Polymorphism in the apolipoprotein(a) gene, plasma lipoprotein(a), cardiovascular disease, and low-dose aspirin therapy

ObjectivesTo review the pathophysiology of COVID-19 disease, potential aspirin targets on this pathogenesis and the potential role of aspirin in patients with COVID-19.DesignNarrative review.SettingThe online databases PubMed, OVID Medline and Cochrane Library were searched using relevant headlines from 1 January 2016 to 1 January 2021. International guidelines from relevant societies, journals and forums were also assessed for relevance.ParticipantsNot applicable.ResultsA review of the selected literature revealed that clinical deterioration in COVID-19 is attributed to the interplay between endothelial dysfunction, coagulopathy and dysregulated inflammation. Aspirin has anti-inflammatory effects, antiplatelet aggregation, anticoagulant properties as well as pleiotropic effects on endothelial function. During the COVID-19 pandemic, low-dose aspirin is used effectively in secondary prevention of atherosclerotic cardiovascular disease, prevention of venous thromboembolism after total hip or knee replacement, prevention of pre-eclampsia and postdischarge treatment for multisystem inflammatory syndrome in children. Prehospital low-dose aspirin therapy may reduce the risk of intensive care unit admission and mechanical ventilation in hospitalised patients with COVID-19, whereas aspirin association with mortality is still debatable.ConclusionThe authors recommend a low-dose aspirin regimen for primary prevention of arterial thromboembolism in patients aged 40–70 years who are at high atherosclerotic cardiovascular disease risk, or an intermediate risk with a risk-enhancer and have a low risk of bleeding. Aspirin’s protective roles in COVID-19 associated with acute lung injury, vascular thrombosis without previous cardiovascular disease and mortality need further randomised controlled trials to establish causal conclusions.

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Public health impact of low-dose aspirin on colorectal cancer, cardiovascular disease and safety in the UK – Results from micro-simulation model

IJC Heart & Vasculature ◽

10.1016/j.ijcha.2021.100851 ◽

2021 ◽

Vol 36 ◽

pp. 100851

Author(s):

Jorne Biccler ◽

Kaatje Bollaerts ◽

Pareen Vora ◽

Elodie Sole ◽

Luis Alberto Garcia Rodriguez ◽

...

Keyword(s):

Public Health ◽

Colorectal Cancer ◽

Cardiovascular Disease ◽

Simulation Model ◽

Low Dose ◽

Health Impact ◽

Dose Aspirin ◽

Low Dose Aspirin ◽

Micro Simulation ◽

The Uk

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Chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilation in middle-aged humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.91215.2008 ◽

2009 ◽

Vol 106 (2) ◽

pp. 500-505 ◽

Cited By ~ 20

Author(s):

Lacy A. Holowatz ◽

W. Larry Kenney

Keyword(s):

Low Dose ◽

Aspirin Therapy ◽

Oral Temperature ◽

Middle Aged ◽

Doppler Flowmetry ◽

Healthy Humans ◽

Cutaneous Vasodilation ◽

Dose Aspirin ◽

Low Dose Aspirin ◽

Reflex Cutaneous Vasodilation

Full expression of reflex cutaneous vasodilation is dependent on cyclooxygenase- (COX) and nitric oxide synthase- (NOS) dependent mechanisms. Low-dose aspirin therapy is widely prescribed to inhibit COX-1 in platelets for atherothrombotic prevention. We hypothesized that chronic COX inhibition with daily low-dose aspirin therapy (81 mg) would attenuate reflex vasodilation in healthy human skin. Two microdialysis fibers were placed in forearm skin of seven middle-aged (57 ± 3 yr), normotensive, healthy humans with no preexisting cardiovascular disease, taking daily low-dose aspirin therapy (aspirin: 81 mg), and seven unmedicated, healthy, age-matched control (no aspirin, 55 ± 3 yr) subjects, with one site serving as a control (Ringer) and the other NOS inhibited (NOS inhibited: 10 mM NG-nitro-l-arginine methyl ester). Red cell flux was measured over each site by laser-Doppler flowmetry, as reflex vasodilation was induced by increasing core temperature (oral temperature) 1.0°C using a water-perfused suit. Cutaneous vascular conductance (CVC) was calculated (CVC = flux/mean arterial pressure) and normalized to maximal CVC (CVCmax; 28 mM sodium nitroprusside). CVCmax was not affected by either aspirin or NOS inhibition. The plateau in cutaneous vasodilation during heating (change in oral temperature = 1.0°C) was significantly attenuated in the aspirin group (aspirin: 25 ± 3% CVCmax vs. no aspirin: 50 ± 7% CVCmax, P < 0.001 between groups). NOS inhibition significantly attenuated %CVCmax in both groups (aspirin: 17 ± 2% CVCmax, no aspirin: 23 ± 3% CVCmax; P < 0.001 vs. control), but this attenuation was less in the no-aspirin treatment group ( P < 0.001). This is the first observation that chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilation through both COX- and NOS-dependent mechanisms.

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