Novel Non-Pharmaceutical Advancements in Heart Failure Management: The Emerging Role of Technology

Public Health Burden ◽

Heart Failure Care ◽

Cardiac Devices ◽

Randomized Controlled Studies ◽

Technological Advances ◽

Purpose of Review: To summarise and discuss the implications of recent technological advances in heart failure care. Recent Findings: Heart failure remains a significant source of morbidity and mortality in the US population despite multiple classes of approved pharmacological treatments. Novel cardiac devices and technologies may offer an opportunity to improve outcomes. Baroreflex Activation Therapy and Cardiac Contractility Remodelling may improve myocardial contractility by altering neurohormonal stimulation of the heart. Implantable Pulmonary Artery Monitors and Biatrial Shunts may prevent heart failure admissions by altering the trajectory of progressive congestion. Phrenic Nerve Stimulation offers potentially effective treatment for comorbid conditions. Smartphone applications offer an intriguing strategy for improving medication adherence. Summary: Novel heart failure technologies offer promise for reducing this public health burden. Randomized controlled studies are indicated for assessing the future role of these novel therapies.

Cardiac Contractility Modulation and Baroreflex Activation Therapy in Heart Failure Patients

Current Heart Failure Reports ◽

10.1007/s11897-019-0422-3 ◽

2019 ◽

Vol 16 (1) ◽

pp. 38-46 ◽

Cited By ~ 3

Author(s):

James A. Mann ◽

William T. Abraham

Keyword(s):

Heart Failure ◽

Cardiac Contractility ◽

Cardiac Contractility Modulation ◽

Heart Failure Patients ◽

Baroreflex Activation Therapy (BAT) in Patients with Heart Failure and a Reduced Ejection Fraction (HFrEF): The BeAT-HF Trial

SSRN Electronic Journal ◽

10.2139/ssrn.3452105 ◽

2019 ◽

Cited By ~ 3

Author(s):

Michael Zile ◽

JoAnn Lindenfeld ◽

Fred A. Weaver ◽

Faiez Zannad ◽

Elizabeth Galle ◽

...

Keyword(s):

Heart Failure ◽

Ejection Fraction ◽

Reduced Ejection Fraction ◽

Patients With Heart Failure ◽

Advances in understanding the role of cardiac glycosides in control of sodium transport in renal tubules

Journal of Endocrinology ◽

10.1530/joe-13-0613 ◽

2014 ◽

Vol 222 (1) ◽

pp. R11-R24 ◽

Cited By ~ 5

Author(s):

Syed Jalal Khundmiri

Keyword(s):

Heart Failure ◽

Intracellular Signaling ◽

Cardiac Contractility ◽

Myocardial Cell ◽

Renal Tubules ◽

Intracellular Signaling Pathway ◽

Body Sodium ◽

Membrane Bound ◽

Total Body

Cardiotonic steroids have been used for the past 200 years in the treatment of congestive heart failure. As specific inhibitors of membrane-bound Na+/K+ATPase, they enhance cardiac contractility through increasing myocardial cell calcium concentration in response to the resulting increase in intracellular Na concentration. The half-minimal concentrations of cardiotonic steroids required to inhibit Na+/K+ATPase range from nanomolar to micromolar concentrations. In contrast, the circulating levels of cardiotonic steroids under physiological conditions are in the low picomolar concentration range in healthy subjects, increasing to high picomolar levels under pathophysiological conditions including chronic kidney disease and heart failure. Little is known about the physiological function of low picomolar concentrations of cardiotonic steroids. Recent studies have indicated that physiological concentrations of cardiotonic steroids acutely stimulate the activity of Na+/K+ATPase and activate an intracellular signaling pathway that regulates a variety of intracellular functions including cell growth and hypertrophy. The effects of circulating cardiotonic steroids on renal salt handling and total body sodium homeostasis are unknown. This review will focus on the role of low picomolar concentrations of cardiotonic steroids in renal Na+/K+ATPase activity, cell signaling, and blood pressure regulation.

Abstract 2415: Long-Term Baroreflex Activation Therapy Increases the Threshold for the Induction of Lethal Ventricular Arrhythmias in Dogs with Chronic Advanced Heart Failure

Circulation ◽

10.1161/circ.118.suppl_18.s_722 ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Mengjun Wang ◽

Valerio Zaca ◽

Alice Jiang ◽

Itamar Ilsar ◽

Matthew Ebinger ◽

...

Keyword(s):

Heart Failure ◽

Sudden Cardiac Death ◽

Cardiac Death ◽

Ventricular Arrhythmias ◽

Lv Function ◽

Increased Risk ◽

Lv Remodeling ◽

Heart failure (HF) is associated with a high incidence of ventricular tachycardia (VT) and fibrillation (VF). Patients with HF in whom these lethal arrhythmias can be induced by electrophysiological (EP) testing carry a high risk of sudden cardiac death. We showed that chronic electrical carotid baroreflex activation therapy (BAT) with the Rheos® System (CVRx, Inc.) improves LV function, attenuates LV remodeling and restores autonomic sympathetic-parasympathetic balance in dogs with HF. This study examined the effects of long-term therapy with BAT on the induction of VT or VF in dogs with coronary microembolization-induced HF (LV ejection fraction ~20%). Eleven dogs with HF underwent EP testing at baseline prior to therapy and after 3 and 6 months of therapy with BAT and again 6 weeks after withdrawal of BAT therapy (n = 7) or no therapy at all (Control, n = 4). Programmed ventricular stimulation was performed from the right ventricular apex and included delivery of up to 4 extrastimuli at progressively shorter coupling intervals (in steps of 10 msec). The extrastimuli were delivered following 8 ventricular paced beats with a drive cycle length between 600 and 200 msec. If a sustained monomorphic VT or VF could not be induced, isoproterenol infusion was initiated to increase the sinus rate by ~30% and the EP stimulation protocol was repeated. At baseline, a sustained VT or VF was induced in all 11 dogs (100%). After 3 and 6 months of follow-up, all Control dogs (100%) were induced into sustained VT or VF. After 3 months of BAT, only 3 of 7 dogs (43%) were induced into sustained VT or VF. After 6 months of BAT, only 2 of 7 dogs (29%) were induced into sustained VT or VF. Finally after withdrawal of BAT therapy, all dogs (100%) were again induced into systained VT or VF. In addition to improving LV function and attenuating LV remodeling, long-term monotherapy with BAT markedly increases the threshold for lethal ventricular arrhythmias in dogs with chronic HF. This is a marked improvement over inducibility of lethal arrhythmias seen in historical untreated controls. This benefit of BAT supports the continued exploration of this device as a therapeutic modality for treating patients with chronic HF and increased risk of sudden cardiac death.