Prinzmetal's angina

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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

Iatrogenic

Pathophysiology

  • The exact pathogenesis of coronary vasospasm is not well understood, but some causes and contributing factors are known.
  • 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
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
 - - + -
  • 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
  • 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
Unstable Angina[48][49][50] Acute 10-20 minutes
  • Same as stable angina but often more severe
 - - + -
Myocardial Infarction[10][11][12][13] Acute Commonly > 20 minutes - - + -
  • ST elevation MI (STEMI)
  • Non-ST elevation MI (NSTEMI) or Non Q wave
  • CCTA combined with MPI
Stable Angina[51] Sudden (acute) 2-10 minutes - - +/- -
  • Exercise EKG: ST-segment depression
Aortic Dissection[52][53] Sudden severe progressive pain (common) or chronic (rare) Variable
  • Tearing, ripping sensation, knife like
 - - + -
  • Nonspecific ST and T wave changes
Pericarditis[54][55][56] Acute or subacute May last for hours to days + + + -
Stress (takotsubo)

Cardiomyopathy[57][58][59][60]

Acute Commonly > 20 minutes - - + -
  • Setting of physical or emotional stress or critical illness
 Stress
Aortic Stenosis[61][62][63] Acute, recurrent episodes of angina 2-10 minutes - - + -
Heart Failure[64][65][66] Subacute or chronic Variable
  • Dull
  • Left sided chest pain
 + +/- + + Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes
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
Pulmonary Pulmonary Embolism[67][68] Acute May last minutes to hours + +/- + -  Hormone replacement therapy

Cancer Oral contraceptive pills Stroke  Pregnancy Postpartum  Prior history of VTE Thrombophilia 

Spontaneous Pneumothorax[69][70] Acute May last minutes to hours - - + -
  • 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 - - + -
  • Trauma
  • Significant elevation of the ST-T segment from leads V1 to V4
Pneumonia[73][74][75] Acute or chronic Variable
  • Dull
  • Localized to side of lesion
 + + + +/-
  • Long hospital stay
  • Ill contact exposure
  • Aspiration
Pleuritis Acute or subacute or chronic May last minutes to hours + + + -
  • EKG done to rule out other causes in differential diagnoses
Gastrointestinal GERD, Peptic Ulcer[76][77][78] Acute +/- - - +/-
  • Not any auscultatory findings associated with this disease
  • Enamel erosion or other dental manifestations
Diffuse Esophageal Spasm[79][80][81][82] Acute
  • Minutes to hours
  • 5 to 60 minutes
 + - +/- +/- --- ---
  • 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)
Esophagitis[83][84][85] Acute Variable + + - +/-
  • No auscultatory finding
Eosinophilic Esophagitis[86][87][88][89][90][91] Chronic Variable + - - -
  • No auscultatory finding in the this disease
  • Typically no finding on EKG
Esophageal Perforation[15] Acute Minutes to hours
  • Burning
  • Upper abdominal
 - +/- + -
    • Confirmed by water-soluble contrast esophagram
Mediastinitis[92][93][94][95] Acute, Chronic Variable
  • Retrosternal irritation
 +/- + + -
  • Nonspecific
  • Infection
  • Esophageal perforation
  • Post operative complication
  • 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 - +/- - -
  • 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 - + + +/-
  • Alcohol abuse
  • Smoking
  • Genetic predisposition
  •  Tachypnea
  • Hypoxemia
  • Hypotension
  • Cullen's sign
  • Grey Turner sign 
  • 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 + - + -
  • 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.
  • 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:
  • 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:
  • 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)"

References

  1. ↑ Prinzmetal M, Kennamer R, Merliss R. of angina pectoris. Am J Med 1959;27:375-88. PMID 14434946.
  2. ↑ Oliva PB, Potts DE, Pluss RG (1973). "Coronary arterial spasm in Prinzmetal angina. Documentation by coronary arteriography". N Engl J Med. 288 (15): 745–51. doi:10.1056/NEJM197304122881501. PMID 4688712.
  3. ↑ Ahooja V, Thatai D (2007). "Multivessel coronary vasospasm mimicking triple-vessel obstructive coronary artery disease". J Invasive Cardiol. 19 (7): E178–81. PMID 17620681. Unknown parameter |month= ignored (help)
  4. ↑ Miwa K, Ishii K, Makita T, Okuda N (2004). "Diagnosis of multivessel coronary vasospasm by detecting postischemic regional left ventricular delayed relaxation on echocardiography using color kinesis". Circ. J. 68 (5): 483–7. PMID 15118293. Unknown parameter |month= ignored (help)
  5. ↑ Lanza GA, Careri G, Crea F (2011). "Mechanisms of coronary artery spasm". Circulation. 124 (16): 1774–82. doi:10.1161/CIRCULATIONAHA.111.037283. PMID 22007100.
  6. ↑ Mahemuti A, Abudureheman K, Schiele F, Ecarnot F, Abudureyimu S, Tang B; et al. (2014). "Association between inflammatory markers, hemostatic markers, and traditional risk factors on coronary artery spasm in patients with normal coronary angiography". J Interv Cardiol. 27 (1): 29–35. doi:10.1111/joic.12086. PMID 24345233.
  7. ↑ Maseri A, Severi S, Nes MD, L'Abbate A, Chierchia S, Marzilli M et al. (1978) "Variant" angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia. Pathogenetic mechanisms, estimated incidence and clinical and coronary arteriographic findings in 138 patients. Am J Cardiol 42 (6):1019-35. PMID: 727129
  8. ↑ Kim HL, Lee SH, Kim J, Kim HJ, Lim WH, Seo JB; et al. (2016). "Incidence and Risk Factors Associated With Hospitalization for Variant Angina in Korea". Medicine (Baltimore). 95 (13): e3237. doi:10.1097/MD.0000000000003237. PMC 4998556. PMID 27043695.
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  12. ↑ 12.0 12.1 Bösner S, Becker A, Haasenritter J, Abu Hani M, Keller H, Sönnichsen AC, Karatolios K, Schaefer JR, Seitz G, Baum E, Donner-Banzhoff N (2009). "Chest pain in primary care: epidemiology and pre-work-up probabilities". Eur J Gen Pract. 15 (3): 141–6. doi:10.3109/13814780903329528. PMID 19883149.
  13. ↑ 13.0 13.1 Ebell MH (March 2011). "Evaluation of chest pain in primary care patients". Am Fam Physician. 83 (5): 603–5. PMID 21391528.
  14. ↑ von Kodolitsch Y, Schwartz AG, Nienaber CA (October 2000). "Clinical prediction of acute aortic dissection". Arch. Intern. Med. 160 (19): 2977–82. PMID 11041906.
  15. ↑ 15.0 15.1 Pate JW, Walker WA, Cole FH, Owen EW, Johnson WH (May 1989). "Spontaneous rupture of the esophagus: a 30-year experience". Ann. Thorac. Surg. 47 (5): 689–92. PMID 2730190.
  16. ↑ Fleet RP, Dupuis G, Marchand A, Burelle D, Beitman BD (October 1994). "Panic disorder, chest pain and coronary artery disease: literature review". Can J Cardiol. 10 (8): 827–34. PMID 7954018.
  17. ↑ Bass C, Chambers JB, Kiff P, Cooper D, Gardner WN (December 1988). "Panic anxiety and hyperventilation in patients with chest pain: a controlled study". Q. J. Med. 69 (260): 949–59. PMID 3270082.
  18. ↑ Evans DW, Lum LC (January 1977). "Hyperventilation: An important cause of pseudoangina". Lancet. 1 (8004): 155–7. PMID 64694.
  19. ↑ Ros E, Armengol X, Grande L, Toledo-Pimentel V, Lacima G, Sanz G (July 1997). "Chest pain at rest in patients with coronary artery disease. Myocardial ischemia, esophageal dysfunction, or panic disorder?". Dig. Dis. Sci. 42 (7): 1344–53. PMID 9246027.
  20. ↑ Ben Freedman S, Tennant CC (April 1998). "Panic disorder and coronary artery spasm". Med. J. Aust. 168 (8): 376–7. PMID 9594945.
  21. ↑ Smoller JW, Pollack MH, Wassertheil-Smoller S, Jackson RD, Oberman A, Wong ND, Sheps D (October 2007). "Panic attacks and risk of incident cardiovascular events among postmenopausal women in the Women's Health Initiative Observational Study". Arch. Gen. Psychiatry. 64 (10): 1153–60. doi:10.1001/archpsyc.64.10.1153. PMID 17909127.
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