Shane Nanayakkara

Management of heart failure with preserved ejection fraction: a review.

PURPOSEnThe purpose of this article was to review the clinical management of patients with heart failure with preserved ejection fraction (HFPEF).nnnMETHODSnFor this critical review, electronic databases (MEDLINE, EMBASE, PubMed) were searched for relevant basic research studies and randomized clinical trials recently published or presented at major meetings. Details of in-progress or planned studies were obtained from the ClinicalTrials.gov website. The range of publication dates was the year 2000 to 2015. Search terms included HFPEF, heart failure with preserved ejection fraction, HFPSF, heart failure with preserved systolic function, diastolic heart failure, diastolic dysfunction, HFNEF, heart failure with normal ejection fraction, treatment, management, therapy.nnnFINDINGSnPatients with HFPEF account for up to half of all patients with a clinical diagnosis of HF. Key contributing factors include hypertension, obesity, and atrial fibrillation, and other chronic diseases, including diabetes, chronic obstructive pulmonary disease, and anemia, frequently coexist. To date, large-scale clinical trials, particularly those focused on antagonism of the renin-angiotensin-aldosterone system, have provided limited evidence of clinical benefit.nnnIMPLICATIONSnThe aggressive management of contributing factors, including hypertension, atrial fibrillation, and myocardial ischemia, is key in the management of HFPEF. New insights into the mechanisms and thus the identification of potential therapeutic strategies are urgently required.

Pathogenesis and treatment of the cardiorenal syndrome: Implications of L-arginine-nitric oxide pathway impairment

A highly complex interplay exists between the heart and kidney in the setting of both normal and abnormal physiology. In the context of heart failure, a pathophysiological condition termed the cardiorenal syndrome (CRS) exists whereby dysfunction in the heart or kidney can accelerate pathology in the other organ. The mechanisms that underpin CRS are complex, and include neuro-hormonal activation, oxidative stress and endothelial dysfunction. The endothelium plays a central role in the regulation of both cardiac and renal function, and as such impairments in endothelial function can lead to dysfunction of both these organs. In particular, reduced bioavailability of nitric oxide (NO) is a key pathophysiologic component of endothelial dysfunction. The synthesis of NO by the endothelium is critically dependent on the plasmalemmal transport of its substrate, L-arginine, via the cationic amino acid transporter-1 (CAT1). Impaired L-arginine-NO pathway activity has been demonstrated individually in heart and renal failure. Recent findings suggest abnormalities of the L-arginine-NO pathway also play a role in the pathogenesis of CRS and thus this pathway may represent a potential new target for the treatment of heart and renal failure.

Utility of rotational atherectomy and outcomes over an eight-year period.

To evaluate outcomes of patients undergoing rotational atherectomy (RA) in a multicenter percutaneous coronary intervention (PCI) registry.

The use of the AVERT system to limit contrast volume administration during peripheral angiography and intervention

The AVERTTM Contrast Modulation System (AVERT) (Osprey Medical, MN) is designed to reduce contrast volume administration during angiography. The AVERT provides an adjustable resistance circuit which decreases the pressure head delivering contrast towards the patient. The AVERT has not been previously studied in patients undergoing peripheral digital subtraction angiography (DSA). The purpose of this study was (1) to evaluate contrast savings with the AVERT and (2) to evaluate the ability to generate clinically acceptable DSA images in the process. To better define the mechanism of action in the peripheral circulation, we also developed a bench model to study the effects of the AVERT on the hydrodynamics of contrast delivery.

Mechanisms of the Improvement in Peak VO2 With Exercise Training in Heart Failure With Reduced or Preserved Ejection Fraction

Heart failure (HF) is a major health care burden associated with high morbidity and mortality. Approximately 50% of HF patients have reduced ejection fraction (HFrEF) while the remainder of patients have preserved ejection fraction (HFpEF). A hallmark of both HF phenotypes is dyspnoea upon exertion and severe exercise intolerance secondary to impaired oxygen delivery and/or use by exercising skeletal muscle. Exercise training is a safe and effective intervention to improve peak oxygen uptake (VO2peak) and quality of life in clinically stable HF patients, however, evidence to date suggests that the mechanism of this improvement appears to be related to underlying HF phenotype. The purpose of this review is to discuss the role of exercise training to improve VO2peak, and how the central and peripheral adaptations that mediate the improvements in exercise tolerance may be similar or differ by HF phenotype (HFrEF or HFpEF).

Targets for Heart Failure With Preserved Ejection Fraction

Heart failure (HF) with preserved ejection fraction (HFPEF) is responsible for half of all HF cases and will be the most common form of HF within the next 5 years. Previous studies of pharmacological agents in HFPEF have proved neutral or negative, in part due to phenotypic heterogeneity and complex underlying mechanisms. This review summarizes the key molecular and cellular pathways characterized in HFPEF as well as current and future therapies that target these mechanisms.

Effects of Milrinone on Rest and Exercise Hemodynamics in Heart Failure With Preserved Ejection Fraction

Heart failure with preserved ejection fraction (HFPEF) accounts for a substantial proportion of the population of patients with heart failure, and the prevalence is rising [(1)][1]. The pathophysiology of HFPEF is complex [(2)][2]; a rapid rise in left ventricular diastolic and pulmonary pressures

Mycotic Pseudoaneurysms of the Coronary Arteries.

Mycotic coronary artery aneurysms are rare and are often fatal without early recognition and prompt surgical management.

Impact of atrial fibrillation on rest and exercise haemodynamics in heart failure with mid-range and preserved ejection fraction

Heart failure with preserved (HFpEF) and mid‐range ejection fraction (HFmrEF) are becoming the most prevalent forms of heart failure. Patients with HFpEF/HFmrEF in atrial fibrillation (AF) have poorer survival and quality of life, but the mechanism underpinning this is unknown. We sought to investigate the influence of AF on the haemodynamic profile of HFpEF/HFmrEF patients at rest and during exercise.

The ageing heart: the systemic and coronary circulation

Most cardiovascular disease (CVD) occurs in patients over the age of 60. However, most evidence-based current cardiovascular guidelines lack evidence in an older population, due to the under-representation of older patients in randomised trials. Blood pressure rises with age due to increasing arterial stiffness, and stricter control results in improved outcomes. Myocardial ischaemia is also more common with increasing age, due to a combination of coronary artery disease and myocardial changes. However, despite higher rates of adverse outcomes, older patients are offered guideline-based therapy less frequently. Frailty is an independent predictor of mortality in adults over the age of 60, yet remains poorly assessed; slow gait speed is a key marker for the development of frailty and for adverse outcomes following intervention. Few trials have assessed frailty independent of age; however, there is evidence that non-frail older patients derive significant benefit from therapy, highlighting the urgent need to include frailty as a measure in clinical trials of treatment in CVD. In this review, the authors appraise the literature in regard to the cardiovascular changes with ageing, specifically in relation to the systemic and coronary circulation and with a particular emphasis on frailty and its implication in the evaluation and treatment of CVD.