Key result
Patients with KCNJ5 somatic mutations exhibited more prominent baseline cardiovascular damage (LVMI 59 vs 51 g/m2.7) than wild-type patients, but achieved similar regression of left ventricular hypertrophy and cure of high blood pressure after adrenalectomy.
Why the study?
Does the presence of KCNJ5 somatic mutations affect cardiac remodeling and the regression of left ventricular hypertrophy after adrenalectomy in patients with primary aldosteronism?
Population
129 patients with primary aldosteronism due to an aldosterone-producing adenoma with high-quality…
Comparison
Presence of KCNJ5 somatic mutations (mutAPA, 26%) vs Absence of KCNJ5 somatic mutations (wtAPA, 74%)
Design
Cohort
Follow-up
long-term
Authors
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Adrenalectomy yields comparable LVH regression and BP cure regardless of KCNJ5 status; leaves open genotype-specific mechanisms of baseline damage.
Cohort (n=127)
Yes
Does the presence of KCNJ5 somatic mutations affect cardiac remodeling and the regression of left ventricular hypertrophy after adrenalectomy in patients with primary aldosteronism?
Absolute Event Rate: 59% vs 51%
p-value: p=<0.05
Patients with KCNJ5-mutated aldosterone-producing adenomas have more prominent baseline cardiovascular damage but experience similar regression of left ventricular hypertrophy and cure of hypertension after adrenalectomy compared to wild-type patients.
Rossi et al. (2014) conducted a cohort in Primary aldosteronism (Aldosterone-producing adenoma) (n=127). KCNJ5 somatic mutations vs. Wild-type aldosterone-producing adenoma (wtAPA) was evaluated on Left ventricular mass index (LVMI) at baseline (p=<0.05). Patients with KCNJ5 somatic mutations exhibited more prominent baseline cardiovascular damage (LVMI 59 vs 51 g/m2.7) than wild-type patients, but achieved similar regression of left ventricular hypertrophy and cure of high blood pressure after adrenalectomy.
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