Evan Lau and Allan L. Klein
INTRODUCTION
Pericardial disease is a small but important subset of cardiovascular illness. Clinical trial data and published society guidelines1 are sparse; board questions should focus on the most basic aspects of these diseases. We review the three most common presentations that are encountered by the cardiologist: acute pericarditis, pericardial effusions, and constrictive pericarditis.
Acute Pericarditis
Presentation and Diagnosis
Acute pericarditis is a common chest pain syndrome, occurring in up to 5% of cases presenting with non-myocardial infarction chest pain to an emergency setting.2 The diagnosis of acute pericarditis is made by a constellation of clinical symptoms, presence of a pericardial friction rub, characteristic ECG changes, and the presence of a pericardial effusion (Table 57.1). Elevation of inflammatory biomarkers serves as a supportive criterion for the diagnosis. Reasonable diagnostic certainty of acute pericarditis is present if findings in two of these four categories support the diagnosis. In practice, the transience of a pericardial friction rub makes it an unreliable marker of disease and significant weight is put on the rise of inflammatory markers during periods of symptom activity. The classic symptoms of acute pericarditis include the presence of sharp, pleuritic chest pain that is exacerbated by recumbency and improved by leaning forward. The pain often times radiates to one or both trapezius muscles. A pericardial friction rub is pathognomonic for pericarditis, but its inconsistency and transience make it less reliable as a diagnostic criterion. The electrocardiogram demonstrates a characteristic progression over time, with diffuse ST elevation and PR depression (representing epicardial injury of the ventricles and atria, respectively) early on (Fig. 57.1), followed by symmetric T-wave inversions, which eventually progress to normalization of the ST/T-wave segments. Serologic testing demonstrates elevation in the erythrocyte sedimentation rate (ESR) and/or C-reactive protein (CRP). Finally, echocardiographic demonstration of a pericardial effusion supports the presence of pericardial inflammation. The use of delayed enhancement imaging with gadolinium by cardiac magnetic resonance imaging is emerging as another imaging tool to demonstrate pericardial inflammation (Fig. 57.2).3
TABLE
57.1 Diagnostic Criteria for Acute Pericarditisa
aRise in inflammatory markers, including ESR and CRP are supportive of the diagnosis. Two out of four major criteria are required for reasonable diagnostic certainty.
Adapted from Imazio M, et al. Controversial issues in the management of pericardial disease. Circulation. 2010;121:916–928.
FIGURE 57.1 Classic ECG changes consistent with earliest stage of acute pericarditis. Diffuse ST-segment elevation with ST depression in aVR. Diffuse PR depression (blackarrow) with PR elevation in aVR.
FIGURE 57.2 Cardiac MRI. Delayed imaging following administration of gadolinium, short axis view. There is uptake of contrast in both the visceral (white arrow) and parietal layers (red arrow) of the pericardium, suggesting active inflammation of the pericardium.
Etiology
There is a long differential diagnosis for the etiology of acute pericarditis (Table 57.2).4 The frequency of etiology depends on the geographic population selected. In developed countries, idiopathic pericarditis represents the vast majority of cases. It is believed that most cases of idiopathic pericarditis represent the sequelae of a viral infection. An exhaustive virologic workup is rarely done in clinical practice, so the terms “idiopathic” and “viral” pericarditis are often used synonymously. Systemic autoimmune disease, chest radiation, open heart surgery, neoplastic disease, hypothyroidism, uremia, and acute myocardial infarction occur with enough frequency that they should be entertained in most cases. Tuberculous pericarditis is more common in developing countries and should be considered in patients with the appropriate exposure. Overall, the prognosis for idiopathic pericarditis is good. However, the risk of complications, including recurrence, tamponade, and constriction, is higher in patients with the following characteristics: female gender, large effusion or tamponade, and aspirin/nonsteroidal anti-inflammatory drug (NSAID) failure. Patients who have a specific underlying etiology (as opposed to idiopathic or viral pericarditis) are more likely to present with fevers, subacute onset, large pericardial effusion, elevation in cardiac troponin, and failure of NSAID treatment. These patients are also at increased risk for pericarditis-related complications of recurrence, tamponade, and constriction.5
TABLE
57.2 Etiology of 100 Consecutive, Hospitalized Acute Pericarditis Patients
aDenotes specific etiologies under subcategory. Percentages in parentheses demonstrate how cases are divided within the subcategory. Adapted from Zaya R, et al. Incidence of specific etiology and role of methods for specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol. 1995;75:378–382.
Treatment
The mainstay of treatment for acute pericarditis is the use of nonsteroidal anti-inflammatory medications. The choice of drug is usually based on clinician experience and drug toxicity; there is a lack of head-to-head comparative trials that would demonstrate the superiority of one over the other. Typical regimens include aspirin (2,400 to 3,200 mg daily), indomethacin (150 mg/d), and ibuprofen (3,200 mg/d). Specific circumstances for choosing aspirin over other NSAIDs include acute pericarditis occurring in the postmyocardial infarction period, as well as chronic kidney disease.6,7 The optimal duration of treatment is unknown. One general approach is to maintain the maximum dose of NSAID until normalization of CRP or ESR (usually 1 to 2 weeks), followed by gradual tapering of the medication, usually over a period of 3 to 4 weeks.8,9 Treatment failure and recurrent symptoms are oftentimes related to inadequate dose and duration of NSAID treatment.
Colchicine has been demonstrated to be beneficial by randomized controlled trials in both first presentation and recurrent presentations of pericarditis.8-10 Patients taking colchicine (loading dose 1 to 2 mg on day 1, followed by maintenance dose 0.5 to 1 mg daily thereafter), demonstrate fewer recurrent episodes. The total duration of colchicine should be for at least 3 months, certainly well past the resolution of symptoms and elevation of inflammatory markers. In the special circumstance of acute pericarditis occurring in the postpericardiotomy setting, the COlchicine for the Prevention of the Postpericardiotomy Syndrome (COPPS) trial also demonstrates the efficacy and safety of colchicine in preventing pericarditis and its complications following open heart surgery.11
Corticosteroids are oftentimes used in acute pericarditis but their role is controversial. Observational data would suggest that they may actually increase the risk for recurrent pericarditis.8 Furthermore, the dosages used are controversial, as one retrospective study suggests that lower doses of corticosteroids may be as effective as higher doses (prednisone 0.2 to 0.5 mg/kg/d vs. 1 mg/kg/d), with lower occurrences of side effects.12 In our opinion, their use in patients with acute pericarditis, particularly those thought to be idiopathic or viral, should be restricted to cases with refractory symptoms (particularly when patients have been receiving optimal doses of NSAIDs and colchicine with evidence of ongoing inflammation) or to cases where they are used to treat a systemic autoimmune process. In the post–myocardial infarction setting, glucocorticoids should be avoided, as their use may be associated with the development of free wall rupture.
Recurrent Pericarditis
Recurrent pericarditis manifests in two different patterns, intermittent or incessant. In cases of intermittent pericarditis, patients will have symptom-free intervals of 6 weeks or greater while off all treatment. In contrast, incessant pericarditis is marked by return of symptoms within a 6 week period, either in the tapering or discontinuation phase of some or all anti-inflammatories.13 Incessant pericarditis is particularly common in patients treated with corticosteroids; observational studies would suggest that corticosteroids are a risk factor for this complication of acute pericarditis. Recurrence of symptoms often coincides with objective findings of pericardial inflammation, particularly elevations of CRP and/or ESR. However, in some cases, patients will demonstrate their stereotypic symptoms without objective findings of inflammation. The treatment approach for recurrent pericarditis is similar to acute pericarditis. Nonsteroidal anti-inflammatories should be the backbone of therapy, along with the use of colchicine. Treatment with maximum doses tolerated should be maintained for at least 1 to 2 weeks or until symptoms and inflammatory markers normalize. Tapering of NSAIDs should be performed over at least a 3 to 4 week period. For some patients with recalcitrant disease, the period of tapering may require several months. Colchicine has been demonstrated to decrease the recurrence rate in patients with recurrent pericarditis.10 Patients should take it for 3 months; for those who require longer periods for NSAID taper, colchicine is continued until NSAIDs have been successfully weaned. Corticosteroids should be reserved only for refractory cases; they may also be considered in patients who demonstrate highrisk features, including evidence for transient constrictive pericarditis on echocardiography or CMR. Weaning of corticosteroids can be problematic, as symptoms often recur when doses are being tapered. We recommend the use of concomitant NSAIDs and colchicine when attempting to wean corticosteroids (triple therapy). Minimizing time on glucocorticoids is an important goal. Even in the presence of recurrent symptoms, we recommend continuing to wean doses as long as objective markers of inflammation are controlled by other anti-inflammatory agents. The prognosis for recurrent, idiopathic pericarditis is good, with no reported cases of constrictive pericarditis and approximately 3.5% cases of tamponade (usually occurring during initial attack).
Pericardial Effusion
Pericardial effusions come to attention in a variety of ways: they are discovered incidentally or as part of an evaluation for pericarditis, or they present symptomatically with symptoms and signs of tamponade.
Presentation and Diagnosis
The classic symptoms of tamponade include hypotension and dyspnea; patients may present with lower extremity edema, if the effusion has had a very slow rate of growth. Physical signs include tachycardia, elevated jugular venous pressure, and the presence of an exaggerated pulsus paradoxus. Electrocardiographic manifestations of a pericardial effusion include low voltage and, in extreme cases, electrical alternans. Pericardial effusion can be detected by a variety of testing, including echocardiography, CT, and MRI. Echocardiography is generally the test of choice with its widespread availability and its ability to provide twodimensional (2-D) imaging with concomitant hemodynamic data. The diagnostic echocardiographic findings for tamponade include the presence of a pericardial effusion, evidence of ventricular interdependence (demonstrated by variation of mitral and tricuspid inflow velocities by pulsed-wave Doppler), inferior vena cava (IVC) plethora, and collapse of the right atrium (Fig. 57.3), left atrium, and/or right ventricle (RV) (Fig. 57.4). In clinical practice, the diagnosis of early tamponade is challenging and is made by an appraisal of the clinical scenario and available data. Unfortunately, no single clinical or echocardiographic sign is completely reliable and a summation of all accessible information is necessary. On rare occasions, the diagnosis of tamponade is in question and a Swan–Ganz catheter is used to adjudicate a diagnosis. Classic hemodynamic findings include tachycardia; elevated right atrial (RA) pressure; an “M” pattern in the RA waveform, with a preserved x descent and blunted y descent; equalization of diastolic pressures in the RA, RV, and pulmonary capillary wedge pressure (PCWP); and a low normal or depressed cardiac output/index. No single hemodynamic finding is pathognomonic or completely sensitive for tamponade either. In cases where a patient is symptomatic and has a moderate to large effusion by echocardiography, the demonstration of an elevated RA pressure and a low normal or depressed cardiac index should, without other explanation, be sufficient to make a diagnosis.14
FIGURE 57.3 Transthoracic echocardiography, 4 chamber view. Collapse of the RA free wall (white arrow) during late atrial diastole.
FIGURE 57.4 Transthoracic echocardiography, subcostal view. There is inversion of the RA (white arrow) and RV free wall (red arrow) during mid-diastole.
Etiology
The etiology of pericardial effusions includes the differential diagnosis of acute pericarditis; commonly encountered scenarios being idiopathic or viral pericarditis, malignancy, rheumatologic disease, tuberculosis, myocardial infarction, and post open heart surgery. Iatrogenic causes, including cardiac perforations from interventional and electrophysiology procedures, may manifest dramatically with tamponade from relatively small effusions accumulating within minutes. On occasion, effusion may be present as a result of elevated intracardiac filling pressures, such as in pulmonary hypertension or congestive heart failure. Finally, patients with myxedema or hypothyroidism may occasionally manifest with pericardial effusions. According to published series, compared to cases of acute pericarditis, patients with large pericardial effusions often have specific etiologies that are identifiable rather than the majority of cases being idiopathic (Table 57.3).15
TABLE
57.3 Differences in Etiologic Diagnosis of Large Pericardial Effusions in Two Major Series
Adapted from Imazio M, et al. Medical therapy of pericardial disease Part II: noninfectious pericarditis, pericardial effusion and constrictive pericarditis. J Cardiovasc Med. 2010;11:785–794.
Cases of suspected tamponade in the post–open heart surgery setting deserve special attention. These cases are particularly challenging as effusions or hemorrhagic pericardial collections are frequently localized and the imaging by surface echocardiography is often suboptimal. Findings usually seen in tamponade, particularly relating to ventricular interdependence, such as pulsus paradoxus, and mitral and tricuspid inflow variation, are not reliable for a variety of reasons. They may be exaggerated or obliterated by changes in pulmonary and intrathoracic dynamics (pleural effusions, mechanical ventilation). Furthermore, localized collections, causing collapse of the right or left atria, may not manifest with ventricular interdependence. In this setting, for patients who have unexplained hemodynamic instability, chamber compression and/or a localized pericardial collection is the most important finding. When imaging by routine surface echocardiography is inadequate, further imaging, such as with transesophageal echocardiography, is recommended.
Treatment
Clinical tamponade, with hemodynamic compromise, is an absolute indication to drain a pericardial effusion. Relative indications include pretamponade physiology (typically seen by echocardiography), large effusions that fail to regress with medical therapy, and the need for diagnostic sampling (particularly to make a diagnosis of bacterial or neoplastic pericarditis). There are multiple approaches that may be taken. Percutaneous drainage via pericardiocentesis is the most expedient and least morbid procedure. This may be accomplished via echocardiographic or fluoroscopic guidance; the two general approaches are via the subxiphoid or para-apical spaces. Surgical drainage is pursued for a variety of reasons: the expectation for recurrence and need for ongoing drainage (neoplastic pericarditis), inability to safely access the pericardial space via pericardiocentesis (typically posteriorly located effusions), the need for a pericardial biopsy, and loculated effusions. In surgical procedures, a portion of the pericardium is excised to create a “window,” through which fluid may continually drain. The two incisional approaches include a subxiphoid window and via left thoracotomy (or thoracoscopy). There is a percutaneous option to more durable drainage: balloon pericardiotomy, where a balloon is used to create a tear in the pericardium (similar to a pericardial window) that may be performed by selected practitioners.
Constrictive Pericarditis
Constrictive pericarditis is one of the most challenging diagnoses to make in cardiology because it is rare, has a variety of presentations, and the diagnostic criteria are nonspecific and insensitive.
Presentation and Diagnosis
The classic and most typical presentation of constrictive pericarditis is predominant right-sided heart failure, with symptoms of lower extremity edema and abdominal distension, usually from ascites. Other common presentations include dyspnea (from left-sided heart failure or pleural effusions), abnormal liver function tests, and cirrhosis. Patients oftentimes are treated by noncardiologists for a prolonged period of time before the diagnosis of constriction becomes evident. In truth, patients with constriction have a wide spectrum of disease severity, spanning from patients with subclinical disease to severe refractory heart failure.
The diagnosis of constrictive pericarditis requires the appraisal of clinical, imaging and hemodynamic data. On clinical examination, the patient should demonstrate signs of right-sided heart failure, including elevated jugular venous pressure, lower extremity edema, and/or signs of ascites. The absence of all of these would make clinically significant constrictive physiology highly unlikely. The presence of a pericardial knock, a diastolic heart sound similar to an S3, is helpful but insensitive. Chest x-ray, particularly the left lateral view, may demonstrate calcified pericardium, though this finding is not universal to all cases of constrictive pericarditis (Fig. 57.5). Transthoracic echocardiography is the initial test of choice and is ideally performed with a respirometer. Relevant findings include conical compression of the chambers, increased pericardial thickening/calcification, “tethering” of the atria and/or ventricles, diastolic septal bounce, mitral and tricuspid inflow, and pulmonary vein and hepatic vein flow variation (Fig. 57.6) by pulsedwave Doppler, normal or exaggerated mitral annular tissue Doppler velocities (Fig. 57.7A and B), IVC plethora, and increased hepatic vein flow reversal with expiration. The preservation (or even exaggeration) of tissue Doppler velocities deserves some special attention, as annular velocities are generally reduced in cardiomyopathies that are part of the differential diagnosis.18,19 In other conditions, as the left ventricular pressure rises, the tissue velocities (e′) fall and the resulting ratio of E/e′ becomes elevated. Conversely, in constrictive pericarditis, increased left ventricular pressure results in paradoxical elevation in tissue velocity; this phenomenon is known as annulus paradoxus and is unique to constriction. Cardiac MRI may show findings of diastolic septal bounce, diastolic restraint, conical deformity of the ventricles (Fig. 57.8), thickening of the pericardium (>4 mm, Fig. 57.9), and exaggerated septal motion with inspiration (Fig. 57.10A,B). There are a number of hemodynamic findings by cardiac catheterization, including but not limited to elevation and equalization of diastolic pressures, “square root sign,” and “M” pattern of the RA pressure tracing with prominent Y descent. The most specific hemodynamic findings for constrictive pericarditis include discordance of RV and LV systolic pressure variation with respiration (Fig. 57.11) and a decrease in pulmonary–capillary wedge pressure to LV end-diastolic pressure gradient with inspiration.20 It should be emphasized that no single test or finding is completely sensitive or diagnostic for constrictive pericarditis. Often, a diagnosis is made with the help of multiple tests and with only some of the characteristic findings present. In considering the entities that are causing the patient’s symptoms, the typical differential diagnoses that present similarly to constriction are right ventricular failure, severe tricuspid regurgitation, and infiltrative cardiomyopathies (most commonly cardiac amyloidosis). Much attention is paid toward differentiating “constrictive” versus “restrictive” physiology (Table 57.4). Although many of the hemodynamic findings overlap, in clinical practice, the distinction is made by the clinical context and echocardiography appearance of the heart. The exception to this rule is in the setting of patients who have had previous chest radiation. For these patients, both constriction (pericardial involvement) and restriction (by myocardial involvement) are real diagnostic possibilities; they may even coexist in a particular patient. Discerning the dominant pathology in these cases is extraordinarily challenging.
FIGURE 57.5 Chest x-ray, left lateral view. A patient with constrictive pericarditis who has severe calcification (white arrows) of the pericardium, which can be best seen on the left lateral view of the chest x-ray.
FIGURE 57.6 Transthoracic echocardiography, pulsed-wave Doppler at the mitral valve leaflet tips. Significant respiratory variation of the mitral E velocity (43%), which decreases with onset of inspiration (white arrow) and increases with onset of expiration (red arrow). Insp, inspiration; exp, expiration.
FIGURE 57.7 Transthoracic echocardiography, tissue Doppler imaging recorded at the septal (A) and lateral mitral annulus (B). There is supranormal e’ velocity (white arrow), suggesting rapid early diastolic ventricular filling. The septal e’ velocity (15 cm/s) is greater than the lateral e’ velocity (11 cm/s), a phenomenon known as “annulus reversus." This is unique to constrictive pericarditis and is thought to be related to tethering of the lateral ventricular wall to the pericardium.
FIGURE 57.8 Cardiac MRI,dark-blood sequence, 4 chamber view. There is thickening of the pericardium (white arrows) and conical deformity of the RV (red arrow).
FIGURE 57.9 Cardiac MRI, dark-blood imaging, short axis view. The black border (white arrows) surrounding the ventricles represents severe thickening of the pericardium, measuring 8 mm in maximal thickness.
FIGURE 57.10 A, B: Cardiac MRI, cine sequences taken during one respiratory cycle. Ventricular interdependence, a hallmark of constrictive pericarditis, is demonstrated by the changes in morphology of the interventricular septum during the respiratory cycle. At end expiration (10A), the interventricular septum has its usual morphology. During inspiration, there is an increase in venous return to the RV; the confinements of the pericardial space prohibit RV expansion, except for bowing of the interventricular septum toward the LV, causing impairment LV filling. This is demonstrated by exaggerated interventricular septal flattening (white arrow) during diaphragmatic lowering (red arrow).
FIGURE 57.11 Simultaneous LV and RV pressure tracings. There is discordance in the timing of peak LV (arrows) and RV (arrowheads) pressures, with respect to respiratory variation. This can be quantitatively demonstrated by changes in the areas under the curves of both LV and RV pressures during respiration.
TABLE
57.4 Differential Imaging Characteristics Between Restrictive Cardiomyopathy and Constrictive Pericarditis
Adapted from Klein AL, Asher C. Diseases of the pericardium, restrictive cardiomyopathy and diastolic dysfunction.
In: Topol EJ, ed. Textbook of Cardiovascular Medicine. 3rd ed. Philadelphia, PA. Lippincott, Williams and Wilkins; 2007:420-459.
Once a diagnosis of constrictive pericarditis has been made, an important determination to make is the clinical context of the constrictive physiology. On occasion, patients with acute pericarditis, manifesting with severe pericardial inflammation, may demonstrate constrictive physiology.21 In this setting, the physiology of constriction may be reversible with aggressive anti-inflammatory measures, as it is related to inflammation and tissue edema. In more typical cases, patients with constriction will present with established pericardial scarring that is irreversible. Short of surgical inspection, there is no perfect method of making the distinction between these two entities. Thus, for patients presenting with acute pericarditis symptoms with signs of inflammation (pericardial-type chest pain, ESR and/or CRP elevation, pericardial effusion, and/or MRI enhancement) and constrictive pericarditis, a trial of anti-inflammatories should be considered prior to surgical therapy. In limited experience, pericardiectomy performed in patients with acute inflammation can result in significant postoperative complications.
Effusive–constrictive pericarditis is another clinical entity that deserves special attention. Patients with this condition demonstrate signs of constrictive physiology, clinically and by imaging, in the setting of a significant pericardial effusion. As many of the hemodynamic changes seen in both tamponade and constriction overlap, it is difficult to determine the relative contribution of the pericardial effusion versus the thickened pericardium to the patient’s clinical presentation. When a significant contribution of pericardial effusion is postulated, the patient may require pericardiocentesis in order to determine the significance of pericardial constriction.
As with pericardial effusions, the differential diagnosis of the etiology of constrictive pericarditis is similar to that of acute pericarditis. As pericardial scarring is a process that usually occurs over a period of time, the history usually reveals an episode of pericarditis that occurred remotely. Classically, the separation between initial insult and presentation of constrictive pericarditis is by years, even decades. This is true for patients with constriction as a result of idiopathic pericarditis and radiation-induced pericarditis. However, on occasion, patients may present as soon as months out from their initial episode, particularly following cardiac surgery. Common causes of constriction that are seen in practice include idiopathic/viral pericarditis, postradiation therapy, and post–open heart surgery.
Treatment
Patients with constrictive pericarditis may manifest along a wide spectrum of disease severity, from the asymptomatic patient with detectable constriction by imaging tests to the debilitated patient with severe right heart failure symptoms. As stated previously, the patient with the possibility of transient constriction in the setting of acute pericarditis deserves a several month course of aggressive antiinflammatory treatment to see if their physiology improves. In patients with established pericardial scarring, medical management of constriction revolves around diuretic therapy to relieve congestive symptoms. It is still unclear what the appropriate disease severity threshold should be to recommend surgical pericardiectomy. Most would agree that patients with refractory symptoms, and/or New York Heart Association (NYHA) Class III/IV heart failure should be considered for surgical referral. However, the appropriate management of patients who are discovered earlier in the natural history of the disease course or who have minimal symptoms remains undetermined. Observational data suggest that patients who are operated on later in their disease course have worse outcomes.22,23 Some of the reluctance for surgical referral revolves around an early surgical series demonstrating a high rate of morbidity and mortality following pericardiectomy. However, more contemporary data suggest that surgical risk in a high volume setting is much lower.24,25 In determining a patient’s surgical risk, some consideration should be given to the etiology of pericardial constriction. In one series, constrictive pericarditis related to mantle radiation had significantly worse perioperative and long-term mortality compared with patients with idiopathic constrictive pericarditis undergoing pericardiectomy.25 Those with constriction as a result of previous open heart surgery had an intermediate short and long-term mortality.
ACKNOWLEDGMENT
We would like to thank Marie Campbell this chapter.
REFERENCES
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QUESTIONS AND ANSWERS
Questions
1. A 65-year-old man has just undergone primary percutaneous intervention for an acute, ST elevation myocardial infarction. Several hours following the procedure, he complains of new onset chest pain, different from his presenting complaint, worse with inspiration and radiating to both of his shoulders. His electrocardiogram demonstrates subtle, diffuse ST elevations in the inferior, lateral, and anterior leads. You perform an echocardiogram that demonstrates a small pericardial effusion, without evidence for a mechanical complication following his myocardial infarction. Which of the following would be the next best step?
a. Initiate ibuprofen 800 mg three times daily
b. Initiate prednisone 1 mg/kg daily
c. Initiate aspirin 800 mg four times daily
d. Return to the cardiac catheterization laboratory for repeat coronary angiography
2. A 77-year-old man with a history of end-stage renal disease presents with fevers and chest pain for 2 weeks. He has been on hemodialysis for more than 5 years and has not missed any recent sessions. He appears uncomfortable and diaphoretic. His vital signs are T103F, HR 82, BP 143/96 RR 12. His pulsus paradoxus is 6 mm Hg. His examination is remarkable for a pericardial friction rub. His electrocardiogram demonstrates diffuse ST elevations with PR depression. A complete blood count demonstrates a WBC of 14K. An echocardiogram demonstrates a large pericardial effusion but no signs of tamponade physiology. The next best step in managing this patient is:
a. Initiate ibuprofen 800 mg three times daily with colchicine 0.6 mg twice daily.
b. Initiate prednisone 0.5 mg/kg daily for 4 weeks followed by a tapering regimen over 3 months.
c. Call the referring nephrologist for more intensive hemodialysis.
d. Perform a pericardiocentesis.
3. A 43-year-old woman presents to your office complaining of lower extremity edema and increased abdominal girth. She had undergone mantle radiation for Hodgkin’s lymphoma 20 years prior. On examination, you find an elevated jugular venous pressure, severe lower extremity edema, and a fluid wave suggesting abdominal ascites. The following echocardiographic findings support a diagnosis of constrictive pericarditis except:
a. A septal tissue Doppler velocity of 4 cm/s
b. Plethora of the inferior vena cava
c. A decrease in mitral inflow early (E) velocity with inspiration
d. An increase in tricuspid inflow early (E) velocity with inspiration
e. Increased hepatic vein flow reversal with expiration
4. Central venous pressure examination in tamponade reveals:
a. Prominent X descent (rapid ventricular filling during systole) and absent Y descent (absent diastolic filling)
b. Prominent X and Y descents
c. Prominent Y but blunted X descent
d. These waveforms can only be discerned with right heart catheterization
5. What is the most common cause of constrictive pericarditis in the United States?
a. Previous cardiac surgery
b. Mantle radiation
c. Tuberculosis
d. Idiopathic or viral
Answers
1. Answer C: Although the incidence of acute pericarditis in the postmyocardial infarction setting has decreased with early revascularization, it is still a commonly encountered scenario. In this setting, there is some concern that the use of nonsteroidal antiinflammatory drugs (NSAIDs) and/or corticosteroids may increase the risk of free wall rupture. As such, using high-dose aspirin is the most appropriate therapy in this situation. The presenting symptoms and ECG do not support stent thrombosis or a complication of the revascularization procedure, so there is no indication for repeat angiography.
2. Answer D: A patient who has been on hemodialysis for a prolonged period of time, particularly if they have not missed any hemodialysis sessions, is unlikely to present with uremic pericarditis. In this case, bacterial pericarditis should be considered on the differential diagnosis. Prior to initiating typical anti-inflammatory therapy, a pericardiocentesis should be performed to rule out bacterial seeding of the pericardial space.
3. Answer A: In constrictive pericarditis, the tissue Doppler velocity of the mitral annulus is typically normal or even exaggerated (8 cm/s or greater). This represents normal diastolic function of the myocardium itself; the diastolic abnormalities in pure constrictive pericarditis are related to constraint from the pericardium. Occasionally, pericardial scarring adjacent to the lateral wall of the LV can cause tethering of the mitral annulus to the pericardium; in these cases, the lateral tissue Doppler velocity may be decreased (a phenomenon known as annulus reversus). As such, for constrictive pericarditis, it is more reliable to use the septal measurement of the tissue Doppler velocity. Choices b-e represent typical echocardiographic findings in patients with constrictive physiology.
4. Answer A: Prominent X descent (rapid ventricular filling during systole) and absent Y descent (absent diastolic filling).
5. Answer D: Idiopathic or viral pericarditis. In one series (Bertog et al.), the etiology was idiopathic in 46%, previous cardiac surgery in 37%, mantle radiation in 9%, and miscellaneous (including tuberculosis) in 8% of the patients. In some series, the representation of constriction as a result of previous PiSSSI cardiac surgery is even higher.