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| {{Template:pericardial constriction}}
| | #REDIRECT [[Constrictive pericarditis]] |
| {{CMG}}; '''Associate Editor-In-Chief:''' Atif Mohammad, M.D.
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| '''See also: [[pericarditis]], [[pericardial effusion]], [[cardiac tamponade]]
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| '''
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| ==[[Pericardial constriction overview|Overview]]==
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| ==Epidemiology==
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| Constriction can occur after almost any pericardial process. Historically, the most common etiology was [[tuberculosis]], but in the modern age, this cause now accounts for <2% of cases. In a study of 95 patients undergoing pericardiectomy at Stanford, no cause could be found in 42% of patients. 31% occurred after [[radiotherapy]], particularly following high dose mantle radiation for [[Hodgkin’s disease]]. Pericardial constriction occurred a mean of 85 months after radiotherapy, but occurred as early as 1 month and as late as 244 months.
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| It also occurred post-operatively in 11% of cases. Connective tissue disorders accounted for 4%, [[neoplasm]] 3%, [[uremia]] 2% and [[sarcoidosis]] for 1% of cases.
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| == Pathophysiology ==
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| Constrictive pericarditis is due to a thickened, fibrotic pericardium that forms a non-compliant shell around the heart. This shell prevents the heart from expanding when blood enters it. This results in significant respiratory variation in blood flow in the chambers of the heart.
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| During inspiration, the negative pressure in the [[thoracic cavity]] will cause increased blood flow into the right ventricle. This increased volume in the right ventricle will cause the interventricular septum to bulge towards the left ventricle, leading to decreased filling of the left ventricle. Due to the [[Frank-Starling law of the heart|Frank-Starling law]], this will cause decreased pressure generated by the left ventricle during [[systole]].
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| During expiration, the amount of blood entering the right ventricle will decrease, allowing the interventricular septum to bulge towards the right ventricle, and increased filling of the left ventricle and subsequent increased pressure generated by the left ventricle during systole.
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| This is known as '''ventricular interdependence''', since the amount of blood flow into one ventricle is dependent on the amount of blood flow into the other ventricle.
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| The impairment of diastolic filling uniformly affects both ventricles, especially during the latter third of diastole. The symmetrical constricting effect of the pericardium results in elevation and equilibration of diastolic pressures in all four chambers of the heart. As a result of this constriction and elevated venous filling pressure, most diastolic filling occurs rapidly and early in diastole. This filling abruptly halts when the myocardium encounters the noncompliant pericardium.
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| == Diagnosis ==
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| === History ===
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| Patients often complain of [[shortness of breath]] and [[edema]]. Patients also commonly present with nonspecific complaints of [[weakness]] and [[fatigue]]. Patients may also complain of weight gain, chest pain, abdominal fullness, and atrial arrhythmias (1/3-1/2 will have atrial fibrillation).
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| === Physical Examination ===
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| Physical examination reveals elevation of the JVP (jugular venous pulse). The waveform is characteristic with a prominent x and y descent. [[Kussmaul’s sign]] may be found (13% in the Stanford series). It occurs because the fall in intrathoracic pressure during inspiration is not transmitted to the cardiac chambers and pericardial space.
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| ==== Appearance of the Patient ====
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| ====Vital Signs====
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| [[Pulsus paradoxus]], though more typical in cardiac [[tamponade]], can be seen in 20% of patients.
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| ==== Neck====
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| [[Jugular venous distention]]
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| ==== Heart ====
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| Widely split [[S2]] can be heard and a pericardial knock can be heard in approximately 50% of patients.
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| ==== Abdomen ====
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| Evidence of right heart failure is also common and may mimic findings in chronic liver disease, e.g. pulsatile liver, [[ascites]], scrotal edema.
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| ==== Extremities ====
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| [[Pedal edema]] can be observed
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| === Laboratory Findings ===
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| [[Protein losing enteropathy]], [[nephrotic syndrome]], LFT abnormalities c/w hepatic congestion and chylous [[ascites]] has also been reported.
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| ==== Cardiac Catheterization ====
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| Typically, there is equalization of diastolic pressures in all four chambers. These filling pressures are typically elevated. RVSP is usually moderately elevated but rarely exceeds 60 mmHg.
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| If RVSP is >60 mmHg, restriction is suggested. The RVEDP is usually at least 1/3 of the RVSP. Again, if it is lower, restriction is suggested. Some say that the LVEDP may be slightly higher than the RVEDP in restriction, especially after volume load or exercise.
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| The RV and LV waveforms exhibit a “dip and Plateau or square root” sign, which is another manifestation of the early rapid diastolic filling, followed by abrupt cessation of flow.
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| Discordance between the RVS and LVS pressures can also be seen during inspiration.
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| Diuresis can obscure the hemodynamic findings in the catheterization laboratory, and diuretics should be held and careful IVF rehydration given if the diagnosis is entertained.
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| Perciardial constriction should be differentiated from restriction (which involves the left ventricle more selectively). The clinical features and hemodynamic findings of the two syndromes have significant overlap. One useful test in the cardiac catheterization laboratory to distinguish the two is a volume challenge. On simultaneous LV and RV diastolic pressure tracings, constriction compromises both ventricles equally (the LV and RV diastolic pressures will rise equally). Restriction on the other hand, will affect the LV more than the RV, and the LV diastolic pressure will rise out of proportion to the RV diastolic pressure. If restriction is suspected, one should screen for [[hemochromatosis]], [[sarcoid]], the hypereosinophillic syndrome, [[amyloid]] and [[radiation]] induced-myopathy.
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| Constrctive Pericarditis can also be differentiated from Restrictive Cardiomyopathy during cardiac catheterization using "Systolic Area Index" as a reliable hemodynamic criterion .Systolic Area Index is the ratio of right ventricular to left ventricular systolic area pressure -time (mm Hg X s) area during inspiration and expiration .It is increased (>1.1) in Constrictive Pericarditis as compared to Restrictive Cardiomyopathy which confirms the "ventricular interdependence" phenomenon present in Constrictive Pericarditis.<ref>{{cite journal |author=Talreja DR, Nishimura RA, Oh JK, Holmes DR |title=Constrictive pericarditis in the modern era: novel criteria for diagnosis in the cardiac catheterization laboratory |journal=[[J. Am. Coll. Cardiol.]] |volume=51 |issue=3 |pages=315–9 |year=2008 |month=January |pmid=18206742 |doi=10.1016/j.jacc.2007.09.039 </ref> |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(07)03432-8}}
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| ==== MRI and CT ====
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| [[MRI]] or [[CT]] may demonstrate thickening or [[calcification]] of the [[pericardium]].
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| Below is a video demonstrating MR findings of constrictive pericarditis where, in mid-diastole, the thickened pericardium begins to restrict right ventricular filling, causing a rapid increase in ventricular pressure. Early changes of septal flattening and bowing of the interventricular septum toward the left ventricle (normally concave in shape toward the left ventricle during diastolic filling) are seen. This pressure change results in diastolic septal dysfunction, the septal bounce described in echocardiography.
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| <youtube v=5srXVJdWIAM/>
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| ==== Echo ====
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| [[Echocardiography]] can demonstrate thickening of the pericardium and specific flow patterns across the mitral and tricuspid valves that are evidence of the abnormal diastolic filling in constriction. Collapse of the [[IVC]] and hepatic veins can be seen.
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| ==Complete Differential Diganosis==
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| In many cases, '''constrictive pericarditis''' is a late sequela of an inflammatory condition of the [[pericardium]]. The inflammatory condition is usually an infection that involves the pericardium, but it may be after a [[myocardial infarction|heart attack]] or after [[coronary artery bypass surgery|heart surgery]].
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| Almost half the cases of constrictive pericarditis in the developing world are idiopathic in origin. In regions where [[tuberculosis]] is common, it is the cause in a large portion of cases.
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| Causes of constrictive pericarditis include:
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| * Post Viral [[Pericarditis]]
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| * [[Tuberculosis]]
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| * Postsurgical
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| * Prior mediastinal [[radiation]] therapy
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| * Chronic [[Renal Failure]]
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| * [[Connective Tissue Disorders]]
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| * [[Neoplastic]] pericardial infiltration
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| * Incomplete drainage of purulent [[pericarditis]]
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| * Fungal and [[Parasitic Infection]]s
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| * Following [[pericarditis]] associated with [[ST elevation myocardial infarction]] ([[Dressler's syndrome]])
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| * In Association with pulmonary [[asbestosis]]
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| == Treatment ==
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| Constriction is a progressive disease without spontaneous reversal of thickening or hemodynamic changes. Some patients can be medically managed for several years. [[Edema]] can be controlled with diuretics and slowing heart rate can maximize diastolic filling.
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| Most patients develop significant debility from impaired [[cardiac output]] and elevated right and left sided filling pressures. Treatment is complete excision of the pericardium. This operation is associated with 12% mortality. Some patients do not have complete relief of symptoms and up to 60% will have at least echocardiographic evidence of a restrictive filling pattern at approximately 2 years. Radiation induced disease seems to have a worse prognosis for improvement in functional class. The 5 and 10-year survival after [[pericardiectomy]] is 78 and 57% respectively, but obviously is most correlated with underlying illness.
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| The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart. This procedure has significant risk involved,<ref name="Cinar-2006">{{cite journal | author=Cinar B, Enc Y, Goksel O, Cimen S, Ketenci B, Teskin O, Kutlu H, Eren E. | title=Chronic constrictive tuberculous pericarditis: risk factors and outcome of pericardiectomy | journal=Int J Tuberc Lung Dis | year=2006 | volume=10 | issue=6 | pages=701-6 | id=PMID 16776460}}</ref> with mortality rates of 6% or higher in major referral centers.<ref name="Chowdhury-2006">{{cite journal | author=Chowdhury UK, Subramaniam GK, Kumar AS, Airan B, Singh R, Talwar S, Seth S, Mishra PK, Pradeep KK, Sathia S, Venugopal P | title=Pericardiectomy for constrictive pericarditis: a clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques. | journal=Ann Thorac Surg | year=2006 | volume=81 | issue=2 | pages=522-9 | id=PMID 16427843}}</ref><ref name="Ling-1999">{{cite journal | author=Ling LH, Oh JK, Schaff HV, Danielson GK, Mahoney DW, Seward JB, Tajik AJ | title=Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy | journal=Circulation | year=1999 | volume=100 | issue=13 | pages=1380-6 | id=PMID 10500037}}</ref> The high risk of the procedure is attributed to adherence of the thickened pericardium to the [[myocardium]] and [[coronary arteries]]. In patients who have undergone [[coronary artery bypass surgery]] with pericardial sparing, there is danger of tearing a bypass graft while removing the pericardium. Given the thin wall of the right ventricle, this can be a dangerous procedure and should only be undertaken if the patient's symptoms are incapacitating.
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| If any [[pericardium]] is not removed, it is possible for bands of [[pericardium]] to cause localized constriction which may cause symptoms and signs consistent with constriction.
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| Due to the significant risks involved with pericardial stripping, many patients are treated medically, with judicious use of diuretics.
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| == References ==
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| {{reflist|2}}
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| {{Circulatory system pathology}}
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| {{SIB}}
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| [[nl:Pericarditis constrictiva]]
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| [[sr:Констриктивни перикардитис]]
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| [[Category:Cardiology]]
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