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Biventricular Cardiac Hypertrophy in a Patient with Primary Aldosteronism and Atrial Septal Defect
Patient: Female, 33 Final Diagnosis: Primary aldosteronism • heart failure • atrial septal defect • biventricular cardiac hypertrophy Symptoms: Dyspneu • muscular weakness Medication: Spironolactone • ACE inhibitor Clinical Procedure: Captopril suppression test • adrenalectomy • right cardiac cathet...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5601392/ https://www.ncbi.nlm.nih.gov/pubmed/28878203 http://dx.doi.org/10.12659/AJCR.902271 |
Sumario: | Patient: Female, 33 Final Diagnosis: Primary aldosteronism • heart failure • atrial septal defect • biventricular cardiac hypertrophy Symptoms: Dyspneu • muscular weakness Medication: Spironolactone • ACE inhibitor Clinical Procedure: Captopril suppression test • adrenalectomy • right cardiac catheterization Specialty: Endocrinology and Metabolism • Cardiology OBJECTIVE: Rare co-existance of disease or pathology BACKGROUND: Primary aldosteronism can be caused by adrenocortical adenoma and is usually associated with left ventricular hypertrophy. Biventricular cardiac hypertrophy and heart failure in the presence of a pre-existing atrial septal defect (ASD) are a rare association of primary aldosteronism. CASE REPORT: A 33-year-old woman with resistant hypertension and refractory hypokalemia presented with signs and symptoms of heart failure. She had previously been diagnosed having a right adrenal tumor and ostium secundum type ASD. Transthoracic echocardiography confirmed the location of the ASD, with a left-to-right cardiac shunt, moderate to severe tricuspid insufficiency, moderate pulmonary hypertension (60 mm Hg), four chamber dilatation and biventricular hypertrophy. The left ventricular ejection fraction was 17%. Endocrine function tests showed a raised plasma aldosterone concentration (PAC) to plasma renin activity (PRA) ratio, which supported a diagnosis of primary aldosteronism. A captopril suppression test failed to suppress the patient’s PAC, which confirmed the diagnosis. The patient underwent a right adrenalectomy with subsequent normalization of hypokalemia, PAC, and PAC to PRA ratio and her hypertension was managed successfully with monotherapy. Surgical pathology examination of the tumor revealed an adrenocortical adenoma. At follow-up at 18 months, the patient had a normal potassium level, and her cardiac function and ventricular geometries were improved. CONCLUSIONS: Reversible cardiac hypertrophy is rarely associated with primary aldosteronism, however, it should be recognized. Present findings suggest that aldosteronism contributes to cardiac remodelling and biventricular hypertrophic changes. Administering appropriate treatment in a timely manner, can reverse cardiac changes along with the other symptoms of primary aldosteronism. |
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