Acids Associated With Atherosclerosis

Studies around the world have consistently shown that both short and long term exposures to Particulate Matter (PM) air pollution are associated with a host of cardiovascular diseases, including myocardial ischemia and infarctions, heart failure, arrhythmias, strokes and increased cardiovascular mortality.

Very recently it was published a study in humans confirming the association of the exposure to ambient air pollution and atherosclerosis through the progression of carotid artery intima-media thickness (1).

In an interesting recent paper by Robert Brook (2) he states that there are three putative ‘general’ pathways to explain the biological mechanisms whereby PM exposure may be capable of mediating cardiovascular events: 1) autonomic mechanisms: parasympathetic nervous system withdraw and/or sympathetic nervous system activation; 2) the release of circulating pro-oxidative and/or pro-inflammatory mediators from the lungs (e. g. cytokines and activated immune cells) into the systemic circulation following PM inhalation that, in turn, indirectly mediate CV responses; and; 3) nano-scale particles and/or soluble PM constituents translocating into the systemic circulation after inhalation that then directly interact with the CV system.

According to Robert Brook, chronic actions of PM and the enhancement of atherosclerosis, are most likely to be induced by the generation of a chronic pro-inflammatory state (pathway 2).

Taking in view the results of studies in humans showing that particulate air pollutants continuous exposition decreases the heart rate variability (3,4) and may lead to an impaired autonomic control with potential acceleration in the progression of atherosclerosis (5,6,7), with the due respect, I feel obliged to differ from Brook’s opinion regarding the biological mechanism related to chronic PM exposure and atherosclerosis. In our view the sympathetic over activity may start the whole process of atherosclerosis which ends in the inflammatory state as hypothesized in the acidity theory of atherosclerosis (8) and discussed in our last article in this blog (9)Carlos Monteiro

1. Nino Kunzli, Michael Jerrett, Raquel Garcia-Esteban, Xavier Basagana, Bernardo Beckermann, Frank Gilliland, Merce Medina, John Peters, Howard N. Hodis, Wendy J. Mack. "Ambient Air Pollution and the Progression of Atherosclerosis in Adults." PloS ONE 5(2): e9096. doi:10.1371/journal.pone.0009096, February 8, 2010. Full free text at http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0009096

2. Brook RD, Cardiovascular effects of air pollution. Clinical Science (2008) 115, (175–187) Full free text at http://www.clinsci.org/cs/115/0175/1150175.pdf

3. Duanping Liao, Yinkang Duan, Eric A. Whitsel, Zhi-jie Zheng, Gerardo Heiss, Vernon M. Chinchilli, and Hung-Mo Lin. Association of Higher Levels of Ambient Criteria Pollutants with Impaired Cardiac Autonomic Control: A Population-based Study, Am J Epidemiol 2004;159:768–777

4. C. Arden Pope III, Matthew L. Hansen, Russell W. Long, Karen R. Nielsen, Norman L. Eatough, William E. Wilson, and Delbert J. Eatough. Ambient Particulate Air Pollution, Heart Rate Variability, and Blood Markers of Inflammation in a Panel of Elderly Subjects. Environmental Health Perspectives, V 112; N 3: March 2004

5. Heikki V. Huikuri; Vesa Jokinen; Mikko Syvänne; Markku S. Nieminen; K. E. Juhani et al, Heart Rate Variability and Progression of Coronary Atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:1979-1985.

6. Anders Gottsäter , Åsa Rydén Ahlgren, Soumia Taimour and Göran Sundkvist, Decreased heart rate variability may predict the progression of carotid atherosclerosis in type 2 diabetes Clinical Autonomic Research Volume 16, Number 3 / June, 2006

7. J. C. Longenecker, M. Zubaid, K.V. Johny, A.I. Attia, J. Ali, W. Rashed, C.G. Suresh, M. Omar. Association of low heart rate variability with atherosclerotic cardiovascular disease in hemodialysis patients. Med Princ Pract 2009;18:85-92

8. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at http://www.infarctcombat.org/AcidityTheory.pdf

9. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html