First Report of Rare Heart Disease in Guinea Pigs—Genetic Clues to Non-Compaction Cardiomyopathy

Left Ventricular Non-Compaction Cardiomyopathy in Eight Guinea Pigs (Cavia porcellus)

K. Kraszewska, I. Janus-Ziółkowska, P.R. Fox, K.E. Schober

Background
Left ventricular non-compaction cardiomyopathy (LVNC) is a rare myocardial disorder in humans and scarcely reported in animals. It is characterized by excessive trabeculation and deep intertrabecular recesses in the left ventricular myocardium. This study aimed to describe the clinical, echocardiographic, and histopathologic findings of LVNC in eight Skinny guinea pigs, and explore a possible genetic basis for the condition.

Methods
Between 2018 and 2023, eight Skinny guinea pigs with suspected cardiac abnormalities underwent physical and echocardiographic evaluations. Echocardiographic parameters were compared with eight breed- and age-matched healthy controls. When possible, postmortem histopathology was performed. Diagnosis of LVNC was based on human echocardiographic criteria, particularly the non-compacted-to-compacted (NC-to-C) myocardium ratio ≥2.

Results
All affected animals demonstrated hypertrabeculated myocardium with deep crypts and echocardiographic evidence of LV dilation and systolic dysfunction. Seven had congestive heart failure (CHF); four exhibited pericardial effusion. Median survival after diagnosis was 127 days. Two animals underwent necropsy, which confirmed LVNC and revealed biventricular involvement and mitral valve anomalies. Four affected animals were from two litters, supporting a potential familial or genetic component.

Limitations
Only two animals underwent necropsy, limiting postmortem confirmation. Radiography and electrocardiography were not performed, precluding full assessment of cardiac function and arrhythmias. Treatments were extrapolated from small animal medicine due to the absence of guinea pig-specific cardiac pharmacology data.

Conclusions
This case series represents the first documentation of LVNC in guinea pigs, with echocardiographic and histopathologic validation. Findings suggest both sporadic and familial forms, implying a genetic etiology. Echocardiography proved effective for in vivo diagnosis. Further research is needed to refine diagnostic criteria, evaluate prevalence, and understand its potential as a model for human disease.

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