Statin Therapy Induces Gut Leakage and Neuromuscular Disjunction in Patients With Chronic Heart Failure

Author:

Ahmad Firdos12ORCID,Karim Asima1,Khan Javaidullah3,Qaisar Rizwan14

Affiliation:

1. Basic Medical Sciences, College of Medicine, University of Sharjah, Sharjah, United Arab Emirates;

2. Department of Biomedical Sciences, College of Health Sciences, Abu Dhabi University, Abu Dhabi, United Arab Emirates;

3. Department of Cardiology, Post Graduate Medical Institute, Hayatabad Medical Complex, Peshawar, Pakistan; and

4. Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.

Abstract

Abstract: Statins are commonly used to limit the risk of cardiovascular diseases, including ischemic heart attack and stroke. However, treatment often leads to myopathy and muscle weakness. Therefore, a better understanding of underlying pathomechanism is needed to improve the clinical outcomes. Here, we assessed the physical performance, including handgrip strength (HGS), gait speed (GS), and short physical performance battery, in 172 patients diagnosed with chronic heart failure (CHF) treated with (n = 50) or without (n = 122) statin and 59 controls. The plasma biomarkers, including sarcopenia marker C-terminal agrin fragment-22 (CAF22), intestinal barrier integrity marker zonulin, and C-reactive protein (CRP), were measured and correlated with the physical performance of patients. The HGS, short physical performance battery scores, and GS were significantly compromised in patients with CHF versus controls. Irrespective of etiology, significant elevation of plasma CAF22, zonulin, and CRP was observed in patients with CHF. There were strong inverse correlations of CAF22 with HGS (r2 = 0.34, P < 0.0001), short physical performance battery scores (r2 = 0.08, P = 0.0001), and GS (r2 = 0.143, P < 0.0001). Strikingly, CAF22 and zonulin were positively correlated with each other (r2 = 0.10, P = 0.0002) and with the level of CRP in patients with CHF. Further investigations revealed a significant induction of CAF22, zonulin, and CRP in patients with CHF taking statin versus nonstatin group. Consistently, HGS and GS were significantly lower in the statin versus nonstatin CHF patients' group. Collectively, statin therapy adversely affects the neuromuscular junction and intestinal barrier, which potentially induces systemic inflammation and physical disability in patients with CHF. Further prospective confirmation of the findings is required in a well-controlled study.

Funder

University of Sharjah

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Pharmacology

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