Related Experiment Videos
Cardiac characteristics and postoperative courses in Cushing's syndrome
N Sugihara1, M Shimizu, Y Kita
1Second Department of Internal Medicine, School of Medicine, Kanazawa University, Japan.
Insights
Cushing's syndrome causes severe left ventricular hypertrophy and asymmetric septal hypertrophy, often more pronounced than in other hypertensive conditions. Treatment can reverse these cardiac changes.
Area of Science:
- Cardiology
- Endocrinology
- Internal Medicine
Background:
- Cushing's syndrome is associated with cardiovascular complications.
- Cardiac characteristics in Cushing's syndrome require further investigation.
Purpose of the Study:
- To evaluate cardiac features and postoperative outcomes in Cushing's syndrome.
- To compare cardiac findings with essential hypertension and primary aldosteronism.
Main Methods:
- Electrocardiography and echocardiography were performed on 12 Cushing's syndrome patients.
- Cardiac results were compared to those with essential hypertension and primary aldosteronism.
Main Results:
- Patients exhibited significant left ventricular hypertrophy and asymmetric septal hypertrophy.
- Cardiac abnormalities were more severe in Cushing's syndrome compared to other hypertensive groups.
- Postoperative follow-up showed normalization of electrocardiographic findings and reduction in hypertrophy.
Conclusions:
- Cushing's syndrome leads to severe cardiac hypertrophy, potentially influenced by cortisol levels.
- Left ventricular hypertrophy and asymmetric septal hypertrophy in Cushing's syndrome are largely reversible after treatment.
- Excessive plasma cortisol, alongside hypertension, may contribute to cardiac hypertrophy in Cushing's syndrome.
Abstract:
To assess the cardiac characteristics and postoperative courses in patients with Cushing's syndrome, electrocardiography and echocardiography were performed to study 12 consecutive, unselected patients, and results were compared with those of essential hypertension and primary aldosteronism. Eleven patients had hypertension and 7 had diabetes mellitus. Before adrenalectomy, common electrocardiographic abnormalities consisted of high-voltage QRS complexes (10 patients) and negative T waves (7 patients). Echocardiograms showed left ventricular hypertrophy in 9 patients, and all the patients had evidence of asymmetric septal hypertrophy. In patients with left ventricular hypertrophy, the thickness of the interventricular septum ranged from 16 to 32 mm, whereas the ratio of the thickness of interventricular septum to that of the posterior wall ranged from 1.33 to 2.67. The interventricular septum in Cushing's syndrome was extremely thicker and asymmetric septal hypertrophy occurred more often than essential hypertension and primary aldosteronism. Nine patients could be followed up after operation. In these patients abnormal electrocardiographic findings had normalized, the thickness of interventricular septum had decreased and asymmetric septal hypertrophy had disappeared except in 1 patient. The reason why left ventricular hypertrophy in Cushing's syndrome is severe is still unknown. Because left ventricular hypertrophy is more severe and the frequency of asymmetric septal hypertrophy much greater in Cushing's syndrome than in essential and other secondary hypertension, it is thought that not only increased aortic pressure but excessive plasma cortisol may be etiologic factors in the progression of left ventricular hypertrophy in Cushing's syndrome.