Elevation of Circulating and Ventricular Adrenomedullin in Human Congestive Heart Failure

Jougasaki, Michihisa; Wei, Chao; McKinley, Linda J.; Burnett, John C.

doi:10.1161/01.cir.92.3.286

Cited by 354 publications

(202 citation statements)

References 15 publications

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“…Elevated circulating levels of cardiac troponin 1, a specific marker of myocardial injury [31], have also been reported in cirrhosis without other causes of cardiac disease [32]. Similar elevated levels of adrenomedullin, a hormone involved in the regulation of vascular tone and natriuresis [33] as well as influencing myocardial inotropy [34,35], have been found in cirrhosis without clinical heart disease [36,37] as in patients with heart failure [38,39] and ventricular hypertrophy [40]. Adrenomedullin mediates its effects through its second messenger, cyclic adenosine mono-phosphate (cAMP), which, in turn, increases the production of nitric oxide (NO) [41].…”

Section: Serum Markersmentioning

confidence: 89%

Cirrhotic cardiomyopathy

2008

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Cirrhotic cardiomyopathy is a recently recognized condition in cirrhosis consisting of systolic incompetence under condition of stress, diastolic dysfunction related to altered diastolic relaxation, and electrophysiological abnormalities in the absence of any known cardiac disease. It can be diagnosed by using a combination of electrocardiograph, 2-dimensional echocardiography, and various serum markers such as brain natriuretic factor. The underlying pathogenetic mechanisms include abnormalities in the b-adrenergic signaling pathway, altered cardiomyocyte membrane fluidity, increased myocardial fibrosis, cardiomyocyte hypertrophy, and ion channel defects. Various compounds for which levels are elevated in cirrhosis such as nitric oxide and carbon monoxide can also exert a negative inotropic effect on the myocardium, whereas excess sodium and volume retention can lead to myocardial hypertrophy. Various toxins can also aggravate the ion channel defects, thereby widening the QRS complex causing prolonged QT intervals. Clinically, systolic incompetence is most evident when cirrhotic patients are placed under stress, whether physical or pharmacological, or when the extent of peripheral arterial vasodilatation demands an increased cardiac output as in the case of bacterial infections. Acute volume overload such as immediately after insertion of a transjugular intrahepatic portosystemic shunt or after liver transplantation can also tip these cirrhotic patients into cardiac failure. Treatment of cirrhotic cardiomyopathy is unsatisfactory. There is some evidence that b-blockade may help some cirrhotic patients with baseline prolonged QT interval. Long-term aldosterone antagonism may help reduce myocardial hypertrophy. Future studies should include further elucidation of pathogenetic mechanisms so as to develop effective treatment strategies.

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Section: Serum Markersmentioning

confidence: 89%

Cirrhotic cardiomyopathy

2008

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“…ADM is an adipokine (3) and is expressed in many different tissues, including adipose tissue, adrenal medulla, lung, heart, and kidney (1)(2)(3)(4). Its plasma level is elevated in obesity (5-7), hypertension (8,9), renal failure (8,9), type 2 diabetes (10)(11)(12), and congestive heart failure (8,13). ADM also plays an important regulatory role in both acute and chronic inflammation (14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Plasma adrenomedullin level is related to a single nucleotide polymorphism in the adrenomedullin gene

Cheung

Ong²,

Tso³

et al. 2011

European Journal of Endocrinology

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Objective: Adrenomedullin (ADM) plays an important role in inflammation and is a marker of future cardiovascular events. We studied common single nucleotide polymorphisms (SNPs) in the gene encoding ADM and their relationship with the plasma levels of ADM and other inflammatory markers. Design and methods: Plasma ADM, interleukin 6 (IL6), fibrinogen, and C-reactive protein (CRP) were measured in 476 subjects from the population-based Hong Kong Cardiovascular Risk Factor Prevalence Study-2. Four tag SNPs in ADM were genotyped. Results: Plasma ADM level increased with decreasing plasma IL6 level (bZK0.116, PZ0.014). Plasma ADM level was not related to plasma levels of CRP and fibrinogen, and other clinical characteristics, except age (PZ0.049). The four SNPs, rs3814700, rs11042725, rs34354539, and rs4910118, had minor allele frequencies of 31.1, 28.7, 33.8, and 23.4% respectively. Carriers of the minor allele of rs4910118 had a mean plasma ADM level that was 10.5% (95% confidential interval: 2.5-17.8%) lower than the non-carriers (bZK0.115, PZ0.011). Haplotype analysis revealed a similar significant association with plasma ADM (PZ0.040). In multivariate analysis, the presence of the minor allele of rs4910118, but not plasma IL6, was independently associated with plasma ADM (PZ0.010). Conclusion: Plasma ADM correlates with plasma IL6 level, consistent with its role in inflammation. It is related to an SNP common in Chinese, independent of other covariates. ADM genotype should be included in future studies of cardiovascular risk prediction.

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“…Cardiomyopathy induced by catecholamines Journal of Human Hypertension has been observed in animals as well as in humans after infusion of vasopressor drugs or in association with pheochromocytoma. 4 In congestive heart failure elevation of circulating and ventricular adrenomedullin has been documented, 5 as well as a myocardial stunning-like phenomenon during a crisis of pheochromocytoma. 6 Bradydysrhythmias, for instance sinus node arrest, without systemic hypertension 7 and ventricular arrhythmias, associated with intermittent hypertension 8 can be secondary to pheochromocytoma and disappear after removal of the tumour.…”

Section: Discussionmentioning

confidence: 99%

Cardiac involvement in pheochromocytoma

et al. 2000

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We report the details of a 40-year-old farmer, a cigarette smoker, who was admitted with general malaise, nausea, vomiting, upper abdominal pain, with ST-elevation on ECG suggestive of an acute anterolateral myocardial infarction. He was treated with nitrates, heparin, betablockade and angiotensin-converting enzyme (ACE) inhibitors. Because of the presence of some blood while vomiting no thrombolysis was given and abdominal echography was performed. This revealed a nodular mass at the right adrenal gland. Urinary catecholamines and abdominal magnetic resonance imaging confirmed the suspected diagnosis of pheochromocytoma. Before

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Elevation of Circulating and Ventricular Adrenomedullin in Human Congestive Heart Failure

Cited by 354 publications

References 15 publications

Cirrhotic cardiomyopathy

Cirrhotic cardiomyopathy

Plasma adrenomedullin level is related to a single nucleotide polymorphism in the adrenomedullin gene

Cardiac involvement in pheochromocytoma

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