Hypercortisolism Is Associated With Increased Coronary Arterial Atherosclerosis: Analysis of Noninvasive Coronary Angiography Using Multidetector Computerized Tomography

Neary, Nicola M.; Booker, Oscar Julian; Abel, Brent S.; Matta, Jatin R.; Muldoon, Nancy; Sinaii, Ninet; Pettigrew, Roderic I.; Nieman, Lynnette K.; Gharib, Ahmed M.

doi:10.1210/jc.2012-3754

Cited by 81 publications

(52 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1). The increased morbidity and mortality in these patients is due to the cardiovascular, thrombotic, metabolic, infectious and musculoskeletal complications (1,2,3). To understand, treat and ideally prevent these complications is a major challenge to the treating physician and the multidisciplinary team looking after the patient.…”

Section: Introductionmentioning

confidence: 99%

Metabolic comorbidities in Cushing's syndrome

Ferraú

Korbonits

2015

European Journal of Endocrinology

137

121

View full text Add to dashboard Cite

Cushing's syndrome (CS) patients have increased mortality primarily due to cardiovascular events induced by glucocorticoid (GC) excess-related severe metabolic changes. Glucose metabolism abnormalities are common in CS due to increased gluconeogenesis, disruption of insulin signalling with reduced glucose uptake and disposal of glucose and altered insulin secretion, consequent to the combination of GCs effects on liver, muscle, adipose tissue and pancreas. Dyslipidaemia is a frequent feature in CS as a result of GC-induced increased lipolysis, lipid mobilisation, liponeogenesis and adipogenesis. Protein metabolism is severely affected by GC excess via complex direct and indirect stimulation of protein breakdown and inhibition of protein synthesis, which can lead to muscle loss. CS patients show changes in body composition, with fat redistribution resulting in accumulation of central adipose tissue. Metabolic changes, altered adipokine release, GC-induced heart and vasculature abnormalities, hypertension and atherosclerosis contribute to the increased cardiovascular morbidity and mortality. In paediatric CS patients, the interplay between GC and the GH/IGF1 axis affects growth and body composition, while in adults it further contributes to the metabolic derangement. GC excess has a myriad of deleterious effects and here we attempt to summarise the metabolic comorbidities related to CS and their management in the perspective of reducing the cardiovascular risk and mortality overall.

show abstract

Section: Introductionmentioning

confidence: 99%

Metabolic comorbidities in Cushing's syndrome

Ferraú

Korbonits

2015

European Journal of Endocrinology

137

121

View full text Add to dashboard Cite

show abstract

“…Glucocorticoids increase blood pressure by enhancing sensitivity of vascular smooth muscle to catecholamines and angiotensin II, by increasing angiotensinogen synthesis, by reducing nitric oxidemediated endothelial dilatation and by sodium retention in the distal nephron (2,3). Consequently, chronic exposure to high doses of endogenous or exogenous glucocorticoids often results in an unfavorable metabolic profile and cardiovascular disease (CVD) (4,5,6,7).…”

Section: Introductionmentioning

confidence: 99%

BclI glucocorticoid receptor polymorphism in relation to cardiovascular variables: the Hoorn and CODAM studies

Moorsel

Greevenbroek

Schaper

et al. 2015

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: Excess glucocorticoids are known to cause hypertension and cardiovascular disease (CVD). The BclI glucocorticoid receptor (GR) polymorphism increases glucocorticoid sensitivity and is associated with adverse metabolic effects. Previous studies investigating cardiovascular implications have shown inconsistent results. Therefore, the aim of the present study was to investigate the association of the BclI polymorphism with blood pressure, atherosclerosis, low-grade inflammation, endothelial dysfunction, and prevalent CVD. Design: Observational cohort study, combining two cohort studies designed to investigate genetic and metabolic determinants of CVD. Methods: We genotyped 1228 individuals (aged 64.7 yearsG8.5) from the Cohort on Diabetes and Atherosclerosis Maastricht (CODAM) study and Hoorn study for the BclI polymorphism. We measured blood pressure, ankle-brachial index (ABI), and carotid intima-media thickness (cIMT). Low-grade inflammation and endothelial dysfunction scores were computed by averaging Z-scores of six low-grade inflammation markers and four endothelial dysfunction markers respectively. Prevalent CVD was assessed with questionnaires, hospital records, ECG, and ABI. Results: Homozygous carriers (GG) had higher mean arterial pressure (103.8G12.4 mmHg vs 101.6G12.2 mmHg (meanGS.D.); P!0.05) compared with non-carriers (CC). Homozygous carriers had lower ABI compared with heterozygous carriers (CG) (1.08G0.13 vs 1.11G0.14; P!0.05). After adjustment for all covariates in the full model, the association with ABI was no longer significant. BclI was not associated with systolic blood pressure, cIMT, low-grade inflammation, endothelial dysfunction, and prevalent CVD. Conclusions: The BclI polymorphism of the GR gene may contribute to an unfavorable cardiovascular profile; however, the effects on cardiovascular variables appear to be limited and partly mediated by the metabolic phenotype exerted by BclI.

show abstract

“…Tedavi edilmeyen hastalarda mortalite ve morbidite sağlıklı kişilere göre belirgin artmaktadır (14). Miyokard enfarktüsü, inme ve tromboembolism gibi kardiyovasküler hastalıklar ve osteoporoz en sık mortalite ve morbidite nedenleridir (14)(15)(16). CS'de hipertansiyon, diyabet, kalp yetmezliği, osteoporoz gibi metabolik ve hemodinamik anormalliklerin gelişiminde hiperkortizoleminin şiddeti ve süresi, yaş, genetik yatkınlık gibi bir çok faktör rol oynar.…”

Section: Discussionunclassified

A Case of Cushing’s Syndrome Presented with Severe Heart Failure and Multiple Vertebral Fractures

Arduç¹,

Işık²,

Akbaba³

et al. 2015

Haseki

View full text Add to dashboard Cite

ÖzetCushing sendromunda (CS) kardiyovasküler hastalıklar ve osteoporoz nedeni ile mortalite ve morbidite artmaktadır. Klinik bulgular ve mortalite hiperkortizoleminin şiddeti ve süresi ile ilişkilidir. Biz CS tanısının gecikmesinden kaynaklanan ciddi komplikasyonlarla başvuran bir olguyu sunduk. Elli iki yaşındaki erkek hasta bacaklarda şişlik, nefes darlığı ve bel ağrısı şikayetleri ile başvurdu. Özgeçmisinde 2 yıldır çoklu antihipertansif tedavi ve yoğun insülin tedavisine rağmen kontrol altına alınamayan hipertansiyon ve diyabet ile 6 aydır kalp yetmezliği mevcuttu. Fizik muayenede pletore, bufalo hörgücü, abdominal obezite, karında mor strialar, pretibial ödem saptandı. Laboratuvar incelemesinde adrenokortikotropik hormon (ACTH) <5 pg/ml, sabah plazma kortizolü 26,33 µg/dl, gece plazma kortizolü 26,38 µg/dl, idrar kortizolü 272 µg/24 saat saptandı. Klasik 2 mg ve 8 mg deksametazon supresyon testlerinde plazma kortizolünde baskılanma yoktu (sırası ile 30,7 µg/dl ve 35,54 µg/dl). Ekokardiyografide ejeksiyon fraksiyonu düşük (%40) ölçüldü, direkt grafide vertebralarda kompresyon fraktürleri mevcuttu. Adrenal CT'de sol sürrenalde 4x4 cm boyutlarında adenom ile uyumlu lezyon mevcuttu. Adrenal kaynaklı CS tanısı ile sol surrenalektomi yapıldı ve patolojik incelemede adrenokortikal adenom saptandı. Operasyon sonrası hastanın diyabet, hipertansiyon ve osteoporozunda kısmi düzelme oldu. Vertebra fraktürlerine yönelik operasyon planlandı. Diyabet ve hipertansiyon gibi hastalıkların daha şiddetli seyretmesi ve tedaviye dirençli olmaları durumunda klinisyenin CS varlığı açısından uyanık olması gerekmektedir. Tanının gecikmesi mortalite ile sonuçlanabilecek ağır komplikasyonlara yol açabilir. (Ha se ki T›p Bül te ni 2015; 53: 256-9)Anahtar Sözcükler: Cushing sendromu, kalp yetmezliği, vertebra kırığı Abs tractCushing's syndrome (CS) is associated with increased morbidity and mortality due to cardiovascular diseases and osteoporosis. Clinical findings and mortality are related to degree and duration of hypercortisolism. We report a patient with CS who presented with severe complications resulting from delayed diagnosis. A 52-year-old male with a two-year history of uncontrolled diabetes mellitus and hypertension and a six-month history of heart failure was admitted with leg edema, dyspnea, and back pain. His physical examination revealed plethora, abdominal obesity, and abdominal purple striae. Laboratory analysis revealed the following results: adrenocorticotropic hormone: <5 pg/ml, morning plasma cortisol: 26.33 µg/dl, night plasma cortisol: 26.38 µg/dl, and urine cortisol: 272 µg/24 hour. No suppression was detected in the plasma cortisol of 2 mg and 8 mg dexamethasone suppression tests (30.7 µg/ dl and 35.54 µg/dl, respectively). Echocardiography showed low ejection fraction (40%), X-ray demonstrated vertebral fractures. Adrenal CT revealed a 4x4 cm left adrenal mass. The patient underwent left adrenalectomy. Histopathological diagnosis was adrenocortical adenoma. After the operation, a partial recovery was detected i...

show abstract

Hypercortisolism Is Associated With Increased Coronary Arterial Atherosclerosis: Analysis of Noninvasive Coronary Angiography Using Multidetector Computerized Tomography

Abstract: Increased coronary calcifications and noncalcified coronary plaque volumes are present in patients with active or previous hypercortisolism. Increased atherosclerosis may contribute to the increased rates of cardiovascular morbidity and mortality in patients with glucocorticoid excess.

Cited by 81 publications

References 26 publications

Metabolic comorbidities in Cushing's syndrome

Metabolic comorbidities in Cushing's syndrome

BclI glucocorticoid receptor polymorphism in relation to cardiovascular variables: the Hoorn and CODAM studies

A Case of Cushing’s Syndrome Presented with Severe Heart Failure and Multiple Vertebral Fractures

Contact Info

Product

Resources

About