Premature Diagnostic Closure After Pericarditis Treatment Delays Recognition of ATTR Cardiomyopathy: A Multimodality Case Report

Figures

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  Figure 1. Electrocardiogram on presentation. Twelve-lead ECG showing sinus rhythm. QRS amplitudes are disproportionately modest relative to the significant left ventricular hypertrophy seen on imaging, suggestive of voltage–mass discordance. There are no acute ST-segment deviations suggestive of ischaemia.

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  Figure 2. Transthoracic echocardiography: (A) apical four-chamber: demonstrating left ventricular hypertrophy, biatrial enlargement, thickening of the interatrial septum, and trace pericardial effusion. (B) Subcostal four-chamber: demonstrating marked right ventricular hypertrophy and trace pericardial effusion. (C) Global longitudinal strain plot showing reduced global longitudinal strain with relative preservation of apical segments compared to basal segments.

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  Figure 3. Coronary angiography. (A) RAO caudal view showing no obstructive disease or thrombus. (B) LAO view showing no obstructive disease or thrombus.

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  Figure 4. Cardiac magnetic resonance imaging. (A) Four-chamber late gadolinium enhancement imaging demonstrating diffuse subendocardial enhancement. (B) Four-chamber late gadolinium enhancement view showing diffuse subendocardial enhancement and an incidental right ventricular mass that is hypointense on late gadolinium enhancement, consistent with a cardiac fibroma. (C) Short-axis late gadolinium enhancement image confirming diffuse circumferential subendocardial enhancement with patchy transmural extension. (D) Native T1 map demonstrating diffusely elevated myocardial T1 values; the calculated extracellular volume was 48% (normal 25%–30%).

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  Figure 5. Endomyocardial biopsy: (A) right ventricular biopsy with Congo red staining under polarized light. (B) High-magnification electron micrograph showing randomly arranged, non-branching fibrils ∼8–10 nm in diameter.