Amarin Corp Plc (AMRN)

[HinduKush]

The theory of causation and acceleration of atherosclerosis in all vascular circuits is well accepted. What you rightly say about SARS-CoV2 is true of HIV and Inflenza viruses also..

Maybe someday Vascepa will be seen as the go to drug to treat not only CVD caused by normal aging but also treat the CVD caused
(or perhaps accelerated) by COVID-19.

Here is a nice summary in the cardiovascular literature by a panel of world experts:
https://documentcloud.adobe.com/link/review?uri=urn:aaid:scds:US:f9132973-cb85-4c57-a219-0552ddc33259
The other issue is the persistence of the virus eg SARS-CoV2 in the body eliciting a pathological Chronic Inflammation response. This can result from from one of the following mechanistic scenarios:

Failure of eliminating the agent causing an acute inflammation such as infectious organisms including Mycobacterium tuberculosis, protozoa, fungi, and other parasites that can resist host defenses and remain in the tissue for an extended period.
Exposure to a low level of a particular irritant or foreign material that cannot be eliminated by enzymatic breakdown or phagocytosis in the body including substances or industrial chemicals that can be inhaled over a long period, for example, silica dust.
An autoimmune disorder in which the immune system recognizes the normal component of the body as a foreign antigen, and attacks healthy tissue giving rise to diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE).
A defect in the cells responsible for mediating inflammation leading to persistent or recurrent inflammation, such as auto-inflammatory disorders (Familial Mediterranean Fever).
Recurrent episodes of acute inflammation. However, in some cases, chronic inflammation is an independent response and not a sequel to acute inflammation for example diseases such as tuberculosis and rheumatoid arthritis.
Inflammatory and biochemical inducers cause oxidative stress and mitochondrial dysfunction such as increased production of free radical molecules, advanced glycation end products (AGEs), uric acid (urate) crystals, oxidized lipoproteins, homocysteine, and others.