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Fig. 6.7 The systolic area index (SAI) differentiating constrictive pericarditis from restrictive car­diomyopathy as demonstrated by Talreja and associates in 2008. (a) Simultaneous left ventricle (LV) and right ventricle (RV) pressure tracing in a patient with constrictive pericarditis showing an increase in the area of RV pressure curve during inspiration as compared with expiration. However, the area of the LV pressure curve decreases during inspiration as compared with expiration. (b) Conversely, in a patient with restrictive cardiomyopathy, there is a decrease in the area of the RV pressure curve as compared with expiration. The area of the LV pressure curve remains unchanged during inspiration as compared with expiation
6 Pathophysiology ofChronic Constrictive Pericarditis
6.3 Fluid Retention inChronic Constrictive Pericarditis
As compared to other causes of congestive cardiac failure, the degree of ascites is disproportionate to pedal oedema in chronic constrictive pericarditis. The pathogen­esis of ‘ascites precox’ remains conjectural. High right atrial pressure, increased venous pressure, increased capillary permeability, cardiac cirrhosis, hypoalbumin­emia secondary to protein losing enteropathy and impedance to lymphatic ow are various factors causing ‘ascites precox’ [19–21, 26, 45–49, 56].
Patients with chronic constrictive pericarditis retain more sodium and water than patients with myocardial failure. Limited studies are available in the literature exploring the causative mechanisms of uid retention in chronic constrictive peri­carditis. Anand and associates noted in 16 patients having untreated chronic con­strictive pericarditis that the mechanisms and magnitude of water and sodium retention in constrictive pericarditis was different from congestion secondary to low cardiac output due to failed myocardium. They noted higher volume retention and lower vascular resistance for a comparable reduction in cardiac output in constric­tive pericarditis compared to patients having myocardial disease. They also noted similar renin-angiotensin-aldosterone activation status like other causes of conges­tive cardiac failure [6–8].
References
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Patients having constrictive pericarditis had vefold rise of atrial natriuretic pep­tide levels as compared to normal controls, but the rise was only one-third of that seen in patients with myocardial disease. However, the atrial natriuretic peptide levels in chronic constrictive pericarditis are disproportionately less than the degree of raised right atrial pressure [6–8].
Since atrial natriuretic peptide release is mediated by atrial stretch, the asyn­chrony between the relatively low atrial natriuretic peptide levels and raised right atrial pressure can be explained by less distensible atria caused by a constricting pericardium in chronic constrictive pericarditis. The atrial natriuretic peptide hypothesis has been suggested to explain the greater salt and water retention and lack of pulmonary oedema in chronic constrictive pericarditis despite high right atrial pressure [6, 8, 54, 55].
In chronic constrictive pericarditis, all segments of the autonomic nervous sys­tem have severe autonomic dysfunction as compared with restrictive cardiomyopa­thy and endomyocardial brosis [62].
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29. Komsuoglu B, Goldeli O, Kulan K.Tuberculous pericarditis in north-east Turkey. An echocar­diographic study. Acta Cardiol. 1994;49:157–63.
30. Komsouglu B, Goldeli O, Kulan K, Komsouglu SS.The diagnostic and prognostic value of adenosine deaminase in tuberculous pericarditis. Eur Heart J. 1995;16:1126–30.
31. Leak LV, Ferrans VJ, Cohen SR, Eidbo EE, Jones M. Animal model of acute pericarditis and its progression to pericardial brosis and adhesions: ultrastructural studies. Am J Anat. 1987;180:373–90.
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34. Liu S, Ma C, Ren W, Zhang J, Li N, Yang J, Zhang Y, Qiao W.Regional left atrial function differentiation in patients with constrictive pericarditis and restrictive cardiomyopathy: a study using speckle tracking echocardiography. Int J Cardiovasc Imaging. 2015;31:1529–36.
35. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, Picard MH, Roman MJ, Seward J, Shanewise JS, Solomon SD, Spencer KT, Sutton MS, Stewart WJ. Recommendations for chamber quantication: a report from the American Society of Echocardiographys Guidelines and Standards Committee and the Chamber Quantication Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18:1440–63.
36. Myers RB, Spodick DH.Constrictive pericarditis: clinical and pathophysiologic chararcteris­tics. Am Heart J. 1999;138:219–32.
37. Martinez-Vazquez JM, Ribera E, Ocana I, Segura RM, Serrat R, Sagrista J.Adenosine deami­nase activity in tuberculous pericarditis. Thorax. 1986;41(11):888.
6 Pathophysiology ofChronic Constrictive Pericarditis
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38. Ng TT, Strang JI, Wilkins EG. Serodiagnosis of pericardial tuberculosis. QJM. Int J Med. 1995;88(5):317–20.
39. Oh JK, Hatle LK, Seward JB, Danielson GK, Schaff HV, Reeder GS, Tajik AJ.Diagnostic role of Doppler echocardiography in constrictive pericarditis. J Am Coll Cardiol. 1994;23(1):154–5.
40. Ommen SR, Nishimura RA, Hurrell DG, Klarich KW.Assessment of right atrial pressure with 2-dimensional and Doppler echocardiography: a simultaneous catheterization and echocardio­graphic study. Mayo Clinic Proceedings. 2000;75(1):24–9.
41. Przybojewski JZ.Rheumatic constrictive pericarditis. A case report and review of the litera­ture. S Afr Med J. 1981;59(19):682–6.
42. Reuter H, Burgess L, van Vuuren W, Doubell A.Diagnosing tuberculous pericarditis. Q J Med. 2006a;99:827–39.
43. Reuter H, Burgess LJ, Carstens ME, Doubell AF.Adenosine deaminase activity: more than a diagnostic tool in tuberculous pericarditis. Cardiovasc J South Afr. 2005;16:143–7.
44. Reuter H, Burgess LJ, Schneider J, Van Vururen W, Doubell AF. The role of histopathol­ogy in establishing the diagnosis of tuberculous pericardial effusions in the presence of HIV.Histopathology. 2006c;48:295–302.
45. Shabetai R.The pericardium. NewYork: Grone & Stratton; 1981.
46. Shabetai R. The pathophysiology of constrictive pericarditis. In: Reddy PS, Leon DF, Shavers JA, editors. Pericardial disease. NewYork: Raven Press Books Ltd; 1982. p.272.
47. Shabetai R.Diseases of the pericardium. In: Hurst JW, Schlant RC, Alexander RW, editors. The heart: arteries and veins. 8th ed. NewYork: McGraw-Hill; 1994. p.1654–62.
48. Shabetai R.The pericardium. Boston: Kluwer Academic; 2003. p.191–251.
49. Shabetai R. Pericardial diseases. In: Hurst JW, editor. The heart, arteries and veins. NewYork: McGraw-Hill; 1990. p.1348–74.
50. Shabetai R, Mangiardi L, Bhargava A, Ross J Jr, Higgins CB.The pericardium and cardiac function. Prog Cardiovasc Dis. 1979;22:107–34.
51. Sagrista-Sauleda J, Angel J, Sanchez A, Permanyer-Miralda G, Soler-Soler J. Effusive­constrictive pericarditis. N Engl J Med. 2004;350:469–75.
52. Shefeld EA. The pathology of tuberculosis. In: Davis PDO, editor. Clinical tuberculosis. London: Chapman and Hall Medical; 1994. p.44–54.
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56. Santamore WP, Bartlett R, Van Buren SJ, Dowd MK, Katcher MA.Ventricular coupling in constrictive pericarditis. Circulation. 1986;74:597–602.
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59. Shabetai R. Pathophysiology and differential diagnosis of restrictive cardiomyopathy. Cardiovasc Clin. 1988;19:123–32.
60. Shabetai R.Left ventricular function and myocardial contractility in chronic constrictive peri­carditis. Chest. 1971;59:476–7.
61. Sun JP, Abdalla IA, Yang XS, Rajagopalan N, Stewart WJ, Garcia MJ, etal. Respiratory varia­tion of mitral and pulmonary venous Doppler ow velocities in constrictive pericarditis before and after pericardiectomy. J Am Soc Echocardiogr. 2001;14:1119–26.
62. Singh M, Juneja R, Bali HK, Varma JS.Autonomic functions in restrictive cardiomyopathy and constrictive pericarditis: a comparison. Am Heart J. 1998;136:443–8.
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65. Vaitkus PT, Kussmaul WG.Constrictive pericarditis versus restrictive cardiomyopathy: a reap­praisal and update of diagnostic criteria. Am Heart J. 1991;122(5):1431–40.
66. Williams IP, Hetzel MR.Tuberculous pericarditis in South-west London: an increasing prob­lem. Thorax. 1978;33:816–7.
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70. Wise DE, Conti CR.Constrictive pericarditis. In: Spodick DH, editor. Pericardial diseases. Philadelphia: F.A.Davis; 1976b. Cardiovasc Clin 1976; 7(3): 197–210.
71. Wood P.Chronic constrictive pericarditis. Am J Cardiol. 1961;7:48–61.
72. Yang HS, Song JK, Song JM, Kang DH, Lee CW, Nam GB, etal. Clinical characteristics of constrictive pericarditis diagnosed by echo-Doppler technique in Korea. J Korean Med Sci. 2001;16:558–66.
6 Pathophysiology ofChronic Constrictive Pericarditis
Chapter 7
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Clinical Presentation, Lab Investigations, andEndomyocardial Biopsy
7.1 Clinical Challenges andDiagnostic Dilemma
Constrictive pericarditis is thrice as common in males. Although published litera­ture cites an age range between 7 and 70years, the great majority of affected patients are below 40years of age [3, 10–17, 22–24, 71, 81–87].
The condition has posed a diagnostic dilemma since it was rst recognized. All cases of constrictive pericarditis cannot be diagnosed using a single criterion. In the majority, the diagnosis may be established on the basis of the history, physical nd­ings, chest radiography, and at least two positive multimordality imaging studies including cardiac catheterization.
The hallmark diagnostic tool is the clinical suspicion of constrictive pericarditis in a patient with signs and symptoms of right-sided heart failure that are dispropor­tionate to left sided, pulmonary or heart disease.
Although non-specic, the clinical features of constrictive pericarditis are sec­ondary to elevated systemic venous pressures, debilitating chronic right-sided car­diac failure, and low cardiac output.
In the majority, symptoms develop over several years; however in cases of trauma, mediastinal irradiation, and cardiac surgery, symptoms may appear quicker [20]. The symptoms of tubercular pericarditis are usually non-specic and consists of fever, weight loss, and night sweats. The most common complaints described are exertional dyspnea (78%), ascites (70%), pedal oedema (55%), abdominal discom­fort (35%) and fatigue (30%) [50–52, 84].
In chronic constrictive pericarditis, the degree of ascites is disproportionate to pedal oedema, a sequence opposite to that of other causes of congestive heart fail­ure. The pathogenesis of ‘ascites precox’ in the appearance of ascites followed by pedal oedema remain conjectural. Disproportionately high right atrial pressure, pro­tein losing enteropathy causing hypoalbuminemia, increased capillary permeability, impedance to lymph ow, disproportionately high atrial natriuretic peptide, and
Ltd. 2023 U. K. Chowdhury, L. K. Sankhyan, Surgical Treatment of Chronic Constrictive Pericarditis, https://doi.org/10.1007/978-981-99-5808-5_7
81© The Author(s), under exclusive license to Springer Nature Singapore Pte
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cardiac cirrhosis have been variously implicated as the causative factors for ascites precox [13, 32, 41].
A mechanical constriction around the heart remain the causative factor for right­sided heart failure without severe dyspnoea, thus differentiating it from valvular heart disease, endomyocardial brosis, and cardiomyopathies. Because of elevation and equalization of end-diastolic pressure in all cardiac chambers, systemic conges­tion is more marked than pulmonary congestion. With progression of the disease due to aggravation of hepatic congestion, atrial brillation and tricuspid regurgita­tion, severe fatigue, muscle wasting, cachexia, generalized anasarca and jaundice develops. Symptoms and signs of left-sided heart failure namely dyspnoea, cough, and orthopnoea may also appear at a later stage.
7 Clinical Presentation, Lab Investigations, andEndomyocardial Biopsy
7.2 Physical Examination
Sinus tachycardia and normal arterial blood pressure are generally evident, except in advanced cases, where it may be low. In upto 86% of cases, a markedly elevated jugular venous pressure, presenting as a rapidly collapsing, negative wave of dia­stolic Y-descent combined with a normal X-decent, produces a ‘M’ or ‘W’ shaped contour of Bloomeld [9]. Physical examination reveals two prominent descent with each cardiac cycle.
At times tachycardia, tachypnoea, dyspnoea and atrial brillation limits visual­ization of the typical jugular venous pulse. Depending on the chronicity of the dis­ease, upto one-third of cases present with atrial brillation. White attributed this to compression scars in the right-atrium. In patients with at brillation,x-descent in lost and y-descent remains [85]. Kussmaul’s sign present an increase in jugular venous pressure during inspiration or the pressure may simply fail to decrease dur­ing inspiration. Basically, the Kussmaul’s sign reects loss of normal increase in venous return to the right-side of the heart during inspiration [34, 35].
The Mayo Clinic group detected the presence of Kussmaul’s sign in 28 out of 135 patients with constrictive pericarditis undergoing pericardiectomy [28, 36, 37]. However, Kussmaul’s sign lack specicity as it is also seen in patients with restric­tive cardiomyopathy, tricuspid stenosis, endomyocardial brosis, and right ventric­ular failure [2, 40, 45, 75].
Evidence of pulsus paradoxus is found in about one-third of patients with con­striction, especially those with effusive-constrictive pericarditis [36, 37]. It has been termed paradoxus because of the absence of a radial pulse despite the presence of a corresponding heart beat [34, 35]. The pulse disappears during inspiration and becomes palpable during expiration [5, 30, 31]. A decrease in systolic blood pres­sure by more than 10 mmHg during inspiration suggests the presence of pulsus paradoxus. Physiologically, it is best explained by the lack of transmission of decreased intrathoracic pressure to left-sided cardiac chambers [42, 46].
Kussmaul’s paradoxical pulse is also seen in patients with massive pericardial effusion, cardiac tamponade, acute myocardial infraction, massive pulmonary
7.4 Electrocardiogram
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thromboembolism, restrictive cardiomyopathy, severe chronic obstructive pulmo­nary disease and tension pneumothorax [29, 30].
Due to extensive pericardial adhesion and calcication, the apex beat is impal­pable in the great majority of patients with constriction (90% in Woods series) [81]. The cardiac impulse may fail to change with change in body position and the heart sound appears distant and mufed [81].
Systolic retraction of apical impulse may be present. A diastolic lift (pericardial knock) that coincides with a high-pitched early diastolic sound and sudden inspira­tory splitting of the second heart sound, heard best at the left sternal border or at the cardiac apex are specic clinical signs found in 21% and 36% of patients with con­strictive pericarditis respectively [2].
Diastolic pericardial knock occurs 0.06–0.12seconds after aortic component of second heart sound, has a higher frequency than third heart sound, and corresponds to abrupt cessation of ventricular lling.
Dalton and colleagues reported hepatomegaly (89%), ascites (45%) and periph­eral oedema (76%) in their series of patients. Advanced cases exhibit dusky facial hue, muscle wasting, cachexia of the extremities, huge ascites disproportionate to pedal oedema, and prominent hepatic pulsation [4, 19, 31, 33, 71].
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7.3 Laboratory Investigation
Among the laboratory parameters in constrictive pericarditis, the erythrocyte sedi­mentation rate may be raised. Hypoalbuminemia, hyperbilirubinemia, raised blood urea, and serum creatinine are important incremental risk factors following pericar­diectomy [10–17, 22–27, 33].
7.4 Electrocardiogram
Although electrocardiographic ndings are non-specic, a completely normal elec­trocardiogram is rare in constrictive pericarditis. Low QRS voltage and non-specic S-T wave abnormalities are common [18, 33, 53].
Several investigators including ourselves have reported electrocardiographic ndings of p-mitrale in 19–43% of individuals with constrictive pericarditis [10–18,
21, 38, 39, 72].
Atrial brillation and atrial utter have been reported in upto one-third of cases of constrictive pericarditis. Other unusual electrocardiographic ndings include right ventricular hypertrophy due to brous band narrowing the right ventricular outow tract [10–12, 81–87]. In advanced cases of calcic constrictive pericarditis, Q wave may be noted as a result of myocardial penetration by the calcic specules. [20, 21, 38, 39, 53].
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7 Clinical Presentation, Lab Investigations, andEndomyocardial Biopsy
7.5 Chest Radiography, Echocardiography, Multimodality
Imaging, Cardiac Catheterization Studies
The role of the above-mentioned investigative modalities have been detailed in Chap. 8.
7.6 Endomyocardial Biopsy
This investigative modality is helpful when echocardiographic, hemodynamic and multimodality imaging studies conclusively fails to establish the diagnosis of con­strictive pericarditis [4–8].
The major role of endomyocardial biopsy is to distinguish constrictive pericardi­tis from disease entities like restrictive cardiomyopathy, tropical endomyocardial brosis, eosinophilic cardiomyopathy, amyloidosis, hemochromatosis or other vari­eties of inltrative diseases [1, 5–8, 22–27, 41–44, 46–49, 53–70, 73, 74, 76–80,
88, 89].
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