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Septic shock
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Bryan E. Freeman, Michael R. Foley
Regarding the definition of SIRS, the committee felt that since the clinical signs of inflammation may be quite variable, a specific definition for SIRS was too difficult to formulate. The definition established by conference in 1992 remained unchanged, but with the acknowledgement that it is “overly sensitive and nonspecific” (9). Subcommittees had been assigned to look at common markers found in sepsis, as well as other laboratory derangements brought about by this condition. Increased levels of IL-6, adrenomedullin, soluble CD14, soluble endothelial cell/leukocyte adhesion molecule 1, macrophage inflammatory protein 1α, extracellular phospholipase A2, procalcitonin, and C-reactive protein had been noted by committee members. Although these and other markers may be elevated during times of inflammation, there are no laboratory panels to create from these to function as a diagnostic tool for SIRS. However, understanding of the significance of the individual markers may aid in targeting specific treatment to a given organ, the coagulation cascade, and so on (9).
Pathogenesis of gestational diabetes mellitus
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Adrenomedullin is a newly discovered hypotensive peptide involved in the insulin regulatory system, and it may play a role in modifying diabetes in pregnancy. Di Iorio et al.46 studied its correlation to GDM. Adrenomedullin concentrations were measured in maternal and fetal plasma and in amniotic fluid in diabetic and nondiabetic pregnancies. Overall amniotic fluid concentration was higher in the pregnant diabetic women (type 1 or GDM), but there was no difference between the group in maternal and fetal plasma levels. These findings suggest that placental adrenomedullin production is upregulated in diabetic pregnancy and that it may be important to prevent excessive vasoconstriction of placental vessels.
Thyroid heart disease in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Myron Miller, Steven R. Gambert
Tachycardia is frequently present in hyperthyroidism. Initially, this was felt to be associated with an altered responsiveness to adrenergic input. Other data support a direct effect of thyroid hormone on pacemaker activity through the sinoatrial (SA) node (44). An increased venous return, secondary to a decreased systemic vascular resistance, activated renin–angiotensin–aldosterone system, and subsequently increased blood volume contribute to the increase in preload reported in hyperthyroid states (5,6,43,45–47). Although these findings contribute to the augmented cardiac output associated with hyperthyroidism, cardiac contractility is increased in cardiac myocytes removed from peripheral effects (15,16). Systemic vascular resistance is decreased directly by thyroid hormone’s action on vascular smooth muscle cells as evidenced by invasive measurement after coronary artery bypass surgery (17). This may be mediated through thyroid hormone-stimulated increased activity of adrenomedullin—a potent vasodilatory peptide (7). Afterload is reduced in hyperthyroid patients as a result of direct arterial smooth muscle relaxation, which leads to an improvement in stroke volume and subsequently cardiac output. A comprehensive review evaluated steady and pulsatile components of afterload and hypothesized that pulsatile components of arterial load actually compensate for the reduction in systemic vascular resistance noted in hyperthyroidism. These data cast doubt on the simplified notion of a single factor such as systemic vascular resistance controlling the observed decrease in ventricular afterload in the hyperthyroid patient (43).
Cardiac biomarkers for risk stratification of arrhythmic death in patients with heart failure and reduced ejection fraction
Published in British Journal of Biomedical Science, 2021
AL Burger, S Stojkovic, A Diedrich, J Wojta, S Demyanets, T Pezawas
The precursor fragments CT-ET1, MR-proANP and MR-proADM show more stable plasma levels than the active hormones and are recommended to be used for quantitative measurements [25]. The biomarkers ET1, proANP and proADM have previously been associated with adverse cardiovascular outcome. ET1 is a vasoconstrictive agent released from endothelial cells [26] and is associated with adverse cardiovascular remodelling [27–29]. Previous studies showed that elevated levels of CT-ET1 are associated with increased overall mortality after myocardial infarction and poor prognosis in patients with congestive heart failure [14,15,30]. Pro-ANP is the precursor molecule from ANP that is released by atrial myocytes in response to increased volume load and wall stretch [11]. Elevated plasma levels of MR-proANP have been associated with adverse outcome in patients with coronary heart disease and heart failure [19,31,32]. MR-proADM is a precursor peptide of ADM that is involved in the function of endothelial cells, causes long-lasting vasodilatation, carries natriuretic properties and might have positive inotropic effects on the contractility of the myocardium [33–35]. Elevated plasma levels of adrenomedullin have been proposed to be upregulated as a protective mechanism in patients with advanced cardiac disease [36,37]. Previous studies demonstrated that elevated levels of MR-proADM are associated with a poor prognosis in patients with acute and chronic heart failure [17,18,38]. So far, the potential role of these biomarkers in risk stratification for arrhythmic death was unclear.
Heart failure risk estimation based on novel biomarkers
Published in Expert Review of Molecular Diagnostics, 2021
Feven Ataklte, Ramachandran S. Vasan
Adrenomedullin (ADM) is an amino acid peptide that is synthesized by endothelial and vascular smooth cells. Its concentration is increased in circulation during left ventricular volume overload [19,20]. Mid-regional pro-adrenomedullin (MR-proADM) is a more stable form of ADM that has a longer plasma half-life [18,19]. MR-proADM is expressed in many tissues including the heart, kidney and blood vessels. It exerts its biological effect as a vasodilator, positive inotrope, diuretic, and natriuretic role. High circulating levels of MR-proADM have been observed in patients with HF and hypertension, and also in non-cardiac diseases, e.g. sepsis and kidney failure [19]. The non-cardiac conditions associated with elevated levels of MR-proADM and HF share common underlying mechanisms of vascular leakage and systemic or pulmonary edema, suggesting ADM’s specific role in vascular congestion [20].
The effect of swimming training on adrenomedullin levels, oxidative stress variables, and gastrocnemius muscle contractile properties in hypertensive rats
Published in Clinical and Experimental Hypertension, 2021
ECE KOC Yildirim, Zahide Dedeoglu, Mehmet Kaya, Aykut G. Uner
Aerobic exercise training can reduce blood pressure via improving vascular stiffness and endothelial function (42) and altering the balance between vasodilation- and vasoconstriction-related compounds such as NO (19), prostacyclin, and thromboxane (43). As a product of cardiovascular system, adrenomedullin may also have played important roles in the regulation of blood pressure. Even though the studies on the relationship between exercise and adrenomedullin levels are contradictory, it seems like adrenomedullin responses depending on the severity of cardiovascular diseases (44,45) and the type of the exercise as demonstrated by the fact that dynamic, static, and maximal exercises affect adrenomedullin levels differently (46-48). The results of several studies (49,50) indicate that the reduction in the levels of ADM may play an important role in the pathogenesis of L-NAME-induced hypertension. However, our correlation analysis indicates that there is no relationship with ADM levels and SP and DP. The studies by Sugo et al. (4, 50) may explain the absence of ADM response to exercise. They reported that the synthesis of ADM in vascular endothelial cells was regulated by gene expression and its secretion occurred in constitutive manner. Our exercise protocol may not have been long enough to stimulate the synthesis and secretion of ADM by gene expression.