Abstract
Pericardial disease may present as an isolated condition or as a manifestation of systemic illness. Recognition of the clinical signs and symptoms of pericardial disorders in the primary care setting is critical for appropriate, and potentially lifesaving, triage and management. This chapter considers acute pericarditis and its potential complications relevant to the primary care provider: recurrent pericarditis, pericardial effusion, and constrictive pericarditis.
1 Introduction
Pericardial disease may present as an isolated condition or as a manifestation of systemic illness. Recognition of the clinical signs and symptoms of pericardial disorders in the primary care setting is critical for appropriate, and potentially lifesaving, triage and management. This chapter considers acute pericarditis and its potential complications relevant to the primary care provider: recurrent pericarditis, pericardial effusion, and constrictive pericarditis.
2 Anatomy/Physiology
The pericardium is a fibroserous sac that consists of two layers. The outer fibrous layer (the parietal pericardium) is composed of collagen and elastic fibers, which allow the pericardium to gradually expand if subjected to chronic stretch. The internal portion of the fibrous pericardium is composed of a serous layer, which reflects onto the epicardial surface of the heart, forming the visceral pericardium [1]. The space between the parietal and visceral layers normally contains 15–35 mL of serous fluid, providing lubrication to the heart’s movements. The pericardium is well innervated with nerve afferents so that acute inflammation produces pain and vagal reflexes [2].
The pericardium attaches to the diaphragm, sternum, and neighboring structures in the anterior mediastinum and, in this manner, serves to anchor the heart within the thorax. Additionally, the pericardium is thought to limit acute dilatation of the heart [3]. The ability to restrain myocardial expansion is likely one of the most important functions of the pericardium. Despite these presumed actions, the complete absence of the pericardium (e.g., congenitally) is generally without clinical consequence [4].
The fibrous pericardium has the tensile strength of rubber [5]. As such, a sudden increase in volume within the pericardial space results in an equal external pressure against each of the cardiac chambers, which can lead to hemodynamic instability, as described below. Conversely, a slow increase in volume, over weeks to months, allows gradual stretching and accommodation of greater volume before chamber compression occurs.
3 Acute Pericarditis
3.1 Case Study 1
A 51-year-old woman with a history of Hodgkin lymphoma presents to the outpatient office with the gradual onset of left anterior pleuritic chest pain and mild dyspnea. The chest pain is non-radiating, dull, and worse with chest and arm movements and is relieved by sitting forward. She also reports 2 weeks of malaise and fatigue accompanied by low-grade fever. On physical examination, she appears uncomfortable and anxious. The temperature is 99 °F, pulse rate 120 bpm, and blood pressure 125/70 mmHg, with pulsus paradoxus of 6 mmHg. The jugular venous pressure is 7 cm water. Her chest is clear to percussion and auscultation. On cardiac examination there is no retrosternal dullness. No murmurs, gallops, or rubs are auscultated. The electrocardiogram (Fig. 22.1) demonstrates ST-segment elevation in most of the ECG leads. A transthoracic echocardiogram (Fig. 22.2) obtained at the outpatient center reveals a small circumferential pericardial effusion with no signs of cardiac tamponade physiology.
3.1.1 Epidemiology and Etiology
Case Study 1 depicts the classic presentation of acute pericarditis, an inflammatory condition of the pericardial sac, the differential diagnosis of which is broad (Table 22.1). As many as 90% of cases of acute pericarditis are considered to be post-viral or of unknown (“idiopathic”) origin [6]. The majority of idiopathic cases are actually likely due to undetected viral infection, often with enteroviruses (e.g., coxsackievirus, echovirus) [7]. Less common viral causes of acute pericarditis include herpesviruses (CMV, Epstein–Barr virus, HHV-6), adenovirus, and parvovirus B19. Acute pericarditis can also result from non-viral infections, autoimmune disorders, malignancy (most commonly lung or breast carcinoma or lymphoma), and uremia, following transmural myocardial infarction, cardiac surgery, or chest irradiation therapy or as a result of specific medications such as isoniazid and hydralazine [5, 7, 8].
Tuberculosis (TB) is only rarely encountered as a cause of pericarditis in industrialized countries . However, it is an important etiology in immunocompromised patients and in less developed regions of the world. In Africa, TB is the most common source of pericardial disease in patients with HIV infection [8].
Echocardiographic or postmortem evidence of pericardial inflammation is very common in autoimmune disorders such as rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis with reported prevalences of 40–80%. However, symptomatic manifestations of acute pericarditis occur in <30% of patients with these conditions [9, 10].
A form of post-MI pericarditis that may be encountered in the primary care office is Dressler syndrome , which can arise weeks or months following an acute myocardial infarction and is thought to be of autoimmune origin, resulting from exposure to antigens released from necrotic myocardial cells. This form of pericarditis has become rare in the era of acute reperfusion therapies for acute ST-segment elevation myocardial infarction. A more common similar syndrome, post-pericardiotomy pericarditis , may present weeks following cardiac surgical procedures [7].
3.1.2 Clinical Presentation
Patients with acute pericarditis typically present with chest discomfort that may mimic more serious conditions such as myocardial infarction or pulmonary embolism [6]. However, the pain is typically pleuritic and positional in nature, worsening with recumbency and improving when the patient sits and leans forward. The discomfort can radiate widely; however, localization to the trapezius ridge is highly suggestive of pericardial irritation, as the phrenic nerve innervates both the pericardium and the trapezius muscle [2]. The discomfort tends to be rapid in onset and can last for hours to days [11].
Symptoms of a viral syndrome, including low-grade fever and malaise, may precede post-viral pericarditis. In cases of pericarditis that develop more gradually (e.g., uremia, collagen vascular conditions, tuberculosis, neoplastic disease), the patient may not describe any chest pain at all. High fever and more severe symptomatology are typical of bacterial (purulent) pericarditis.
A thorough review of systems and past history can help identify specific etiologies of acute pericarditis. For example, drug-induced pericarditis should be considered in a patient taking isoniazid, diphenylhydantoin, or hydralazine. A history of HIV or mycobacterium infection should lead to consideration of those pathogens or associated complications. A prior malignancy may raise the concern of recurrence manifesting as pericardial involvement.
3.1.3 Physical Examination
Approximately one-third of patients with acute pericarditis manifest a pericardial friction rub [8]. It is best auscultated over the left mid-to-lower sternal border, while the patient leans forward [12]. The character of the rub can be scratchy, leathery, or the crunchy sound of walking in snow and can be distinguished from a pleural rub by a breath hold, which extinguishes the latter [7, 12]. It is most often triphasic, representing the phases of rapidly changing cardiac volumes: ventricular ejection, rapid ventricular filling in early diastole, and atrial systole [5, 12]. The mechanism that produces the rub may not solely be the interaction between the inflamed pericardial layers as the finding can be detected even in patients with large pericardial effusions, in whom the layers are widely separated from one another [12]. In any patient with acute pericarditis, it is important to inspect for potential signs of cardiac tamponade described in more detail below: hypotension, distended neck veins, and distant heart sounds.
3.1.4 Electrocardiogram
The electrocardiogram can help distinguish pericarditis from other forms of chest discomfort. There are usually diffuse ST-segment elevations in the limb and precordial leads, typically with the exception of lead aVR. This is commonly accompanied by PR-segment deviation opposite to the direction of the P-wave. These findings reflect epicardial irritation of both the ventricles and the atria [13]. The electrocardiographic abnormalities typically evolve in four stages [2, 14, 15]:
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Stage 1—Diffuse ST-segment elevations and PR-segment deviations (see Fig. 22.1)
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Stage 2—Normalization of the ST- and PR-segments
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Stage 3—Diffuse T-wave inversions (often weeks later)
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Stage 4—Complete resolution
More than 60% of patients with acute pericarditis present with Stage 1 electrocardiographic findings [8]. Anti-inflammatory treatment has been shown to prevent further progression of the ECG abnormalities [16].
There are several characteristics that distinguish the ECG findings of pericarditis from those of acute myocardial infarction. In patients with acute ST-segment elevation myocardial infarction (STEMI), the ST-segment elevation is localized to the region of the involved myocardium and is accompanied by ST depression in the opposite leads. The direction of the ST-segment elevation is typically concave upward in pericarditis but convex upward in STEMI. In addition, in infarction, T-wave inversions develop, while the ST-segments are still elevated, whereas this occurs many days later in pericarditis, after the ST-segments have returned to baseline (Stage 3). Finally, acute myocardial infarction does not cause deviations of the PR-segment.
Individuals with the common ECG variant known as early repolarization display baseline ST elevations that can mimic Stage 1 pericarditis. However, in distinction to those with early repolarization, the height of the ST-segment in acute pericarditis tends to be >25% of the height of the T-wave.
3.1.5 Chest X-Ray
The chest radiograph may be normal in uncomplicated pericarditis . However, the presence of a large effusion (>250–300 mL) is manifest as a symmetrically enlarged cardiac silhouette [7].
3.1.6 Blood Studies
Measurement of acute and convalescent serum viral titers, or virus identification by polymerase chain reaction (PCR) testing, is not of practical value in the diagnosis of pericarditis as most patients will have recovered before such results are available. Indicators of systemic inflammation are often elevated in acute pericarditis, and while there is no consensus on the utility of measuring markers, such as C-reactive protein or erythrocyte sedimentation rate (ESR), they can be helpful in establishing the diagnosis or following the course of disease [7]. In general, a modestly elevated ESR is consistent with idiopathic or post-viral pericarditis, while higher levels are suggestive of underlying inflammatory states such as rheumatoid arthritis, systemic lupus erythematosus, or tuberculosis. Similarly, a mild leukocytosis is typical of viral or idiopathic pericarditis, whereas a markedly elevated white blood cell count is more consistent with purulent pericarditis. In 35–50% of patients with pericarditis, troponin levels are increased due to extension of inflammation to the adjacent myocardium [17,18,19]. However, elevation of cardiac-specific troponins is not a negative prognostic marker in acute pericarditis [20,21,22].
3.1.7 Echocardiogram
Current guidelines recommend that a transthoracic echocardiogram be obtained in patients with suspected pericardial disease to assess for effusion, contributing pathology, and evidence of impending hemodynamic compromise [7]. In patients with uncomplicated pericarditis, the echocardiogram may be completely normal. If a pericardial effusion has formed, it is visualized as an echo-free space external to the cardiac chambers, as in Fig. 22.2 [6]. The smallest effusions appear posterior to the left ventricle because of the effect of gravity. Larger effusions wrap around the sides of the heart and, if more than approximately 250 mL has accumulated , appear anterior to the right ventricle as well.
3.1.8 Treatment
Idiopathic or post-viral pericarditis is a self-limited condition that tends to improve spontaneously within 1–3 weeks. Drug therapies are employed for earlier symptomatic relief. The European Society of Cardiology has published guidelines with management strategies [7]. The mainstay of acute treatment is oral nonsteroidal anti-inflammatory agent (NSAIA) therapy such as aspirin (2–4 g daily), ibuprofen (1600–3200 mg daily), or indomethacin (75–225 mg daily) [7]. No one NSAIA appears to be more effective than others; ibuprofen is used frequently in North America, and aspirin tends to be preferred in Europe. For individuals who have sustained a recent myocardial infarction, aspirin is the drug of choice given a concern of impairment of healing of infarcted tissue by other NSAIAs in animal models [6]. In addition to oral NSAIAs, parenteral ketorolac has been shown to be effective at resolving symptomatic acute pericarditis [23].
Colchicine, in combination with an NSAIA, has been shown to shorten initial symptoms and reduce the recurrence rate of acute pericarditis. The prospective ICAP trial randomized patients with a first episode of acute pericarditis to colchicine (0.5 mg twice daily or 0.5 mg once daily for weight ≤70 kg for 3 months) or placebo in addition to NSAIA therapy. Colchicine reduced the rate of recurrent pericarditis (16.7% compared to 37.5% in the placebo-treated patients) and shortened the duration of initial symptoms [24]. Conversely, corticosteroids are not recommended as first-line agents in uncomplicated pericarditis as their use predisposes to relapses [7, 25, 26].
Symptoms typically resolve within days of treatment, often after the first few doses. NSAIAs are usually continued for 7–14 days followed by gradual reduction in dosage over 1–2 weeks for a total treatment time of 3–4 weeks. If colchicine is used, it should be continued for 3 months, as was the protocol in clinical trials. Acute pericarditis is not an absolute contraindication to concurrent anticoagulation therapy in patients with atrial fibrillation or intracardiac thrombus. However, the risks and benefits of continued anticoagulation must be evaluated on a patient-by-patient basis.
3.1.9 Triage
Identification of high-risk features is important in the triage of patients with acute pericarditis. Findings that warrant hospitalization and close observation include a large circumferential pericardial effusion, cardiac tamponade, patients who are on anticoagulation therapy, high fever, underlying immunosuppressed state, evidence of accompanying myocarditis, or trauma-associated pericarditis (Fig. 22.3) [21, 27]. There is no consensus on triage of patients who do not exhibit such high-risk features. In general, patients with uncomplicated idiopathic/post-viral pericarditis can be safely treated in an observation setting for several hours, have an echocardiogram performed, and, if stable, return home [21].
4 Recurrent Pericarditis
Between 15% and 30% of patients treated for acute pericarditis experience relapses after a symptom-free interval [11, 24]. Symptoms are similar to the initial episode, characterized by fever, pleuritic chest pain, pericardial rub, and elevation of inflammatory markers [28]. Recurrences may relate to an immune-mediated reaction following the initial episode or may be the manifestation of a previously undiagnosed and ongoing inflammatory condition such as an autoimmune disorder [6, 11].
Relapses can be challenging to suppress. The first defense is prevention of recurrent episodes by optimizing treatment of the index presentation. As noted above, the ICAP trial demonstrated a decreased recurrence rate in patients with acute pericarditis treated with NSAIA therapy plus colchicine compared with an NSAIA alone [24]. Once a recurrence develops, symptoms often respond to renewed therapy with an NSAIA agent plus colchicine. In the prospective Colchicine for Recurrent Pericarditis (CORE) trial, 84 patients with a first bout of recurrent pericarditis were randomized to aspirin alone versus aspirin in addition to colchicine (1.0–2.0 mg on the first day and then 0.5–1.0 mg daily for 6 months). Compared with aspirin alone, the combination reduced further recurrences by 50%, and symptom persistence at 72 h fell by approximately 33% [29]. Recurrent episodes with refractory symptoms may require the addition of a corticosteroid [7]. Of note, a retrospective review of 100 patients with recurrent pericarditis concluded that lower steroid doses (prednisone 0.2–0.5 mg/kg/day) were better tolerated and were associated with fewer subsequent recurrences than historically used higher dosages [7, 30]. Patients with persistent symptoms or recurrent episodes that fail to cease with these measures should be referred to a specialist for consideration of advanced approaches, such as more powerful immunosuppressive regimens or pericardiectomy [7].
5 Pericardial Effusion
5.1 Case Study 2
The 51-year-old woman from Case Study 1 returns to her primary care doctor 2 weeks after her initial presentation. Her symptoms had responded initially to a course of ibuprofen plus colchicine. The colchicine was discontinued after a few days due to diarrhea. Her current symptoms are increasing dyspnea on exertion and chest fullness when she leans toward her left side. She denies fevers, sweats, or chills.
On physical examination , the temperature is 98 °F, heart rate 115 bpm, and blood pressure 112/70 mmHg with a pulsus paradoxus of 15 mmHg. The jugular venous pressure is 12 cm water. The chest is clear to auscultation. On cardiac exam, there is retrosternal dullness, and a pericardial friction rub is auscultated. There is no abdominal distension, hepatomegaly, or peripheral edema. The patient undergoes an urgent echocardiogram (Fig. 22.4), which demonstrates a large circumferential pericardial effusion with right atrial and right ventricular diastolic collapse.
5.1.1 Etiology
A pericardial effusion results from the accumulation of fluid within the potential space between the visceral and parietal pericardial layers. Fluid accumulation can result from an inflammatory reaction, direct trauma, or obstruction of lymphatic drainage [11]. The etiologies of acute pericardial disease in Table 22.1 are all potential causes of pericardial effusion accumulation. Large effusions are most commonly idiopathic, neoplastic, or uremic in origin [29, 31]. As many as 15% of patients with idiopathic pericarditis and 60% of patients with purulent or malignant disease present with an effusion [32].
Effusions that are most likely to progress to tamponade are those caused by trauma, non-viral infections (bacterial, fungal), and malignancy. It is unusual for idiopathic/post-viral pericarditis to lead to tamponade.
5.1.2 Pathophysiology
The pericardium has only a limited potential for expansion. A sudden increase in pericardial volume, even of small quantity, can lead to hemodynamic instability due to external compression of the cardiac chambers, resulting in diminished cardiac output and possible cardiogenic shock. Conversely, a slowly accumulating effusion (over weeks or months) can stretch the pericardium and accommodate a much larger volume (e.g., >1 L) before tamponade physiology develops [5].
5.1.3 Clinical Presentation
In the primary care setting , a pericardial effusion may come to light in the setting of known pericarditis, as an incidental finding on an imaging study, or in an individual who presents with symptoms of tamponade [2, 33]. In the absence of tamponade physiology, a patient with a pericardial effusion may not have symptoms attributable to it. Conversely, patients with tamponade typically manifest dyspnea, chest discomfort, cough, and evidence of decreased cardiac output [11, 33].
5.1.4 Physical Examination
Patients with a small pericardial effusion may not have any abnormal findings on exam. The only clue to its presence may be distant heart sounds on auscultation and retrosternal dullness to percussion. A pericardial rub may be present [12]. Conversely, in patients who have developed tamponade, the triad of hypotension, distant heart sounds, and elevated jugular venous pressure is expected [34]. Furthermore, tamponade physiology produces pulsus paradoxus, an abnormal decline in blood pressure with normal inspiration (see Section 22.6) [2, 34]. One review analyzed five features observed in patients with tamponade: dyspnea, tachycardia, pulsus paradoxus, elevated jugular venous pressure, and cardiomegaly on chest radiography. Of these features a pulsus paradoxus >10 mmHg identified the presence of tamponade with a sensitivity of 98% and specificity of 70% [34, 35]. Of note, pulsus paradoxus may not appear in tamponade when coexisting conditions impede respiratory alterations in left ventricular filling, including left ventricular dysfunction, aortic regurgitation, and atrial septal defects. Conversely, conditions that cause large alterations in intrathoracic pressure (e.g., advanced obstructive airway disease or pulmonary embolism) can produce pulsus paradoxus in the absence of tamponade.
6 Pulsus Paradoxus
Measurement of pulsus paradoxus at the bedside is of great value in assessing the hemodynamic significance of a pericardial effusion. During the respiratory cycle in healthy patients, inspiration draws blood from the systemic veins into the thorax and the right side of the heart, causing the interventricular septum to bow toward the left, which transiently reduces LV filling. As a result, LV stroke volume declines, and systolic blood pressure normally falls slightly (<10 mmHg) with inspiration. In tamponade, this mechanism is exaggerated by the presence of high-pressure pericardial effusion compressing the cardiac chambers. The more marked inspiratory decline in LV filling in tamponade reduces the LV stroke volume to a greater extent, and the systolic blood pressure falls >10 mmHg.
6.1 Procedure to Measure Pulsus Paradoxus
The arm sphygmomanometer is inflated to a level greater than the systolic pressure. As the cuff is slowly deflated, note the pressure at which the first Korotkoff sound is heard. Next listen as the Korotkoff sound at that level disappears with inspiration. Then continue to deflate the cuff slowly until the Korotkoff sounds stop drifting in and out, i.e., they are heard during both inspiration and expiration. The difference in pressure between the first Korotkoff sound and when the Korotkoff sounds are heard during both inspiration and expiration is the pulsus measurement.
6.2 Electrocardiogram
A large pericardial effusion decreases transmission of electrical forces from the myocardium resulting in decreased voltage on the ECG [34]. In addition, a sufficiently large effusion allows the heart to swing back and forth within the pericardial sac. This is manifest as beat-to-beat variation in the axis of the QRS complex on the ECG, causing electrical alternans (Fig. 22.5) [36].
6.3 Chest X-Ray
If a pericardial effusion is greater than ~250–300 mL in volume, the cardiac silhouette enlarges, typically in a symmetrical fashion.
6.4 Echocardiogram
Echocardiography is the most useful noninvasive modality in the diagnosis of pericardial effusion and cardiac tamponade [37, 38]. The location and size of the pericardial effusion as well as its hemodynamic impact can be readily assessed. Important signs of tamponade include diastolic collapse of the right ventricle and the right atrium, distention of the inferior vena cava, and exaggerated reciprocal respiratory variations in mitral and tricuspid diastolic Doppler velocities. Magnetic resonance imaging and computed tomography can also help localize and characterize pericardial effusions but rarely add to the clinical information afforded by echocardiography in the evaluation of tamponade physiology [39].
6.5 Treatment of Pericardial Effusion with Cardiac Tamponade
Cardiac tamponade is a medical emergency requiring rapid recognition and management. Patients who present in the primary care setting with findings consistent with this diagnosis should be immediately triaged to the hospital for consideration of urgent pericardiocentesis. When performed, pericardial fluid analysis for diagnostic purposes should include cytology and bacterial, fungal, and mycobacterial cultures [8, 40]. However, the diagnostic yield of pericardial fluid culture for M. tuberculosis is low. If TB is suspected, a more rapid diagnosis from the pericardial fluid can be accomplished by polymerase chain reaction or by the finding of an elevated level of adenosine deaminase [41].
6.6 Management of Pericardial Effusion Without Tamponade
Asymptomatic patients with small- to moderate-sized effusions can be followed with serial echocardiograms to ensure ultimate resolution. Pharmacologic treatment aimed at decreasing pericardial inflammation should be considered (e.g., NSAIA and/or colchicine; see Section 22.3) [7]. When the cause of effusion is not clear from the clinical presentation, investigating for specific etiologies should be undertaken, such as testing for tuberculosis; serologic evaluation (e.g., antinuclear antibodies) for collagen vascular diseases; mammography and chest CT for screening of breast and lung cancers, respectively; and, in the appropriate clinical contexts, assessing for Lyme disease or hypothyroidism.
Patients with asymptomatic large chronic pericardial effusions who are being followed in the outpatient setting may occasionally develop tamponade unexpectedly [42]. Reassuringly, in one series of 45 patients with large pericardial effusions managed conservatively, no progression to tamponade was demonstrated [40].
7 Constrictive Pericarditis
7.1 Etiology and Pathophysiology
Constrictive pericarditis is characterized by a thickened and/or scarred pericardium with abnormal rigidity that impairs filling of the cardiac chambers [7, 43]. Any of the etiologies of acute pericarditis listed in Table 22.1 can result in constrictive pericarditis. The most common causes are idiopathic pericarditis, post-cardiac surgery, and prior mediastinal radiation therapy [44]. Tuberculous pericarditis, no longer a common cause of constrictive pericarditis in the developed world, remains an important etiology in developing countries [7].
In constriction, pericardial compliance becomes the limiting factor of ventricular filling leading to elevation and equalization of diastolic intracardiac pressures [5]. In early diastole (just after the mitral and tricuspid valves open), the ventricles actually begin to fill quite briskly because atrial pressures are typically elevated. However, as soon as the ventricles fill to the limit imposed on them by the surrounding rigid pericardium, filling abruptly ceases. Venous congestion results from the elevated diastolic pressures, and the reduced LV filling impairs ventricular stroke volume and forward cardiac output.
7.2 Clinical Presentation
Clinical findings in constrictive pericarditis develop insidiously over a period of months to years. Patients typically present with systemic congestion out of proportion to pulmonary congestion. Symptoms of right-sided heart failure in constriction include elevated jugular venous pressure, hepatic congestion, early satiety, ascites, and peripheral edema. Dyspnea in the absence of pulmonary congestion is also common [7]. Late in the disease, signs of reduced cardiac output become manifest including cachexia and muscle wasting.
7.3 Physical Exam
The jugular venous pressure is markedly elevated with two prominent descents during each cardiac cycle (x and y descents), creating a distinctive filling and collapsing pattern that is often evident from across the room. In distinction to normal individuals, the degree of jugular venous distention fails to decrease, or may increase further, with inspiration (Kussmaul sign). In normal individuals, inspiration decreases intrathoracic pressure resulting in increased venous return to the heart and a decline in jugular venous pressure. Conversely, in pericardial constriction the inspiratory decrease in intrathoracic pressure is not transmitted through the rigid pericardium to the cardiac chambers, resulting in an increased jugular venous pressure instead. On cardiac auscultation there may be a pericardial knock. This is a high-pitch sound that is best heard at the left sternal border or the apex in early diastole. It corresponds to the abrupt cessation of ventricular filling in early diastole. Additional physical findings include abdominal distension , ascites, and peripheral edema.
7.4 Laboratory Studies
There are no specific findings of constrictive pericarditis on the electrocardiogram, usually simply nonspecific ST- and T-wave abnormalities . However, atrial arrhythmias such as atrial fibrillation are common, and about one-third of patients manifest low QRS voltage. The chest radiograph may show a rim of pericardial calcification, particularly in those with chronic tuberculous pericarditis, best observed at the right heart border on a lateral projection. Echocardiography may demonstrate a thickened pericardium, but this is often difficult to visualize by a standard transthoracic study. Doppler analysis reveals a characteristic pattern that can be differentiated from other causes of diastolic dysfunction such as restrictive cardiomyopathy (see Table 22.2) [45, 46]. Cardiac magnetic resonance imaging and computed tomography are superior to echocardiography in visualizing pericardial anatomy. Pericardial thickness is usually increased at >2 mm in patients with constrictive pericarditis, though nearly 20% of patients with proven constriction have normal thickness [47]. Cardiac catheterization demonstrates elevation and equalization of right and left ventricular diastolic pressures with abrupt cessation of diastolic filling as ventricular volumes reach the limit imposed by the constricting pericardium.
7.5 Treatment
Complete surgical pericardiectomy is the mainstay of treatment in patients with advanced constrictive pericarditis [7]. Pericardiectomy results in symptomatic improvement rapidly in many patients, but recovery may be more gradual in those with associated myocardial stiffness or fibrosis. Patients with constriction due to viral/idiopathic pericarditis have the best outcomes after surgery, while results are less favorable in those with radiation-associated constriction [44].
7.6 Constrictive Pericarditis Versus Restrictive Cardiomyopathy
The clinical findings of constrictive pericarditis can closely resemble those of restrictive cardiomyopathy (e.g., cardiac amyloidosis). Both of these pathologies result in impaired diastolic ventricular filling. The distinction is important as constrictive pericarditis is treatable with surgical resection, while options for restrictive cardiomyopathies are much more limited. Table 22.2 lists common features that cardiologists consider in differentiating these entities.
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Saldana, F., Lilly, L.S. (2019). Pericardial Diseases. In: Toth, P., Cannon, C. (eds) Comprehensive Cardiovascular Medicine in the Primary Care Setting. Contemporary Cardiology. Humana Press, Cham. https://doi.org/10.1007/978-3-319-97622-8_22
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