variant angina pectoris



OVERVIEW

Definition

Variant angina is angina due to spasm of the coronary arteries, causing myocardial ischemia.

In severe cases, it may lead to acute myocardial infarction, severe arrhythmia or even sudden death.

Incidence

The prevalence of the disease is not clear, and epidemiologic surveys in different countries have shown different results, but according to research studies, the prevalence of variant angina is significantly higher in Japan than in Caucasians.

Variant angina is most common in middle-aged men, with a prevalence in the middle of the night and early morning hours [1].

Causes

Causes

Coronary artery endothelial damage

Increased local blood concentrations of vasoactive substances such as 5-hydroxytryptamine, tissue and various vasoconstrictor factors stimulate vascular smooth muscle to become more responsive to contraction, inducing variant angina.

Coronary atherosclerotic plaque

The site of variant angina is often located in the vicinity of an atherosclerotic plaque, suggesting that the evolution of an atherosclerotic plaque may affect the contractile properties of the arteries in its vicinity and stimulate adrenergic receptors, causing variant angina.

Physical and Chemical Factors

Abnormal concentrations of certain substances in the blood, such as decreased concentrations of magnesium ions and cocaine, may also induce variant angina.

Autonomic Nerve Dysfunction

Autonomic nerves are capable of regulating the functions of many organs in the body. Autonomic nerve dysfunction can lead to abnormal regulation of vascular smooth muscle contraction, resulting in coronary artery spasm and variant angina.

Genetic factors

It has been found that a number of genetic variations can lead to the development of variant angina pectoris.

Pathogenesis

Vascular endothelial cell dysfunction

Vascular endothelial cells are part of the body that makes up the coronary arteries. It releases nitric oxide and endothelin, which cause blood vessels to dilate and endothelin to constrict.

When the vascular endothelium is damaged and dysfunctional, the release of nitric oxide decreases and the release of endothelin increases, causing the coronary arteries to contract excessively, resulting in coronary artery spasm.

Vascular smooth muscle cell contractile hyperresponsiveness

Vascular smooth muscle cells are also part of the composition of the coronary arteries.

Stimulated by factors such as inflammation, vascular smooth muscle cells produce an excessive contractile response, leading to coronary artery spasm.

Oxidative Stress

Oxidative stress in the body produces oxygen free radicals, which damage vascular endothelial cells and degrade nitric oxide, leading to coronary artery spasm.

Inflammatory reaction

Inflammation of the coronary artery periphery and surrounding adipose tissue is associated with this disease.

Autonomic dysfunction

During rest or sleep, vagal activity is increased and sympathetic nerves are stimulated to release norepinephrine, which stimulates alpha receptors in the coronary arteries and induces coronary artery constriction [2].

Genetic alterations

Genetic variants that are clearly associated with coronary artery spasm include Glu298Asp, 786T/C, eNOS intron 4b/a , endothelin-1 and esterase C-51 protein-related genes of endothelial-type nitric oxide synthase, etc. Alterations in these genes affect some of the cellular functions, which ultimately lead to coronary artery spasm [2-3].

Symptoms

Clinical symptoms

Angina pectoris occurs at rest, often in periodic episodes, often in the second half of the night or upon awakening in the early morning.

The site of pain is often in the precordial region or retrosternal.

The pain is crushing or constricting, accompanied by dyspnea and a sense of near death, lasting several minutes or even longer, and may be accompanied by severe arrhythmias or syncope [4].

Complications

Acute myocardial infarction

Severe and persistent precordial or retrosternal crushing pain with dyspnea and a sense of dying, which is not completely relieved by rest and nitrates.

Arrhythmia

Myocardial ischemia and reperfusion lead to arrhythmia, including ventricular tachycardia, ventricular fibrillation, etc., manifested by panic, chest tightness, palpitation, shortness of breath, dizziness, sweating, and even fainting.

Heart Failure

Severe angina and extensive ischemia can lead to complications such as cardiac dysfunction and heart failure, manifested by dyspnea, dizziness, fatigue, swelling of the lower limbs and even the whole body.

Sudden cardiac death

Variant angina pectoris is often complicated by acute myocardial infarction and malignant arrhythmia, resulting in sudden cardiac death [5], which manifests as cardiac arrest.

Consultation

Department of Medicine

Cardiovascular medicine

Chest pain that occurs in a calm state, with patients experiencing tight, crushing pain in the precordial area, which may be accompanied by pain in the left shoulder, left hand, jaw, abdomen, etc., please go to the Department of Cardiovascular Medicine.

Feeling dizziness, blurred vision, lightheadedness, and unsteadiness, please go to Cardiovascular Medicine.

If you experience a decrease in physical strength, such as shortness of breath after walking 1 kilometer at a normal speed or walking up a flight of stairs, please consult the Cardiovascular Medicine Department.

Emergency Medicine

Chest pain that persists without relief and difficulty breathing, go to the Emergency Department.

Shock, or early signs of shock: pale and cold skin, profuse sweating, shallow and rapid breathing, even purple lips, unconsciousness, go to the Emergency Department.

Fainting, loss of consciousness, slow or no response to external stimuli (e.g., shouting, shaking, pinching skin with hands), go to the emergency department.

Preparation for medical treatment

Preparing for a visit: registering, preparing information, common problems

Tips for seeking medical treatment

Keep your mood stable, don’t stay up late, and don’t over-exercise before going to the doctor.

Preparation Checklist

Pay particular attention to the time of onset of symptoms, special performance, etc.

Are there symptoms of chest tightness or chest pain? How long have the symptoms been present? How long does it last? How was it relieved?

Has there been any loss of consciousness?

Was there a significant drop in blood pressure?

Is there any difficulty in breathing?

Any previous history of angina?

Is there a history of heart disease?

Is there any family history of related diseases?

Test results in the last 6 months to bring with you to the doctor’s office

Blood biochemistry (cardiac enzyme profile, markers of myocardial injury, brain natriuretic peptide, etc.)

Electrocardiogram (including routine electrocardiogram, 24-hour ambulatory electrocardiogram, etc.)

Echocardiogram

Electrocardiogram exercise test

Coronary angiography

Medication use in the last 3 months, carry the box or package with you to the doctor if available

Nitrates: nitroglycerin, isosorbide mononitrate

Calcium channel blockers: diltiazem

Antiplatelet therapy: aspirin

Statins: Atorvastatin, Simvastatin

Beta-blockers: metoprolol succinate

Diagnosis

Diagnosis is based on

Medical history

The patient may have a family history of variant angina.

Clinical manifestations

Angina pectoris occurs at rest, often in periodic episodes, often in the second half of the night or upon awakening in the early morning hours.

The site of pain is often in the precordial region or retrosternal.

The pain is crushing or constricting, accompanied by dyspnea and a sense of dying, lasting several minutes or longer, and may be accompanied by severe arrhythmias or syncope.

Related examination

When myocardial ischemia and hypoxia are severe enough to cause myocardial necrosis, myocardial enzyme tests will show characteristic changes.

This test helps to determine the severity and nature of the disease.

The ST segment is elevated in the corresponding leads during an attack, while the corresponding leads show ST segment depression.

In some patients, ST-segment elevation and depression with alternating upright and inverted T-waves are the result of ischemic conduction delays, which can progress to fatal arrhythmias, and the presence of this phenomenon is often indicative of a poor prognosis.

Coronary artery stenosis can be differentiated from spasm by injecting a contrast medium into the coronary arteries to visualize them on x-ray.

At the end of the imaging, an atraumatic drug provocation test can be performed to further diagnose coronary artery spasm in patients who do not have stenosis [6].

Screening for underlying disease, such as coronary atherosclerosis, allows for a more definitive diagnosis.

Clarifying the presence of myocardial injury and clarifying myocardial blood supply can observe the severity of coronary artery spasm.

Hyperventilation combined with cold pressor test confirms the presence of coronary artery spasm syndrome.

Combination of hyperventilation and exercise test to confirm the presence of coronary artery spasm syndrome.

It is mainly used in patients with chest pain or chest tightness who do not have a significant fixed stenosis on coronary angiography, and can be used to make a differential diagnosis of vasospastic angina pectoris

It mainly includes ergometrine provocation test and acetylcholine provocation test, and the diagnosis is made by whether the two drugs can induce coronary artery spasm.

Differential diagnosis

Acute pericarditis

Similarities: ST-segment changes and pain in the precordial area are present on the ECG.

Differences: Patients with pericarditis may have fever and an increased white blood cell count before the pain, and the pain is often exacerbated by deep breathing and coughing [7].

Acute pulmonary embolism

Similarities: both present with chest pain.

Differences: The electrocardiogram in pulmonary embolism indicates a rightward deviation of the electrical axis and inversion of the Q and T waves [8].

Aortic dissection

Similarities: both present with severe chest pain.

Difference: aortic dissection often radiates to the back, ribs, abdomen, waist, and lower extremities, and the diagnosis of aortic dissection can also be confirmed by X-ray, ultrasonography, and MRI [9].

Treatment

The purpose of treatment: to relieve the spasm of coronary artery, timely management of complications, and avoid recurrent attacks.

Treatment principle: symptomatic treatment in the acute stage and prevention of recurrence in the stabilization stage.

Acute phase treatment

Drug treatment

Nitroglycerin can prevent vasoconstriction, promote vasodilation, and relieve symptoms.

Calcium channel blockers, such as Diltiazem, can promote coronary vasodilation.

Antiplatelet therapy, commonly used aspirin, persistent spasm may develop into acute myocardial infarction or sudden death, and antiplatelet therapy should be initiated as soon as possible.

Stabilization treatment

Control of risk factors and predisposing factors

Cessation of smoking and alcohol consumption.

Control blood pressure.

Maintain appropriate body weight, neither overweight nor too thin.

Correct blood sugar and lipid metabolism disorders.

Avoid overwork and mental stress.

Medication

Commonly used drugs are diltiazem, nifedipine, amlodipine, benidipine and so on.

They can promote coronary vasodilation.

Allergy to these drugs is prohibited; long-term use may cause nausea and vomiting and other symptoms.

Commonly used drugs are nitroglycerin, isosorbide mononitrate and so on.

They can prevent vasoconstriction, promote vasodilation, and relieve symptoms.

Oral can also play a role in the effect, sublingual effect is faster, in addition to allergy to this drug should be prohibited, while patients with low blood pressure is also prohibited.

The commonly used drug is Nicorandil.

It can increase coronary blood flow without affecting blood pressure, heart rate and cardiac conduction system, and will not be resistant to the drug, which can relieve nervousness, reduce myocardial oxygen consumption and relieve angina pectoris.

Commonly used drugs include aspirin and clopidogrel.

May prevent acute coronary events.

May present with bleeding, skin petechiae and ecchymosis.

Commonly used drugs include atorvastatin, simvastatin.

Effective in preventing coronary spasm and may improve endothelial function.

Other treatments

Some patients may be combined with moderate to severe coronary artery stenosis, percutaneous coronary intervention can be used.

It is indicated for patients with sustained tachycardia induced by coronary artery spasm or ventricular fibrillation leading to cardiac arrest. After ineffective pharmacologic therapy, a buried automated defibrillation pacemaker may be considered [10].

Prognosis

Cure.

Untreated disease progression may occur, resulting in acute myocardial infarction, malignant arrhythmia, and in severe cases, cardiac arrest, leading to life-threatening conditions.

Patients who adhere to long-term medication based on strict smoking and alcohol cessation generally have a favorable prognosis.

Harmfulness

Daily life

Long-term symptoms such as chest tightness and chest pain may affect life.

Mental health

The disease has a long course, but is prone to recurrence, and patients are prone to worry and other adverse emotions.

Lethality

It may cause myocardial infarction, etc., and is prone to life-threatening conditions and even death.

Daily

Daily management

Dietary management

The principle of diet is low salt and low fat diet.

You can eat more green vegetables and fresh fruits.

At the same time, consume sufficient amount of high quality protein and less cholesterol-containing food, such as fried food and fatty meat.

Do not eat too much at each meal and recommend eating small meals to avoid overeating.

Lifestyle management

Quit smoking and drinking.

Ensure reasonable sleep time.

Avoid excessive pressure and relaxation.

Obese people should carry out appropriate and regular exercise to reduce weight scientifically. Normal weight people also need to exercise regularly to control their weight.

Avoid catching colds and exertion.

Exercise appropriately to enhance physical fitness, but avoid doing strenuous exercise.

Mood Management

Positively adjust bad moods and maintain a good mindset.

Special management

Monitor blood pressure, heart rate, etc., and review regularly. Prompt medical attention is required for obvious discomfort.

Disease monitoring

Patients with abnormal blood pressure should monitor their blood pressure regularly at home for a long period of time, and observe and record their blood pressure control.

Patients with diabetes can follow the doctor’s instructions to measure and record their blood glucose at home.

Follow-up

Regular follow-up as prescribed by the doctor may include routine examinations such as electrocardiogram to observe the progress of the disease.

Prevention

Stop smoking and drinking.

Ensure reasonable sleep time and avoid late night, exertion and emotional stress.

Regular medical checkups and timely treatment of the disease.