Springer Science and Business Media LLC

Patients with heart failure (HF) have an increased symptom burden and complex psychosocial and decision-making needs that necessitate the integration of palliative care. However, in the current era, palliative care is frequently evoked for these patients only at the end-of-life or in the inpatient setting; rarely is palliative care proactively utilized in outpatients with HF. The purpose of this review is to evaluate the current state of palliative care and heart failure and to provide a roadmap for the integration of palliative care into outpatient HF care. Recent studies, including PAL-HF, CASA, and SWAP-HF, have demonstrated that structured palliative care interventions may improve quality of life, depression, anxiety, understanding of prognosis, and well-being in HF. HF is associated with high mortality risk, significant symptom burden, and impaired quality of life. Palliative care can meet many of these needs; however, in the current era, palliative care consultations in HF occur late in the disease course and too often in the inpatient setting. Primary palliative care should be provided to all outpatients with heart failure based on their needs, with referral to secondary palliative care provided based on certain triggers and milestones.

The feasibility, safety, and efficacy of transcatheter heart valve (THV) therapies such as MitraClip and transcatheter aortic valve implantation (TAVI) have made them valid therapeutic options in high-risk or inoperable patients with heart failure (HF). Randomized controlled trials (RCTs) demonstrated noninferiority and superiority in terms of efficacy for 12 months of TAVI versus surgical replacement and optimal medical therapy, respectively. With regard to MitraClip, noninferiority was first demonstrated in four subgroups at 12 months and then later at 4-year follow-up. This difference in clinical outcomes between the two therapies is consistent with the discrepancy in the level of recommendation and class of evidence for TAVI and MitraClip according to recent international guidelines (IB vs. IIbC, respectively). Data from ongoing RCTs and national registries will help establish the reciprocal role and hierarchy among THV therapies, surgery, and medical treatment in patients with HF.

Atrial fibrillation (AF) and heart failure (HF) are commonly encountered clinical disorders that often co-exist, accelerating disease progression and adverse outcomes. It is known that restoration of sinus rhythm positively impacts this population; however, the complex comorbidity profile associated with HF introduces intricacies not encountered in other patient populations. The current review focuses on the safety and efficacy of an interventional-based management for atrial tachyarrhythmias in HF. While pharmacotherapy has been the standard treatment of cardiac dysrhythmias in the HF population, recent evidence suggests catheter ablation is more effective and causes less harm than antiarrhythmic drugs (AADs) in the HF population. For the maintenance of sinus rhythm, catheter ablation results in improved freedom from recurrent arrhythmia, with secondary benefit on mortality and hospitalization in those with HF and reduced ejection fraction. For those with permanent AF, cardiac resynchronization therapy and atrioventricular junction ablation result in improved quality of life, physical functioning, and cardiac function.

Transthyretin amyloidosis (ATTR) is either a hereditary disease related to a mutation in the transthyretin gene that leads to neuropathy and/or cardiomyopathy or an acquired disease of the elderly that leads to restrictive cardiomyopathy. The prevalence of this disease is higher than once thought and awareness is likely to increase amongst physicians and in particular cardiologists. Until recently there have been no treatment options for this disease except to treat the heart failure with diuretics and the neuropathy symptomatically. However, there are several emerging pharmacologic therapies designed to slow or stop the progression of ATTR. This article reviews novel therapeutic drugs that work at different points in the pathogenesis of this disease attempting to change its natural history and improve outcomes.

Although cardiac resynchronization therapy (CRT) has been of unquestioned therapeutic benefit to many patients with heart failure identified by a widened QRS complex on an electrocardiogram, many patients do not respond favorably. Several studies using echocardiographic methods to measure abnormalities of mechanical activation, known as dyssynchrony, have been proposed to improve patient selection for CRT. Many single-center studies from institutions with special expertise have demonstrated the feasibility of echocardiographic dyssynchrony to potentially assist with patient selection. However, the PROSPECT trial, a recent large multicenter study, highlighted the technical challenges in echocardiographic dyssynchrony analysis in mainstream clinical practice. Accordingly, a uniform clinical approach has not been established, and refinements of echocardiographic approaches and methods are constantly evolving. This article reviews current echocardiographic methods to quantify ventricular dyssynchrony, their strengths and limitations, and the proposed and potential expanding clinical applications.

Both nonischemic and ischemic dilated cardiomyopathy are associated with an increased risk of sudden cardiac death, most commonly as a result of ventricular tachyarrhythmias. The pathophysiology of sudden death is complex and results from the interplay of scarred myocardium with physiologic and environmental triggers. Clinical trials completed within the past decade have clarified the role of implantable defibrillators in prolonging survival and have expanded the indications for the use of these devices in patients with heart failure. This article examines the pathophysiology of sudden cardiac death and reviews the clinical trials that have defined the role of device therapy in current practice.

The kidney natriuretic peptide urodilatin (ie, ularitide) decreases pulmonary capillary wedge pressure (PCWP) but does not cause diuresis in persons with congestive heart failure (CHF). Thirty-three percent of patients with CHF treated with 30 ng/kg/min ularitide develop hypotension with systolic blood pressures below 90 mmHg. Nesiritide and atrial natriuretic peptide lower PCWP and cause hypotension. They do not produce diuresis or natriuresis in patients with CHF. The best natriuretic peptide for treating CHF is the cardiac hormone vessel dilator which decreases PCWP and decreases systemic and pulmonary vascular resistance while simultaneously increasing cardiac output and cardiac index. What makes the vessel dilator markedly better than atrial natriuretic peptide, nesiritide, and ularitide for treatment of CHF is that it enhances sodium excretion fivefold and causes a fivefold enhanced diuresis in patients with CHF with its biologic effects lasting over 6 hours compared with less than 30 minutes for the above peptides.

Heart failure readmissions result in significant costs to the health care system and to patients’ quality of life, but programs to reduce readmissions have met with mixed success. Successful strategies have included multidisciplinary hospital-based quality initiatives, disease management programs, and care transition interventions. Devices like telemonitors and indwelling catheters, however, have met with mixed success. Research is still needed to elucidate the most effective interventions for readmission reduction in the HF population.

Left ventricular (LV) noncompaction cardiomyopathy (LVNC) is a form of cardiomyopathy in which trabeculations fail to “compact” with the left ventricular endocardium during fetal cardiac development and is classically associated with subsequent impairment of LV function, significant mortality, ventricular dysrhythmias, and embolic phenomena. As awareness and medical imaging quality have improved, it is becoming easier to identify trabeculations that traverse the LV cavity and serve as a distinguishing feature of this disorder. Differentiating true noncompaction from mild increases in trabeculations requires prudent imaging and clinical correlation. This review seeks to discuss the potential methods of evaluating left ventricular trabeculations, the role of increased trabeculations in cardiovascular disease, and how their presence may affect clinical management.