Various provocative stimulants were used to test the spasm: methacholine, adrenaline (with / without propranolol), phenylephrine, serotonin, histamine, dopamine, methylergometrine, and hyperventilation using TRIS infusion buffer. The two most commonly used in modern practice are acetylcholine and ergonovine. Intracoronary acetylcholine is administered as an incremental selective slow bolus injection into the right (25-50 μg) and left (25-100 μg) coronary arteries, often requiring stimulation due to transient cholinergic bradycardia. Occasionally, slow intracoronary bolus injections of 20–60 µg ergonovin into the right and left coronary arteries were used, while others used incremental intravenous bolus injections (25–300 µg) at 5-minute intervals. The presence of induced coronary spasm is assessed based on chest pain, ECG changes and / or severe coronary constriction in response to the use of a stimulant.

Differential diagnoses for patients with suspected variable angina (for example, in the presence of back pain with an increase in ST) include developing myocardial infarction, mixed-type angina, tacocubi cardiomyopathy, and coronary microvascular disorders. Although vasospastic angina can be perceived as a myocardial infarction with ST elevation, the former has a history of recurrent chest pain and positive effects of nitrates.

Angina of the mixed type (both painful and painless) was presented by Maseri [3 - Maseri A: Variant Angina. In Ischemic Heart Disease A Case for Clinical Practice and Clinical Research. New York: Churchill Livingstone; 1995: 559-588] represents a wide range of coronary diseases from angina pectoris due to fixed obstructive coronary artery disease to dynamic spasm. This is often observed in case of variant angina.

Tacocubi cardiomyopathy can manifest itself in the form of rest angina associated with an increase in ST. Although the classic apical attack can distinguish it from variant angina, some researchers suggest that this pathology is caused by multivessel spasm. Coronary microvascular disorders can cause rest angina in patients with normal angiography, which can be distinguished from variant angina, excluding coronary artery spasm with provocative spasm testing. In the absence of confirmed ischemia, it is necessary to take into account other non-cardiac causes of pain at rest (for example, a spasm of the esophagus).

Diagnostic criteria

Diagnosis of variant angina is based on two approaches.

1. The first is based on the clinical criteria of Prinzmetal for the diagnosis of vasospastic angina pectoris:

1.1 Angina alone.

1.2 Short-term increase in ST.

1.3 Improvement in the use of sublingual nitrates.

Many early studies have used this clinical approach, but with the appearance of images of the coronary arteries using selective angiography, the focus has been on a diagnosis based on provocative testing of coronary spasm.

2. The second approach under the term “vasospastic angina pectoris” was developed with the following diagnostic criteria:

2.1 Anginal state at rest.

2.2 Reversible ST changes (increased or depressed).

2.3 Spontaneous / provoked coronary spasm during angiography.

Although these diagnostic approaches differ from each other, there is considerable agreement, since validation studies reported 90% sensitivity and 99% specificity in provoked angiography spasm with Pritzmetal’s clinical diagnostic criteria.Guidelines for the diagnosis and treatment of vasospastic angina pectoris were developed by the Japanese Circulation Society, although they still need to be improved in other countries.

Treatment and prognosis

Treatment guidelines for vasospastic angina pectoris are focused on the following:

  • Avoiding predisposing factors, such as smoking.
  • Prevention of coronary angiospasm with vasodilation therapy.

In approximately 10% of cases, spastic coronary artery disease can be resistant to optimal vasodilator therapy, and then very high doses of calcium antagonists or nitrates should be used.

Short-acting nitrates are used to relieve acute angina attacks, while long-acting nitrates are used to prevent vasospastic attacks.

In some cases, calcium channel blockers are added to background nitrate therapy, which reduce the risk of seizures in patients with variant angina.

A number of studies have shown that potassium channel activating drugs, like nicoradil and Rho-kinase inhibitor, fasudil, are effective in preventing episodes of coronary angiospasm and are useful agents for treating this condition.

If no conservative treatment of vasospastic angina does not help, then balloon angioplasty or stenting is performed, which can help prevent coronary spasm. Also, depending on the indications, coronary artery bypass grafting is used to create a workaround for the blood flow.

Forecast

Vasospastic angina may be associated with significant morbidity and mortality due to the development of myocardial infarction. The probability of developing such a complication is 60-95% after 5 years. Ways to reduce the risk of developing heart attack include the use of calcium channel blockers, controlling the degree and severity of coronary artery disease, and preventing the development of multi-vascular spasm.

Key points

  • Attacks of vasospastic angina often short and occur in the morning (5-8 hours).
  • Among all risk factors, tobacco smoking most often contributes to the occurrence of vasospastic angina.
  • Vasospastic angina pectoris can be easily diagnosed by evaluating clinical criteria and / or provocative spasm testing.
  • The course of vasospastic angina may be complicated by myocardial infarction, arrhythmia, and even sudden death.
  • Treatment of vasospastic stenocardia is based on the use of nitrates of short and prolonged action.

Video: Vasospastic Angina


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