Key result
Pathogenic cardiomyopathy variants are linked to a ~68% lower rate of LVEF normalization versus noncarriers.
Why the study?
Clinical presentation and long-term outcomes of myocarditis are heterogeneous, and a complex interaction between pre-existing genetic background and inflammation might be involved.
Does the presence of pathogenic genetic variants in cardiomyopathy-causing genes reduce the likelihood of left ventricular ejection fraction normalization in patients with active lymphocytic myocarditis?
Cohort (n=36)
No
Does the presence of pathogenic genetic variants in cardiomyopathy-causing genes reduce the likelihood of left ventricular ejection fraction normalization in patients with active lymphocytic myocarditis?
Absolute Event Rate: 18% vs 56%
p-value: p=0.035
A significant proportion of patients with biopsy-proven lymphocytic myocarditis carry pathogenic genetic variants, which are associated with a lower rate of left ventricular ejection fraction normalization over time.
The clinical presentation of myocarditis is extremely heterogeneous, ranging from asymptomatic to overt heart failure (HF). The long-term scenario varies between healing and evolution to dilated cardiomyopathy. A complex interaction between pre-existing genetic background and inflammation might be
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Artico et al. (2020) conducted a cohort in Lymphocytic Myocarditis (n=36). Pathogenic or likely pathogenic variants in cardiomyopathy-causing genes vs. Noncarriers was evaluated on Left ventricular ejection fraction (LVEF) normalization (p=0.035). Carriers of pathogenic variants in cardiomyopathy-causing genes had a significantly lower rate of left ventricular ejection fraction normalization compared with noncarriers (18% vs 56%, p=0.035).
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