Angiotensin-converting enzyme 2 ( ACE2), as a key negative regulator of the RAAS, hydrolyze respectively angiotensin I/II (Ang I/II) into Ang (1–9)/Ang (1–7), and Ang (1–7) further acts on the Mas receptor, forming the ACE2/Ang(1–7)/Mas axis. It is well known that the occurrence and development of T2D is associated with renin–angiotensin–aldosterone system (RAAS) activation, and through entire chain of diabetic related cardiovascular events (e.g., AF ). Here, early genetic risk evaluation of individual’s at greater risk of AF and CS will provide a possible strategy for precision prevention of AF and CS in patients with T2D. Although optimal glycemic management and integrated control of these reversible risk factors (e.g., unhealthy diet, smoking, physical inactivity, obesity, and obstructive sleep apnea syndrome, dyslipidemia, etc.) have been related to lower incidence of AF and CS, the benefit could be dampened or offset by inherently greater genetic risk. More Studies indicated that the risk of cardioembolic stroke (CS) is increased when both conditions coexist, becoming a major public health problem in China. The incidence of AF is then increasing with the diabetes epidemic.

Currently, the prevalence of diabetes in China has rapidly increased over the past decade, and has been ranked top one around the world. The exact mechanisms underlying the increased risk of AF in T2D patients are not fully elucidated, but are thought to involve structural and electrical remodeling of atria, inflammation, oxidative stress, and glycemic fluctuation. In particular, ACE2 rs4646188 was associated with higher levels of ACE ( P = 0.017 and 0.037), Ang I ( P = 0.002 and 0.001), Ang II (both P < 0.001) and ALD ( P = 0.005 and 0.011).Ītrial fibrillation (AF) is the most common arrhythmia worldwide, and type 2 diabetes (T2D) is an independent risk factor for AF.

The 3 ACE2 variants exhibited heterogeneity on circulating RAAS activation. The 3 ACE2 variants were related to larger left atrial end-systolic diameter (LAD) (all P < 0.05), but not all of the 3 ACE2 variants were related to increased levels of serum sodium (rs4240157 and rs4646188, all P < 0.05), HsCRP (rs4240157 and rs4646188, all P < 0.05) as well as decreased serum potassium levels (rs2074192 and rs4646188, all P < 0.05). If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.

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