Key result
Pregnancy number shows no association with worse phenotype or RVOT enlargement in arrhythmogenic cardiomyopathy.
Why the study?
The relation between number of pregnancies and cardiac structure, function, and arrhythmic events in women with arrhythmogenic cardiomyopathy was unclear.
Does a higher number of pregnancies worsen cardiac structure, function, or arrhythmic events in women with arrhythmogenic cardiomyopathy?
Cross-Sectional (n=77)
Does a higher number of pregnancies worsen cardiac structure, function, or arrhythmic events in women with arrhythmogenic cardiomyopathy?
A higher number of pregnancies is not associated with a worse phenotype, including cardiac structure, function, or arrhythmic events, in women with arrhythmogenic cardiomyopathy.
Answers are grounded in this paper and cite their sources.
No association with pregnancy number should not alter AC counseling; leaves open need for prospective longitudinal confirmation.
Aims: We aimed to assess the relation between number of pregnancies and cardiac structure, function, and arrhythmic events in women with arrhythmogenic cardiomyopathy (AC). Methods and results: We included female AC patients in a cross-sectional study. Number of pregnancies and pregnancy related symptoms were recorded. Ventricular arrhythmias were defined as aborted cardiac arrest, sustained ventricular tachycardia, or appropriate implantable cardioverter-defibrillator therapy. Right and left ventricular dimensions and function, including strain analyses, were assessed by echocardiography and magnetic resonance imaging. We created a new AC severity score to grade the severity of AC disease. We included 77 women (age 47 ± 16, 43 probands and 34 AC mutation positive female relatives), 19 ± 14 years after last pregnancy. Median number of pregnancies was 2 (0-4); 19 had no previous pregnancies, 16 had 1 pregnancy, 30 had 2, and 12 had ≥3 pregnancies. Presence of a definite AC diagnosis (P = 0.36), severity of AC disease (P = 0.53), and arrhythmic events (P = 0.25) did not differ between groups of pregnancies. Number of pregnancies was related to increased right ventricular outflow tract diameter in single variable analyses [odds ratio (OR) 1.76, 95% confidence interval (CI) 1.08-2.87; P = 0.02], but not when adjusted for body surface area and age (OR 1.56, 95% CI 0.91-2.66; P = 0.11). The number of pregnancies was not associated with any other measures of cardiac structure and function. Conclusion: Higher number of pregnancies did not seem to relate to a worse phenotype in women with AC.
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Castrini et al. (2018) conducted a cross-sectional in Arrhythmogenic cardiomyopathy (n=77). Number of pregnancies vs. Fewer or no pregnancies was evaluated on Increased right ventricular outflow tract diameter (adjusted for body surface area and age) (OR 1.56, 95% CI 0.91-2.66, p=0.11). In women with arrhythmogenic cardiomyopathy, the number of pregnancies was not associated with a worse phenotype or adjusted right ventricular outflow tract diameter.
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