Myocardial lysis in acute rheumatic fever followed by regeneration of cardiac muscle and origin of Aschoff bodies.

Abstract

In acute rheumatic heart disease, lysis of cardiac muscle fibres with or without retention of sarcolemma is found to be the most damaging feature in many cases. In deeper myocardium the cellular lysis often forms anastomosing clefts or sinus-like spaces between surviving muscle bundles and in the outer portion of myocardium cellular lysis may leave the sarcolemma more or less intact. From lysing cardiac muscle fibres there arise dedifferentiated cells with remarkable potentiality for regeneration. For the origin of these dedifferentiated cells, which are often indistinguishable from lymphocytes, no mitosis is seen in cardiac muscle cells. The successive stages of development of muscle cell from these dedifferentiated cells within the remaining or newly formed sarcolemma have been observed in this study. This study infers that the increased number of fibrous septa, when seen, denotes the tracks of previous muscle degeneration and subsequent replacement of it with incomplete muscle regeneration and fibrous tissue formation. In an area of muscle lysis the origin of Aschoff bodies from these dedifferentiated cells has been followed. Ashoff bodies arising in this was behave as an abortive and atypical growth of muscle fibres in a nodular fashion specific to rheumatic fever.

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“…Posteriormente a Goerttler e Ferraz de Carvalho, não se detectou na literatura à qual se teve acesso nenhum autor que fizesse menção sobre os CC como estruturas normais do miocárdio, o que permitiu que se aventasse a hipótese que os mesmos seriam na verdade alterações estruturais decorrentes de patologias do miocárdio, como a fibrose miocárdica (WHITAKER et al, 1989, BURKE e VIRMANI, 2007BHAR-AMATO, 2017), a febre reumática (ASCHOFF, 1904;WEDUN e MCGUIRE, 1963;MCDONALD, 1975, FREANT et al, 1997, a cardiomiopatia dilatada (RADU et al, 2012), a cardiomiopatia hipertrófica (TEARE, 1958;MCKENNA et al, 1990;HIGUCHI et al, 1999;VARNAVA, 2000;MARIAN E BRAUNWALD, 2017), e a cardiomiopatia chagásica intensa e difusa com ocorrência de necrose (MARIN-NETO et al, 1999;HIGUCHI et al,2003).…”