WORKUP	Section 5 of 11
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Lab Studies:

• No laboratory data are diagnostic of constrictive pericarditis. However, as a result of the universal findings of a chronically elevated right atrial pressure and passive congestion of the liver, kidneys, and gastrointestinal tract, resultant abnormalities may be present. These include elevations in both conjugated and unconjugated bilirubin levels and elevated levels as determined by hepatocellular function tests.

• Hypoalbuminemia may be a result of both a protein-losing enteropathy and proteinuria that may approach nephrotic range.

• If active or chronic inflammation is present, nonspecific markers, such as an elevated sedimentation rate or a normocytic normochromic anemia, may be present.

• If an associated collagen vascular disorder is suggested, antinuclear antibody or rheumatoid factor should be measured.

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

• Expect an elevation in the white blood cell count with an associated left shift in cases of bacterial pericarditis.

• Cytologically examining the pericardial fluid, if present, helps diagnose a malignant cause (if not otherwise apparent).

• The levels of brain natriuretic peptide (BNP), a cardiac hormone released in response to increased wall stretch, are often mildly increased in constrictive pericarditis. BNP levels are even higher in restrictive cardiomyopathy and may be useful in differentiating these disorders.

Imaging Studies:

• Chest radiography

• Although findings are insensitive for the presence of constrictive pericarditis, some classic findings are suggestive of the diagnosis when present within a compatible clinical context.

• Severe pericardial calcification is common (see Image 1); however, it is not specific and does not prove pericardial constriction.

• If no significant pericardial effusion is present, the cardiac silhouette may appear normal.

• The superior vena cava, azygous veins, 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.

• 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 echocardiography 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.

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

• CT scanning and MRI are considered the procedures of choice for imaging the pericardium, in particular its thickness and degree of encasement. Dynamic cardiac physiology can be interrogated. For example, the posterior motion of the otherwise normal interventricular septum relative to the less compliant ventricular walls (which are encased by the pericardium) correlates with the auscultatory pericardial knock.

• Two-dimensional echocardiography can show evidence of right-sided pressure overload such as atrial septal shifting to the left with inspiration or dilated inferior and superior vena cavae and hepatic veins. These are nonspecific signs that can also occur in right heart failure as a result of other causes.

• Doppler echocardiography provides important hemodynamic information.
  • Early rapid diastolic filling can be imaged by interrogating forward flow at the mitral and tricuspid valve levels. Termed the E (for early filling) and the A (for atrial filling) waves, they may have shortened durations, increased velocity, and rapid decelerations from their peak velocity, reflecting constrictive physiology. These velocities usually decrease with inspiration and increase with expiration.

  • The transtricuspid velocities show an opposite pattern to the transmitral (ie, increasing with inspiration and decreasing 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, with its diastolic inflow being greater than systolic inflow, which itself may even reverse. These Doppler findings are sensitive when present, but, like many echocardiographic signs, their absence does not exclude constrictive hemodynamics.

  • 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.

  • Always keep in mind that 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.

  • 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.

  • Although technically challenging, Doppler ventricular inflow patterns can help distinguish constrictive from restrictive cardiac physiology. From a Doppler perspective, constriction limits ventricular filling and enhances ventricular interaction. Conversely, restriction generally limits ventricular distensibility. Put another way, in constriction, presumably normal myocardium is present, but the ventricles are encased together, whereas in restriction, abnormal myocardium is present with no such restraint. Therefore, both physiologies have abnormal early diastolic filling with early atrial ventricular pressure equilibration.

  • The respiratory variations are usually greater in constriction than in restriction (probably because of the normal intraventricular septum), usually with greater than 25% changes at the onset of inspiration and expiration. Reflecting this, the deceleration time of the mitral Doppler inflow E wave is usually less than 150 ms with constriction, with a further decrease with inspiration. 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.

  • A recent innovation that may improve this differentiation is tissue Doppler echocardiography, in which the actual endocardial and epicardial tissue velocities are measured. Because myocardial relaxation itself is preserved in pure constrictive pericarditis, the early relaxation myocardial velocity (Em, also known as Ea) is normal, whereas it is abnormal with restriction (when intrinsic myocardial disease is present). For example, given that a normal Em is more than 10 cm/s, a near-normal (>8 cm/s) Em supports constriction, whereas a much lower Em supports restriction. Only contemporary echocardiography equipment can be used to measure this.

• 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, degree of calcification, and distribution of these findings are easily measured.

• The normal pericardium is 1-2 mm thick. An abnormal pericardial thickness is considered 3-4 mm thick or thicker.

• Pericardial thickening of more than 4 mm assists in differentiating constrictive disease from restrictive cardiomyopathy, and a thickening of more than 6 mm adds even more specificity for constriction.

• 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.

• If the hemodynamics and presentation are otherwise compatible, the diagnosis must still be entertained despite unremarkable pericardial imaging.

• Magnetic resonance imaging

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

• As can be done with CT scanning, an MRI can be used to measure the pericardium for thickness, calcification, and distribution of abnormalities.

• A thickened pericardium does not prove that constrictive pericarditis is present; it must be clinically correlated. Likewise, constriction can occur in a scarred fibrous pericardium of normal thickness.

• Gated MRI has an advantage in determining whether pericardial fluid is hemorrhagic.

• Obtaining CT scan images may be advantageous compared to performing MRI when calcium levels are significantly elevated.

Other Tests:

• Electrocardiogram

• Chronic pericarditis is not associated with the classic ECG findings seen with acute pericarditis.

• Findings of acute pericarditis (see Pericarditis, Acute) 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. In addition, if a history of these findings exists, the later development of constrictive pericarditis should be considered.

• 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, 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 (see Cardiac Tamponade) must be considered.

Procedures:

• Cardiac catheterization hemodynamics

• Despite best efforts to diagnose constrictive pericarditis using noninvasive testing, the diagnosis may still be uncertain. The differentiation between constrictive pericarditis and restrictive cardiomyopathy is often a major consideration and can be as difficult in the catheterization laboratory as in the echocardiography laboratory.

• The hemodynamic changes seen in constrictive pericarditis are based on impaired ventricular diastolic blood flow that leads to an equalization of intraventricular diastolic pressures and an abrupt cessation of ventricular filling after early diastole. The right atrial pressure tracings may show this.

• Normally, with inspiration, the mean right atrial pressures should decline as returning venous blood flows into the pulmonary vasculature. Failure to do so or an actual pressure increase with inspiration is known as the Kussmaul sign. While this can be seen with constrictive pericarditis, it also can be seen with right heart failure, severe tricuspid regurgitation, or systemic venous congestion.

• Closer inspection of the atrial waveforms reveals the Y descent becoming exaggerated and, thus, appearing deeper and steeper than its X-descent counterpart (see Image 2). This is in contrast to the Y descent in cardiac tamponade, which becomes attenuated or even up-sloping.

• Measuring right ventricular pressures is vital in determining if a patient has constrictive pericarditis, and a right heart catheterization is included in any hemodynamic evaluation.

• Traditional teachings have focused on (1) the equalization of pressures between the 2 ventricles (see Image 3), (2) the relationship of the right ventricular systolic to diastolic pressure, and (3) the pulmonary artery pressures.

• Generally, a difference between the left and right ventricular end-diastolic pressures of less than 5 mm Hg, a right ventricular diastolic pressure of greater than one third the right ventricular systolic pressure, or a pulmonary artery pressure of less than 50 mm Hg favors a diagnosis of constrictive pericarditis rather than restrictive cardiomyopathy.

• When making or excluding a diagnosis of constrictive pericarditis, these criteria are neither sensitive nor specific enough to rely on solely. However, the further they are to either extreme, the more reliable they are.

• The classic dip-and-plateau (also known as the square-root sign) that has been described in abnormal ventricular diastolic filling patterns can occur in both constrictive and restrictive disorders. In constrictive pericarditis, this pattern represents early rapid ventricular filling followed by a sudden halt in ventricular filling as the pericardium is restrained from the end of the first third of diastole onward.

• In 1989, a landmark study by Hatle et al (and later by Hurrell et al) was published. It elucidated both the echocardiographic and hemodynamic variations that occur in both right and left ventricular filling patterns during normal respiration with constrictive pericarditis.
  • Using the presence or absence of (1) ventricular pressure interdependence and (2) intrathoracic/intracardiac pressure disassociation, they were able to increase the sensitivity and specificity of hemodynamic testing to greater than 90%. That is, in constrictive pericarditis, with inspiration, the right ventricular inflow is increased, which is believed to cause the interventricular septum to shift toward the left, thus further diminishing left ventricular filling.

  • As a result of this preload mismatch, stoke volume is augmented in the right ventricle and reduced in the left ventricle. Hemodynamic tracings obtained simultaneously in both ventricles show that the left ventricular pressure falls with inspiration while the right ventricular pressure rises. The opposite is true during expiration. These ventricular pressure responses have been termed discordant. This phenomenon does not occur in congestive heart failure or restrictive disorders.

  • With inspiration, the intrathoracic pressure also drops. This causes a subsequent drop in pulmonary capillary wedge pressure (and mean left atrial pressure). However, because of the constricting pericardium, this drop in pressure cannot be transmitted to the left ventricle during diastole. The result is a decrease in the pressure gradient for filling the left ventricle. This intrathoracic/intracardiac dissociation occurs commonly (although not exclusively) in constrictive pericarditis. This dissociation does occur, although to a much lesser extent, in restrictive cardiomyopathy. Hurrell et al showed a sensitivity of 93% and a specificity of 81% for diagnosing pericardial constriction with this finding.

• Although these signs are useful, in practice, uncertainty always exists when attempting to diagnose constrictive pericarditis. Fluid-filled catheters render notoriously poor fidelity tracings, which can lead to a misinterpretation of the data. Irregular rhythms, such as atrial fibrillation, may alter ventricular filling pressures based on the varying RR intervals. Variations in respiration patterns may affect hemodynamics, and patients should be instructed to breathe smoothly and uniformly during hemodynamic recordings. 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 to unmask occult constrictive pericarditis. Conversely, if the filling pressures are too high, the more subtle respiratory variations in pressure may be missed.

• Etiologies of diastolic pressure equalization include constrictive pericarditis, restrictive cardiomyopathy, cardiac tamponade, COPD and pneumothorax (pulmonary hyperinflation), dilated cardiomyopathy (if severe, all filling pressures are high), atrial septal defect, and volume depletion (all filling pressures are low).

• Pericardial and endomyocardial biopsy

• Occasionally, direct inspection and pericardial biopsy may be required to diagnose constriction.

• If constriction is strongly suggested clinically, the pericardium may be thin, and, after careful consideration, direct surgical inspection, biopsy, and pericardectomy may be required to diagnose definitively or to exclude the diagnosis.

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

	TREATMENT	Section 6 of 11
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Medical Care:

• Medical management is generally ineffective in the vast majority of cases unless a prominent inflammatory component is present.

• This is in contrast with acute pericarditis (see Pericarditis, Acute), in which the use of nonsteroidal anti-inflammatory agents, cyclooxygenase-2 inhibitors, colchicine, corticosteroids, or a combination thereof may provide benefit. However, even after optimal therapy of acute pericarditis, over time, the possibility of developing constriction exists. Other medical considerations are as follows:

• Subacute constrictive pericarditis may respond to steroids if treated before pericardial fibrosis occurs.

• Diuretics are commonly used to relieve congestion if ventricular filling pressures are clinically elevated. However, this may decrease cardiac output and requires careful monitoring.

• Any therapy directed toward the causative disease is appropriate, such as antituberculosis medication.

• Complications, such as atrial arrhythmias, require their own therapy as needed.

• In general, beta-blockers should be avoided because the sinus tachycardia that commonly occurs in constrictive pericarditis is compensatory in nature.

Surgical Care:

• Complete pericardectomy is the definitive therapy and is a potential cure.

• Results are generally better if the procedure is performed earlier in the course, when less calcification is present and when the chance of abnormal myocardium or advanced heart failure is reduced.

• Some judgment is required because patients who are asymptomatic (NYHA class I) or who have early NYHA stage II symptoms may be clinically stable for years.

• Pericardial decortication should be as extensive as possible, especially at the diaphragmatic-ventricular contact regions.

• The surgical procedure can be long and is often technically complex. Complications may include excessive bleeding and atrial and ventricular arrhythmias.

• Poor surgical results are observed in patients with organ failure (especially renal and hepatic), ascites, uncorrected coronary artery disease, myocardial fibrosis, older age, NYHA class IV, or postradiation pericarditis.

• The published surgical mortality rates range from 5-15%. Significantly, 80-90% of patients who undergo pericardectomy postoperatively achieve NYHA class I or II.

• Even though the symptoms following a pericardiectomy are commonly improved, evidence of abnormal diastolic filling (which can be correlated with clinical status) often remains.

• A recent study found that some diastolic filling abnormalities remained in a substantial number of patients after pericardectomy for constriction.

• In 58 patients who underwent total pericardectomy for constriction, 30% still had some significant symptoms after 4 years. These patients were more likely to have a persistent restrictive or constrictive pattern to their transmitral and transtricuspid Doppler signals as determined by respiratory recording.

• Although some improved with time, persistent diastolic filling abnormalities tended to occur in patients who had a longer history of preoperative symptoms, supporting the concept of early operation in patients who are symptomatic.

• New experimental devices are being investigated to access the pericardial space, including in patients without significant effusion.

• One is the PerDUCER, which is a percutaneous sheath-needle pericardial access device.

• Hopefully, the development of such devices can improve diagnostic and therapeutic options in patients with pericardial disease.

Consultations:

• A cardiologist can assist with obtaining and interpreting echocardiographic imaging, hemodynamic measurements, and, if necessary, endocardial or pericardial biopsies.

• Consultation with a cardiothoracic surgeon is appropriate when a pericardial procedure is being considered.

Diet:

• No specific dietary recommendations are necessary.

Activity:

• Although no specific restrictions are needed, activity can often be severely limited by symptoms.

	MEDICATION	Section 7 of 11
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Surgical pericardectomy is clearly the treatment of choice for patients with constrictive pericarditis. Diuretics have been used in the early stages of the disease to improve pulmonary and systemic congestion. However, these should be used cautiously because any drop in intravascular volume may cause a corresponding drop in cardiac output.

Drug Category: Diuretics -- These agents may improve pulmonary and systemic congestion. These should be used cautiously because any drop in intravascular volume may cause a corresponding drop in cardiac output.

Drug Name	Furosemide (Lasix) -- Any loop diuretics may be used to treat volume overload. Always start at minimal dose necessary.
Adult Dose	20 mg/d PO/IV
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
Interactions	Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN level determinations during first few months of therapy and periodically thereafter

	FOLLOW-UP	Section 8 of 11
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Further Inpatient Care:

• Given the invasive nature of certain diagnostic procedures, inpatient care is often warranted in the workup.

Further Outpatient Care:

• Outpatient care may be appropriate in the early stages, particularly when the diagnosis is still uncertain and the symptoms are relatively stable.

In/Out Patient Meds:

• Commonly, diuretics (particularly loop-type) are titrated to optimal clinical volume status.

• Any other medications used to treat patients with constrictive pericarditis would be specific to the underlying etiology of the pericardial disease.

Transfer:

• If adequate diagnostic or therapeutic modalities are not available, transfer to an appropriate facility is warranted.

Complications:

• Complications arise with failure to diagnose or treat constrictive pericarditis adequately, including any existing underlying etiology. Surgical intervention poses separate and significant complication risks (see Surgical Care).

Prognosis:

• Long-term prognosis with medical therapy alone is poor.

• With surgery, the long-term outcome of patients with constrictive pericarditis has been shown to be independently less favorable with advanced age, poor renal function, abnormal left ventricular systolic function, high pulmonary artery systolic pressure, lower serum sodium level, worsening NYHA classification, and, most notably, with a postradiation cause. Pericardial calcification has shown no effect on survival.

• A recent study showed postpericardiectomy survival rates of 71% and 52% at 5 and 10 years, respectively.

• Long-term survival after pericardiectomy depends on the underlying cause. Of common causes, idiopathic constrictive pericarditis has the best prognosis, followed by constriction due to cardiac surgery.

Patient Education:

• Patients should discuss any unexplained dyspnea, abdominal swelling, or edema with their doctor.

	MISCELLANEOUS	Section 9 of 11
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Medical/Legal Pitfalls:

• Constrictive pericarditis is a potentially curable disease if diagnosed early, but it is potentially fatal if overlooked.

• The clinician must always keep constrictive pericarditis in the differential of any patient who presents with unexplained dyspnea, gastrointestinal symptoms, ascites, or edema.

Special Concerns:

• 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, Charleston, South Carolina.

	PICTURES	Section 10 of 11
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Caption: Picture 1. Constrictive pericarditis. Anteroposterior and lateral chest radiograph from a patient with tuberculous constrictive pericarditis (arrows denote marked pericardial calcification).
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Picture Type: X-RAY

Caption: Picture 2. Right atrial pressure tracing showing marked Y descents (arrows) in a patient with constrictive pericarditis.
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Picture Type: Graph

Caption: Picture 3. Simultaneous right and left ventricular pressure tracings showing diastolic equalization of pressures in both ventricles in a patient with constrictive pericarditis.
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Picture Type: Graph

	BIBLIOGRAPHY	Section 11 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

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Pericarditis, Constrictive excerpt