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Constrictive Pericarditis Workup

  • Author: John L Parks, MD; Chief Editor: Richard A Lange, MD, MBA  more...
 
Updated: Dec 23, 2014
 

Approach Considerations

No laboratory data are diagnostic of constrictive pericarditis. However, as a result of the nearly universal findings of a chronically elevated right-sided atrial pressure and passive congestion of the liver, kidneys, and gastrointestinal (GI) tract, resultant abnormalities may be present (see Laboratory Studies below). Examples include elevations in both conjugated and unconjugated bilirubin levels, elevated levels of hepatocellular transaminases, and elevated serum creatinine.

A number of ancillary tests usually must be used to aide in diagnosis. These include chest radiography, computed tomography (CT), magnetic resonance imaging (MRI), echocardiography, and invasive hemodynamic measurements. Given the invasive nature of certain diagnostic procedures, inpatient care is often warranted in the workup. As mentioned, one of the most common issues arising from diagnostic testing is distinguishing restrictive cardiomyopathy from constriction.

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Laboratory Studies

A complete blood count (CBC) may reveal evidence of dilutional anemia when congestive heart failure (CHF) is also present. Leukocytosis may be evident if an infectious, bacteriologic, or rheumatologic source is the etiology or if patients are receiving treatment with steroid therapy. Leukopenia may be present in patients in whom chemotherapeutic agents are administered for malignancy.

Dilution secondary to CHF may demonstrate hyponatremia or pseudohyponatremia. Contraction alkalosis (ie, hypochloremia with hypercarbia) may occur when diuretics are aggressively used. With renal insufficiency, short-term elevation of blood urea nitrogen (BUN) levels and long-term elevation of serum creatinine levels are observed.

On arterial blood gas measurement, metabolic acidosis (ie, low pH and low bicarbonate), with or without compensatory respiratory alkalosis (ie, decreased partial pressure of carbon dioxide), is frequently observed with right-sided CHF.

Passive hepatic congestion from cor pulmonale may cause elevated transaminase levels. Hypoalbuminemia is the hallmark of a protein-losing enteropathy (PLE) that results from increased central venous pressure in the portal system of patients with hepatomegaly and ascites (as well as of proteinuria that may approach the nephrotic range). When PLE is suspected, stool α1 -antitrypsinase levels should be measured.

If active or chronic inflammation is present, nonspecific markers, such as an elevated sedimentation rate (ESR) or a normocytic normochromic anemia, may be present. In postpericardiotomy syndrome, both the ESR and the C-reactive protein (CRP) level may be elevated.

The level of brain natriuretic peptide (BNP), a cardiac hormone released in response to increased ventricular wall stretch, is often mildly increased in constrictive pericarditis (usually below 150 ng/L). BNP levels are generally higher in restrictive cardiomyopathy (diagnostic if exceeding 650 ng/L) and may be useful in differentiating these disorders.[11, 12]

If an associated collagen vascular disorder is suggested, antinuclear antibody (ANA) or rheumatoid factor (RF) levels should be measured.

Results from a purified protein derivative (PPD) skin test should be positive in cases of tuberculous pericarditis (unless the patient is anergic).

Cytologic examination of the pericardial fluid, if present, helps diagnose a malignant cause (if such a cause is not otherwise apparent).

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Chest Radiography

Radiographic findings are commonly unremarkable. However, certain classic findings, though not sensitive for the presence of constrictive pericarditis, are suggestive of the diagnosis when present within a compatible clinical context. For example, severe pericardial calcification is found in 20-30% of patients (see the image below); however, it is not specific and does not prove pericardial constriction.[13]

Constrictive pericarditis. Anteroposterior and lat Constrictive pericarditis. Anteroposterior and lateral chest radiograph from a patient with tuberculous constrictive pericarditis (arrows denote marked pericardial calcification).

If no significant pericardial effusion is present, the cardiac silhouette may appear normal. The superior vena cava, the azygos vein, or both may be dilated. Pleural effusions are common and are usually bilateral. Pulmonary edema is rare and might suggest other cardiac or lung disease

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Echocardiography

Echocardiography has been used for many years to help diagnose constrictive pericarditis and, in particular, to differentiate it from restrictive and other cardiomyopathies. Unfortunately, no echocardiographic finding is pathognomonic for constriction. However, when all the echocardiographic data are taken together within a clinical context, the likelihood of constriction can usually be accurately assessed.

As a general principle, pericardial imaging by echocardiography is not sensitive and is not considered a reliable technique to visualize the pericardium. Admittedly, the pericardium can be echodense, but this is not always the case. CT scanning and MRI are considered the procedures of choice for imaging the pericardium.

Transesophageal echocardiography (TEE) is more reliable than transthoracic echocardiography (TTE) for helping to detect a thickened pericardium, especially if the pericardium is thick or very echogenic, but it is not nearly as accurate as CT or MRI.

A study by Welch et al indicated that echocardiography can be used to differentiate constrictive pericarditis from restrictive myocardial disease and severe tricuspid regurgitation. The study compared echocardiograms in 130 patients with constrictive pericarditis with those of 36 patients with either of the other two conditions. The investigators determined that if ventricular septal shift was present with either a medial mitral annular e’ velocity of 9 cm/sec or greater or a hepatic vein expiratory diastolic reversal ratio of 0.79 or greater, constrictive pericarditis could be diagnosed with a sensitivity of 87% and a specificity of 91%. If all three factors coexisted, the diagnosis could be made with a specificity of 97%, but with a sensitivity of only 64%.[14]

Two-dimensional echocardiography

On two-dimensional echocardiography, systemic veins may be dilated. The echocardiogram may reveal diminished intraventricular volumes. Pericardial effusions are easily detected with this modality.

Interventricular septal motion may be paradoxic or the septum may have a flattened appearance as a sign of ventricular interdependence. The inspiratory increase in chamber size is larger in patients with constrictive pericarditis than in those with restrictive cardiomyopathy.

The posterior motion of the interventricular septum relative to the less compliant ventricular walls (which are encased by the pericardium) correlates with the auscultatory pericardial knock (which can be seen on M-mode and two-dimensional echocardiography as an early diastolic septal notch or “septal bounce”).[15] This septal bounce is considered a finding consistent with constrictive physiology, with sensitivity of 62% and specificity of 93%.[16]

Two-dimensional echocardiography can show evidence of right-sided pressure overload, such as atrial septal shifting to the left with inspiration. There also may be dilation of the inferior and superior venae cavae and hepatic veins, with diminished collapse with inspiration. These are nonspecific signs that can also occur in right-sided heart failure as a result of other causes.

Doppler echocardiography

Doppler echocardiography provides important hemodynamic information. A number of Doppler findings are sensitive for pericardial constriction when present, but as with many echocardiographic signs, their absence does not exclude constrictive hemodynamics.[17, 18]

Early rapid diastolic filling can be determined by interrogating forward flow at the mitral and tricuspid valve levels. The resulting waves are termed the E (for early filling) and A (for atrial filling) waves.

The transtricuspid velocities show an opposite pattern to the transmitral velocities. Across the tricuspid valve, velocities increase with inspiration and decrease with expiration, whereas across the mitral valve, velocities decrease with inspiration and increase with expiration. The shortened deceleration time from these peak velocities is felt to correspond to the dip-and-plateau hemodynamics seen with limited early diastolic flow.

The pulmonary vein Doppler inflow pattern also has respiratory variation; its diastolic inflow is greater than its systolic inflow, and this inequality may even reverse. During constriction, the pulmonary venous flow pattern demonstrates systolic and diastolic forward flow, with a marked decrease in diastolic flow on inspiration and an increase on expiration. This measurement may help determine if a pseudonormalized diastolic pattern is present on the mitral inflow tracing.

Pulsed-wave Doppler of the hepatic venous flow mimics right-sided atrial pressure curves. In constriction, there is often marked diastolic flow reversal that increases with expiration when compared with inspiration. However, in severe constriction or a mixed constrictive-restrictive picture, there may be hepatic diastolic flow reversal in inspiration as well as expiration. This contrasts to restrictive cardiomyopathy, in which hepatic flow reversal is more prominent in inspiration.[16]

Doppler ventricular inflow patterns can help distinguish constrictive from restrictive cardiac physiology, though the distinction may be technically challenging to make.

From a Doppler perspective, constriction limits ventricular filling and enhances ventricular interaction; conversely, restriction generally limits ventricular distensibility. Respiratory variation is usually greater in constriction than in restriction (probably because of the normal intraventricular septum), with changes usually exceeding 25%. With restriction, the E/A ratio frequently is greater than 2, the deceleration time is less than 150 ms, and the relaxation time is less than 60 ms. Unfortunately, when such Doppler findings are not present, the diagnostic reliability decreases. If a concomitant pericardial effusion is present, it may account for some respiratory variation.[13]

Tissue Doppler echocardiography (TDE) measures the actual endocardial and epicardial tissue velocities. Because myocardial relaxation itself is preserved in pure constrictive pericarditis, the early relaxation myocardial velocity (Ea, also known as Em) is normal, whereas it is abnormal with restriction (when intrinsic myocardial disease is present). For example, given that a normal Ea is higher than 10 cm/s, a near-normal (approximately 8 cm/s) Ea supports constriction, whereas a much lower Ea supports restriction.[19]

The newer method of speckle tracking of B-mode images measures cardiac longitudinal and circumferential deformation. Patients with constrictive pericarditis were found to have decreased circumferential deformation (however, this may also be decreased in restrictive cardiomyopathy). Longitudinal strain and longitudinal early diastolic velocity remain preserved in constriction but are decreased in restriction.[16, 20]

Doppler interrogation can be limited if patients cannot adequately vary their respiration or if concomitant myocardial disease, atrial fibrillation, or severe lung disease (eg, chronic obstructive pulmonary disease [COPD], which can lead to false-positive findings) is present. Because Doppler transmitral inflow respiratory variation can occur in COPD, other differences must then be examined. For example, the marked increase in inspiratory superior vena cava systolic flow seen in COPD is not seen in constriction.[21]

Measurements of diastolic function are load-dependent (ie, dependent on preload and afterload). If atrial and ventricular filling pressures are low, Doppler interrogation findings may be falsely negative. Likewise, if atrial and ventricular filling pressures are high, respiratory variation may be masked. In such cases, preload may be reduced with either medication or dynamic maneuvers, such as tilting the patient’s head up or having the patient sit. These maneuvers may unmask respiratory variation.

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Computed Tomography

Conventional CT scanners may not help adequately visualize the parietal pericardium. However, the parietal pericardium can be visualized well using high-resolution CT. The pericardial thickness, the degree of calcification, and the distribution of these findings are easily measured.

The normal pericardium is 1-2 mm thick. A pericardial thickness of 3-4 mm or more is considered abnormal. Pericardial thickening that exceeds 4 mm assists in differentiating constrictive disease from restrictive cardiomyopathy, and thickening that exceeds 6 mm adds even more specificity for constriction.

CT is perhaps the best modality at identifying pericardial calcification. While neither completely sensitive nor specific, pericardial calcification is often associated with constriction.

Supportive findings suggesting impaired right ventricular filling include dilation of the vena cava, hepatic vein, and right atrium as well as ascites or hepatosplenomegaly. Cine imaging (from a retrospective gated study) may demonstrate the early diastolic interventricular septal bounce or inflammatory pericardial tethering.

False-negative results may occur if a long-standing thin pericardial scar without appreciable thickening is present. That is, normal pericardial thickness does not exclude pericardial constriction, and the clinical situation must always be taken in account. Therefore, if the hemodynamics and presentation are otherwise compatible, the diagnosis of constrictive pericarditis must still be entertained even when pericardial imaging yields unremarkable results.

In those patients who have an established diagnosis of constriction, CT scanning may provide helpful information for preoperative planning. This is particularly true in individuals with previous cardiothoracic surgery, helping to identify anatomic relationships, adhesions, and bypass graft locations. Coronary calcium as well as potential coronary stenoses may be identified. Pericardial calcification location and severity may lead the surgeon towards a particular approach or help identify regions of the pericardium needing particular attention at the time of resection.

CT scanning may also be used to identify associated radiation lung injury in radiation-induced constriction.

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Magnetic Resonance Imaging

The development of real-time, high-resolution MRI and the ability to acquire images in 50 ms or less makes MRI a sensitive method for imaging the pericardium.[22, 23]

Like CT scanning, MRI can be used to measure the pericardium for thickness (see the image below), calcification, and other anatomic abnormalities. Features notable on MRI and associated with constriction include an elongated, narrow right ventricle (“tubing of the ventricle”), atrial dilation, and a characteristic intraventricular septal “bounce” in early diastole. This septal bounce is associated with ventricular interdependence. The septum may have a sigmoid appearance. Gated MRI has an advantage in determining whether pericardial fluid is hemorrhagic. CT scanning may be preferable when pericardial calcification is particularly prominent.[24]

MRI shows constrictive pericarditis in 13-year-old MRI shows constrictive pericarditis in 13-year-old patient with otherwise structurally normal heart. Infectious workup was negative. (Image courtesy of Tal Geva, MD.)

A thickened pericardium does not prove that constrictive pericarditis is present; it must be clinically correlated. Likewise, the absence of pericardial thickening does not rule out hemodynamically significant restrictive pericarditis; constriction can occur in a scarred fibrous pericardium of normal thickness.

MRI with gadolinium administration may identify those patients with constrictive pericarditis with a reversible component. A small study examining myocardial inflammation using MRI with gadolinium noted association of greater pericardial thickness and increased degree of qualitative late gadolinium enhancement as being associated with reversible constrictive pericarditis. It was thought that increased pericardial thickness and increased gadolinium enhancement correlated with increased inflammation that would respond to traditional anti-inflammatory therapy (nonsteroidal anti-inflammatory drugs [NSAIDs] and corticosteroids).[25, 26]

A study by Amaki et al indicated that when it comes to differentiating constrictive pericarditis from restrictive cardiomyopathy, comparable diagnostic information can be derived from left ventricular mechanics using either cine MRI – based or two-dimensional echocardiography – based tissue tracking.[27]

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Electrocardiography

No electrocardiographic signs are diagnostic for constriction. The electrocardiogram in constriction most often shows nonspecific ST-T segment abnormalities. The diagnostician might be tempted to look for findings similar to those in pericarditis. However, chronic pericarditis (sometimes associated with constriction) is not associated with the classic electrocardiographic (ECG) findings seen with acute pericarditis.

Findings of acute pericarditis generally include diffuse concave ST-segment elevation that must be distinguished from other causes of ST elevation with PR depression. In most instances of acute pericarditis, the magnitude of the ST elevation is greater than one fourth of the T-wave height in the lateral V leads. If a history of these findings exists, the later development of constrictive pericarditis should be considered. The above findings are contrasted with the patient with restrictive cardiomyopathy who may have diffuse low-voltage tracings, bundle-branch block, or AV conduction abnormalities.

Over time, even if chronic pericarditis develops, no specific ECG patterns develop. Inverted T waves may persist, or all ECG findings may resolve to normal. In long-standing cases, atrial fibrillation may occur, but this is certainly nonspecific.

If a pericardial effusion develops, a low QRS voltage may be present in the limb and chest leads. This must be distinguished from other causes of low voltage, such as long-standing myocardial infarction (MI), pleural effusion, postoperative state, or various cardiomyopathies.

When electrical alternans (a beat-to-beat cyclic shift in the QRS axis that may also involve the P and T waves) is present, cardiac tamponade must be considered.

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Right-Sided Heart Catheterization

Despite data from the history, physical findings, laboratory results, and noninvasive testing, an accurate diagnosis of constrictive pericarditis may be difficult to make. When this diagnosis is not absolute, despite all of the available information, invasive procedures, such as right heart catheterization, can help make or exclude the diagnosis.

The traditional hemodynamic criteria for constrictive pericarditis are as follows:

  • Elevated left and right ventricular diastolic pressures equalized within 5 mm Hg (See the image below)
  • Right ventricular systolic pressure less than 55 mm Hg
  • Mean right arterial pressure greater than 15 mm Hg
  • Right ventricular end-diastolic pressure greater than one third of the right ventricular systolic pressure (narrow pulse pressure)

In the absence of these criteria, a diagnosis of restrictive pericarditis is favored.[28]

Simultaneous right and left ventricular pressure t Simultaneous right and left ventricular pressure tracings showing diastolic equalization of pressures in both ventricles in a patient with constrictive pericarditis.

In addition, one would expect to see an exaggerated x descent with a steep y descent on right arterial pressure waveforms (W sign), as well as the square root sign (dip-and-plateau) on right or left ventricular tracings, which distinguishes this diagnosis from cardiac tamponade (see the image below). Another hemodynamic parameter is the Kussmaul sign, which is failure of the right arterial pressure to decrease with inspiration. However, this can also be seen in right-heart failure, severe tricuspid regurgitation, and systemic venous congestion.[4]

Right atrial pressure tracing showing marked y des Right atrial pressure tracing showing marked y descents (arrows) in a patient with constrictive pericarditis.

The respiratory variations in intrathoracic pressures are not transmitted to the cardiac chambers in constriction, and this leads to decreased left-side filling on inspiration in comparison with the right side.

Talreja et al, in a study examining the areas under the right and left ventricular curves during inspiration and expiration, found a 100% positive predictive accuracy, a 97% sensitivity, and a 100% specificity for constriction with a systolic area index greater than 1.1 (comparing expiration with peak inspiration). This was not a randomized controlled clinical study, and there was selection bias; however, this may prove to be another standard diagnostic criterion in the future.[29]

Although these signs are useful, in practice there is always some uncertainty when they are used in efforts to diagnose constrictive pericarditis. Fluid-filled catheters render notoriously poor fidelity tracings, which can lead to a misinterpretation of the hemodynamic data. Irregular rhythms, such as atrial fibrillation, may alter ventricular filling pressures on the basis of the varying RR intervals.

The patient’s diastolic filling pressures can affect hemodynamic measurements, and some authors advocate infusing isotonic sodium chloride solution if the patient’s left ventricular end-diastolic pressure is less than 15 mm Hg in order to unmask occult constrictive pericarditis. Conversely, if the filling pressures are too high, subtle respiratory variations in pressure may be missed.[8]

Important causes of diastolic pressure equalization that should be considered in the differential diagnosis include the following:

  • Restrictive cardiomyopathy
  • Cardiac tamponade
  • Chronic obstructive pulmonary disease (COPD) and pneumothorax (pulmonary hyperinflation)
  • Dilated cardiomyopathy (which, if severe, may cause all filling pressures to be high)
  • Atrial septal defect
  • Volume depletion (when all filling pressures are low)
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Pericardial and Endomyocardial Biopsy

Occasionally, direct inspection and pericardial biopsy may be required to diagnose constriction. Myocardial histologic findings include fibrotic thickening, chronic inflammation, granulomas, and calcification.

If constriction is strongly suggested on clinical grounds (despite imaging and hemodynamic data), direct surgical inspection, biopsy, and pericardiectomy may be required. This should only be undertaken after careful consideration to establish or exclude the diagnosis.[30]

Despite the best attempts at diagnosing constrictive pericarditis, confirming the diagnosis may be impossible until the time of surgical evaluation. Patients and their families need to be mindful of this fact and aware that, in some cases, surgery may be considered exploratory.

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Contributor Information and Disclosures
Author

John L Parks, MD Fellow, Division of Cardiology, Medical University of South Carolina College of Medicine

John L Parks, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Terrence X O'Brien, MD, FACC Professor of Medicine/Cardiology, Director, Clinical Cardiovascular Research, Medical University of South Carolina; Director, Echocardiography Laboratory, Veterans Affairs Medical Center of Charleston

Terrence X O'Brien, MD, FACC is a member of the following medical societies: American College of Cardiology, American Society of Echocardiography, Heart Failure Society of America, American Heart Association, South Carolina Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Acknowledgements

Hugh D Allen, MD Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Stuart Berger, MD Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Charles I Berul, MD Professor of Pediatrics and Integrative Systems Biology, George Washington University School of Medicine; Chief, Division of Cardiology, Children's National Medical Center

Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, and Society for Pediatric Research

Disclosure: Johnson & Johnson Consulting fee Consulting

Christopher Johnsrude, MD, MS Chief, Division of Pediatric Cardiology, University of Louisville School of Medicine; Director, Congenital Heart Center, Kosair Children's Hospital

Christopher Johnsrude, MD, MS is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology

Disclosure: St Jude Medical Honoraria Speaking and teaching

Renee E Margossian, MD Instructor, Department of Cardiology, Children's Hospital, Harvard University; Consulting Staff, Department of Cardiology, Boston Medical Center and Brigham and Women's Hospital

Renee E Margossian, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Society of Echocardiography, and Heart Failure Society of America

Disclosure: Nothing to disclose

Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center

Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society

Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx Clinical Trials + honoraria; Bayer Grant/research funds Consulting

Weems R Pennington III, MD Cardiology Fellow, Department of Medicine, Medical University of South Carolina

Disclosure: Nothing to disclose.

Kurt Pflieger, MD, FAAP Active Staff, Department of Pediatrics, Lake Pointe Medical Center

Kurt Pflieger, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Darren S Sidney, MD, MS Electrophysiology Fellow, Department of Medicine, Medical University of South Carolina

Disclosure: Nothing to disclose.

Brian D Soriano, MD, FASE, Associate Professor of Pediatrics, Cardiology Division, Adjunct Assistant Professor of Radiology, University of Washington School of Medicine; Attending Physician, Pediatric Cardiology and Cardiac Imaging, Seattle Children’s Hospital

Brian D Soriano is a member of the following medical societies: American Heart Association, American Medical Association, and American Society of Echocardiography

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Eric Vanderbush, MD, FACC Chief, Department of Internal Medicine, Division of Cardiology, Harlem Hospital Center; Clinical Assistant Professor of Cardiology, Columbia University College of Physicians and Surgeons

Eric Vanderbush, MD, FACC is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Acknowledgments

Acknowledgments for this work include support by the Office of Research and Development, Medical Research Service, Ralph H. Johnson Department of Veterans Affairs Medical Center, and the Gazes Cardiac Research Institute, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina.

References
  1. Brockington GM, Zebede J, Pandian NG. Constrictive pericarditis. Cardiol Clin. 1990 Nov. 8(4):645-61. [Medline].

  2. Shabetai R. Constrictive pericarditis. Shabetai R, ed. The Pericardium. New York, NY: Grune & Stratton; 1981.

  3. Hancock EW. On the elastic and rigid forms of constrictive pericarditis. Am Heart J. 1980 Dec. 100(6 Pt 1):917-23. [Medline].

  4. Shabetai R. Pericardial Disease: etiology, pathophysiology, clinical recognition, and treatment. New York NY: Churchill Livingstone; 1995. 1024-35.

  5. Chen CA, Lin MT, Wu ET, et al. Clinical manifestations and outcomes of constrictive pericarditis in children. J Formos Med Assoc. 2005 Jun. 104(6):402-7. [Medline].

  6. Bertog SC, Thambidorai SK, Parakh K, et al. Constrictive pericarditis: etiology and cause-specific survival after pericardiectomy. J Am Coll Cardiol. 2004 Apr 21. 43(8):1445-52. [Medline].

  7. Imazio M, Brucato A, Maestroni S, et al. Risk of constrictive pericarditis after acute pericarditis. Circulation. 2011 Sep 13. 124(11):1270-5. [Medline].

  8. Griffin BP, Topol EJ. Pericardial Disease. Manual of Cardiovascular Medicine. 2nd ed. Philadelphia, Pennsylvania: Lippincott Williams and Wilkins; 2004. 372-396.

  9. Kleynberg RL, Kleynberg VM, Kleynberg LM, Farahmandian D. Chronic constrictive pericarditis in association with end-stage renal disease. Int J Nephrol. 2011. 2011:469602. [Medline]. [Full Text].

  10. Thompson JL, Burkhart HM, Dearani JA, Cetta F, Oh JK, Schaff HV. Pericardiectomy for pericarditis in the pediatric population. Ann Thorac Surg. 2009 Nov. 88(5):1546-50. [Medline].

  11. Babuin L, Alegria JR, Oh JK, Nishimura RA, Jaffe AS. Brain natriuretic peptide levels in constrictive pericarditis and restrictive cardiomyopathy. J Am Coll Cardiol. 2006 Apr 4. 47(7):1489-91. [Medline].

  12. Leya FS, Arab D, Joyal D, et al. The efficacy of brain natriuretic peptide levels in differentiating constrictive pericarditis from restrictive cardiomyopathy. J Am Coll Cardiol. 2005 Jun 7. 45(11):1900-2. [Medline].

  13. Yazdani K, Maraj S, Amanullah AM. Differentiating constrictive pericarditis from restrictive cardiomyopathy. Rev Cardiovasc Med. 2005. 6(2):61-71. [Medline].

  14. Welch TD, Ling LH, Espinosa RE, et al. Echocardiographic diagnosis of constrictive pericarditis: Mayo Clinic criteria. Circ Cardiovasc Imaging. 2014 May. 7(3):526-34. [Medline].

  15. Sengupta PP, Mohan JC, Mehta V, Arora R, Khandheria BK, Pandian NG. Doppler tissue imaging improves assessment of abnormal interventricular septal and posterior wall motion in constrictive pericarditis. J Am Soc Echocardiogr. 2005 Mar. 18(3):226-30. [Medline].

  16. Dal-Bianco JP, Sengupta PP, Mookadam F, Chandrasekaran K, Tajik AJ, Khandheria BK. Role of echocardiography in the diagnosis of constrictive pericarditis. J Am Soc Echocardiogr. 2009 Jan. 22(1):24-33; quiz 103-4. [Medline].

  17. Appleton CP, Hatle LK, Popp RL. Cardiac tamponade and pericardial effusion: respiratory variation in transvalvular flow velocities studied by Doppler echocardiography. J Am Coll Cardiol. 1988 May. 11(5):1020-30. [Medline].

  18. Hurrell DG, Nishimura RA, Higano ST, et al. Value of dynamic respiratory changes in left and right ventricular pressures for the diagnosis of constrictive pericarditis. Circulation. 1996 Jun 1. 93(11):2007-13. [Medline].

  19. Sohn DW, Kim YJ, Kim HS, et al. Unique features of early diastolic mitral annulus velocity in constrictive pericarditis. J Am Soc Echocardiogr. 2004 Mar. 17(3):222-6. [Medline].

  20. Veress G, Feng D, Oh JK. Echocardiography in pericardial diseases: new developments. Heart Fail Rev. 2012 Jul 1. [Medline].

  21. Oh JK, Hatle LK, Seward JB, et al. Diagnostic role of Doppler echocardiography in constrictive pericarditis. J Am Coll Cardiol. 1994 Jan. 23(1):154-62. [Medline].

  22. Zurick AO, Bolen MA, Kwon DH, Tan CD, Popovic ZB, Rajeswaran J, et al. Pericardial Delayed Hyperenhancement With CMR Imaging in Patients With Constrictive Pericarditis Undergoing Surgical Pericardiectomy A Case Series With Histopathological Correlation. JACC Cardiovasc Imaging. 2011 Nov. 4(11):1180-91. [Medline].

  23. Amal L, Nawal D, Abdellah Z, Anis S, Fouad Amal W, Abdellatif B, et al. Use of magnetic resonance imaging in assessment of constrictive pericarditis: a Moroccan center experience. Int Arch Med. 2011 Oct 19. 4(1):36. [Medline].

  24. Ariyarajah V, Jassal DS, Kirkpatrick I, Kwong RY. The utility of cardiovascular magnetic resonance in constrictive pericardial disease. Cardiol Rev. 2009 Mar-Apr. 17(2):77-82. [Medline].

  25. Imazio M, Brucato A, Mayosi BM, et al. Medical therapy of pericardial diseases: part II: Noninfectious pericarditis, pericardial effusion and constrictive pericarditis. J Cardiovasc Med (Hagerstown). 2010 Nov. 11(11):785-94. [Medline].

  26. Feng D, Glockner J, Kim K, et al. Cardiac magnetic resonance imaging pericardial late gadolinium enhancement and elevated inflammatory markers can predict the reversibility of constrictive pericarditis after antiinflammatory medical therapy: a pilot study. Circulation. 2011 Oct 25. 124(17):1830-7. [Medline].

  27. Amaki M, Savino J, Ain DL, et al. Diagnostic concordance of echocardiography and cardiac magnetic resonance-based tissue tracking for differentiating constrictive pericarditis from restrictive cardiomyopathy. Circ Cardiovasc Imaging. 2014 Sep. 7(5):819-27. [Medline].

  28. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation. 1989 Feb. 79(2):357-70. [Medline].

  29. Talreja DR, Nishimura RA, Oh JK, Holmes DR. Constrictive pericarditis in the modern era: novel criteria for diagnosis in the cardiac catheterization laboratory. J Am Coll Cardiol. 2008 Jan 22. 51(3):315-9. [Medline].

  30. Talreja DR, Edwards WD, Danielson GK, et al. Constrictive pericarditis in 26 patients with histologically normal pericardial thickness. Circulation. 2003 Oct 14. 108(15):1852-7. [Medline].

  31. Imazio M, Antonio B, Roberto C, Ferrua S, Belli R, Maestroni S, et al. Colchicine treatment for recurrent pericarditis (CORP): a randomized trial. Ann Intern Med. 2011 Oct 4. 155(7):I28. [Medline].

  32. Tuna IC, Danielson GK. Surgical management of pericardial diseases. Cardiol Clin. 1990 Nov. 8(4):683-96. [Medline].

  33. Ling LH, Oh JK, Schaff HV, et al. Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation. 1999 Sep 28. 100(13):1380-6. [Medline].

  34. [Guideline] Maisch B, Seferovic PM, Ristic AD, Erbel R, Rienmuller R, Adler Y, et al. Guidelines on the diagnosis and management of pericardial diseases. European Society of Cardiology. 2004.

  35. Clare GC, Troughton RW. Management of constrictive pericarditis in the 21st century. Curr Treat Options Cardiovasc Med. 2007 Dec. 9(6):436-42. [Medline].

 
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Constrictive pericarditis. Anteroposterior and lateral chest radiograph from a patient with tuberculous constrictive pericarditis (arrows denote marked pericardial calcification).
Right atrial pressure tracing showing marked y descents (arrows) in a patient with constrictive pericarditis.
Simultaneous right and left ventricular pressure tracings showing diastolic equalization of pressures in both ventricles in a patient with constrictive pericarditis.
MRI shows constrictive pericarditis in 13-year-old patient with otherwise structurally normal heart. Infectious workup was negative. (Image courtesy of Tal Geva, MD.)
Left ventricular volume curve in constrictive pericarditis.
 
 
 
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