Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 320, Issue 2, Pages H475-H486Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00573.2020
Keywords
gut microbiota; heart failure; hypertension; inflammation; short-chain fatty acids
Funding
- University College Dublin
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Heart failure is a major cause of mortality and morbidity in the modern world, with increasing prevalence of HFpEF being of particular concern. Pressure overload caused by hypertension is the predominant driver of HFpEF.
Heart failure (HF) is one of the leading causes of mortality and morbidity in the modern world whose increasing prevalence is associated with Western diet and sedentary lifestyles. Of particular concern is the increasing burden of HF with preserved ejection fraction (HFpEF) that involves complex pathophysiology and is difficult to treat. Pressure overload caused by hypertension (HTN) is the predominant driver of cardiac injury, left ventricular hypertrophy, and fibrosis that progresses to diastolic dysfunction and ultimately HFpEF. Although pharmacological control of blood pressure may affect the degree of pressure overload, such therapies are largely ineffective in established HFpEF, and there is a need to modulate the festering inflammatory and fibrotic response to injury to halt and perhaps reverse pathology. An emerging literature indicates potentially important links between the gut microbiota, dietary soluble fiber, and microbiota-derived metabolites that modulate blood pressure and the immune response. In particular, high-fiber diets demonstrate protective properties in systemic hypertension and left-sided cardiac pathology, and this action is closely associated with short-chain fatty acid (SCFA)-producing bacteria. Mechanisms underlying the beneficial action of SCFAs in immunity and the systemic circulation could potentially be applied to the treatment of hypertension and the cardiac damage it causes. In this review, we discuss the potential beneficial effects of SCFAs, with an emphasis on mechanisms that are involved in cardiac responses to pressure overload.
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