The Detrimental Potential of Arrhythmia-Induced Cardiomyopathy

Figures

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  Figure 1. (A) Time course of important laboratory findings revealing a recovery of initially affected organ functions. (B) Surface electrocardiogram showing tachycardiac atrial flutter and successful restoration of normofrequent sinus rhythm after electrical cardioversion. GOT, glutamic oxaloacetic transaminase; GPT, glutamic pyruvic transaminase; INR, international normalized ratio.

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  Figure 2. (A) Short tau inversion recovery sequence in short cardiac axis of initial magnetic resonance imaging (left). Despite artefacts due to large pleural effusions, myocardial oedema can be excluded. Late‐enhancement sequence in four‐chamber view of follow‐up magnetic resonance imaging (right). There is no pathological late enhancement, hence no evidence of myocardial scar or fibrosis. (B) Histology revealed mild hypertrophic cardiomyocytes with enlarged nuclei and a mild subendocardial fibrosis in the haematoxylin and eosin staining (a, ×200); immunohistologically isolated CD3 positive lymphocytes could be found in the interstitium (b, ×200); an increased positivity for major histocompatibility complex II was evident (c) as well as a slight increased number of CD68 positive macrophages (d). Ultrastructurally, increased number of mitochondria near the intercalated discs was found (e); in the interstitium, macrophages could be shown (f).