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| LETTER TO THE EDITOR |
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| Year : 2015 | Volume
: 3
| Issue : 4 | Page : 121-122 |
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Acute Rheumatic Valvulitis with Palisading: A Rare but Classic Histopathological Finding in a Surgical Specimen
Amita Radhakrishnan Nair1, Sandhyamani Samavedam1, Jagan Mohan Tharakan2, Jayakumar Karunakaran3
1 Department of Pathology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India
2 Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India
3 Department of Cardiothoracic and Vascular Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India
| Date of Web Publication | 21-Dec-2015 |
Correspondence Address:
Sandhyamani Samavedam
Department of Pathology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram - 695 011, Kerala
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2321-449X.172360
How to cite this article:
Nair AR, Samavedam S, Tharakan JM, Karunakaran J. Acute Rheumatic Valvulitis with Palisading: A Rare but Classic Histopathological Finding in a Surgical Specimen. Heart India 2015;3:121-2 |
How to cite this URL:
Nair AR, Samavedam S, Tharakan JM, Karunakaran J. Acute Rheumatic Valvulitis with Palisading: A Rare but Classic Histopathological Finding in a Surgical Specimen. Heart India [serial online] 2015 [cited 2021 Dec 2];3:121-2. Available from: https://www.heartindia.net/text.asp?2015/3/4/121/172360 |
Sir,
Rheumatic fever is still the leading cause of acquired heart disease in children and young adults. Surgical intervention is performed mainly in patients with chronic valve deformities. In recent years, pathological examination of such specimens has been given less importance. In this setting, we recently had the opportunity to see a rare but classic histopathological finding of acute rheumatic valvulitis in a surgical specimen.
A 17-year-old girl with history of dyspnea on exertion and palpitation of 20 days was admitted for evaluation. There was no history of joint pain or swelling or respiratory tract infection in the preceding 1 month. She was afebrile and pale with icterus and bilateral pedal edema. There was tachycardia and with normal blood pressure. The cardiovascular system examination showed normal heart sounds, S1 soft, 3/6 presystolic murmur at the apex radiating to the axilla, 2/6 systolic murmur at the left lower sternal border and in the pulmonary area, and 2/6 diastolic murmur in the apex and left ventricle S3. The jugular venous pressure was elevated with no peripheral signs of infective endocarditis. Air entry was reduced in the right lower zone with fine crepitations. The abdomen was distended, with palpable liver and spleen.
Investigations showed low hemoglobin and mild leukocytosis with neutrophil dominance; erythrocyte sedimentation rate was 25 mm at the end of 1 h (Westergren method). Chest x-ray showed cardiomegaly, cardiothoracic ratio of 156/243, with right atrial enlargement and right-sided pleural effusion. Electrocardiogram (ECG) showed sinus rhythm, PR 145, axis +70, normal QRS duration. In echocardiography (echo) the various gradients were: Left ventricle (LV) 49/32, left atrium-to-aortic (LA/AO) 53/21, ejection fraction 65%, 6 mm pericardial effusion (PE) posterior to LV, and restricted posterior mitral leaflet opening with doming of the anterior leaflet. Liver function tests showed direct hyperbilirubinemia and hypoalbuminemia.
The possibility of acute rheumatic fever was considered but antistreptolysin O (ASO) titer was only 52 units (normal value: Up to 200 units). The patient was treated for heart failure and the symptoms improved.
One year later, she underwent mitral valve replacement with preservation of the posterior leaflet. Grossly, the mitral leaflet was opaque and thickened with granularity along the line of valve closure. Microscopic examination showed dense perivascular mononuclear infiltrates, fibrinous material surrounded by palisaded arrangement of histiocytes [Figure 1], sclerosis, and neovascularization by bunches of thin- and thick-walled vessels [Figure 2]. The features were suggestive of acute rheumatic vegetation superimposed on chronic valve disease. Stains for organisms were negative, ruling out infective endocarditis. ASO titer was 300 units, thus confirming acute rheumatic activity. The postoperative period was uneventful. ECG showed no fresh changes. Echo showed good left and right ventricular functions. She was asked to gradually resume normal activities over a period of 3 months. She has been under regular follow-up for the last 1 year and is doing well. | Figure 1: Histology showing features of acute valvulitis (a) Dense inflammatory infiltrate x100 (b) Foci of "fibrinoid" material with histiocytic palisading x100 (c) Palisaded lesion showing histiocytes admixed with a few lymphocytes x400. (a, b, c: H and E)
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 | Figure 2: Histology of the mitral valve showing features of chronic rheumatic disease (a) Neovascularization with thick- and thin-walled vessels (b) Sclerosis (H and E x100)
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The histologic hallmark of acute rheumatic carditis is the Aschoff nodule. Three stages are described in the development of Aschoff nodule. The early or exudative stage is characterized by swelling and edema of the collagen (fibrinoid degeneration), intermediate or proliferative/granulomatous stage shows infiltration by lymphocytes, histiocytes, fibroblasts, and Anitschkow cells. The prominent palisading by histiocytes around the fibrinoid area gives it a granuloma-like appearance. This phase lasts up to the 13th week of disease following which healing of the lesion occurs (late/senescent phase). [1]
Surgical intervention is rare in the acute phase and is restricted to very intense valve damage, usually with ruptured valve chordae due to acute valvulitis[2] and so the histopathological material showing acute lesions of rheumatic fever (RF) is scarce. In 1909, Coombs [3] reported the earliest detailed histologic description of acute rheumatic valvular lesions and in 1936, Gross and Friedberg [4] presented the gross and microscopic findings in acute rheumatic valvulitis in two patients. Most of the histopathology descriptions of acute rheumatic valvulitis come from autopsy series. [5],[6] Fraser et al. (1995) [7] studied 15 cases of acute rheumatic valvulitis; the microscopic findings seen were fibrinoid necrosis or lymphoid aggregates with occasional macrophages.
The latest case series (2007) [8] is a cohort of 25 young rheumatic heart disease (RHD) patients who underwent surgery during an acute RF episode. The microscopic findings included fibrosis, neovascularization, calcification, inflammatory infiltrates (sparse, patchy, or dense), and the presence of fibrin deposits (verrucae) on the endocardial surface. Rasheed et al. (2007) [9] retrospectively analyzed the pathological changes in the excised mitral valve from 25 patients who had undergone surgery for RHD. The findings included "fibrinoid areas, lymphocytic infiltrate, and presence of Anitschkow cells."
In all these series, the classically described stage of "palisaded lesion" finds no mention, asserting the infrequency of this finding. Our case showed extensive palisading by macrophages around fibrin, allowing a confident diagnosis to be made on histopathology. The acute rheumatic activity was confirmed with the raised ASO titers.
We present this case as a reminder of the now rare but classically described histopathological findings of palisading lesions in acute rheumatic valvulitis, similar to the descriptions given in the old literature.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Kissane JM. Anderson's Pathology. Vol. 1. 9 th ed. St. Louis: The CV Mosby and Company; 1990. p. 639-49.  |
| 2. | Hillman ND, Tani LY, Veasy LG, Lambert LL, Di Russo GB, Doty DB, et al. Current status of surgery for rheumatic carditis in children. Ann Thorac Surg 2004;78:1403-8. |
| 3. | Coombs C. The histology of rheumatic endocarditis. Lancet 1909;1:1377. |
| 4. | Gross L, Friedberg CK. Lesions of the cardiac valves in rheumatic fever. Am J Pathol 1936;12:855-910.9. |
| 5. | Deshpande J, Vaideeswar P, Amonkar G, Vasandani S. Rheumatic heart disease in the past decade: An autopsy analysis. Indian Heart J 2002;54:676-80. |
| 6. | Josselson A, Bagnall JW, Virmani R. Acute rheumatic carditis causing sudden death. Am J Forensic Med Pathol 1984;5:151-4. |
| 7. | Fraser WJ, Haffejee Z, Cooper K. Rheumatic Aschoff nodules revisited: An immunohistological reappraisal of the cellular component. Histopathology 1995;27:457-61. |
| 8. | Sampaio RO, Fae KC, Demarchi LM, Pomerantzeff PM, Aiello VD, Spina GS, et al. Rheumatic heart disease: 15 years of clinical and immunological follow-up. Vasc Health Risk Manag 2007; 3:1007-17. |
| 9. | Rashed MM, Nagem MA, Galal MK, Ragab NM. Clinical and histopathologic study of surgically excised mitral valves in children. Int J Pathol 2006;5. |
[Figure 1], [Figure 2]
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