Pericardial constriction: Difference between revisions
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{{ | {{CMG}}; '''Associate Editor-In-Chief:''' Atif Mohammad, M.D. | ||
'''Associate Editor:''' Atif Mohammad, | |||
'''See also: [[pericarditis]], [[pericardial effusion]], [[cardiac tamponade]] | |||
''' | |||
==Overview== | ==Overview== | ||
Revision as of 18:09, 26 June 2011
| Constrictive pericarditis | ||
| ICD-10 | I31.1 | |
|---|---|---|
| MeSH | C14.280.720.595 | |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Atif Mohammad, M.D.
See also: pericarditis, pericardial effusion, cardiac tamponade
Overview
Pericardial constriction occurs when a fibrotic, adherent pericardium restricts diastolic filling of the heart. It mainly occurs after an episode of acute pericarditis, which may or may not have been symptomatic. There is fibrous scarring of the pericardium and usually fusion of the visceral and parietal pericardium. [1] [2] [3]
Epidemiology
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.
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.
Pathophysiology
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.
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, this will cause decreased pressure generated by the left ventricle during systole.
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.
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.
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.
Diagnosis
History
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).
Physical Examination
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.
Appearance of the Patient
Vital Signs
Pulsus paradoxus, though more typical in cardiac tamponade, can be seen in 20% of patients.
Neck
Heart
Widely split S2 can be heard and a pericardial knock can be heard in approximately 50% of patients.
Abdomen
Evidence of right heart failure is also common and may mimic findings in chronic liver disease, e.g. pulsatile liver, ascites, scrotal edema.
Extremities
Pedal edema can be observed
Laboratory Findings
Protein losing enteropathy, nephrotic syndrome, LFT abnormalities c/w hepatic congestion and chylous ascites has also been reported.
Cardiac Catheterization
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.
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.
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. Discordance between the RVS and LVS pressures can also be seen during inspiration.
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.
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.
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.[4] |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(07)03432-8}}
MRI and CT
MRI or CT may demonstrate thickening or calcification of the pericardium
Echo
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.
Complete Differential Diganosis
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 heart attack or after heart surgery.
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.
Causes of constrictive pericarditis include:
- Post Viral Pericarditis
- Tuberculosis
- Postsurgical
- Prior mediastinal radiation therapy
- Chronic Renal Failure
- Connective Tissue Disorders
- Neoplastic pericardial infiltration
- Incomplete drainage of purulent pericarditis
- Fungal and Parasitic Infections
- Following pericarditis associated with ST elevation myocardial infarction (Dressler's syndrome)
- In Association with pulmonary asbestosis
Treatment
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.
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.
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,[5] with mortality rates of 6% or higher in major referral centers.[6][7] 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.
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.
Due to the significant risks involved with pericardial stripping, many patients are treated medically, with judicious use of diuretics.
References
- ↑ Mehta A, Mehta M, Jain AC. Constrictive pericarditis. Clin Cardiol 1999; 22:334-44.
- ↑ Cameron J, Oesterle SN, Baldwin JC, Hancock EW. The etiologic spectrum of constrictive pericarditis. Am Heart J 1987; 113:354-60.
- ↑ Ling LH, Oh JK, Schaff HV, et al. Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation 1999; 100:1380-6.
- ↑ {{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
- ↑ Cinar B, Enc Y, Goksel O, Cimen S, Ketenci B, Teskin O, Kutlu H, Eren E. (2006). "Chronic constrictive tuberculous pericarditis: risk factors and outcome of pericardiectomy". Int J Tuberc Lung Dis. 10 (6): 701–6. PMID 16776460.
- ↑ Chowdhury UK, Subramaniam GK, Kumar AS, Airan B, Singh R, Talwar S, Seth S, Mishra PK, Pradeep KK, Sathia S, Venugopal P (2006). "Pericardiectomy for constrictive pericarditis: a clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques". Ann Thorac Surg. 81 (2): 522–9. PMID 16427843.
- ↑ Ling LH, Oh JK, Schaff HV, Danielson GK, Mahoney DW, Seward JB, Tajik AJ (1999). "Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy". Circulation. 100 (13): 1380–6. PMID 10500037.
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