Aims: Comorbidities 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 results: Arterial 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). Conclusions: This 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.

Purpose of Review: To provide an overview of the potential iatrogenic causes of acute decompensated heart failure (AHF) and an evidence-based management strategy to address this.Recent Findings: As the heart failure (HF) population continues to age and become burdened with greater comorbidities and polypharmacy, patients become more susceptible to the iatrogenic precipitants of HF. The following clinical scenarios are familiar to clinicians, but the sequelae to AHF are often unanticipated: HF medications withdrawn during an intercurrent illness and not restarted, cardiotoxic therapy prescribed for cancer without timely and regular monitoring of left ventricular function, excessive intravenous fluids administered for sepsis or postoperatively, a blood transfusion volume not adjusted for body weight, iatrogenic anaemia that goes unnoticed or an inappropriate type of pacemaker implanted in a patient with underlying left ventricular systolic dysfunction.Summary: Iatrogenic decompensated HF is a phenomenon that is infrequently documented in the literature but increasingly confronted by clinicians of all specialties. It is associated with a high mortality and morbidity rate. By having greater awareness of these triggers, iatrogenic AHF should be one that is prevented rather than managed when it occurs.

Background : There is already extensive literature on the natural history of hypertensive heart disease (HHD) and aortic stenosis (AS). Once these patients develop severe left ventricular systolic dysfunction (LVSD) despite guideline-directed therapy for heart failure (HF), it is often thought to be end-stage from irreversible adverse remodelling. Our case series challenges this traditional paradigm. A more holistic model that factors in the interactions between the ventricle and vasculature is required. Based on a novel hypothetical concept of myocardial fatigue, we propose that occasionally LVSD is not an inherent myocardial or valvular disease but a consequence of an arterial afterload mismatch. By addressing this, the ventricle may recover and contract efficiently in unison with the arterial system. Case summary : We present two cases of severe LVSD in a young lady with long-standing essential hypertension and a gentleman with stable severe AS. Both patients were already established on HF medications. After optimizing their blood pressure control, repeat echocardiography revealed normalization of left ventricular ejection fraction within 3 months, along with a demonstrable improvement in ventricular–arterial coupling and for AS, a reduction in valvular-arterial impedance. Discussion : Just as Frank–Starling’s law was discovered by initially drawing analogies to skeletal muscle behaviour, it is biologically plausible that cardiac fatigue can occur in the setting of afterload mismatch. The chance of recovery rests upon early recognition before it transitions to irreversible myocardial damage. Only by testing new emerging theories of HF can we galvanize original research and find new avenues to understanding this complex syndrome.

Functional substrate mapping has emerged as an essential tool for electrophysiologists, overcoming many limitations of conventional mapping techniques and demonstrating favourable long-term outcomes in clinical studies. However, a consensus on the definition of ‘functional substrate’ mapping remains elusive, hindering a structured approach to research in the field. In this review, we highlight the differences between ‘functional mapping’ techniques (which assess tissue response to the ‘electrophysiological stress’ using short coupled extrastimuli) and those highlighting regions of slow conduction during sinus rhythm. We also address fundamental questions, including the optimal degree of electrophysiological stress that best underpins the critical isthmus and the role of wavefront activation in determining the most effective ablation site.