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Lipoprotein-associated phospholipase A2, a marker of vascular inflammation and systemic vulnerability - Figure 1

Eur. Heart J. (2009), 30 (23), 2829-2831; 10.1093/eurheartj/ehp311 - Click here to view abstract

The controversial role of Lp-PLA2. The enzyme hydrolyses a number of mediators potentially involved in atherogenesis, such as oxidized low-density lipoproteins (oxLDL) and platelet-activating factor (PAF), thus reducing their negative impact. At the same time, products of Lp-PLA2-mediated degradation of these molecules may also have proinflammatory, proliferative, and ultimately proatherogenic roles. Notably, Lp-PLA2 is itself hyperexpressed in the setting of inflammation, and it is inhibited by peroxynitrite (ONOO). What causes this equilibrium to tip from a beneficial role for Lp-PLA2 to a proatherogenic role of the enzyme remains unknown.



Post-traumatic stress disorder: breaking hearts - Figure 1

Eur. Heart J. (2011), 32 (6), 668-669; 10.1093/eurheartj/ehq404 - Click here to view abstract


Potential mechanisms of increased aortic stiffness and cardiovascular risk in people with post-traumatic stress disorder.



Genes and cardiovascular risk - Figure 1

Eur Heart J (2013) 34 (13): 949-950; 10.1093/eurheartj/ehs439 - Click here to view abstract

Most variations in regulatory and transcribed regions of DNA are weakly and inconsistently associated with variation in phenotypes such as risk of common complex diseases, plasma concentrations of lipoproteins, and the manner in which statins affect both, probably because we are still only beginning to understand how ∼80% of DNA regulates the way in which transcribed regions (‘genes’), in <2% of DNA, are turned on and off.



Airborne pollution and cardiovascular disease: burden and causes of an epidemic - Figure 1

Eur Heart J (2013) 34 (17): 1251-1253; 10.1093/eurheartj/eht045 - Click here to view abstract

Mechanisms of action of the inhalation of particulate matter on cardiac functions and cardiovascular disease.

 

Renal dysfunction and heart failure: things are seldom what they seem - Figure 1

Eur Heart J (2014) 35 (7): 416-418; 10.1093/eurheartj/eht515 - Click here to view the abstract

Potential pathogenetic pathways linking heart failure with renal dysfunction. RAS, renin–angiotensin system.

 

Renal dysfunction and heart failure: things are seldom what they seem - Figure 2

Eur Heart J (2014) 35 (7): 416-418; 10.1093/eurheartj/eht515 - Click here to view the abstract

Determinants and forms of worsening renal function in heart failure.

 

Serelaxin: insights into its haemodynamic, biochemical, and clinical effects in acute heart failure - Figure 1

Eur Heart J (2014) 35 (7): 410-412; 10.1093/eurheartj/eht477 - Click here to view the abstract

Pathophysiology of acute heart failure and effects of serelaxin. AHF, acute heart failure; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CV, cardiovascular; eGFR, estimated glomerular filtration rate; hsTnT, high sensitive troponin T; NT-proBNP, N-terminal pro brain natriuretic peptide; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure.

 

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