key: cord-0915962-0rjsmq06
authors: Koulaouzidis, George; Charisopoulou, Dafni; Koulaouzidis, Anastasios
title: Collateral Casualties of COVID-19
date: 2021-05-25
journal: J Am Coll Cardiol
DOI: 10.1016/j.jacc.2021.01.058
sha: 57cefac21b32e93db987269e2fdaca9d96d7a845
doc_id: 915962
cord_uid: 0rjsmq06

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connecting pressure to these changes remain, however, to be explored. Hypertension-induced alteration in flow velocity and pattern, as suggested by Dr. Aslanger, leading to local changes in shear stress is certainly a hypothesis with merit and should be examined in future research.

Dr. Aslanger also points out that absolute pressures do not predict the rate of atherogenesis across the body. Importantly, this is not the same as to say that increases in pressures may not be proatherogenic.

Under physiologic conditions, each artery is developed to cope with the particular local pressures and lumen diameters that are needed for distribution of blood. The guiding principle is to keep the load on arterial smooth muscle cells constant by varying the number of these cells (2) . Thus, arterial cells do not sense the absolute luminal pressure, but will sense relative increases in pressure that will increase tensile stress and require restructuring of the arterial wall to normalize the mechanical load per cell. We propose that these restructuring processes, detected by histology and proteomics in our experiment, are at the heart of hypertensionaccelerated atherogenesis.

In conclusion, at this stage we are left with more questions than answers. Future experiments will tell which path the story will take. 

We read with interest the recent paper by Einstein 

We appreciate the thoughtful comments by Dr. 

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