A prospective study of biopsy-proven myocarditis: prognostic relevance of clinical and aetiopathogenetic features at diagnosis

Caforio, Alida L.P.; Calabrese, Fiorella; Angelini, Annalisa; Tona, Francesco; Vinci, Annalisa; Bottaro, Stefania; Ramondo, Angelo; Carturan, Elisa; Iliceto, Sabino; Thiene, Gaetano; Daliento, Luciano

doi:10.1093/eurheartj/ehm076

Cited by 415 publications

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“…[2,9,10] Myocarditis has been found to have a male predominance, with symptoms of shortness of breath, chest pain or palpitations. [11] Despite having serious consequences, cardiac involvement has not been associated with poor prognosis when treated in a timely manner. [12] In our case, the delay in diagnosis was attributed to myocarditis manifesting as the presenting symptom of Still's disease.…”

Section: Discussionmentioning

confidence: 99%

Adult onset still’s disease masquerading as acute coronary syndrome

Jayakumar

Ash

Lobo

et al. 2016

IJDI

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Adult onset still's disease (AOSD) is a rare inflammatory disorder characterized by high fevers, arthralgia, salmon rash and leukocytosis. It is a diagnosis of exclusion and popularly diagnosed by the Yamaguchi criteria. Cardiac involvement in AOSD causing myocarditis is seldom seen. Echocardiography is an important measure of cardiac manifestation, but a more characteristic confirmation is obtained by the cardiac MRI. It is an increasingly recognized noninvasive alternative to the gold standard endomyocardial biopsy. In this case, mid myocardial enhancement in the absence of left ventricular dysfunction was consistent with a diagnosis of myocarditis in AOSD. The delay in diagnosis was caused by AOSD masquerading as acute coronary syndrome. This case highlights the importance of early recognition of myocarditis in an atypical presentation of AOSD which results in early immunomodulatory therapy and an improved clinical outcome.

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Section: Discussionmentioning

confidence: 99%

Adult onset still’s disease masquerading as acute coronary syndrome

Jayakumar

Ash

Lobo

et al. 2016

IJDI

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“…Si tratta di marcatori di malattia autoimmune cardiaca sia nelle miocarditi che nella cardiomiopatia dilatativa. In un nostro recente studio, questi marcatori sono stati riscontrati nel 56% dei pazienti con miocardite, a sostegno dell'ipotesi immunomediata [18].…”

Section: Bem = Biopsia Endomiocardicaunclassified

A case of peripartum heart failure

Vinci

Caforio

2008

CMI

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Un caso di scompenso cardiaco nel peripartum CASO CLINICODescriviamo il caso di una giovane donna di 32 anni che anamnesticamente presentava familiarità per cardiopatia ischemica; inoltre un cugino di 55 anni era affetto da cardiomiopatia dilatativa idiopatica. L'anamnesi fisiologica e patologica remota erano negative.Al V mese della sua prima gravidanza, si segnalava l'insorgenza di un episodio di cardiopalmo autorisoltosi. Nell'ultimo mese di gravidanza comparivano edemi declivi e tosse stizzosa, soprattutto in clinostatismo.Tre giorni dopo il parto, per la persistenza di edemi declivi e comparsa di dispnea e polipnea notturne e un isolato episodio di iperpiressia della durata di 24 ore a risoluzione spontanea, la paziente veniva ricoverata presso l'Unità Coronarica della città AbstractA 32-year-old woman was admitted in congestive heart failure (CHF) 3 days after delivery. She had no history of cardiovascular disease and impaired left ventricular Ejection Fraction (EF 35%). She underwent complete heart catheterisation, selective coronary angiography and right ventricular endomyocardial biopsy (EMB).Coronary arteries were normal and EMB revealed active virus negative myocarditis. Serum was positive for anti-heart autoantibodies (AHA). Thus myocarditis was classified as autoimmune and the patient was treated with immunosuppressive therapy, with clinical and hemodynamic improvement. At 27 months follow-up EMB showed healed myocarditis. Peripartum cardiomyopathy (PPCM) is a rare disorder in which left ventricular dysfunction and heart failure occur in the peripartum period in previously healthy women. The etiology is still unknown but a sizable proportion of patients may have an underlying organ-specific autoimmune myocarditis.Keywords: peripartum cardiomyopathy, heart failure, myocarditis, immunosuppressive therapy A case of peripartum heart failure. CMI 2008; 2(1): 7-15 1 Divisione di Cardiologia, Dipartimento di Scienze Cardiologiche, Toraciche e Vascolari, Centro "V. Gallucci", Università di Padova di origine. All'esame obiettivo era presente ritmo di galoppo, soffio sistolico puntale 1-2/6. L'ECG mostrava tachicardia sinusale e onde T negative diffuse. Un ecocardiogramma metteva in evidenza la presenza di un ventricolo sinistro marcatamente dilatato con marcata ipocinesia globale e funzione di pompa severamente depressa (VTD = 116 ml/m 2 , FE = 36%), insufficienza mitralica di grado moderato-rilevante. La paziente si presentava ipotesa, veniva quindi trattata

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“…Other clinical manifestations of myocarditis are chest pain and/or arrhythmias [3][4][5] . The cases presenting with heart failure symptoms have a poorer prognosis than those with chest pain or arrhythmias 6 . Clinical suspicion of myocarditis is raised by the presence of any of the described symptoms and simultaneous fulfillment of at least one of the diagnostic criteria from examinations such as ECG, laboratory findings, echocardiographic or magnetic resonance imaging as described elsewhere 4 .…”

Section: Introductionmentioning

confidence: 99%

“…A myocardial sample is commonly obtained transvascularly from the right or left ventricle using endomyocardial biopsy (EMB). EMB is considered the gold standard for myocarditis diagnosis and is also the only method able to confirm a final diagnosis in vivo [6][7][8][9][10] . According to the WHO / ISCF definition of 1995 diagnosis of myocarditis is based on histological, immunological and immunohistochemical criteria 11 .…”

Section: Introductionmentioning

confidence: 99%

“…There are a number of factors that play a role in the course of the disease, for instance type of myocarditis, grade of initial myocardial injury, hormonal factors, physical stress during the acute phase of the disease, the intensity and duration of the inflammatory process and persistence or replication of the virus in the myocardium 5,7,9,10,[28][29][30] . Although a number of studies have focused on prognostic indicators 6,25,[29][30][31][32] , we have no clear and convincing evidence that will allow us to stratify patients at the time of diagnosis and to tailor additional medical care, including the use of advanced and expensive methods of current medicine, i.e. device therapy and heart transplantation.…”

Section: Introductionmentioning

confidence: 99%

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Improvement of left ventricular systolic function in inflammatory cardiomyopathy: What plays a role?

Krejčí¹,

Hude²,

Ozábalová³

et al. 2016

BIOMED PAP

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, Lenka Spinarova aAims. To compare the differences between patients with inflammatory cardiomyopathy (ICM) with and without improvement in left ventricular (LV) systolic function and to identify the relevant predictors of LV improvement. Patients and Methods. The study included 63 patients with biopsy-proven ICM and heart failure symptoms of at least NYHA II, symptom duration ≤ 6 months, LV ejection fraction (LVEF) ≤ 40% assessed by echocardiography and presence of >14 mononuclear leukocytes (LCA+ cells)/mm 2 in biopsy samples. Patients were evaluated at baseline and after 6 months. Results. In the group with LVEF improvement of ≥ 10% (I+ group, n = 41), LVEF increased from 24 ± 7% to 47 ± 8% (P < 0.001). In 22 patients (group I-), there was no or minimal LVEF increase (< 10%). In the I+ group, there were more LCA+ cells/mm 2 at baseline (25.1 ± 16.5 vs. 18.5 ± 4.4 cells/mm 2 ; P = 0.032) and a more significant decrease in LCA+ cells in the follow-up (reduction of 13.6 ± 14.3 cells/mm 2 vs. 5.0 ± 7.7 cells/mm 2 in the I-group; P = 0.009). The univariate logistic regression showed a possible association of number of LCA+ cells, LV end-diastolic diameter and N-terminal fragment of pro-brain natriuretic peptide (NTproBNP) value with LVEF improvement. In the multivariate analysis, only NTproBNP at diagnosis was confirmed as an independent predictor of LVEF improvement (OR=1.2; 1.003 to 1.394; P = 0.046). Conclusion. The LV systolic function improvement was observed in 65% of the patients. In these patients, the number of inflammatory cells at baseline was higher and decreased more but the higher baseline NTproBNP value was the only independent predictor of LVEF improvement.

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A prospective study of biopsy-proven myocarditis: prognostic relevance of clinical and aetiopathogenetic features at diagnosis

Cited by 415 publications

References 35 publications

Adult onset still’s disease masquerading as acute coronary syndrome

Adult onset still’s disease masquerading as acute coronary syndrome

A case of peripartum heart failure

Improvement of left ventricular systolic function in inflammatory cardiomyopathy: What plays a role?

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