Rising arterial stiffness with accumulating comorbidities associates with heart failure with preserved ejection fraction

Author:

Ali Danish1,Tran Patrick23ORCID,Ennis Stuart14,Powell Richard4,McGuire Scott1,McGregor Gordon14,Kimani Peter K.1,Weickert Martin O.13,Miller Michelle A.1,Cappuccio Francesco P.13,Banerjee Prithwish123

Affiliation:

1. Warwick Medical School University of Warwick Coventry UK

2. Centre for Sport, Exercise and Life Sciences, Faculty of Health and Life Sciences Coventry University Coventry UK

3. University Hospitals Coventry and Warwickshire Coventry UK

4. Department of Cardiopulmonary Rehabilitation, Centre for Exercise and Health University Hospitals Coventry and Warwickshire NHS Trust Coventry UK

Abstract

AbstractAimsComorbidities play a significant role towards the pathophysiology of heart failure with preserved ejection fraction (HFpEF), characterized by abnormal macrovascular function and altered ventricular–vascular coupling. However, our understanding of the role of comorbidities and arterial stiffness in HFpEF remains incomplete. We hypothesized that HFpEF is preceded by a cumulative rise in arterial stiffness as cardiovascular comorbidities accumulate, beyond that associated with ageing.Methods and resultsArterial stiffness was assessed using pulse wave velocity (PWV) in five groups: Group A, healthy volunteers (n = 21); Group B, patients with hypertension (n = 21); Group C, hypertension and diabetes mellitus (n = 20); Group D, HFpEF (n = 21); and Group E, HF with reduced ejection fraction (HFrEF) (n = 11). All patients were aged 70 and above. Mean PWV increased from Groups A to D (PWV 10.2, 12.2, 13.0, and 13.7 m/s, respectively) as vascular comorbidities accumulated independent of age, renal function, haemoglobin, obesity (body mass index), smoking status, and hypercholesterolaemia. HFpEF exhibited the highest PWV and HFrEF displayed near‐normal levels (13.7 vs. 10 m/s, P = 0.003). PWV was inversely related to peak oxygen consumption (r = −0.304, P = 0.03) and positively correlated with left ventricular filling pressures (E/e′) on echocardiography (r = −0.307, P = 0.014).ConclusionsThis study adds further support to the concept of HFpEF as a disease of the vasculature, underlined by an increasing arterial stiffness that is driven by vascular ageing and accumulating vascular comorbidities, for example, hypertension and diabetes. Reflecting a pulsatile arterial afterload associated with diastolic dysfunction and exercise capacity, PWV may provide a clinically relevant tool to identify at‐risk intermediate phenotypes (e.g. pre‐HFpEF) before overt HFpEF occurs.

Publisher

Wiley

Subject

Cardiology and Cardiovascular Medicine

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