Constrictive pericarditis occurs when a thickened fibrotic pericardium, of whatever cause, impedes normal diastolic filling. This usually involves the parietal pericardium, although it can involve the visceral pericardium (see Constrictive-Effusive Pericarditis). Acute and subacute forms of pericarditis (which may or may not be symptomatic) may deposit fibrin, which, in turn, can evoke a pericardial effusion. This often leads to pericardial inflammation, chronic fibrotic scarring, calcification, and restricted cardiac filling.[1]
Constrictive pericarditis symptoms overlap those of diseases as diverse as myocardial infarction (MI), aortic dissection, pneumonia, influenza, and connective tissue disorders. This overlap can confuse the most skilled diagnostician. An increased suspicion of constriction helps move constrictive pericarditis to the top of a lengthy differential diagnosis list and facilitates correct diagnosis and timely therapy.
The classic diagnostic conundrum associated with constrictive pericarditis is the difficulty distinguishing this condition from restrictive cardiomyopathy (see Restrictive Cardiomyopathy) and other syndromes associated with elevated right-sided pressure that all share similar symptoms, physical findings, and hemodynamics.
Although obtaining a careful history and performing a physical examination remain the cornerstones of evaluation, technologic advances have facilitated diagnosis, particularly with the appropriate use of Doppler echocardiography, high-resolution computed tomography (CT), magnetic resonance imaging (MRI), and invasive hemodynamic measurement.
Pericardiectomy is the predominant definitive treatment. Hemodynamic and symptomatic improvements are rapid. Medical management, such as careful observation or symptomatic treatment, has been suggested in less severe cases; however, this option is controversial. The underlying disease usually determines the prognosis. Poorer prognoses are associated with malignancy and New York Heart Association (NYHA) class III or IV heart failure symptoms.
The normal pericardium is composed of 2 layers: the tough fibrous parietal pericardium and the smooth visceral pericardium. Usually, approximately 50 mL of fluid (plasma ultrafiltrate) is present in the intrapericardial space to minimize friction during cardiac motion.[2]
Acute and subacute forms of pericarditis (which may or may not be symptomatic) may deposit fibrin, which, in turn, can evoke a pericardial effusion. This often leads to pericardial organization, chronic fibrotic scarring, and calcification, most often involving the parietal pericardium (see Constrictive-Effusive Pericarditis for visceral pericardial disease).[3]
In constrictive pericarditis, the easily distensible, thin parietal and visceral pericardial linings become inflamed, thickened, and fused. Because of these changes, the potential space between the linings is obliterated, and the ventricle loses distensibility. Venous return to the heart becomes limited, and ventricular filling is reduced, with associated inability to maintain adequate preload. Filling pressures of the heart tend to become equal in both the ventricles and the atria.
Since the myocardium is unaffected, early ventricular filling during the first third of diastole is unimpeded. After early diastole, the stiff pericardium affects flow and hemodynamics. Accordingly, the ventricular pressure initially decreases rapidly (producing a steep y descent on right atrial pressure waveform tracings) and then increases abruptly to a level that is sustained until systole (the “dip-and-plateau waveform” or “square root sign” seen on right or left ventricular pressure waveform tracings).[4]
The preservation of myocardial function in early diastole aids in distinguishing constrictive pericarditis from restrictive cardiomyopathy. Systolic function is rarely affected until late in the course of the disease, presumably secondary to infiltrative processes that affect the myocardium, atrophy, or scarring or fibrosis of the myocardium from the overlying adjacent pericardial disease.
Experimental models indicated that a change in volume-elasticity curves (see the image below) was the fundamental pathophysiologic change associated with the disease. During development of the constriction, right and left ventricular diastolic pressure increased, and stroke volume decreased. A small increase in volume resulted in a considerable increase in end-diastolic pressure.
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Constrictive pericarditis. The image depicts a left ventricular volume curve in constrictive pericarditis.
Symptoms consistent with congestive heart failure (CHF), especially right-sided heart failure, develop as a result of the inability of the heart to increase stroke volume.[5] Over time, cardiac output gradually becomes inadequate (see the Cardiac Output calculator), at first with exercise and then at rest.
The clinical symptoms and classic hemodynamic findings of constrictive pericarditis can be explained by the early rapid diastolic filling and elevation, with eventual equalization of the diastolic pressures in all of the cardiac chambers. This restricts late diastolic filling, leading to venous engorgement and decreased cardiac output, all secondary to a confining pericardium.
Chronic constrictive pericarditis is a disease that has multiple possible causes and is associated with variable clinical findings, depending on its severity. It develops insidiously, and in many cases, no etiology is ever determined. In some patients (approximately 10%), an antecedent acute pericarditis is present. Other cases of constriction are postulated to have been preceded by a subclinical, or occult, form of pericarditis.
All forms of pericarditis may eventually lead to pericardial constriction. They may be broadly classified into common, less common, and rare forms. The top 3 causes of constrictive pericarditis are idiopathic (presumably viral), cardiothoracic surgery, and radiation therapy, which, according to one study, are responsible for 46%, 37%, and 9% of cases of constrictive pericarditis, respectively (in patients who underwent surgical therapy of their constriction).[6]
Common forms
Idiopathic
In many cases, particularly in developed countries, no antecedent diagnosis can be found. These cases are termed idiopathic. Reports by many authors indicate that a high percentage of idiopathic cases of constrictive pericarditis may be related to previously recognized or unrecognized viral pericarditis (see below).
Infection (bacterial and viral)
Tuberculosis is the leading cause of constrictive pericarditis in developing nations but represents only a minority of causes in the United States and other developed countries.
Bacterial infections that lead to purulent pericarditis are also declining in frequency. In the past, purulent pericarditis associated with pneumococcal pneumonia was the most common presentation of a bacterial source. However, the widespread use of antibiotics has drastically changed the frequency and spectrum of purulent pericarditis such that the most common presentation now occurs following cardiac surgery. It should be noted that the progression from acute pericarditis to constrictive pericarditis can occur more rapidly after bacterial pericarditis (eg, ≤6 months in some cases).
An increasing number of gram-positive organisms, including multiple resistant strains of staphylococci, may be isolated. Group A and B streptococci and gram-negative rods (eg, Pseudomonas species, Escherichia coli, and Klebsiella species) have also been documented.
Although the absolute number of tuberculous and bacterial pericarditis cases are decreasing, it must be recognized that these processes remain closely associated with constrictive pericarditis. A prospective analysis determined that the incidence of constrictive pericarditis was 0.76 cases per 1,000 person-years after acute idiopathic/viral pericarditis but 31.7 cases per 1,000 person-years for acute tuberculous pericarditis and 52.7 cases per 1,000 person-years for purulent pericarditis.[7]
Viral pathogens that can cause constrictive pericarditis include coxsackievirus, hepatitis, adenovirus, and echovirus.[8]
Radiation
The long-term effects of thoracic and mediastinal radiation therapy (as used in the treatment of hematologic, breast, and other malignancies) are increasingly being realized. The common features of radiation-induced cardiac complications stem from microcirculation injury with endothelial damage, capillary rupture, and platelet adhesion. This sets up an inflammatory response, which may either resolve or organize to form adhesions between the visceral pericardium and the parietal pericardium. This cascade potentially leads to constriction.
Generally, radiation-induced constrictive pericarditis presents 5-10 years after radiation therapy and is more likely to present with an associated pericardial effusion. In a study by Bertog, the median time between radiation and pericardiectomy was 11 years, with a broad range of 2-30 years. These findings were consistent with those of other previous studies.[6]
Cardiac surgery
Any operative or invasive procedure in which the pericardium is opened, manipulated, or damaged may invoke an inflammatory response, leading to constrictive pericarditis (postpericardiotomy syndrome). The most common example is constrictive pericarditis in the setting of previous coronary artery bypass grafting (CABG) when only part of the pericardium is resected.
Less common forms
Infection (fungal)
Fungal infections are an uncommon source of constrictive pericarditis in patients who are immunocompetent. Nocardia species can be causative organisms, especially in endemic areas such as the Ohio Valley. Aspergillus, Candida, and Coccidioides species are important pathogens in patients infected with HIV and in other immunocompromised hosts.
Neoplasms
Malignant involvement may also manifest as pericardial effusion (with or without tamponade) or as an encased heart with thickening of both visceral and parietal layers, resulting in constrictive physiology. Although many types of neoplasms have been reported, breast and lung carcinomas and lymphomas are the metastatic malignancies most commonly associated with constrictive pericarditis. Other malignancies that involve the pericardium with relative frequency include melanoma and mesothelioma.
Uremia
Uremia with long-term hemodialysis can lead to constrictive pericarditis and is usually associated with a pericardial effusion.
Connective tissue disorders
Autoimmune disorders that involve the pericardium are not unusual, typically manifesting as a small pericardial effusion or as an episode of acute pericarditis. Chronic pericardial involvement is less common but can occur in patients with rheumatoid arthritis, usually associated with the presence of subcutaneous nodules. Systemic lupus erythematosus (SLE) and scleroderma also may lead to constrictive pericarditis; in the latter case, the prognosis is poor.
Drugs
Procainamide and hydralazine have been reported to cause constrictive pericarditis through a drug-induced lupuslike syndrome. Methysergide therapy also has been implicated as a cause of constrictive pericarditis.
Trauma
Blunt and penetrating injuries to the chest wall have been reported to cause constrictive pericarditis, presumably through an inflammatory mechanism. Trauma-induced constrictive pericarditis is generally uncommon.
Myocardial infarction
Post-MI constrictive pericarditis has been reported. The patient typically has a history of Dressler syndrome or hemopericardium after thrombolytic therapy.
Rare forms
Constrictive pericarditis after implantation of an epicardial pacemaker or automated implantable cardiac defibrillator is a rare but reported phenomenon.
Mulibrey nanism is an autosomal recessive disorder characterized by multiple abnormalities, including dwarfism, constrictive pericarditis, abnormal fundi, and fibrous dysplasia of the long bones.
In rare instances, constrictive pericarditis may occur after sclerotherapy for esophageal varices.
Chylopericardium is a rare cause of constrictive pericarditis.
As with many diseases that once were predominantly infectious in origin, the clinical spectrum of constrictive pericarditis has changed. Approximately 9% of patients with acute pericarditis from any cause go on to develop constrictive physiology.[8] The true frequency is dependent on the incidence of the specific causes of pericarditis, but given that acute pericarditis is clinically diagnosed in only 1 in 1000 hospital admissions, the frequency of a diagnosis of constrictive pericarditis is likely to be less than 1 in 10,000 admissions.
In a 2019 report of annual trends of patients admitted to US hospitals with constrictive pericarditis from 2005 to 2014, investigators found a stable prevalence of 9-10 cases per million.[9]
In the developing world, infectious etiologies remain more prominent (tuberculosis has the highest total incidence).
Age-, sex-, and race-related demographics
Although pediatric data are lacking for epidemiologic analysis, it is clear that the condition is rare in adults and even more rare in children. In all age groups, prevalence is increased among patients who are hospitalized and among patients who have undergone cardiac surgery. Cases have been reported in persons aged 8-70 years. Predilection is likely reflective of the underlying disease. Historical studies suggest a median age of 45 years, whereas more recent studies suggest a median age of 61 years (possibly reflecting ongoing demographic changes).
There appears to be a male predominance, with some studies report a male-to-female ratio of 3:1. No racial predilection exists for this disorder.
Between 2005 and 2014, patients with constrictive pericarditis who underwent pericardiectomy were younger, more likely to be male, and had fewer comorbidities than those who received medical management.[9]
Because the disease is rare, prognostic data are relatively scant. Constrictive pericarditis is a potentially curable disease if diagnosed early, but it is potentially fatal if overlooked. The prognosis is also dependent on the disease severity. One study showed postpericardiectomy survival rates of 71% and 52% at 5 and 10 years, respectively. The long-term prognosis with medical therapy alone is poor. Life expectancy is reduced in untreated children and in patients with relatively acute onset of symptoms.
Between 2005 and 2014, in-hospital mortality for patients with constrictive pericarditis was 7.3% for those who underwent pericardiectomy and 6.8% for those who received medical management.[9]
Long-term survival after pericardiectomy depends on the underlying cause. Of common causes, idiopathic constrictive pericarditis has the best prognosis (88% survival at 7 years), followed by constriction due to cardiac surgery (66% at 7 years). The worst postpericardiectomy prognosis occurs in postradiation constrictive pericarditis (27% survival at 7 years), probably as a reflection of confounding comorbidities. Occasionally, the etiology of the constriction may cause coincident myocardial dysfunction.
With surgical treatment, the long-term outcomes of patients with constrictive pericarditis have 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, as noted above, radiation therapy as the cause of the constrictive pericarditis.[6, 10] The degree of pericardial calcification has shown no effect on survival.
Failure of conventional medical therapy for CHF often follows an extensive diagnostic workup, leading to the final diagnosis of constrictive pericarditis. Decline in function is a result of decreased cardiac output (see the Cardiac Output calculator) with symptoms of CHF, along with morbidity stemming from chronic systemic venous congestion.
Multisystem failure can develop into an end-stage of illness when global tissue hypoxia leads to worsening metabolic acidemia.
Because constrictive pericarditis presents with a myriad of symptoms, making a diagnosis solely on the basis of the clinical history is virtually impossible. Patients' symptoms may develop slowly over a number of years, so that they may not be aware of all of their symptoms until questioned. These symptoms are often similar to those associated with right-side congestive heart failure (CHF). Thus, the patient's history may add constriction to the differential diagnosis.
Dyspnea tends to be the most common presenting symptom and occurs in virtually all patients. Fatigue and orthopnea are common. Lower-extremity edema and abdominal swelling and discomfort are also common. Nausea, vomiting, and right upper quadrant pain, if present, are thought to be due to hepatic congestion, bowel congestion, or both.
The initial history may be more compatible with liver disease (cryptogenic cirrhosis) than with pericardial constriction because of the predominance of findings related to the venous system.
Chest pain, presumably due to active inflammation, may be present, though it is observed in only a minority of patients. Other symptoms that may be noted include the following:
Easy fatigability
Fever
Tachycardia
Palpitations
Paroxysmal nocturnal dyspnea
Diaphoresis
In a single-center review of pediatric patients who underwent pericardiectomy between 1978 and 2008, 11 patients underwent surgery for pericardial constriction; presenting complaints included chest pain in 4 (36%), shortness of breath in 2 (18%), and heart failure symptoms in 3 (27%).[11]
In the early stages, physical findings may be subtle, necessitating close examination to ensure that the diagnosis is not missed. In more advanced stages, the patient may appear ill, with marked muscle wasting, cachexia, or jaundice. Constriction should be considered in the presence of otherwise unexplained jugular venous distention, pleural effusion, hepatomegaly, or ascites.
Cardiovascular findings
Elevated jugular venous pressures are an almost universal finding. Avoid examining the patient only in the supine position, because venous pressures may be above the angle of the jaw and inadvertently mistaken for normal.
Sinus tachycardia is common while the blood pressure is normal or low, depending on the stage of the disease process.
The apical impulse is often impalpable, and the patient may have distant or muffled heart sounds. A friction rub is usually not found.
A pericardial knock, which corresponds with the sudden cessation of ventricular filling early in diastole, occurs in approximately half the cases. It is usually heard along the left sternal border and may be mistaken for an S3 gallop. However, a knock is of higher frequency than an S3 gallop and occurs slightly earlier in diastole.
A cardiac murmur is typically not present unless concomitant valvular heart disease or a fibrous band that constricts the right ventricular outflow tract is present.
Pulsus paradoxus is a variable finding. If present, it rarely exceeds 10 mm Hg unless a concomitant pericardial effusion with an abnormally elevated pressure exists.
The Kussmaul sign (ie, elevation of systemic venous pressures with inspiration) is a common nonspecific finding, but this sign is also observed in patients with right ventricular failure, restrictive cardiomyopathy, right ventricular infarction, and tricuspid stenosis—although, notably, not in patients with cardiac tamponade.
Right-sided heart cardiac catheterization provides direct assessment of cardiac filling pressures and can be invaluable in diagnosing constriction, helping to correlate physical examination findings with quantitative data. Ventricular pressure waveform typically demonstrates a steep y descent after systole, followed by rapid diastolic filling (during early diastole) until a plateau is reached. There is little additional filling of the ventricle despite atrial contraction. This corresponds to a normally compliant ventricle opening and rapid filling initially until the stiff pericardium impedes late diastolic filling (forming the so-called “dip-and-plateau” sign).
Gastrointestinal, pulmonary, and other organ system findings
Hepatomegaly with prominent hepatic pulsations can be detected in as many as 70% of patients. Other signs that result from chronic hepatic congestion include ascites, spider angiomata, and palmar erythema, which can contribute to the common but erroneous diagnosis of primary liver disease.
Peripheral (dependent) edema is a common finding, though it may be less prominent in younger patients with competent venous valves.
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.
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.[12, 13]
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).
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.[14] The European Society of Cardiology recommends chest radiography (frontal and lateral) with adequate technical features in all patients with suspected constrictive pericarditis.[15]
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Constrictive pericarditis. These images are anteroposterior and lateral chest radiographs from a patient with tuberculous constrictive pericarditis (a....
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
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. Computed tomography (CT) scanning and magnetic resonance imaging (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 scanning or MRI.[16] The European Society of Cardiology recommends TTE in all patients with suspected constrictive pericarditis.[15]
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%.[17]
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”).[18] This septal bounce is considered a finding consistent with constrictive physiology, with sensitivity of 62% and specificity of 93%.[19]
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.[20, 21]
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.[19]
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.[14]
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.[22]
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.[19, 23]
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.[24]
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.
Conventional computed tomography (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. Although 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.
The development of real-time, high-resolution magnetic resonance imaging (MRI) and the ability to acquire images in 50 ms or less makes MRI a sensitive method for imaging the pericardium.[25, 26] The European Society of Cardiology recommends both computed tomography scanning (CT) and MRI as second-level imaging techniques for the evaluation of constrictive pericarditis, including assessing calcifications (CT scanning), pericardial thickness, and degree and extent of pericardial involvement, with class I, level C level of evidence.[15] Cardiac MRI also has high diagnostic accuracy in the setting of recurrent pericarditis and for identifying patients at higher risk of complications).[27]
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. Real-time, steady-state free-procession (SSFP) imaging can be used to assess ventricular coupling, which allows assessment of changes in the ventricular septal shape and motion over the respiratory cycle. Gated MRI has an advantage in determining whether pericardial fluid is hemorrhagic. CT scanning may be preferable when pericardial calcification is particularly prominent.[15, 28]
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Constrictive pericarditis. The magnetic resonance image shows constrictive pericarditis in 13-year-old patient with an otherwise structurally normal h....
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).[29, 30] In patients who may have inflammatory constriction that would resolve with anti-inflammatory therapy, cardiac MRI may be helpful in the diagnostic workup.[31]
Cremer et al looked at pericardial delayed hyperenhancement as a predictor of clinical improvement in patients with constrictive pericarditis.[32] They were able for the first time to quantify improvement in patients treated with anti-inflammatory agents who had increased pericardial delayed hyperenhancement.[32]
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 tissue tracking or two-dimensional echocardiography–based tissue tracking.[33]
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.
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.[15] .
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.[34]
View Image
Constrictive pericarditis. The simultaneous right and left ventricular pressure tracings shows diastolic equalization of pressures in both ventricles ....
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]
View Image
Constrictive pericarditis. This right atrial pressure tracing shows 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.[35]
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)
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.[36]
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.
Definitive care is primarily surgical (ie, pericardiectomy). Operative therapy typically leads to rapid hemodynamic and symptomatic improvements. Medical management, such as careful observation or symptomatic treatment, has been suggested in less severe cases; however, this option is controversial.
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 (see the Cardiac Output calculator). Complications may arise with failure to diagnose or treat constrictive pericarditis (and any existing underlying etiology) adequately.
Outpatient care may be appropriate in the early stages, particularly when the diagnosis is still uncertain and the symptoms are relatively stable. A low salt, fluid-restricted diet is probably beneficial. Although no specific restrictions are needed, activity can often be severely limited by symptoms.
In the vast majority of cases, medical management is ineffective unless a prominent inflammatory component is present. In this respect, constrictive pericarditis differs from acute pericarditis, in which the use of nonsteroidal anti-inflammatory agents (NSAIDs), cyclooxygenase (COX)-2 inhibitors, colchicine, corticosteroids, or a combination thereof may provide benefit.[37] However, even after optimal therapy of acute pericarditis, constriction may develop over time. Transient constrictive pericarditis has been described, so those individuals with a diagnosis of constriction who are medically stable may be given a trial of conservative treatment for 2-3 months (using NSAIDs and/or steroids). This should be only considered in those individuals with an optimized volume status and controlled symptoms.[29]
Other considerations related to medical treatment of constrictive pericarditis are as follows:
Subacute constrictive pericarditis may respond to steroids if treated before pericardial fibrosis occurs
Diuretics (particularly loop diuretics) are the mainstay to relieve congestion and optimize clinical volume status; however, they may decrease preload to the point of reducing cardiac output and thus require careful monitoring (see the Cardiac Output calculator)
Any other medications used to treat patients with constrictive pericarditis would be specific to the underlying cause of the pericardial disease
Any therapy directed toward the causative disease (eg, antituberculosis medication) is appropriate
Complications (eg, atrial arrhythmias) require their own therapy as appropriate
In general, beta-blockers and calcium channel blockers should be avoided, because the sinus tachycardia that commonly occurs in constrictive pericarditis has a compensatory function, maintaining cardiac output in a setting of fixed stroke volume (secondary to fixed diastolic filling)
Individuals with significantly advanced symptoms related to constriction may derive little benefit from pericardiectomy; these are often the same patients who have particularly high surgical risk.[29]
Complete pericardiectomy is the definitive therapy and is a potential cure.[38, 39, 40] 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 must be exercised because patients who are in New York Heart Association (NYHA) class I (ie, asymptomatic) or who have early NYHA stage II symptoms may be clinically stable for years.
Pericardiectomy can be a long and often technically complex procedure. The 2 standard approaches are via an anterolateral thoracotomy and via a median sternotomy. Pericardial decortication should be as extensive as possible, especially at the diaphragmatic-ventricular contact regions. An excimer laser can be used should severe adhesions occur between the pericardium and epicardium.[40] Complications may include excessive bleeding, atrial and ventricular arrhythmias, and ventricular wall ruptures.
In published reports, surgical mortality ranges from 5% to 15%, with one report citing a 30-day perioperative mortality of 6.1%. The causes of death include progressive heart failure, sepsis, renal failure, respiratory failure, and arrhythmia. Between 80% and 90% of patients who undergo pericardiectomy achieve NYHA class I or II postoperatively.
To evaluate the clinical outcome of pericardiectomy, investigators studied 99 consecutive patients who underwent pericardiectomy at the Montreal Heart Institute over a 20-year period. They found that hospital mortality was 7.9% in the case of isolated pericardiectomy and that the patients who were operated on within 6 months of symptom onset showed a lower mortality risk. Preoperative clinical conditions and associated comorbidities were critical in predicting mortality risk, and pericardiectomy was able to improve functional status in the majority of late survivors.[41]
Even though symptoms are commonly alleviated after a pericardiectomy, evidence of abnormal diastolic filling (which can be correlated with clinical status) often remains. One study found that only 60% of patients showed complete normalization of cardiac hemodynamics.[40] Although some patients improved with time, persistent diastolic filling abnormalities tended to occur in those who had a longer history of preoperative symptoms, supporting the view that early operation is advisable in symptomatic patients. Those patients who have symptoms that persist even after successful pericardiectomy may have a more mixed constrictive-restrictive picture.
Of 58 patients who underwent total pericardiectomy 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.
In a study comprising 25 patients who underwent pericardiectomy due to symptomatic chronic constrictive pericarditis (reduced exercise capacity and sleep-disordered breathing), there was improvement in peak rate of oxygen uptake, quality of life, and sleep, but no significant change in sleep disordered breathing.[42]
Different methods of accessing the pericardial space, such as video-assisted thoracoscopy, are being investigated. Further development of such devices may help improve diagnostic and therapeutic options in patients with pericardial disease.[43]
Cardiac mortality and morbidity seem to be related to preoperative myocardial atrophy or fibrosis, which can be detected by means of computed tomography (CT) scanning. Excluding these patients keeps the mortality rate at the lower end of the range (5%).[40]
Postoperatively, low cardiac output may occur in patients who are debilitated and who have ascites or other findings of fluid retention. Patients with low cardiac output may require maintenance of high left atrial pressure, sympathomimetic infusions, or both. Mechanical support of the circulation, such as extracorporeal membrane oxygenation (ECMO) or intra-aortic balloon counterpulsation, can be used in patients who are critically ill.
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.
Referral to a specialized center may be required. If adequate diagnostic or therapeutic modalities are not available, transfer to an appropriate facility is warranted.
The ESC released updated guidelines for the diagnosis and treatment of constrictive pericarditis in 2015, which are summarized below.[15] All of these recommendations are based on class I, level C evidence, unless noted otherwise.
Transthoracic echocardiography as well as frontal and lateral chest radiography with adequate technical characteristics are recommended in all patients with suspected constrictive pericarditis.
Computed tomography (CT) scanning and/or cardiac magnetic resonance imaging (CMRI) are indicated as second-level imaging techniques to assess calcifications (CT scanning), pericardial thickness, and degree and extension of pericardial involvement.
Cardiac catheterization is indicated when noninvasive diagnostic methods do not provide a definite diagnosis of constriction.
The mainstay of treatment of chronic constriction is pericardiectomy.
Medical therapy for specific etiologies of pericarditis is recommended to prevent progression of constriction, as well as for advanced cases or in the setting of a high risk of surgery or mixed forms with myocardial involvement.
Empiric anti-inflammatory therapy may be considered in cases with transient or a new diagnosis of constriction with concomitant evidence of pericardial inflammation on CT/CMRI or results of laboratory studies suggestive of inflammation (eg, elevated C-reactive protein [CRP] or erythrocyte sedimentation rate [ESR]) (class IIb, level C evidence).
No medications are required when the diagnosis of constrictive pericarditis is definitive, because the patient is usually referred for surgical management. To help maintain a euvolemic state, diuretics and afterload-reducing medications should be used cautiously; decreasing preload or afterload can cause greater compression of the heart and sudden cardiac decompensation, especially when general anesthetic agents are administered just before the pericardiectomy is performed.
Clinical Context:
Aspirin is a mainstay of treatment for acute pericarditis. The European Society of Cardiology recommends a dosing regimen of 750-1000 mg every 8 hours for 1-2 weeks.[41] Consider tapering by decreasing the doses by 250-500 mg every 1-2 weeks.
Clinical Context:
Ibuprofen is also a mainstay of treatment for acute pericarditis. The European Society of Cardiology recommends a dosing regimen of 600 mg every 8 hours for 1-2 weeks.[41] Consider tapering by decreasing the doses by 200-400 mg every 1-2 weeks.
Clinical Context:
The European Society of Cardiology recommends cochicine as an adjunct first-line drug added to conventional anti-inflammatory therapies (eg, aspirin, ibuprofen) in individuals with a first or recurrent episode of pericarditis for improvement in therapeutic response, increase in remission rates, and reduction in recurrences/[41]
The dosing regimen is 0.5 mg once (< 70 mg) or 0.5 mg twice daily (≥70 kg) for 3 months. Although tapering is not mandatory, consider tapering by alternating 0.5 mg every other day (< 70 kg) or 0.5 mg once (≥70 kg) in the last weeks.[41] Provide gastroprotection for patients administered colchine.
Other medical therapy is dependent on the etiology of the constrictive pericarditis such as nonsteroidal anti-inflammatory agents (NSAIDs) in early constriction with an inflammatory component. Relatively recently a variant, "transient constrictive pericarditis," has been named because of its reversible pattern after spontaneous recovery or medical therapy (ie, NSAIDs or colchicine, steroids, or other immune-modulating agents in refractory cases).[15, 44]
Clinical Context:
Furosemide increases excretion of water by interfering with the chloride-binding co-transport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. If a switch is made from IV to oral administration, an equivalent oral dose should be used. Doses vary depending on the patient's clinical condition and renal function.
Clinical Context:
Torsemide increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. It increases excretion of water, sodium, chloride, magnesium, and calcium. If a switch is made from IV to oral administration, an equivalent oral dose should be used. Doses vary depending on the patient's clinical condition and renal function.
Diuretics may improve pulmonary and systemic congestion. They should be used cautiously because any drop in intravascular volume may cause a corresponding drop in cardiac output. Any loop diuretics may be used to treat volume overload. Always start at the minimal dose necessary.
William M Edwards, Jr, MD, Assistant Professor of Medicine, Department of Cardiology, Medical University of South Carolina College of Medicine
Disclosure: Nothing to disclose.
Chief Editor
Terrence X O'Brien, MD, MS, FACC, Professor of Medicine/Cardiology, Director, Clinical Cardiovascular Research, Medical University of South Carolina College of Medicine; Director, Echocardiography Laboratory, Veterans Affairs Medical Center of Charleston
Disclosure: Nothing to disclose.
Additional Contributors
John L Parks, MD, Fellow, Division of Cardiology, Medical University of South Carolina College of Medicine
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
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.
[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.
[Guideline] Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. European Heart Journal. August 29, 2015. 36:2937-2944.
Constrictive pericarditis. The image depicts a left ventricular volume curve in constrictive pericarditis.
Constrictive pericarditis. These images are anteroposterior and lateral chest radiographs from a patient with tuberculous constrictive pericarditis (arrows denote marked pericardial calcification).
Constrictive pericarditis. The magnetic resonance image shows constrictive pericarditis in 13-year-old patient with an otherwise structurally normal heart. Infectious workup was negative. (Image courtesy of Tal Geva, MD.)
Constrictive pericarditis. The simultaneous right and left ventricular pressure tracings shows diastolic equalization of pressures in both ventricles in a patient with constrictive pericarditis.
Constrictive pericarditis. This right atrial pressure tracing shows marked y descents (arrows) in a patient with constrictive pericarditis.
Constrictive pericarditis. These images are anteroposterior and lateral chest radiographs from a patient with tuberculous constrictive pericarditis (arrows denote marked pericardial calcification).
Constrictive pericarditis. This right atrial pressure tracing shows marked y descents (arrows) in a patient with constrictive pericarditis.
Constrictive pericarditis. The simultaneous right and left ventricular pressure tracings shows diastolic equalization of pressures in both ventricles in a patient with constrictive pericarditis.
Constrictive pericarditis. The magnetic resonance image shows constrictive pericarditis in 13-year-old patient with an otherwise structurally normal heart. Infectious workup was negative. (Image courtesy of Tal Geva, MD.)
Constrictive pericarditis. The image depicts a left ventricular volume curve in constrictive pericarditis.
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