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Giant-Cell Myocarditis: a Rare Cause of Rapidly Evolved Stenosis of the Mitral Valve

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Giant-Cell Myocarditis: a Rare Cause of Rapidly Evolved Stenosis of the Mitral Valve Hellenic J Cardiol 44: 355-359, 2003 Giant-Cell Myocarditis: A Rare Cause of Rapidly Evolved Stenosis of the Mitral Valve CHRISTOS E. CHARITOS1, MICHALIS ARGIRIOU1, DIMITRA RONTOGIANNI2, CHRISTOFOROS KOTOULAS2 1Second Cardiothoraric Surgery Department and 2Pathologoanatomic Laboratory, “Evangelismos” Hospital, Athens, Greece Key words: An aged anemic woman was operated on for mitral valve stenosis that had rapidly progressed in a few Idiopathic giant-cell months. Surgical and histological findings of the replaced valve proved the unexpected diagnosis of giant- myocarditis, mitral valve stenosis. cell myocarditis. This atypical clinical presentation of mitral stenosis associated with systemic manifestations must raise suspicions for other underlying illnesses. In such cases, a preoperative endomyocardial biopsy can be helpful. The patient succumbed few days later from low cardiac output syndrome. Repair or replacement of an infiltrated by giant-cells myocardium and mitral valve should not be attempted. Instead, combined immunosuppression or mechanical support and heart transplantation should be applied to save these patients. Manuscript received: itral valve stenosis of origin 25 years ago, for which she was receiving December 11, 2003; other than rheumatic fever is a replacement therapy. There was no hi- Accepted: July 10, 2003. M rare entity. Giant-cell myo- story of rheumatic fever during childhood carditis is an extremely rare, with poor or adolescent years. The symptoms began prognosis, probably autoimmune, granu- 7 months earlier with a dyspnea on exer- Address: lomatous disease of the heart. Progres- tion, moderate fever, substernal aches, Christos E. Charitos sive congestive heart failure, intraventri- and anemia (Ht=23%). The echocar- cular conduction defects and ventricular diogram revealed normal cardiac funct- 11 Filippoupoleos St., arrhythmias, which in many cases can be ion, a well functioning mitral valve, and 171 23, Nea Smirni, fatal, are the usual manifestations of this only minor accumulation of pericardial Athens, Greece 1 e-mail: disease . On the contrary, mitral valve fluid. The clinical findings were attri- [email protected] stenosis has not been observed as an ini- buted to a viral pericarditis, and the ane- tial clinical presentation of giant-cell mia treated as pernicious. Four months myocarditis. The present case report later, the symptoms relapsed. The find- regards a patient with the clinical pre- ings of a new echocardiogram were in- sentation of a rapidly evolved mitral valve teresting: mitral valve stenosis with a stenosis, due to giant-cell infiltration of valve area of 1.65 cm2 (Figure 1) and pul- the myocardium and the mitral appa- monary hypertension with a systolic ratus. pulmonary artery pressure of 57.6 mmHg. Relief of the symptoms was observed after administration of digitalis and diu- Case report retics, and blood transfusions. Two A 71-year old female patient, (married months later, the patient presented with and mother of five children), was referred orthopnea and severe anemia. The echo- for surgical correction of a critical mitral cardiogram that was immediately per- valve stenosis. The patient’s medical formed showed critical mitral stenosis record reported hypothyroidism diagnosed with an impressive decrease of the valve (Hellenic Journal of Cardiology) HJC ñ 355 Ch. Charitos et al Figure 1. Calculation of the mitral valve area by the pressure half-time technique. At the A echocardiogram the mitral valve area was measured to 1.65 cm2. At the B, two months later, the area was decreased to 1.04 cm2. There are also E>A and blood flow indicating mitral damage. area to 1.04 cm2 (Figure 1b). The mean left atri- mechanical Sorin_ No 27 valve, sutured with multiple oventricular pressure gradient was measured to 16.8 mattress sutures of Ethybond_ 2-0, reinforced with mmHg and the pulmonary artery systolic pressure Teflon_ pledgets. Cardiopulmonary bypass weaning was increased to 67.6 mmHg. Preoperative cardiac was achieved with high inotropic support. A few catheterization confirmed the diagnosis of severe hours later acute pulmonary edema emerged ne- stenosis of the mitral valve, pulmonary hyperten- cessitating reintubation, mechanical respiratory sion and right heart failure. No lesions were ob- support and increased doses of inotropes. The served in the coronary angiography. Physical exami- patient succumbed on the 12th postoperative day nation revealed a pale skin, distension of the jugular from low cardiac output syndrome. Mechanical veins, absence of a mitral face, tachycardia, diastolic circulatory assistance as a bridge to heart trans- rumbling murmur, and signs of stasis at both lung plantation was not attempted, due to the patient’s bases. Electrocardiogram showed sinus node ta- age, and the rarity of donor hearts in our country. chycardia with 1st degree AV block, without right A limited autopsy confined to the thorax was ventricular hypertrophy, mitral or pulmonary P wa- performed which revealed that, the heart weighed ves. Chest x-rays revealed an enlargement of the 700 gr and was hypertrophic. The prosthetic me- cardiac silhouette and pulmonary congestion with- chanical valve was intact with no paravalvular leaks out any other abnormal findings from the lung pa- or limitations at the movement of its leaflets. The renchyma. other valves were normal and there was no thrombus The patient was operated on with the indication in any of the cardiac chambers. Multiple cross sect- of replacement of the stenosed mitral valve. Intra- ions of the heart revealed notable hypertrophy of the operatively, there was an active pericardial inflam- left ventricle with a severe limitation of its cavity. mation, loose adhesions and moderate accumulation Many white global lesions of various diameters dif- of pericardial fluid. The mitral valve was approached fusely occupied the myocardium. There were no via the traditional left vertical atriotomy. The inspec- atheromatic lesions in the coronary arteries. The tion through the small left atrium revealed a heavy pericardium was edematous and thickened. invasion of the mitral apparatus by a white firm tis- The surgical specimen with the mitral valve was sue, which resulted in a total destruction of its ar- fixed in buffered formalin and after dehydration was chitecture. The tissue extended from the mitral embedded in paraffin. The specimen was studied by annulus to the basis of both papillary muscles, light microscopy. Sections were stained with hema- creating a solid tubular mass, thus obstructing the toxylin-eosin, Masson trichrome, Pas, Giemsa, atrioventricular opening. This tissue and the in- Ziehl-Nielsen, and Grocott stains, as well as immu- filtrated native mitral valve were removed with great nohistochemically with the ABC method. The an- difficulty. The diseased valve was replaced with a tibodies utilized were against T cells (CD3), B cells 356 ñ HJC (Hellenic Journal of Cardiology) Mitral Valve Stenosis Due to Giant-Cell Myocarditis Figure 2. Active granulomatous process of giant-cell myocarditis with (A) scattered giant-cells (white arrow, H+Eá200), and (B) interstitial inflammation with focal development of collagen fibers (H+Eá100). (CD20) and CD68 antigen (myelomonocytic marker Therefore, the mean age of patients undergoing – Dako). The histological examination showed surgery for symptomatic mitral stenosis is appro- active granulomatous process with multiple giant- ximately 40-50 years2. In this case report, the ad- cells, scattered foci of necrosis and a mild increase in vanced age, the absence of rheumatic history during collagen deposition (Figure 2). In addition to the childhood and adolescent years, the absence of granulomatous lesions, there was a heavy interstitial calcifications of the mitral apparatus, the functional inflammation (lymphocytes, mononuclear and and pathological integrity of the other valves, and plasma cells) with degeneration of the myofibers. the rapidly evolved stenotic process based on the Results of the special stains with CD68 antibodies echo findings (no stenosis observed seven months (myelomonocytic marker) were positive for multi- before surgery, and mitral valve area of 1.65 cm2 and nucleate giant cells. The interstitial lymphocytic 1.04 cm2 before four and two months) does not favor population was composed mainly of CD3+ (T) and the rheumatic origin of the disease. few CD20+ (B) lymphocytes. These histological Rare causes, other than rheumatic fever, can findings established the diagnosis of giant-cell myo- lead to functional or anatomical stenosis of the carditis. mitral valve. These include myxoma3, sarcoma4, or Histological examination of the explanted heart free-floating thrombus of the left atrium5, hydatid revealed the same findings, in addition to focal cysts6, vegetations from infective endocarditis7, mu- development of fibrous collagen tissue. The degree of inflammation and the extent of the granuloma- tous process were more severe in the left ventricle, especially in the vicinity of the mitral annulus (Fig- ure 3). The study of the lungs showed congestion, a finding compatible with the clinical picture of pul- monary edema. No granulomata or other patholo- gical lesions were observed in the pulmonary pa- renchyma. Discussion Mitral valve stenosis is the result of the rheumatic fever in almost all adult patients. Between acute rheumatic fever during the adolescent years and the appearance of symptoms from leaflet calcification Figure 3. Granulomata (white arrows) in the vicinity of the
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