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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

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


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

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

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

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

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

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.

 

Alcohol consumption and incident cardiovascular disease: not just one unifying hypothesis

Eur Heart J (2014) 36 (15): 897-898 - 10.1093/eurheartj/ehv021

Schematic illustration of the relationships between alcohol intake and several major cardiovascular disease outcomes. The small boxes represent the approximate relationship between alcohol intake and the corresponding cardiovascular endpoint, the dashed line indicating the risk among non-drinkers as the reference group.

 

IMPROVEd quality of life and lower cost with an endovascular strategy for ruptured abdominal aortic aneurysms - impact on daily practice

Eur. Heart J. (2015), 36 (31), 2031-2033, Fig 1; 10.1093/eurheartj/ehv221 - click here to view abstract

Streamlined care and swift management begins with rapid emergency transfer to a certified emergency care centre followed by diagnostic imaging. Diagnostic CT images may be shared with the surgical/interventional team in another hospital or directly fed into the hybrid theatre for optimal care e.g. an EVAR first strategy if anatomy allows.

 

Marfan and Sartans: time to wake up!

Eur. Heart J. (2015), 36 (32), 2131-2133, Fig 1; 10.1093/eurheartj/ehv228  - click here to view abstract

Concept of mechanobiology underlying homeostasis in the thoracic aorta. Alterations, either due to higher imposed forces (hypertension) or due to (genetic) alterations in the various components required for proper sensing and/or transduction of the signal, may lead to aneurysms/dissections. In Marfan syndrome (MFS), mutations in fibrillin-1 affect the mechanical properties of the microfibrils, leading to an altered mechanotransduction signal and initiation of cellular response mechanisms including increased transforming growth factor-β (TGFβ) signalling. AngII, angiotensinII; ECM, extracellular matrix; Erk, extracellular signal regulated kinase; Jnk, c-JunNH2-terminal kinase; LAP, latency associated protein; LLC, large latency complex; MMP, matrix metalloproteinase; Smad, mothers against decapentaplegic; SLC, small latency complex; TGFβ, transforming growth factorβ; TGFβR, transforming growth factor β receptor; VSMC, vascular smooth muscle cell.

 

Hypertrophic cardiomyopathy: single gene disease or complex trait?

Eur. Heart J. (2015), Fig 1; 10.1093/eurheartj/ehv562 - click here to view abstract

Penetrance of a sarcomere mutation increases with age and males tend to be diagnosed earlier compared with females. Genetic modifiers could either exacerbate or dampen the effects of the primary sarcomere mutation leading to earlier or delayed onset of clinical disease, respectively. Comorbid conditions, such as hypertension, obesity, diabetes, obstructive sleep apnoea, and sedentary lifestyle, are likely to have cumulative effects and be most influential in increasing disease penetrance and severity in older individuals. Conversely, healthy lifestyle choices and stringent adherence to treatment of comorbid disease could positively impact the natural history of HCM in sarcomere mutation carriers.

 

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