Reversible Biventricular Heart Failure Due to Primary Adrenal Insufficiency

Devareddy, Ankita; Sawicki, Konrad Teodor; Choudhury, Lubna; Wilcox, Jane E.

doi:10.1016/j.jaccas.2019.12.039

Cited by 6 publications

(2 citation statements)

References 8 publications

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“…In the case of drycold type heart failure, cortisol followed by thyroid hormone replacement therapy is considered to be appropriate, in addition to extracellular fluid and inotropic drugs for heart failure. Hormone replacement therapy has been reported to be effective in heart failure with hypothyroidism and adrenocorticism (10,11); however, the pathophysiology and molecular basis of endocrine abnormalities that cause heart failure have not been fully elucidated. Further studies are required to establish solid evidence for the management of patients with hypopituitarism, particularly those with severe disorders.…”

Section: Discussionmentioning

confidence: 99%

Decompensated Heart Failure Secondary to Hypopituitarism in an Elderly Patient

Yoshino,

Harano,

Shibata

et al. 2024

Intern. Med.

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Hypopituitarism is difficult to diagnose because of its non-specific symptoms, especially in the presence of comorbidities. A 77-year-old woman with worsening anorexia and exertional dyspnea was initially diagnosed with decompensated dry cold-type heart failure. Hormonal laboratory tests indicated secondary hypothyroidism as a part of the evaluation of heart failure. Furthermore, pituitary magnetic resonance imaging revealed thickening of the pituitary stalk and a loss of signal intensity in the posterior pituitary, thus suggesting lymphocytic hypophysitis. Oral hydrocortisone and levothyroxine improved the persistent anorexia. In this case, hypopituitarism occasionally presented as dry cold-type heart failure, thus making a prompt diagnosis challenging in the setting of concurrent heart failure.

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Section: Discussionmentioning

confidence: 99%

Decompensated Heart Failure Secondary to Hypopituitarism in an Elderly Patient

Yoshino,

Harano,

Shibata

et al. 2024

Intern. Med.

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“…In support of cardiovascular protective actions of cortisol, accumulating evidence suggests that glucocorticoid receptor signaling in cardiomyocytes is critical for normal heart function, and cardiomyocyte-specific glucocorticoid receptor–knockout mice die prematurely from cardiac hypertrophy that progresses to dilated cardiomyopathy and heart failure [ 2 , 27-29 ]. In this context, there are also several reports of patients with adrenal insufficiency who suffered from heart failure and responded to hydrocortisone treatment with rapid improvement of ventricular function [ 30 ]. Various other potentially beneficial effects of cortisol on cardiovascular diseases such as certain anti-atherosclerotic or anti-inflammatory properties have been described [ 9 , 16 ].…”

Section: Discussionmentioning

confidence: 99%

Associations of Serum Cortisol with Cardiovascular Risk and Mortality in Patients Referred to Coronary Angiography

Pilz

Theiler‐Schwetz

Trummer

et al. 2021

Journal of the Endocrine Society

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Context Serum cortisol may be associated with cardiovascular risk factors and mortality in patients undergoing coronary angiography, but previous data on this topic are limited and controversial. Objective We evaluated whether morning serum cortisol is associated with cardiovascular risk factors, lymphocyte subtypes and mortality. Design and Setting This is a prospective cohort study performed at a tertiary care centre in south-west Germany between 1997 and 2000. Participants We included 3052 study participants who underwent coronary angiography. Main Outcome Measures Primary outcome measures were cardiovascular risk factors, lymphocyte subtypes and all-cause and cardiovascular mortality. Results Serum cortisol was associated with an adverse cardiovascular risk profile, but there was no significant association with coronary artery disease or acute coronary syndrome. In a subsample of 2107 participants, serum cortisol was positively associated with certain lymphocyte subsets including CD16+CD56+ (natural killer) cells (p<0.001). Comparing the fourth versus the first serum cortisol quartile, the crude Cox proportional hazard ratios (with 95% confidence intervals) were 1.22 (1.00 to 1.47) for all-cause and 1.32 (1.04 to 1.67) for cardiovascular mortality, respectively. After adjustments for various cardiovascular risk factors, these associations were attenuated to 0.93 (0.76 to 1.14) for all-cause, and 0.97 (0.76 to 1.25) for cardiovascular mortality, respectively. Conclusions Despite significant associations with classic cardiovascular risk factors and natural killer cells, serum cortisol was no significant and independent predictor of mortality in patients referred to coronary angiography. These findings might reflect that adverse cardiovascular effects of cortisol could be counterbalanced by some cardiovascular protective actions.

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