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[Scientific news] Arterial-ventricular coupling, more than a life-long love story

 

Our hearts endlessly pump the life-giving blood required by our organs to keep them running smoothly.

And they do this day after day after day, about 3.5 billion times over an average lifetime. Due to disease, environmental factors, or just old age, cardiovascular components start to deteriorate progressively. With international collaborators, IHU-ICAN researchers have used advanced magnetic resonance imaging (MRI) imaging to examine the life-long relationship between the arteries and heart chambers. Such high-resolution imaging techniques can help determine cardiovascular age to better predict future health.

 

Our hearts are tireless muscular pumps. With every heartbeat the ascending aorta carries newly oxygen-enriched blood to the heart, and is tightly coupled to the left ventricular chamber, which steadily pushes oxygenated blood throughout our bodies. Clinician scientists and researchers from the IHU-ICAN community including Sorbonne UniversityLIBicv INSERM, Pitie Salpetriere hospital and HEGP (AP-HP) collaborated with other cardiac MRI imaging experts at Johns Hopkins in the United States as well as Taiwan and Norway, to find out how this relationship can impact disease progression, as well as healthy aging.

It’s known that as we age, our arteries gradually stiffen, reducing the ability of the heart to function correctly under all conditions. Certain diseases such as diabetes or other environmental, lifestyle, or nutritional factors can exacerbate this deterioration. These factors can also damage or stiffen the ventricles (the pumping chambers) of the heart and impede its proper function.

The thoracic aorta has an important role in channeling oxygenated blood from the heart for peripheral distribution and must maintain an equal pressure to function correctly. As the aorta progressively stiffens, the left ventricle compensates by increasing contractility and heart chamber wall thickness (remodeling). However this makes the heart work much harder, reducing its ability to adapt to further increased loading conditions, which may ultimately lead to heart failure.

 

Using cutting-edge MRI imaging to delve into artery-ventricle relationships

Using advanced MRI imaging techniques to measure both aortic and left ventricular strain and flow in 100 healthy men and women volunteers aged over 18 years, the authors discovered that:

  1. Aortic stiffening appears earlier in life than left ventricle remodeling and dysfunction, at all ages
  2. In individuals younger than 45 years old, decreased left ventricular deformation (strain) and increased remodeling is linked to aortic deformation relative to the driving pressure (distensibility=strain divided by pulse pressure), whereas it is linked to aortic impedance, a measure of the pulsatile resistance component in the ascending aorta in individuals older than 45 years of age.
  3. The static resistance component measured as total peripheral resistance was however consistently related to cardiac deformation and remodeling across the age spectrum. It is important to distinguish the different components contributing to blood flow “resistance” (such as from the ventricle to the aorta, and organs). Therefore different strategies related to each of the different components could be used to slow the accelerated aging and stiffening seen is some patients, and thus protect the efficiency of the heart-aorta couple.

 

Central arterial elasticity is the best predictor of cardiac health

Maintaining arterial flexibility as we age determines our future cardiac health (Hypertension 2010), whereas diseases or environmental/nutritional factors that stiffen our arteries are linked to a poorer cardiac outcome (JACC 2014). However, there is good news, as it is possible to reverse aortic stiffness, by changing habits to encourage weight loss, in combination with diet modifications and increasing exercise. Several existing blood-pressure lowering drugs can also have potential benefits.

 

Relevant links

https://www.ncbi.nlm.nih.gov/pubmed/30978118

https://www.physiology.org/doi/abs/10.1152/ajpheart.00694.2018