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Revision as of 17:09, 15 April 2020

For patient information, click here
For main page on Acute coronary syndrome, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2],Amandeep Singh M.D.[3] Roukoz A. Karam, M.D.[4] Synonyms and keywords: Variant angina; angina inversa; vasospastic angina

Overview

Vasospastic angina was previously referred to as Prinzmetal or variant angina. Vasospastic angina is a syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in periodic cycles. Vasospastic angina is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than fixed narrowings of the coronary arteries due to atherosclerosis (buildup of fatty plaque and hardening of the arteries).

Historical Perspective

Printzmetal's angina was first described as a variant form in 1959 by the American cardiologist Dr. Myron Prinzmetal.^[1]

It was first documented by coronary arteriography in 1973.^[2]

Classification

Classification by Location

Coronary artery spasm can be classified according to the location of vasoconstriction:

Focal coronary spasm

Focal coronary spasm is limited to a localized segment of the coronary artery.

Multifocal coronary spasm

Multifocal coronary spasm involves several localized segments of the same coronary artery.

Multivessel coronary spasm

Multivessel coronary spasm involves several coronary arteries.^[3]^[4]

Classification by Clinical Syndrome

Coronary artery vasospasm can be classified into either spontaneous or iatrogenic.

Spontaneous

A subtype of epicardial coronary artery spasm is known as Prinzmetal's angina. Prinzmetal's angina is characterized by the sudden onset of chest pain at rest with ST elevation on ECG. Click here for more information about Prinzmetal's angina.

Iatrogenic

Coronary vasospasm can be secondary to PCI. Click here for more information about PCI-induced coronary vasospasm.

Pathophysiology

The exact pathogenesis of coronary vasospasm is not well understood, but some causes and contributing factors are known.

Coronary spasm can be explained by a hyperreactivity to vasoconstrictor stimuli that results from endothelial dysfunction or primary hyperreactivity of smooth muscle cells. Vasoconstrictor stimuli include changes in the autonomic nervous system, inflammation, and calcium availability in the myocardium.^[5]^[6] Dysfunction of the autonomic nervous system and endothelial dysfunction can lead to chronic intermittent vasospasm, which usually occurs where a fixed, non-calcified stenosis is located.

A significant group of patients with variant angina have underlying obstructive coronary artery disease.^[7]

Epidemiology and Demographics

Incidence or prevalence of Prinzmetal angina is still unknown.
Young patients with fewer cardiovascular risk factors (with the exception of smoking) are at a higher risk for coronary vasospasm, as are noncalcified lesions and eccentric plaques.
Some studies show that the Japanese population has an increased risk of developing vasospastic angina when compared with Caucasian populations.
The average age of presentation of vasospastic angina is around the fifth decade of life.^[8]

Risk Factors

Smoking^[9]
Genetic factors and insulin resistance
- There is some evidence that genetic factors and insulin resistance are associated with vasospastic angina
Patients with vasospastic angina are often younger and exhibit fewer classic cardiovascular risk factors (except smoking).
Vasospastic angina may be associated with other vasospastic disorders, such as Raynaud's phenomenon and migraine headache or its treatment [54-56].
A history of drug abuse such as cocaine may be present.
Hyperventilation can precipitate attacks of vasospastic angina [57].

Differential diagnosis

Differentiating the Life Threatening and Ischemic Causes of Chest Pain from other Disorders

The following table outlines the major differential diagnoses of chest pain:^[10]^[11]^[12]^[13]^[14]^[15]^[16]^[17]^[18]^[19]^[20]^[21]^[22]^[23]^[24]^[25]^[26]^[27]^[28]^[29]^[30]^[31]^[32]^[33]^[34]^[35]^[36]^[37]^[38]^[39]^[40]^[41]^[42]^[43]^[44]^[45]

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell); Coronary CT angiography (CCTA); multidetector row scanners (MDCT); Cardiovascular magnetic resonance — CMRI; Myocardial perfusion imaging (MPI); single-photon emission CT (SPECT); Positron emission tomography (PET) scanning; Magnetic resonance (MR) angiography, Computed tomographic (CT) angiography, and Transesophageal echocardiography (TEE), late gadolinium enhancement (LGE); right ventricular hypertrophy (RVH), right atrial enlargement (RAE), functional tricuspid regurgitation (TR), Pulmonary artery systolic pressure (PASP; adenosine deaminase (ADA); Serum amyloid A (SAA), soluble interleukin-2 receptor (sIL2R); High-resolution CT (HRCT) scanning

Differentials on the Basis of Etiology	Disease	Clinical Manifestations										Diagnosis
		Symptoms								Risk Factors	Physical Exam	Lab Findings	EKG	Imaging	Gold Standard
		Onset	Duration	Quality of Pain	Cough	Fever	Dyspnea	Weight Loss	Associated Features	Risk Factors	Physical Exam	Lab Findings	EKG	Imaging	Gold Standard
Cardiac	Vasospastic/ Prinzmetal/ Variant Angina^[46]^[47]	Gradual in onset and offset	Episodic, gradual in onset and offset	Chest discomfort described as squeezing, tightness, pressure, constriction, strangling, burning, heart burn, fullness in the chest, a band-like sensation, knot in the center of the chest, lump in the throat, ache, and heavy weight on chest	-	-	+	-	Nausea, diaphoresis, dizziness, dyspnea, and palpitations Associated with other vasospastic disorders, such as Raynaud's phenomenon and migraine headache	Multiple drugs (ephedrine-based products, cocaine, marijuana, alcohol, butane, sumatriptan, and amphetamines) Food-born botulism Guide wire or balloon dilatation while doing PCI Magnesium deficiency	Tachycardia, hypertension, diaphoresis, and a gallop rhythm	Urine drug screen may be positive for cocaine or other drugs	Transient (less than 15 minutes) ischemic ST changes in multiple leads A tall and broad R wave, Disappearance of the S wave A taller T wave Negative U waves	Stress testing: normal noninvasive stress test, exercise-induced spasm with ST-segment elevation, Stress echocardiography with ergonovine provocation: Vasospasm of coronory vessels Coronary arteriography: Epicardial spasm	Coronary arteriography
	Unstable Angina^[48]^[49]^[50]	Acute	10-20 minutes	Same as stable angina but often more severe	-	-	+	-	Nausea and vomiting Diaphoresis Presyncope Palpitations	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	Reverse splitting of the second heart sound Rales or crackles Elevated jugular venous pressure	Cardiac biomarkers [Cardiac troponin I, cardiac troponin T and MB isoenzyme of creatine kinase (CK-MB)] normal	ST-depression New T wave inversions Transient ST-elevation	Echocardiography: Ejection fraction <50 percent Exercise Stress Testing: Decreased myocardial perfusion	Invasive coronary angiography
	Myocardial Infarction^[10]^[11]^[12]^[13]	Acute	Commonly > 20 minutes	Same as stable angina but often more severe	-	-	+	-	Nausea and vomiting Diaphoresis Presyncope Palpitations Lateral displacement of the apical impulse	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	Hypotension Tachycardia S4 gallop Paradoxical splitting of S2 Mitral regurgitation murmur	Elevated cardiac enzymes ↑B-Type Natriuretic Peptide	ST elevation MI (STEMI) Non-ST elevation MI (NSTEMI) or Non Q wave	Echocardiography: ↓ EF CCTA: Coronory artery stenosis CMRI: Coronory vessels stenosis MPI on SPECT or PET scanning: Decreased myocardial perfusion.	CCTA combined with MPI
	Stable Angina^[51]	Sudden (acute)	2-10 minutes	Heaviness/pressure/ tightness/squeezing/ burning (Levine's sign) Retrosternal or left sided chest pain	-	-	+/-	-	Nausea and vomiting Diaphoresis	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	Transient third heart sound (S3 - ventricular filling sound) and fourth heart sound (S4 - atrial filling sound)	Cardiac enzymes normal	Exercise EKG: ST-segment depression	Exercise Stress Testing: Decreased myocardial perfusion Transthoracic echocardiography: Ejection fraction <50 percent	Coronary angiography
	Aortic Dissection^[52]^[53]	Sudden severe progressive pain (common) or chronic (rare)	Variable	Tearing, ripping sensation, knife like	-	-	+	-	Focal neurologic deficit Hypotension	Hypertension Genetically mediated collagen disorders Preexisting aortic aneurysm Bicuspid aortic valve Aortic coarctation Turner syndrome Vasculitis (giant cell arteritis, Takayasu arteritis, rheumatoid arthritis, syphilitic aortitis)	Pulse deficit New diastolic murmur Diastolic decrescendo murmur Focal neurologic deficit Hypotension	D-dimer <500 ng/mL rules out aortic dissection ↑Soluble ST2 (sST2) Measurements of soluble elastin fragments, smooth muscle myosin heavy chain, high-sensitivity C-reactive protein, fibrinogen, and fibrillin fragments	Nonspecific ST and T wave changes	CXR: Mediastinal and/or aortic widening CTA: A compressed true lumen MRA: Detects differential flow between the true and false lumens, widening of the aorta with a thickened wall TEE: Intimal dissection flaps, true and false lumens, thrombosis in the false lumen Aortography: Distortion of the normal contrast column, Flow reversal or stasis into a false channel, Failure of major branches to fill, and Aortic valvular regurgitation	CT angiography Digital subtraction aortography (if high suspicion)
	Pericarditis^[54]^[55]^[56]	Acute or subacute	May last for hours to days	Sharp & localized retrosternal pain	+	+	+	-	Pericardial friction rub	HIV TB Immunosuppression Acute trauma	Pericardial friction rub heard with the diaphragm of stethoscope	Leukocytosis ↑Troponin level ↑Erythrocyte sedimentation rate ↑C-reactive protein level	EKG changes (typically widespread ST segment elevation or PR depressions)	Chest x-ray typically normal Echocardiogram: normal or pericardial effusion CT scan: Noncalcified pericardial thickening with pericardial effusion CMR: inflamed pericardium and myocarditis	Pericardiocentesis Pericardial biopsy
	Stress (takotsubo) Cardiomyopathy^[57]^[58]^[59]^[60]	Acute	Commonly > 20 minutes	Substernal heaviness or tightness	-	-	+	-	Setting of physical or emotional stress or critical illness	Stress	Murmurs and rales may be present on auscultation in the setting of acute pulmonary edema	Catecholamines transiently elevated ↑TnT level ↑BNP level	ST segment elevation ST depression QT interval prolongation, T wave inversion, abnormal Q waves	Radionuclide myocardial perfusion imaging: Transient perfusion abnormalities in the left ventricular apex	Ventriculography and invasive coronary angiography
	Aortic Stenosis^[61]^[62]^[63]	Acute, recurrent episodes of angina	2-10 minutes	Heaviness/pressure/ tightness/squeezing/ burning (Levine's sign) Retrosternal	-	-	+	-	Dyspnea and decreased exercise tolerance Dizziness and syncope Angina pectoris	HTN Old age	S2 is soft, single and paradoxically split A2 delayed and tends to occur simultaneously with P2 Aortic ejection click Fourth heart sound (S4) can also be heard Crescendo–decrescendo murmur	Schistiocytes on peripheral blood smear	Non specific (the voltage of the QRS complex is increased showing the presence of left ventricular hypertrophy)	Echocardiography: aortic leaflets thickened and calcified, ↑ pulmonary artery pressure) CMR: Myocardial fibrosis, evaluation of aortic anatomy and size MDCT: Degree of aortic valve calcification PET: Measures active mineralization which correlates with stenosis severity	Echocardiography
	Heart Failure^[64]^[65]^[66]	Subacute or chronic	Variable	Dull Left sided chest pain	+	+/-	+	+	Orthopnea Peripheral edema Hemoptysis	Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes	S3 Elevated JVP Peripheral edema	Hyponatremia Hypoalbuminemia ↑ Serum brain natriuretic peptide (BNP) or NT-proBNP level A mild elevation in serum bilirubin (total bilirubin <3 mg/dL)	EKG findings are specific according to each cause of heart failure Q waves, ST and T wave abnormalities in patients with prior MI New onset arrhythmias (atrial fibrillation and ventricular tachycardia)	CXR: Cardiomegaly Echocardiography: ↓ EF Right heart catheterization: Pulmonary capillary wedge pressure >20 mmHg, right atrial pressure ≥12 mmHg) and/or decreased cardiac index (≤2.2 L/min/m2	Echocardiography
Differentials on the Basis of Etiology	Disease	Clinical Manifestations										Diagnosis
		Symptoms								Risk Factors	Physical Exam	Lab Findings	EKG	Imaging	Gold Standard
		Onset	Duration	Quality of Pain	Cough	Fever	Dyspnea	Weight Loss	Associated Features	Risk Factors	Physical Exam	Lab Findings	EKG	Imaging	Gold Standard
Pulmonary	Pulmonary Embolism^[67]^[68]	Acute	May last minutes to hours	Sharp or knifelike or pleuritic pain Localized to side of lesion	+	+/-	+	-	Hemoptysis History of venous thromboembolism or coagulation abnormalities.	Hormone replacement therapy Cancer Oral contraceptive pills Stroke Pregnancy Postpartum Prior history of VTE Thrombophilia	S3 or S4 gallop Low grade fever Tachycardia Tachypnea Hypoxia	↑D-dimer ≥500 ng/mL Arterial blood gases (Respiratory alkalosis) ↑Troponin levels Hypercoagulation workup	Tachycardia and nonspecific ST-segment and T-wave changes (70 percent) S1Q3T3 pattern New right bundle branch block Inferior Q-waves (leads II, III, and aVF)	Duplex Ultrasonography: DVT CXR: Westermark sign, Hampton hump, Palla's sign Echocardiography: RV dilation (ratio of apical 4-chamber RV diameter to left ventricle (LV) diameter > 0.9) RV systolic dysfunction Ventilation-Perfusion Scanning: High probability	CT pulmonary angiography
	Spontaneous Pneumothorax^[69]^[70]	Acute	May last minutes to hours	Sharp Localized pleuritic	-	-	+	-	Respiratory distress Tachypnea Asymmetric lung expansion Hyperresonance on percussion Decreased tactile fremitus Tachycardia Cardiac apical displacement	Smoking Positive family history Marfan syndrome Homocystinuria Thoracic endometriosis.	Decreased breath sounds on involved side Lung sounds transmitted from the unaffected hemithorax are minimal with auscultation at the midaxillary line Adventitious lung sounds (crackles, wheeze; an ipsilateral finding) Pulsus paradoxus	Respiratory alkalosis on ABGs	Rightward shift in the mean electrical axis Loss of precordial R waves Diminution of the QRS voltage Precordial T wave inversions	CXR: White visceral pleural line on the chest radiograph CT: small amounts of intrapleural gas, atypical collections of pleural gas, and loculated pneumothoraces	CT scan
	Tension Pneumothorax^[71]^[72]	Acute	May last minutes to hours	Sharp Pleuritic	-	-	+	-	Hypotension Jugular venous distention Respiratory distress	Trauma	Decreased breath sounds on involved side Lung sounds transmitted from the unaffected hemithorax are minimal with auscultation at the midaxillary line Adventitious lung sounds (crackles, wheeze; an ipsilateral finding) Pulsus paradoxus	Respiratory alkalosis on ABGs	Significant elevation of the ST-T segment from leads V1 to V4	CXR: A distinct shift of the mediastinum to the contralateral side, collapse of the ipsilateral lung, and flattening or inversion of the ipsilateral hemidiaphragm	CT scan
	Pneumonia^[73]^[74]^[75]	Acute or chronic	Variable	Dull Localized to side of lesion	+	+	+	+/-	Altered mental status Tachycardia Rust-colored sputum Green sputum Red currant-jelly sputum Central cyanosis	Long hospital stay Ill contact exposure Aspiration	Wheezing Rhonchi Rales Decreased breath sounds Pleural friction rub	Arterial blood gas : Hypoxia, hypoxemia ↑ Procalcitonin Leukocytosis Sputum evaluation Positive blood cultures	Sinus tachycardia Nonspecific ST-segment or T-wave changes	CXR: Interstitial infiltrates, lobar consolidation, cavitation	CXR
	Pleuritis	Acute or subacute or chronic	May last minutes to hours	Sharp Localized pleuritic	+	+	+	-	Sharp chest pain with breathing Itching in sites on the back Dizziness	Autoimmune conditions Infections	Tachypnea Tachycardia Pleural Rubs Decreased breath sounds	Leukocytosis Arterial blood gas (ABG): Hypoxia Thoracocentesis	EKG done to rule out other causes in differential diagnoses	Chest X Ray: Pleural fluid on one or both sides Computerized tomography (CT) scan: Pleural effusions	CXR
Gastrointestinal	GERD, Peptic Ulcer^[76]^[77]^[78]	Acute	Minutes to hours (gastroesophageal reflux) Prolonged (peptic ulcer) 5 to 60 minutes	Burning Substernal Epigastric	+/-	-	-	+/-	Visceral, substernal, worse with recumbency, no radiation, relief with food, antacids Hematemesis or melena resulting from gastrointestinal bleeding Dyspepsia	Prolonged NSAIDs intake Smoking Alcohol abuse Spicy foods H-pylori infection	Not any auscultatory findings associated with this disease Enamel erosion or other dental manifestations	↑Serum Gastrin Level Secretin Stimulation Test H-Pylori testing	EKG usually normal but may show T wave inversions in leads V2 through V4 consistent with myocardial ischemia in patients with peptic ulcer perforation	Upper Gastrointestinal Endoscopy: Biopsy Esophageal Manometry: To exclude an esophageal motility disorder Esophageal impedance pH testing: Monitors esophageal pH	Upper Gastrointestinal Endoscopy
	Diffuse Esophageal Spasm^[79]^[80]^[81]^[82]	Acute	Minutes to hours 5 to 60 minutes	Burning Pressure Visceral, spontaneous, substernal	+	-	+/-	+/-	Associated with cold liquids Relief with nitroglycerin	---	---	Barium swallow: Multiple areas of spasm throughout the length of the esophagus Impedance testing: Higher amplitudes and better transit of swallowed boluses	No ECG findings associated with DES, but ECG is done to exclude variant angina due to higher concurrent association of variant angina with DES	Esophageal manometry : ≥20 percent premature contractions (distal latency <4.5 seconds)	Esophageal manometry
	Esophagitis^[83]^[84]^[85]	Acute	Variable	Burning Epigastric	+	+	-	+/-	Heartburn Abdominal pain	HIV Immunosuppression	No auscultatory finding	Troponin or other cardiac markers Leukopenia ↓CD4 count Human immunodeficiency virus (HIV) test	ECG is done to rule out acute coronary syndrome	Double-contrast esophageal barium study (esophagography) Endoscopy: Biopsy	Endoscopy
	Eosinophilic Esophagitis^[86]^[87]^[88]^[89]^[90]^[91]	Chronic	Variable	Burning Retrosternal Abdominal	+	-	-	-	Dysphagia Food impaction GERD	Allergic diseases Asthma Rinitis Eczema	No auscultatory finding in the this disease	Elevated IgE (>114,000 units/L) Elevated peripheral eosinophils	Typically no finding on EKG	Barium studies: Strictures and a ringed esophagus Endoscopy: Stacked circular rings ("feline" esophagus) ●Strictures ●Linear furrows ●Whitish papules Esophageal biopsy: More than 15 eosinophils per high-power field	Esophageal biopsy
	Esophageal Perforation^[15]	Acute	Minutes to hours	Burning Upper abdominal	-	+/-	+	-	Eating disorders such as bulimia Repeated episodes of retching and vomiting with either recent excessive dietary or alcohol intake Subcutaneous emphysema	Instrumentation/surgery Penetrating or blunt trauma Medications, other ingestions, foreign body Violent retching/vomiting Hernia/intestinal volvulus/obstruction Inflammatory bowel disease Appendicitis Peptic ulcer disease	Mild tachycardia or hypothermia Hamman crunch (crackling sound upon chest auscultation occurs due to pneumomediastinum)	↑Serum amylase ↑C-reactive protein levels	EKG may be indicated to assess for myocardial ischemia due to acute gastrointestinal bleeding, especially if there is coexisting:Cardiovascular disease, significant anemia and advanced age	Plain chest films or chest CT: Pneumomediastinum, Free air under the diaphragm, •Pleural effusion •Pneumothorax (Macklin effect). •Subcutaneous emphysema Plain abdominal films (or abdominal CT scout film):The appearance of pneumoperitoneum -Free air under the diaphragm -Cupola sign (inverted cup) -Rigler sign (double-wall sign) -Psoas sign -Urachus sign	Confirmed by water-soluble contrast esophagram
	Mediastinitis^[92]^[93]^[94]^[95]	Acute, Chronic	Variable	Retrosternal irritation	+/-	+	+	-	Nonspecific	Infection Esophageal perforation Post operative complication	Dysphagia Dysphonia Stridor Hamman sign	Positive organisms in sternal culture Leukocytosis Positive blood cultures	Diffuse ST elevation	CT: Localize the infection and extent of spread MRI: Assesses vascular involvement and complications	CT scan
	Cholelithiasis^[96]^[97]^[98]^[99]	Acute, subacute	Minutes to hours	Burning Colicky Right upper abdomen Substernal epigastric	-	+/-	-	-	Obesity Fertile females in 40's	The presence of a common bile duct stone on transabdominal ultrasound •Clinical acute cholangitis •A serum bilirubin greater than 4 mg/dL (68 micromol/L)	Murphy sign negative Jaundice	↑ALT ↑AST ↑Amylase levels ↑ALP	Typically not indicated	Transabdominal ultrasound (TAUS): shows gallstones EUS: Detects biliary sludge MRCP: Detects stones >6mm Endoscopic Retrograde Cholangiopancreatography (ERCP): Diagnostic and therapeutic removal of stones	Endoscopic ultrasound and MECP
	Pancreatitis^[100]^[101]^[102]^[103]^[104]	Acute, Chronic	Variable	Epigastric Upper left side of the abdomen Pressure like	-	+	+	+/-	Primary cirrhosis Primary sclerosing cholangitis Cystic fibrosis Autoimmune diseases	Alcohol abuse Smoking Genetic predisposition	Tachypnea Hypoxemia Hypotension Cullen's sign Grey Turner sign	↑Amylase levels ↑Lipase levels ↑ALT ↑ALP Leukocytosis	T-wave inversion ST-segment depression ST-segment elevation rarely Q-waves	CT: focal or diffuse enlargement of the pancreas MRI: Pancreatic enlargement	CT Scan
	Sliding Hiatal Hernia^[105]^[106]^[107]	Acute	Variable	Epigastric Burning	+	-	+	-	Obstruction Cameron ulcers GERD Dysphagia	Trauma Iatrogenic Congenital malformation	Bowel sounds may be heard in the chest	Non specific	T wave inversion in anterior lead.	Barium swallow: At least three rugal folds traversing the diaphragm Upper endoscopy: A greater than 2-cm separation between the squamocolumnar junction and the diaphragmatic impression High resolution manometry: The separation of the crural diaphragm from the lower esophageal sphincter (LES) by a pressure trough	Upper endoscopy High resolution manometry (for smaller hernias)
Musculoskeletal	Costosternal syndromes (costochondritis)^[108]^[109]^[110]^[111]	Acute, subacute	Days to weeks	Pressure like on anterior part of chest wall	-	+	-	-	History of repeated minor trauma or unaccustomed activity (eg, painting, moving furniture)	Trauma	Pain by palpation of tender areas Maneuvers, such as the "crowing rooster" and horizontal arm flexion maneuver	Non specific	EKG is done to rule out other cardiovascular causes	CXR: To rule out fracture	Pain by palpation of tender areas

Natural History, Complications and Prognosis

There are no findings characteristic for vasospastic angina. However, during an episode, tachycardia, hypertension, diaphoresis, and a gallop rhythm may be present.
Bradycardia and hypotension can be observed if the sinus nodal, atrioventricular nodal, and right ventricular arteries are involved during proximal right coronary artery vasospasm.
If left untreated, 25% of patients with prinzmetal angina may progress to develop myocardial infarction and life threatening arrhythmias.^[112]^[113]
Two-thirds of patients have concurrent atherosclerosis of a major coronary artery. This is often mild or not in proportion to the degree of symptoms.
Coronary vasospasm can lead to life-threatening arrhythmias, depending on the vessel that is involved.
- Right coronary artery spasm can lead to sinus arrest or complete heart block.
- Left anterior descending artery spasm can lead to ventricular tachycardia or fibrillation.
- Multivessel spasm can also lead to ventricular arrhythmias.
Once detected, aggressive management of coronary vasospasm is necessary, as vasospasm can provoke fatal arrhythmias or myocardial infarction.^[114]
Patients who have coronary artery disease in addition to coronary vasospasm have an overall worse prognosis.^[115]
The prognosis of vasospastic angina depends on the extent of underlying coronary artery disease (CAD).

History and Symptoms

While the symptoms of chronic stable angina occur with exertion, the symptoms of Prinzmetal's angina typically occur at rest. The symptoms may occur reproducibly at certain times of the day or night. In the classic description, the symptoms often come on at night.

Characteristic pain features for vasospastic angina include:

Discomfort better describes the spasms than pain. Other common ways to describe the episodes: squeezing, tightness, pressure, constriction, strangling, burning, heart burn, fullness in the chest, a band-like sensation, knot in the center of the chest, lump in the throat, ache, and heavy weight on chest.
Each episode is typically gradual in onset and offset.
There is no change in the quality of pain with respiration or position.
The patient may have some difficulty in describing the location of the pain, although the substernal location is common. Radiation to the neck, throat, lower jaw, teeth, upper extremity, or shoulder is common.
During each episode, symptoms of nausea, sweating, dizziness, dyspnea, and palpitations may be present.

Diagnosis

Physicians should suspect vasospasm if ST segment elevation is detected in patients experiencing angina, and if the ECG completely returns to baseline upon resolution of symptoms.
- These changes are usually transient (less than 15 minutes) and may occur in multiple leads of a 12-lead ECG.
Patients who develop cardiac chest pain are generally treated empirically as an "acute coronary syndrome" patient, and are generally evaluated with serial testing of cardiac enzymes such as creatine kinase isoenzymes or troponin I or T. These may in some cases be abnormal or positive, as coronary spasm can lead to myocardial necrosis in severe cases.

The gold standard test is coronary angiography including the administration of provocative agents, such as acetylcholine or ergonovine, via the intracoronary route. The definitive diagnosis of coronary vasospasm is made angiographically by demonstration of reduction of luminal diameter in a discrete segment of the vessel, which is proven to be reversible. Reversibility may be demonstrated by previous or subsequent enlargement of luminal diameter, often after the administration of intracoronary vasodilators.

It should be noted that two-thirds of patients with Prinzmetal's angina have concurrent atherosclerosis of a major coronary artery, but the extent of the atherosclerosis is generally mild, and the symptoms are out of proportion to the extent of disease. Depending on the local protocol, provocative testing may utilize either ergonovine, methylergonovine or acetylcholine. Exaggerated spasm is diagnostic of Prinzmetal's angina. Care should be taken to have nitrates and calcium channel agents readily available to reverse the spasm.

Electrocardiogram

Prinzmetal's angina is associated with transmural injury and ST segment elevation rather than ST segment depression.

The most important ECG change during a focal proximal coronary spasm is in around 50% of cases the appearance of peaked and symmetrical T wave that is followed, if the spasm persist, by progressive ST-segment elevation that last for a few minutes, and later progressively resolve.^[116]

The most frequent ECG changes associated with ST-segment elevation are:

Increased height of the R wave
Coincident S-wave diminution
Upsloping TQ in many cases
Alternans of the elevated ST-segment
Negative T wave deepness
- In 20% of cases.

Treatment

Prinzmetal angina typically responds to nitrates and calcium channel blockers. Patients with multivessel spasm, refractory spasm, spasm that results in sudden death may benefit from dual calcium channel blocker therapy.

Calcium channel blockers:
- Generally, well tolerated and can aid with hypertension control.^[117]
- A combination of dihyropyridine and non-dihydropyridine calcium channel blockers should be used in patients with refractory coronary vasospasm, particularly if it has resulted in ventricular arrhythmia.
- Multiple calcium channel blockers may be required in patients with refractory or multi-vessel spasm.
- A patient who has suffered ventricular tachycardia or ventricular fibrillation due to spontaneous vasospasm (not due to acute infarction) should also likely undergo ICD placement.
  - Diltiazem 240-360 mg PO qd
  - Verapamil 240-480 mg PO qd
  - Nifedipine XL 60-120 mg PO qd
  - Nicardipine 40-160 mg PO qd
Long-acting nitrates:
- Generally, well tolerated and can aid with hypertension control.^[118]
  - Isosorbide mononitrate (Imdur) 60-240 mg PO qd
  - Isosorbide dinitrate (Isordil) 20-40 mg PO tid
Statins:
- May improve endothelial dysfunction and lower inflammation. A small, randomized control trial showed that fluvastatin 30 mg daily reduced rates of vasospasm. Statins also provide benefits of LDL lowering and plaque stabilization.^[119]
  - Fluvastatin 30 mg PO qd
Hormone replacement therapy:
- This remains controversial, particularly due to the risk of concern of increased cardiac events.
Smoking cessation:
- Should be emphasized in all patients, as it contains non-cardiac benefits as well. It lowers future event rates of vasospasm and acute coronary syndromes.^[120]
Percutaneous coronary intervention:
- While resolution occurs following PTCA/stenting in some cases, spasm can propagate to a new location, proximal or distal to the stented site.^[121]
- PCI is not commonly indicated for patients with focal spasm and minimal obstructive disease. However, it may be helpful if significant obstructive coronary disease is present and thought to be a potential trigger for focal spasm.
ICD placement:
- As described above for patients with ventricular tachycardia or ventricular fibrillation due to spontaneous coronary vasospasm without other provocation that may be treated.
Surgical autonomic denervation/plexectomy:
- Can be useful in cases that are refractory to medical therapy or percutaneous intervention. It's reserved only for the most refractory cases.

Making a Selection

Treatment of chronic vasospasm should be performed in this order (step-wise fashion): medical therapy, percutaneous intervention, and then, surgery.

Medical Therapy

Risk factor modification (smoking cessation, lipid control) is recommended for all patients.
Begin pharmacologic therapy with oral calcium channel blockers (diltiazem, verapamil, nifedipine) and/or nitrates. If monotherapy is ineffective, begin combination therapy which is generally well tolerated (10% of patients may require 2 calcium channel blockers). If refractory or multi-vessel spasm is present, multiple CCBs are likely necessary, as these patients are at high risk for ventricular arrhythmias. Alpha blockers may also be useful if there is incomplete response to CCB and nitrates.
Due to their ability to improve endothelial function, statins should be considered for vasospasm.
Certain medications should be avoided: nonselective beta blockers, aspirin, and sumatriptan can exacerbate vasospasm. Hormone replacement therapy (estrogen-progestin) have been associated with an increase in cardiac events (HERS-II and WHI trials) and should also be avoided.

Percutaneous Intervention (PCI)

If vasospasm has a clearly definable area that is associated with coronary artery disease and refractory to medical therapy, stenting may be an effective strategy. However, stenting may simply propagate the spasm to a proximal or distal location in the vessel.
Following any PCI, adjunctive medical therapy must be continued.
Resolution of symptoms, ECG changes, and angiographic vasospasm is usually apparent within one minute post-procedure.
Refractory spasm occurring during PCI is likely secondary to dissection, which requires stenting unless the artery is small and the patient is clinically stable.
The role of revascularization in the setting of multivessel vasospasm is uncertain.

Surgery

In the rare circumstance that a patient is refractory to pharmacologic and percutaneous therapy, surgical denervation and plexectomy have been effective.

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes (DO NOT EDIT) ^[122]

Recommendations for Prizmental's angina

Class I
"1.CCBs alone or in combination with long-acting nitrates are useful to treat and reduce the frequency of vasospastic angina.(Level of Evidence: B)"
"2.Treatment with HMG-CoA reductase inhibitor, cessation of tobacco use, and additional atherosclerosis risk factor modification and are useful in patients with vasospastic angina. (Level of Evidence: B)"
"3.Coronary angiography (invasive or noninvasive) is recommended in patients with episodic chest pain accompanied by transient ST-elevation to rule out severe obstructive CAD. (Level of Evidence: C)"

Class IIb
"1. Provocative testing during invasive coronary angiography†† may be considered in patients with suspected vasospastic angina when clinical criteria and noninvasive testing fail to establish the diagnosis (Level of Evidence: B)"

ESC Guidelines for Diagnostic Tests in Suspected Vasospastic Angina (DO NOT EDIT)^[123]

Class I
"1. ECG during angina if possible. (Level of Evidence: B)"
"2. Coronary arteriography in patients with characteristic episodic chest pain and ST-segment changes that resolve with nitrates and/or calcium channel blockers to determine the extent of underlying coronary disease. (Level of Evidence: B)"

Class IIa
"1. Intracoronary provocative testing to identify coronary spasm in patients with normal ﬁndings or nonobstructive lesions on coronary arteriography and the clinical picture of coronary spasm. (Level of Evidence: B)"
"2. Ambulatory ST Segment Monitoring to identify ST-deviation. (Level of Evidence: C)"

ESC Guidelines for Pharmacological Therapy of Vasospastic Angina (DO NOT EDIT)^[123]

Class I
"1. Treatment with calcium channel blocker and if necessary nitrates in patients whose coronary arteriogram is normal or shows only non-obstructive lesions. (Level of Evidence: B)"

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@@ Line 950: / Line 950: @@
 |Pain by palpation of tender areas
 |- style="background: #DCDCDC; padding: 5px;" |
-!Lower rib pain syndromes<ref name="pmid8344569">{{cite journal |vauthors=Scott EM, Scott BB |title=Painful rib syndrome--a review of 76 cases |journal=Gut |volume=34 |issue=7 |pages=1006–8 |date=July 1993 |pmid=8344569 |pmc=1374244 |doi= |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |Chronic
-| style="background: #F5F5F5; padding: 5px;" |Variable
-| style="background: #F5F5F5; padding: 5px;" |
-*Aching
-*Lower chest
-*Upper abdomen
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*Common in women with a mean age in the mid-40s
-| style="background: #F5F5F5; padding: 5px;" | ---
-| style="background: #F5F5F5; padding: 5px;" |
-*Hooking maneuver
-*Reproduces pain by pressing a tender spot on the costal margin
-| style="background: #F5F5F5; padding: 5px;" |
-*Non specific
-*The workup is done for excluding cardiac disorders and other causes of chest pain
-| style="background: #F5F5F5; padding: 5px;" |
-*EKG is done to rule out other cardiovascular causes
-| style="background: #F5F5F5; padding: 5px;" |
-*CXR: To rule out fracture
-| style="background: #F5F5F5; padding: 5px;" | ---
-|- style="background: #DCDCDC; padding: 5px;" |
-!Sternalis syndrome
-| style="background: #F5F5F5; padding: 5px;" |Chronic
-| style="background: #F5F5F5; padding: 5px;" |Variable
-| style="background: #F5F5F5; padding: 5px;" |Pressure like pain
-*Over the body of sternum
-*Sternalis muscle
-*Left or middle side of the chest wall
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Heart|Cardiac]] diseases
-| style="background: #F5F5F5; padding: 5px;" |
-* Daily activities
-* Emotional [[distress]]
-* [[Anxiety]]
-| style="background: #F5F5F5; padding: 5px;" |
-*Localized [[tenderness]] is found directly over the body of the sternum or overlying sternalis muscle
-| style="background: #F5F5F5; padding: 5px;" |
-*No specific diagnostic test for this disease
-*The workup is done for excluding cardiac disorders and other causes of chest pain
-| style="background: #F5F5F5; padding: 5px;" |
-*EKG is done to rule out other cardiovascular causes
-| style="background: #F5F5F5; padding: 5px;" |
-*[[X-rays|X-ray]] : To rule out fracture
-| style="background: #F5F5F5; padding: 5px;" |
-*Physical exam
-|- style="background: #DCDCDC; padding: 5px;" |
-![[Tietze's syndrome]]<ref name="pmid1697801">{{cite journal |vauthors=Aeschlimann A, Kahn MF |title=Tietze's syndrome: a critical review |journal=Clin. Exp. Rheumatol. |volume=8 |issue=4 |pages=407–12 |date=1990 |pmid=1697801 |doi= |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |Acute
-| style="background: #F5F5F5; padding: 5px;" |Weeks
-| style="background: #F5F5F5; padding: 5px;" |Pressure like pain over
-*Costosternal joint
-*[[Sternoclavicular articulation|Sternoclavicular]] joint
-*[[Costochondral joint|Costochondral]] joint
-*Second and third ribs
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*Most often involve the areas of 2nd and 3rd ribs
-*More common in young adults
-*Sternocostoclavicular hyperostosis
-*Ankylosing spondylitis
-| style="background: #F5F5F5; padding: 5px;" |
-* Upper respiratory infections
-* Excessive coughing
-| style="background: #F5F5F5; padding: 5px;" |
-*Painful and localized swelling of the costosternal, [[Sternoclavicular articulation|sternoclavicular]], or [[Costochondral joint|costochondral joints]] most often involving 2nd and 3rd [[ribs]]
-| style="background: #F5F5F5; padding: 5px;" |
-*No specific diagnostic test for this disease
-*The workup is done for excluding cardiac disorders and other causes of chest pain
-| style="background: #F5F5F5; padding: 5px;" |
-*EKG is done to rule out other cardiovascular causes
-| style="background: #F5F5F5; padding: 5px;" |
-*[[X-rays|X-ray]]: To rule out fracture
-| style="background: #F5F5F5; padding: 5px;" |
-*Tests are done to rule out other diseases
-|- style="background: #DCDCDC; padding: 5px;" |
-![[Xiphoidalgia]]<ref name="pmid13266001">{{cite journal |vauthors=LIPKIN M, FULTON LA, WOLFSON EA |title=The syndrome of the hypersensitive xiphoid |journal=N. Engl. J. Med. |volume=253 |issue=14 |pages=591–7 |date=October 1955 |pmid=13266001 |doi=10.1056/NEJM195510062531403 |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |Acute
-| style="background: #F5F5F5; padding: 5px;" |Variable
-| style="background: #F5F5F5; padding: 5px;" |Pressure like pain over
-*Over the xiphoid process
-*Sternum
-*Xiphisternal joint
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*Symptoms are aggravated by twisting and bending movements
-| style="background: #F5F5F5; padding: 5px;" |
-* Cough
-* Heavy work
-| style="background: #F5F5F5; padding: 5px;" |
-*Provocative test
-| style="background: #F5F5F5; padding: 5px;" |
-*No specific diagnostic test for this disease
-*The workup is done for excluding cardiac disorders and other causes of chest pain
-| style="background: #F5F5F5; padding: 5px;" |
-*EKG is done to rule out other cardiovascular causes
-| style="background: #F5F5F5; padding: 5px;" |
-*X-ray: To rule out fracture
-| style="background: #F5F5F5; padding: 5px;" |
-*Tests are done to rule out other diseases
-|- style="background: #DCDCDC; padding: 5px;" |
-!Spontaneous [[sternoclavicular]] [[subluxation]]<ref name="pmid1458785">{{cite journal |vauthors=van Holsbeeck M, van Melkebeke J, Dequeker J, Pennes DR |title=Radiographic findings of spontaneous subluxation of the sternoclavicular joint |journal=Clin. Rheumatol. |volume=11 |issue=3 |pages=376–81 |date=September 1992 |pmid=1458785 |doi= |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |Acute, Chronic
-| style="background: #F5F5F5; padding: 5px;" |Variable
-| style="background: #F5F5F5; padding: 5px;" |Aching pain over [[Sternoclavicular articulation|Sternoclavicular joint]]
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*More common in middle age [[women]]
-*Occurs in dominant hands with repetitive tasks of heavy or moderate quality
-| style="background: #F5F5F5; padding: 5px;" |
-* Trauma
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Palpation]] of tender areas
-| style="background: #F5F5F5; padding: 5px;" |
-*No specific diagnostic test for this disease
-*The workup is done for excluding cardiac disorders and other causes of chest pain
-| style="background: #F5F5F5; padding: 5px;" |
-*EKG is done to rule out other cardiovascular causes
-| style="background: #F5F5F5; padding: 5px;" |
-*[[X-rays|X-ray]]: Sclerosis of the medial clavicle
-| style="background: #F5F5F5; padding: 5px;" |
-*X-ray
-|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
-! rowspan="3" |Differentials on the Basis of Etiology
-! rowspan="3" |Disease
-! colspan="10" |Clinical Manifestations
-! colspan="4" |Diagnosis
-|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
-| colspan="8" |Symptoms
-| rowspan="2" |Risk Factors
-! rowspan="2" |Physical Exam
-! rowspan="2" |Lab Findings
-! rowspan="2" |EKG
-! rowspan="2" |Imaging
-! rowspan="2" |Gold Standard
-|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
-!Onset
-!Duration
-!Quality of Pain
-!Cough
-!Fever
-!Dyspnea
-!Weight loss
-!Associated Features
-|- style="background: #DCDCDC; padding: 5px;" |
-| rowspan="7" |Rheumatic
-![[Fibromyalgia]]<ref name="pmid20380956">{{cite journal |vauthors=Almansa C, Wang B, Achem SR |title=Noncardiac chest pain and fibromyalgia |journal=Med. Clin. North Am. |volume=94 |issue=2 |pages=275–89 |date=March 2010 |pmid=20380956 |doi=10.1016/j.mcna.2010.01.002 |url=}}</ref><ref name="pmid7979843">{{cite journal |vauthors=Disla E, Rhim HR, Reddy A, Karten I, Taranta A |title=Costochondritis. A prospective analysis in an emergency department setting |journal=Arch. Intern. Med. |volume=154 |issue=21 |pages=2466–9 |date=November 1994 |pmid=7979843 |doi= |url=}}</ref><ref name="pmid1543409">{{cite journal |vauthors=Wise CM, Semble EL, Dalton CB |title=Musculoskeletal chest wall syndromes in patients with noncardiac chest pain: a study of 100 patients |journal=Arch Phys Med Rehabil |volume=73 |issue=2 |pages=147–9 |date=February 1992 |pmid=1543409 |doi= |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |[[Chronic (medical)|Chronic]]
-| style="background: #F5F5F5; padding: 5px;" |Variable
-| style="background: #F5F5F5; padding: 5px;" |
-*Raynaud phenomenon (RP)
-*Deep [[Pain|ache]] and burning pain on
-**[[Shoulder|Shoulders]]
-**Back of the [[Neck]]
-**[[Chest]]
-**Lower [[Human back|Back]]
-**[[Elbow|Elbows]]
-**[[Hip (anatomy)|Hips]]
-**Shin
-**[[Knee|Knees]]
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Somatization]]
-*[[Depression]]
-*IBS
-| style="background: #F5F5F5; padding: 5px;" | ---
-| style="background: #F5F5F5; padding: 5px;" |
-*Presence of [[tenderness]] in soft-tissue anatomic locations
-| style="background: #F5F5F5; padding: 5px;" |
-*Non specific
-*Normal [[Blood, Sweat & Tea|Blood]] and [[Urine|urine test]] (mandatory to rule out other diseases)
-| style="background: #F5F5F5; padding: 5px;" |
-*P-wave dispersions (Pd)
-| style="background: #F5F5F5; padding: 5px;" | ---
-| style="background: #F5F5F5; padding: 5px;" | ---
-|- style="background: #DCDCDC; padding: 5px;" |
-![[Rheumatoid arthritis]]<ref name="pmid23335586">{{cite journal |vauthors=Rodríguez-Henríquez P, Solano C, Peña A, León-Hernández S, Hernández-Díaz C, Gutiérrez M, Pineda C |title=Sternoclavicular joint involvement in rheumatoid arthritis: clinical and ultrasound findings of a neglected joint |journal=Arthritis Care Res (Hoboken) |volume=65 |issue=7 |pages=1177–82 |date=July 2013 |pmid=23335586 |doi=10.1002/acr.21958 |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |[[Chronic (medical)|Chronic]]
-| style="background: #F5F5F5; padding: 5px;" |Years
-| style="background: #F5F5F5; padding: 5px;" |Symmetrical joint pain in
-*Wrist
-*Fingers
-*[[Knee|Knees]]
-*Feet
-*Ankles
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" |
-*Extra-articular involvement of other organ systems
-*[[Carpal tunnel syndrome]]
-*[[Tarsal tunnel syndrome]]
-| style="background: #F5F5F5; padding: 5px;" |
-* Old age
-* Smoking
-* Autoimmune conditions
-| style="background: #F5F5F5; padding: 5px;" |
-*Reduced grip strength
-*[[Rheumatoid nodules]]
-| style="background: #F5F5F5; padding: 5px;" |
-*Positive Rheumatic Factor
-*Anti-CCP body
-*Synovial fluid analysis: WBC between 1500 and 25,000/cubicmm, low glucose, low C3 and C4 complement level.
-*Thrombocytosis
-*Anemia
-*Mild leukocytosis
-| style="background: #F5F5F5; padding: 5px;" |
-*ECG is done rule out the heart failure as RA is one of the causes of heart failure
-| style="background: #F5F5F5; padding: 5px;" |
-*Plain film radiography: periarticular osteopenia, joint space narrowing, and bone erosions
-*MRI: Bone erosions
-*Ultrasonography: Degree of inflammation and the volume of inflamed tissue
-| style="background: #F5F5F5; padding: 5px;" | ---
-|- style="background: #DCDCDC; padding: 5px;" |
-![[Ankylosing spondylitis]]<ref name="pmid22798267">{{cite journal |vauthors=Ramonda R, Lorenzin M, Lo Nigro A, Vio S, Zucchetta P, Frallonardo P, Campana C, Oliviero F, Modesti V, Punzi L |title=Anterior chest wall involvement in early stages of spondyloarthritis: advanced diagnostic tools |journal=J. Rheumatol. |volume=39 |issue=9 |pages=1844–9 |date=September 2012 |pmid=22798267 |doi=10.3899/jrheum.120107 |url=}}</ref><ref name="pmid23678156">{{cite journal |vauthors=Wendling D, Prati C, Demattei C, Loeuille D, Richette P, Dougados M |title=Anterior chest wall pain in recent inflammatory back pain suggestive of spondyloarthritis. data from the DESIR cohort |journal=J. Rheumatol. |volume=40 |issue=7 |pages=1148–52 |date=July 2013 |pmid=23678156 |doi=10.3899/jrheum.121460 |url=}}</ref><ref name="pmid1488919">{{cite journal |vauthors=Jurik AG |title=Seronegative anterior chest wall syndromes. A study of the findings and course at radiography |journal=Acta Radiol Suppl |volume=381 |issue= |pages=1–42 |date=1992 |pmid=1488919 |doi= |url=}}</ref><ref name="pmid19604431">{{cite journal |vauthors=Guglielmi G, Cascavilla A, Scalzo G, Salaffi F, Grassi W |title=Imaging of sternocostoclavicular joint in spondyloarthropaties and other rheumatic conditions |journal=Clin. Exp. Rheumatol. |volume=27 |issue=3 |pages=402–8 |date=2009 |pmid=19604431 |doi= |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |[[Chronic (medical)|Chronic]]
-| style="background: #F5F5F5; padding: 5px;" |Years
-| style="background: #F5F5F5; padding: 5px;" |Intermittent pain in
-*[[Vertebral column|Spine]] joint
-*[[Sacroiliac joint|Sacroiliac]] joint
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*Patients with [[Human leukocyte antigen|HLA]]-27 variant
-*Extra-articular joint involvements
-*[[Restrictive lung disease|Restrictive pulmonary disease]]
-*Acute coronary syndromes (ACS), strokes, venous thromboembolism, conduction abnormalities
-| style="background: #F5F5F5; padding: 5px;" |
-* Genetics (Monozygotic twins)
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Tenderness]] of the SI
-*Limited spinal [[Range of motion|ROM]]
-*[[Schober's test|Schober test]]
-| style="background: #F5F5F5; padding: 5px;" |
-*↑ESR
-*↑CRP
-*↑ALP
-*↑IgA
-*[[Antigen]] HLA-27 positive
-*Negative Rheumatic Factor
-| style="background: #F5F5F5; padding: 5px;" |
-*ECG is done to rule out conductions defects and aortic insufficiency
-| style="background: #F5F5F5; padding: 5px;" |
-*Plain radiography: Erosions, ankylosis, changes in joint width, or sclerosis.
-*Magnetic resonance imaging (MRI): Osteitis" or "bone marrow edema" (BME)
-| style="background: #F5F5F5; padding: 5px;" |
-*Plain films of the sacroiliac joints
-|- style="background: #DCDCDC; padding: 5px;" |
-![[Psoriatic arthritis]]<ref name="pmid1488919">{{cite journal |vauthors=Jurik AG |title=Seronegative anterior chest wall syndromes. A study of the findings and course at radiography |journal=Acta Radiol Suppl |volume=381 |issue= |pages=1–42 |date=1992 |pmid=1488919 |doi= |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |[[Chronic (medical)|Chronic]]
-| style="background: #F5F5F5; padding: 5px;" |Years
-| style="background: #F5F5F5; padding: 5px;" |Asymmetrical intermittent pain in
-*[[Interphalangeal articulations of hand|Interphalangeal joints]]
-*Nails
-*Wrist
-*[[Knee|Knees]]
-*Ankles
-*Lower [[Human back|Back]]
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Psoriasis]]
-*[[Enthesitis]]
-*[[Tenosynovitis]]
-*[[Dactylitis]]
-| style="background: #F5F5F5; padding: 5px;" |
-* Psoriasis
-* HLA-B*27 positive
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Dactylitis]] with sausage [[digits]]
-*Onycholysis
-*Pitting edema
-*Ocular involvement
-| style="background: #F5F5F5; padding: 5px;" |Non specific
-| style="background: #F5F5F5; padding: 5px;" |
-*Longer PR interval
-| style="background: #F5F5F5; padding: 5px;" |
-*X-ray: "pencil-in-cup" deformity, erosive changes and new bone formation, lysis of the terminal phalanges; fluffy periostitis
-*MRI: Detects articular, periarticular, and soft-tissue inflammation, enthesitis
-| style="background: #F5F5F5; padding: 5px;" |
-*X-ray
-|- style="background: #DCDCDC; padding: 5px;" |
-!Sternocostoclavicular [[hyperostosis]] (SAPHO syndrome)<ref name="pmid1488919">{{cite journal |vauthors=Jurik AG |title=Seronegative anterior chest wall syndromes. A study of the findings and course at radiography |journal=Acta Radiol Suppl |volume=381 |issue= |pages=1–42 |date=1992 |pmid=1488919 |doi= |url=}}</ref><ref name="pmid8484129">{{cite journal |vauthors=Saghafi M, Henderson MJ, Buchanan WW |title=Sternocostoclavicular hyperostosis |journal=Semin. Arthritis Rheum. |volume=22 |issue=4 |pages=215–23 |date=February 1993 |pmid=8484129 |doi= |url=}}</ref><ref name="pmid19772827">{{cite journal |vauthors=Magrey M, Khan MA |title=New insights into synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome |journal=Curr Rheumatol Rep |volume=11 |issue=5 |pages=329–33 |date=October 2009 |pmid=19772827 |doi= |url=}}</ref><ref name="pmid19479702">{{cite journal |vauthors=Colina M, Govoni M, Orzincolo C, Trotta F |title=Clinical and radiologic evolution of synovitis, acne, pustulosis, hyperostosis, and osteitis syndrome: a single center study of a cohort of 71 subjects |journal=Arthritis Rheum. |volume=61 |issue=6 |pages=813–21 |date=June 2009 |pmid=19479702 |doi=10.1002/art.24540 |url=}}</ref><ref name="pmid23597971">{{cite journal |vauthors=Carneiro S, Sampaio-Barros PD |title=SAPHO syndrome |journal=Rheum. Dis. Clin. North Am. |volume=39 |issue=2 |pages=401–18 |date=May 2013 |pmid=23597971 |doi=10.1016/j.rdc.2013.02.009 |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |[[Chronic (medical)|Chronic]]
-| style="background: #F5F5F5; padding: 5px;" |Years
-| style="background: #F5F5F5; padding: 5px;" |Recurrent and multifocal pain in
-[[Sternoclavicular articulation|Sternoclavicular]] joint
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*Palmoplantar [[pustulosis]] (PPP)
-| style="background: #F5F5F5; padding: 5px;" |
-Positive family history of:
-* Spondyloarthritis
-* IBD
-* Psoriasis
-* Rheumatoid arthritis
-* Other autoimmune/autoinflammatory disease
-| style="background: #F5F5F5; padding: 5px;" |
-*Hyperostosis
-*Osteitis
-*Synovitis
-*Pustular eruptions
-*Inflammatory nodules or plaques
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Serology|Serologic]] testing to exclude other diseases
-*Non specific
-| style="background: #F5F5F5; padding: 5px;" |
-*ECG is done to rule out conductions defects and aortic insufficiency
-| style="background: #F5F5F5; padding: 5px;" |
-*Plain radiography: Hyperostotic changes (thickening of periosteum, cortex, and endosteum), sclerotic lesions, osteolysis, periosteal reaction, and osteoproliferation
-*Bone scan: "bull's head" change
-*Magnetic resonance imaging: Osteitis and soft tissue involvement
-*Fluorodeoxyglucose positron emission tomography (FDG-PET)/CT: Differentiates active versus inactive lesions
-| style="background: #F5F5F5; padding: 5px;" |
-*Bone scan
-|- style="background: #DCDCDC; padding: 5px;" |
-![[Systemic lupus erythematosus]]<ref name="pmid6749397">{{cite journal |vauthors=Turner-Stokes L, Turner-Warwick M |title=Intrathoracic manifestations of SLE |journal=Clin Rheum Dis |volume=8 |issue=1 |pages=229–42 |date=April 1982 |pmid=6749397 |doi= |url=}}</ref> <ref name="pmid5015911">{{cite journal |vauthors=Hunder GG, McDuffie FC, Hepper NG |title=Pleural fluid complement in systemic lupus erythematosus and rheumatoid arthritis |journal=Ann. Intern. Med. |volume=76 |issue=3 |pages=357–63 |date=March 1972 |pmid=5015911 |doi= |url=}}</ref><ref name="pmid17283581">{{cite journal |vauthors=Porcel JM, Ordi-Ros J, Esquerda A, Vives M, Madroñero AB, Bielsa S, Vilardell-Tarrés M, Light RW |title=Antinuclear antibody testing in pleural fluid for the diagnosis of lupus pleuritis |journal=Lupus |volume=16 |issue=1 |pages=25–7 |date=2007 |pmid=17283581 |doi=10.1177/0961203306074470 |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |[[Chronic (medical)|Chronic]]
-| style="background: #F5F5F5; padding: 5px;" |Years
-| style="background: #F5F5F5; padding: 5px;" |
-*Skin
-*[[Joint|Joints]] (fingers, wrist, knees)
-*[[Kidney|Kidneys]]
-*SLE can affect any organ of the body
-| style="background: #F5F5F5; padding: 5px;" | +/-
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Human leukocyte antigen|HLA]]-genetic mutations
-*[[Female]] gender
-*Being younger than 50
-| style="background: #F5F5F5; padding: 5px;" |
-* Autoimmune conditions
-* Genetic predisposition
-* Positive family history
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Malar rash]]
-*[[Photosensitive]] [[rash]]
-*[[Discoid lupus|Discoid rash]]
-*[[Arthritis]] of the [[Proximal interphalangeal joints|proximal interphalangeal (PIP)]] and [[Metacarpophalangeal joint|metacarpophalangeal (MCP) joints]] of the [[hands]]
-*[[Pleural friction rub|Pleuro-pericardial friction rubs]]
-*[[Systolic murmurs]]
-| style="background: #F5F5F5; padding: 5px;" |
-*Elevation of [[Autoantibody|autoantibodies]] ([[Antinuclear antibodies|ANA]], [[Anti-dsDNA antibody|anti-dsDNA]], [[Anti-SM antibody|anti-SM]], [[Antiphospholipid antibodies|antiphospholipid]])
-*[[Complement]] levels decreased
-*Anemia
-| style="background: #F5F5F5; padding: 5px;" |
-* [[Sinus tachycardia]], [[ST segment changes]], and [[Ventricular arrhythmias|ventricular conduction disturbances]]
-| style="background: #F5F5F5; padding: 5px;" |
-*Related to specific organ involvent
-| style="background: #F5F5F5; padding: 5px;" |
-*Anti-dsDNA antibody test
-|- style="background: #DCDCDC; padding: 5px;" |
-![[Relapsing polychondritis]]<ref name="pmid23597963">{{cite journal |vauthors=Chopra R, Chaudhary N, Kay J |title=Relapsing polychondritis |journal=Rheum. Dis. Clin. North Am. |volume=39 |issue=2 |pages=263–76 |date=May 2013 |pmid=23597963 |doi=10.1016/j.rdc.2013.03.002 |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |[[Chronic (medical)|Chronic]]
-| style="background: #F5F5F5; padding: 5px;" |Years
-| style="background: #F5F5F5; padding: 5px;" |Intermittent pain in:
-*[[Tissue (biology)|Tissues]] that cover the end of the [[Joint|joints]]
-*[[Cartilage]] of costal rib
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Hodgkin's lymphoma|Hodkin's lymphoma]]
-*[[Myelodysplastic syndrome|Myelodysplastic]] syndromes
-*[[Digestive disease|Gastrointestinal disorders]]
-*Type 1 [[Diabetes mellitus]]
-*[[Auricular appendage|Auricular]] [[chondritis]]
-| style="background: #F5F5F5; padding: 5px;" |
-* Autoimmune diseases
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Physical examination|Physical examinations]] findings are seen related to [[nasal]] [[chondritis]], [[ocular]] [[inflammation]], [[cardiovascular disease]], [[skin disease]], [[CNS]] and [[Pulmonary|pulmonary system]]
-| style="background: #F5F5F5; padding: 5px;" |
-*Negative [[Rheumatoid factor|rheumatoid]] factor
-*Anti-type II collagen antibodies
-*Antineutrophil cytoplasmic antibodies
-| style="background: #F5F5F5; padding: 5px;" |
-* ECG is done to rule out the cardiovascular complications of this disease
-| style="background: #F5F5F5; padding: 5px;" |
-*Non specific
-*Related to specific organ involvent
-| style="background: #F5F5F5; padding: 5px;" |
-*No gold standard test for this disease
-|- style="background: #DCDCDC; padding: 5px;" |
-|Psychiatric
-![[Panic attack]]/ Disorder<ref name="pmid10906353">{{cite journal |vauthors=Fleet RP, Martel JP, Lavoie KL, Dupuis G, Beitman BD |title=Non-fearful panic disorder: a variant of panic in medical patients? |journal=Psychosomatics |volume=41 |issue=4 |pages=311–20 |date=2000 |pmid=10906353 |doi=10.1176/appi.psy.41.4.311 |url=}}</ref><ref name="pmid7954018">{{cite journal |vauthors=Fleet RP, Dupuis G, Marchand A, Burelle D, Beitman BD |title=Panic disorder, chest pain and coronary artery disease: literature review |journal=Can J Cardiol |volume=10 |issue=8 |pages=827–34 |date=October 1994 |pmid=7954018 |doi= |url=}}</ref><ref name="pmid8068393">{{cite journal |vauthors=Simpson RJ, Kazmierczak T, Power KG, Sharp DM |title=Controlled comparison of the characteristics of patients with panic disorder |journal=Br J Gen Pract |volume=44 |issue=385 |pages=352–6 |date=August 1994 |pmid=8068393 |pmc=1238951 |doi= |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |Acute or subacute or chronic
-| style="background: #F5F5F5; padding: 5px;" |Variable
-| style="background: #F5F5F5; padding: 5px;" |Variable
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*History of [[Depression]]
-*[[Panic attack|Panic attacks]]
-*[[Agoraphobia]]
-| style="background: #F5F5F5; padding: 5px;" |
-*Psychiatric disorders
-| style="background: #F5F5F5; padding: 5px;" |
-*Anxious
-*Tachypneic
-| style="background: #F5F5F5; padding: 5px;" |
-*Thyroid function tests
-*Complete blood count
-*Chemistry panel
-| style="background: #F5F5F5; padding: 5px;" |
-*Sinus Tachycardia
-| style="background: #F5F5F5; padding: 5px;" |
-*No any specific radiographic test is done
-| style="background: #F5F5F5; padding: 5px;" | ---
-|- style="background: #DCDCDC; padding: 5px;" |
-| rowspan="2" |
-Others
-!Substance abuse
-([[Cocaine abuse|Cocaine]])<ref name="pmid26039070">{{cite journal |vauthors=Grant BF, Goldstein RB, Saha TD, Chou SP, Jung J, Zhang H, Pickering RP, Ruan WJ, Smith SM, Huang B, Hasin DS |title=Epidemiology of DSM-5 Alcohol Use Disorder: Results From the National Epidemiologic Survey on Alcohol and Related Conditions III |journal=JAMA Psychiatry |volume=72 |issue=8 |pages=757–66 |date=August 2015 |pmid=26039070 |pmc=5240584 |doi=10.1001/jamapsychiatry.2015.0584 |url=}}</ref><ref name="pmid17592911">{{cite journal |vauthors=Cosci F, Schruers KR, Abrams K, Griez EJ |title=Alcohol use disorders and panic disorder: a review of the evidence of a direct relationship |journal=J Clin Psychiatry |volume=68 |issue=6 |pages=874–80 |date=June 2007 |pmid=17592911 |doi= |url=}}</ref><ref name="pmid2183544">{{cite journal |vauthors=George DT, Nutt DJ, Dwyer BA, Linnoila M |title=Alcoholism and panic disorder: is the comorbidity more than coincidence? |journal=Acta Psychiatr Scand |volume=81 |issue=2 |pages=97–107 |date=February 1990 |pmid=2183544 |doi= |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |Acute (hours)
-| style="background: #F5F5F5; padding: 5px;" |Minutes to hours
-| style="background: #F5F5F5; padding: 5px;" |Pressure like pain in the center of chest
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Anxiety]]
-*[[Dyspnea]]
-*[[Nausea and vomiting|Nausea]]
-*[[Palpitation|Palpitations]]
-| style="background: #F5F5F5; padding: 5px;" |
-*Psychiatric disorders
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Signs]] of [[injection]] [[drug use]]
-*[[Signs]] of [[drug]] [[inhalation]]
-*Poor [[personal hygiene]]
-| style="background: #F5F5F5; padding: 5px;" |
-*Serum [[Cardiac biomarkers|biomarkers]] ([[Troponin I]], [[Troponin T]])
-*Toxicologic tests or drug screens of bodily fluids (blood, urine, saliva) and hairs
-| style="background: #F5F5F5; padding: 5px;" |
-**QT prolongation
-**Sinus Tachycardia
-**Arrhythmias
-**Cardiac conduction abnormalities
-| style="background: #F5F5F5; padding: 5px;" | ---
-| style="background: #F5F5F5; padding: 5px;" |
-*Gold standard test depends on the type of substance is abuse
-|- style="background: #DCDCDC; padding: 5px;" |
-![[Herpes Zoster]]<ref name="pmid17143845">{{cite journal |vauthors=Dworkin RH, Johnson RW, Breuer J, Gnann JW, Levin MJ, Backonja M, Betts RF, Gershon AA, Haanpaa ML, McKendrick MW, Nurmikko TJ, Oaklander AL, Oxman MN, Pavan-Langston D, Petersen KL, Rowbotham MC, Schmader KE, Stacey BR, Tyring SK, van Wijck AJ, Wallace MS, Wassilew SW, Whitley RJ |title=Recommendations for the management of herpes zoster |journal=Clin. Infect. Dis. |volume=44 Suppl 1 |issue= |pages=S1–26 |date=January 2007 |pmid=17143845 |doi=10.1086/510206 |url=}}</ref><ref name="pmid8545018">{{cite journal |vauthors=Oxman MN |title=Immunization to reduce the frequency and severity of herpes zoster and its complications |journal=Neurology |volume=45 |issue=12 Suppl 8 |pages=S41–6 |date=December 1995 |pmid=8545018 |doi= |url=}}</ref><ref name="pmid15897984">{{cite journal |vauthors=Jumaan AO, Yu O, Jackson LA, Bohlke K, Galil K, Seward JF |title=Incidence of herpes zoster, before and after varicella-vaccination-associated decreases in the incidence of varicella, 1992-2002 |journal=J. Infect. Dis. |volume=191 |issue=12 |pages=2002–7 |date=June 2005 |pmid=15897984 |doi=10.1086/430325 |url=}}</ref>
-| style="background: #F5F5F5; padding: 5px;" |Acute or Chronic
-| style="background: #F5F5F5; padding: 5px;" |Variable
-| style="background: #F5F5F5; padding: 5px;" |Burning pain on
-*Chest
-*Upper back
-*Lower back
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | +
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" | -
-| style="background: #F5F5F5; padding: 5px;" |
-*People who had [[chickenpox]]
-| style="background: #F5F5F5; padding: 5px;" |
-* Immunosuppression
-| style="background: #F5F5F5; padding: 5px;" |
-*[[Painful]] grouped herpetiform [[vesicles]] on an [[Erythematous|erythematous base]] distributed in a single [[dermatome]]
-| style="background: #F5F5F5; padding: 5px;" |
-*Viral culture
-*Direct immunofluorescence testing,
-*Polymerase chain reaction assay (PCR)
-| style="background: #F5F5F5; padding: 5px;" |
-*ECG is done to rule out other cardiovascular causes of chest pain
-| style="background: #F5F5F5; padding: 5px;" |
-*Magnetic resonance imaging (MRI): To rule out encephalitis
-| style="background: #F5F5F5; padding: 5px;" |
-*Viral tissue culture
 |}