→increased incidence of angioedema [ ]
Even though real progress has been made in the past decades in the discovery of novel pharmacological treatments for HF, the prevention of premature deaths has only been marginally alleviated. Despite the availability of a plethora of pharmaceutical approaches, proper management of HF is still challenging. Thus, further research, experimental, and clinical studies focusing on the discovery of novel drugs targeting new pathological mechanisms involved in HF are still mandatory.
Recent technological advances have made possible the development of various interventional techniques and device-based approaches for the treatment of cardiovascular diseases. In the following paragraphs, we aimed to summarize the advances made in the development of such procedures and device-based therapies for HF (other than cardiac resynchronization therapy), since these approaches complement and increase the efficiency of the classical drug-based treatments. Moreover, since many of these modern approaches interfere with various well-known described pathological mechanisms in HF, they have a real capability to increase the efficiency of existing medications and improve the prognosis and survival rate. Thus, we consider that among the classical and recently discovered drugs for the treatment of HF, non-pharmacological approaches (other than cardiac resynchronization therapy) must also be discussed.
3.1. neuromodulatory approaches.
The autonomic nervous system (ANS) plays a critical role in the regulation and homeostasis of the human body, particularly of the cardiovascular system. Since in HF ANS dysregulation has a detrimental effect on cardiac function, improving this pathological alteration by various approaches may represent a pillar in the management of HF [ 78 ]. The sympathetic and parasympathetic systems are the two major components of ANS. In the heart, the activation of the parasympathetic nervous system lowers heart rate and decreases contractility, conductance, and myocardial O 2 consumption, resulting in a reduction in cardiac output during relaxation [ 79 ]. Primarily responsible for parasympathetic innervation is the vagus nerve, encompassing all major thoracic organs [ 80 ]. Complex interactions between the sympathetic (SNS) and parasympathetic (PNS) nervous systems, as well as regional responses and feedback from the central nervous system, contribute to the modulation of cardiovascular homeostasis [ 81 ]. Briefly, excitation of the SNS causes nerve terminals to release norepinephrine (NE), whereas the adrenal glands and medulla release both norepinephrine and epinephrine. These catecholamines bind to adrenergic receptors (ARs), which are further subdivided into subtypes α1, α2, β1, β2, and β3 [ 82 ]. In the human heart, β-ARs account for approximately 90% of all ARs, whereas α1-ARs account for almost 10% [ 83 ].
HF is characterized by an imbalance of the ANS, which generates a vicious cycle, meaning that the increased sympathetic activity together with reduced vagal activity promote the progression of ventricular remodeling and worsening of heart failure, and likewise, the development of HF further exacerbates the discrepancy between sympathetic and vagal activity [ 84 ]. High levels of NE over the long-term enhance myocardial stress due to chronic tachycardia increased afterload and oxygen consumption, thereby worsening ventricular remodeling. Increased catecholamines bind with their own cardiomyocyte β-receptors and stimulate G-protein-coupled receptor kinase upregulation, resulting in the downregulation and desensitization of the β1 receptors at the plasma membrane [ 81 , 85 , 86 ]. These processes are thought to be protective mechanisms by which the heart preserves itself against severe catecholaminergic toxicity, which commonly induces cyclic adenosine-monophosphate-mediated calcium overload, leading to cardiomyocyte death [ 81 , 83 , 86 ]. The modulation of the heart PNS is achieved by nicotinic and muscarinic acetylcholine receptors (nAChR and mAChR, respectively) through the neurotransmitter acetylcholine (ACh) [ 81 , 87 ]. Experimental and clinical HF studies have reported that an increased HR, together with a reduced HR variability, is the consequence of PNS dysfunction [ 88 , 89 ].
Cardiac sympathetic denervation (CSD) is a surgical antiadrenergic intervention that has significant antiarrhythmic effects, as demonstrated by both preclinical and clinical studies, being effective in severe ventricular arrhythmias [ 90 , 91 ]. CSD decreases automaticity and repolarization heterogeneity and prolongs repolarization. It exerts its effects by interfering with both efferent and afferent neurons [ 92 ]. Left-sided sympathetic denervation has been utilized effectively in refractory instances of long QT syndrome, catecholaminergic polymorphic ventricular tachycardia [ 93 ], and ventricular arrhythmias in patients with structural heart disease [ 94 , 95 , 96 ].
Renal denervation (RDNx) is a catheter-based procedure used to ablate renal nerves as a solution to ameliorate the pathophysiology of HF by lowering the activity of the sympathetic nervous system. In both HF experimental and clinical studies, RDNx is able to induce antihypertensive effects but also improve adverse cardiac remodeling [ 97 , 98 , 99 , 100 ]. The REACH-pilot study was the first to evaluate the value of RDNx in HF symptomatic patients. In the study, RDNx was related to improvements in both symptoms and exercise ability. There was neither a substantial fall in blood pressure nor a decline in renal function, and some patients were able to limit their usage of diuretics [ 101 ]. In the clinical studies conducted so far, RDNx seems to be safe and well tolerated in patients with HFrEF by improving HF symptoms and modestly lowering systolic and diastolic blood pressure without worsening renal function [ 102 ]. Further insights into the mechanisms by which RDNx improves the physiopathology of HF are required. In this regard, clinical trials with control arms such as RE-ADAPT-HF (A Prospective, Multicenter, Randomized, Blinded, Sham-controlled, Feasibility Study of Renal Denervation in Patients with Chronic Heart Failure) and UNLOAD-HFpEF (Renal Denervation to Treat Heart Failure with Preserved Ejection Fraction) are ongoing, with the results expected in the next years.
Vagus nerve stimulation (VNS) . During an inflammatory response, the vagus nerve acts as an afferent and efferent pathway between the brain and peripheral organs, including the heart [ 103 ]. In the presence of proinflammatory cytokines in the periphery, the sensory afferents of the vagus nerve are activated and transmit the signal to the brain. This signal induces the release of acetylcholine from the vagus nerve efferents into the reticuloendothelial system, which limits inflammation by reducing the synthesis and release of proinflammatory cytokines [ 104 ]. Thus, it is comprehensible that VNS might reduce the proinflammatory state, which is already recognized as a critical pathogenic mechanism in HF, particularly in HFpEF, since it is associated with promoting cardiac remodeling [ 104 ]. Schwartz and colleagues were the first to describe the efficacy of long-term VNS in patients with heart failure. They reported an improvement in functional status, quality of life, and left ventricular volume in HFrEF after vagus nerve stimulation [ 105 ]. However, larger clinical studies of VNS in patients with HFrEF, such as NECTAR-HF (Neural Cardiac Therapy for Heart Failure Study), INOVATE-HF (Increase of Vagal Tone in Chronic Heart Failure), and ANTHEM-HF (Autonomic Neural Regulation Therapy to Enhance Myocardial Function in Heart Failure) have not reliably reproduced the advantages so far [ 106 , 107 , 108 ]. The inconsistency may be the result of extensive variation in stimulation settings, targets, and systems. ANTHEM HFrEF (Autonomic Regulation Therapy to Enhance Myocardial Function and Reduce Progression of Heart Failure with Reduced Ejection Fraction) is an adaptive, open-label, randomized, controlled study that is now enrolling and is expected to provide more insights regarding the efficiency of VNS on HF outcomes [ 109 ].
Tragus nerve stimulation . One of the main drawbacks of vagus stimulation is the invasive nature of this therapy, which is accompanied by surgical risks and low patient tolerance [ 110 ]. Low-level tragus stimulation (LLTS) is a non-invasive transcutaneous approach that may influence autonomic function by stimulating the auricular branch of the vagus nerve (ABVN) [ 111 ]. Currently, ideal LLTS parameters are unclear. In both preclinical and clinical research, LLTS parameters have been empirically determined. In a rat model of heart failure with HFpEF, LLTS lowered both systolic and diastolic blood pressure. Furthermore, left ventricular hypertrophy, circumferential strain, and diastolic function were improved. It has also reduced inflammatory cell infiltration and fibrosis within the ventricle and induced downregulation of pro-inflammatory and pro-fibrotic genes [ 112 ]. Human trials of LLTS in HF patients are very limited. In a prospective, randomized, double-blind, 2 × 2 cross-over trial, 1 h of LLTS improved the longitudinal mechanics of the left ventricle and the heart rate variability (HRV) in patients with HFrEF [ 113 ]. In a pilot, randomized, sham-controlled research including patients with HFrEF, 1 h of LLTS improved microcirculation as assessed by flow-mediated vasodilatation [ 114 ].
Cardiac contractility modulation (CCM) is a novel approach that employs non-excitatory electrical impulses to the interventricular septum during the absolute refractory period [ 115 ]. Implantation is similar to a conventional transvenous pacemaker device, except two right ventricular leads are used. Mechanistic research has shown an increase in left ventricular contractility and positive global effects on reverse remodeling, mostly as a result of calcium handling improvements by phosphorylation of phospholamban and upregulation of SERCA-2A [ 116 ]. Increases in functional ability and quality of life have been shown in clinical trial data, but long-term outcome data are limited [ 117 ]. After two pilot studies to validate the safety and feasibility of CCM in patients with HFrEF [ 118 ], FIX-HF-3 was the first observational trial to evaluate the clinical efficacy of CCM treatment in 25 patients [ 119 ]. At a 2-month follow-up, improvements were found in LVEF, 6 min walk distance (6MWD), NYHA functional class, and quality of life in HFrEF NYHA III patients [ 120 ]. This was accompanied by the first randomized, double-blind crossover trial (FIX-CHF-4), which included patients with severe HFrEF, defined as LVEF < 35%, NYHA class II-III, and a narrow QRS duration. Those who were medically optimized were compared to those who received additional CCM therapy, with measures taken after 12 weeks in each group. Peak VO2 as assessed by cardiopulmonary exercise testing (CPEX) improved similarly in both groups (0.4 mL/kg/min), which strongly indicated a placebo effect. After the 6-month treatment period, however, only those with CCM showed a consistent improvement linked with QoL indicators. In a recent randomized controlled study, FIX-HF-5C (Evaluation of the Safety and Effectiveness of the OPTIMIZER System in Subjects with Heart Failure), which enrolled patients with NYHA class III or IV symptoms, QRS length of 130 ms, and LVEF between 25 and 45%, patients in the CCM arm had statistically significant improvements in NYHA class, 6MWD, and quality of life, as well as a composite reduction in HFrEF hospitalization and cardiovascular mortality. Moreover, a subgroup analysis of the FIX-HF-5 study revealed more substantial treatment advantages, such as that CCM therapy may provide additional benefits in patients with a relatively moderate LVEF decline [ 121 , 122 ].
Baroreceptor activation therapy (BAT). The carotid body and sinus are innervated by both PNS (via the vagus and glossopharyngeal fibers) and SNS (via cervical sympathetic ganglia). Electrical stimulation of carotid sinus baroreceptors generates afferent signals to the dorsal medulla, resulting in SNS reduction and enhanced vagal tone, which reduces blood pressure and heart rate [ 123 , 124 ]. In HF patients, these responses associated with the baroreceptor pathway are partially blunted due to carotid body alterations, leading to baroreflex dysfunction and subsequent SNS overactivation [ 123 ]. Baroreceptor sensitivity impairments in heart failure are related to higher death rates [ 125 ]. In preclinical studies, BAT was shown to diminish sympathetic tone and increase parasympathetic signaling, thus enhancing the autonomic input to the heart [ 126 ]. The BeAT-HF (Baroreflex Activation Therapy for Heart Failure) clinical trial demonstrated that BAT is safe in HFrEF patients and significantly improves patient-centered symptomatic endpoints of the QOL score, exercise capacity, and functional status [ 127 ]. Moreover, a considerable improvement in NT-proBNP levels was achieved with BAT, despite a disproportionate rise in the number of drugs in the control group [ 127 ].
Endovascular Ablation of the Right Greater Splanchnic Nerve (GSN). Exertional dyspnea, decreased aerobic capacity, and higher mortality are all linked to elevated intracardiac filling pressures at rest and during exercise in HF patients with both reduced and preserved ejection fraction [ 128 , 129 , 130 ]. As a result, several cardiovascular therapies aim to lower intracardiac filling pressures in these patients to enhance exertional capacity and QOL and improve cardiovascular morbidity [ 131 ].
Reduced inotropic and chronotropic reserves, as well as impaired relaxation, all contribute to higher filling pressures at rest and during activity. The vascular system is also involved in this process by reducing pulmonary arterial compliance and increasing pulmonary arterial resistance. Excessive blood volume distribution from extrathoracic compartments into the thorax is a major factor in high filling pressures in HF patients [ 131 , 132 ]. Splanchnic vasoconstriction mediated by the SNS causes rapid blood shifts from the splanchnic compartment to the heart and lungs, which is a typical physiological adaptative response mechanism during exercise. These rapid blood volume shifts from the splanchnic to central vasculature, however, cause an exaggerated rise in heart filling pressures in patients with HF, increasing exercise intolerance and possibly leading to HF decompensation [ 133 , 134 ].
Splanchnic nerve activity modulation has thereby been developed as a possible treatment approach in HF patients to reduce volume redistribution and improve symptoms and outcomes. Recent research has explored the impact of temporarily and permanently blocking the GSN over the HF spectrum. Splanchnic nerve modulation has been proven beneficial for both acute decompensated (ADHF) and chronic heart failure (CHF), according to the Splanchnic Nerve Anesthesia in Heart Failure and Abdominal Nerve Blockade in Chronic Heart Failure trials. In 11 ADHF patients with advanced HFrEF who underwent short-term blockade of the greater splanchnic nerve via anesthetic agents, there was a significant decrease in PCWP and an increase in the cardiac index [ 135 ]. Comparable outcomes were yielded from a study including 18 CHF patients who underwent the same procedure [ 136 ]. In HFpEF patients, permanent ablation of the right greater splanchnic nerve led to a decrease in intracardiac filling pressures during exercise as soon as 24 h following the intervention [ 137 ]. The Surgical Resection of the Greater Splanchnic Nerve in Subjects Having Heart Failure with Preserved Ejection Fraction two-center study has shown a substantial decrease in PCWP at the 3-month follow-up and a considerable 12-month improvement in NYHA class and QOL [ 132 ]. To ablate the right-sided GSN, a novel, endovascular, transvenous, minimally invasive procedure (splanchnic ablation for volume management-SAVM) was designed, and it has been proven to be helpful in a small, single-center open-label pilot trial [ 138 ].
REBALANCE-HF (Endovascular Ablation of the Right Greater Splanchnic Nerve in Subjects Having HFpEF) is an ongoing, multicenter, randomized, sham-controlled trial whose objective is to assess the safety of unilateral ablation of the right greater splanchnic nerve and its effectiveness in improving hemodynamics, quality of life, and exercise tolerance in patients with HFpEF [ 139 ]. The preliminary results from this trial show that GSN ablation is efficient in reducing PCWP during exercise, with improving the symptoms, but without a significant change in exercise capacity. The decrease in PCWP is substantial and it is consistent with previous results suggesting that abnormalities in venous capacitance play a significant role in the development of hemodynamic perturbations in HFpEF during exercise [ 140 ]. These findings show for the first time that endovascular GSN ablation can be used to treat HFpEF. All neuromodulatory approaches are summarized in Table 2 .
Neuromodulatory approaches in HF.
Neuromodulatory Approaches | Mechanisms of Action | Clinical Trial/Study | Main Findings | Limitations |
---|---|---|---|---|
surgical antiadrenergic denervation | Vaseghi et al. Schwartz et al. | →antiarrhythmic effects; →improvements in HR variability and autonomic nervous system [ , , , , , , ] | →limited data exist on the benefits of sympathetic denervation in HF patients. | |
frequency-based catheter renal nerve ablation | REACH pilot study | →improvements in both symptoms and exercise ability [ ] | →the RDT-PEF (Renal Denervation in Heart Failure with Preserved Ejection Fraction) trial was prematurely disrupted due to enrollment challenges, leaving it underpowered to determine whether RDN positively affected QOL, exercise function, biomarkers, and left heart remodeling in HFpEF patients [ ]. | |
RE-ADAPT-HF UNLOAD-HFpEF | →enrolling →enrolling | →future randomized, blinded, sham-controlled clinical studies are necessary to establish the impact of RDN on the morbidity of HFrEF and HFpEF patients. | ||
electrical stimulation of the vagus nerve | Schwartz et al. | →improvement in functional status, quality of life (QoL), and left ventricular volume in HFrEF [ ] | ||
NECTAR-HF (NCT01385176) | →favorable long-term safety profile; failed to show that VNS improved clinic outcomes versus OMT [ ] | →VNS has a considerable favorable effect on the functional state of the patient, but with no effect on the prognosis [ ]. | ||
INOVATE-HF (NCT01303718) | →quality of life, NYHA class, and 6 min walking distance were favorably affected by vagus nerve stimulation; failed to show that VNS improved clinic outcomes versus OMT [ ] | →the lack of a control group in the ANTHEM-HF trial is a considerable limitation; to avoid the placebo effect and validate the procedure’s safety, a randomised, controlled clinical trial is required [ ]. | ||
ANTHEM-HF (NCT01823887) | →chronic open-loop left- or right-side VNS is feasible and well tolerated in HFrEF patients [ ] | →no significant echocardiographic improvements nor reduction levels of NTpro BNP have been documented in any study [ ]. | ||
ANTHEM-HFrEF (NCT03425422) | →enrolling; test the impact of Vitaria system on cardiovascular mortality and HF hospitalization in patients with HF and reduced EF (HFrEF) [ ] | |||
non-invasive transcutaneous approach to VNS that stimulates the auricular branch of the vagus nerve | Zhou et al. | →lowered both systolic and diastolic blood pressure; →left ventricular hypertrophy, circumferential strain, and diastolic function; →reduced inflammatory cell infiltration and fibrosis within the ventricle and induced downregulation of pro-inflammatory and pro-fibrotic genes [ ] | →previous research has a number of limitations, including the absence of a well-controlled placebo group and longitudinal data and the limited sample populations; the optimal stimulation settings have yet to be established. →longitudinal data are required to assess the long-term impact of LLTS. | |
Tran et al. | → improved the longitudinal mechanics of the left ventricle and the heart rate variability (HRV) in patients with HFrEF [ ] | →moreover, there is no validated biomarker for measuring the efficacy of LLTS [ ]. | ||
Dasari et al. | → improved microcirculation [ ] | |||
myocardial non-excitatory electrical impulses delivered during the absolute refractory period that increases left ventricular contractility as a result of calcium handling improvements by phosphorylation of phospholamban and upregulation of SERCA-2A | FIX-HF-3 | →improvements in LVEF, 6 min walk distance (6MWD), NYHA functional class, and quality of life in HFrEF NYHA III patients [ , ] | →the impact of CCM on parameters such as left ventricular diastolic volumes has not been investigated systematically. | |
FIX-CHF-4 | →consistent improvement linked with QoL indicators at 6 months of therapy in HFrEF patients who received CCM [ ] | →CCM may only be effective when administered to viable, non-necrotic myocardium; however, this has not been fully investigated in preclinical or clinical research. | ||
FIX-HF-5 (NCT00112125) | →subgroup analysis revealed improvements in ventilatory anaerobic threshold were observed in patients with ejection fraction ranging from 25% to 45% [ , ] | →likewise, the advantages of CCM in CRT “non-responder” patients are inadequately documented. →in the study conducted by Kuschyk et al., there was an increased number of adverse outcomes, including two fatalities. | ||
FIX-HF-5C (NCT01381172) | →statistically significant improvements in NYHA class, 6MWD, QoL, a composite reduction in hospitalization, and cardiovascular mortality [ ] | →prospective trial results are inadequate, and it is essential that this disparity be settled prior to expanding usage in populations with medically optimal adjusted HFrEF, narrow QRS duration, and persistent symptoms [ ]. | ||
electrical stimulation of carotid sinus baroreceptors lowers SNS activity and increases parasympathetic tone | BeAT-HF (NCT02627196) | →BAT is safe and effective; →BAT significantly improved QoL and 6MWD, and reduced NT-proBNP levels [ ] | →BAT requires larger-scale studies with extended follow-up periods, a wider cohort of patients, and defined outcomes, including mortality risks, before this procedure can be included in HF clinical practice [ ]. | |
modulation of splanchnic nerve activity reduces cardiac filling pressures | REBALANCE-HF (NCT04592445) | →the preliminary results from this ongoing trial show that GSN ablation is efficient in reducing PCWP during exercise, with improving the symptoms but without a significant change in exercise capacity [ ] | →the safety and effectiveness of SNM in the management of HF must be explored more extensively; the latest scientific studies are centered on limited patient groups with minimal follow-up; the aforementioned proof-of-concept clinical trials lacked a control group [ ]. |
Sleep-disordered breathing, a widespread condition affecting both the circulatory and respiratory systems, is one element now recognized as contributing to the increased morbidity and mortality in HF. Two primary sleep apnea syndromes have been described: obstructive sleep apnea syndrome (OSA) and central sleep apnea syndrome (CSA) [ 109 ].
Stimulation of Phrenic Nerve. This procedure involves inserting an electrode into a brachiocephalic or pericardiophrenic vein to detect the diaphragm’s contractions throughout breathing and activate the diaphragmatic nerve during apnea, with the purpose to preserve fairly constant pO 2 and pCO 2 levels and avoid SNS and RAAS overactivation [ 141 , 142 ]. In the pivotal trial of the remedé system (Respicardia Inc., Minnetonka, MN, USA) involving 151 patients, the stimulation of the phrenic nerve showed a substantial decrease in the apnea–hypopnea index (AHI), central apnea index, arousal index, oxygen desaturation 4% index, percentage of sleep with rapid eye movement, and sleepiness (Epworth Sleepiness Scale (ESS)) [ 143 ]. A 5-year follow-up investigation confirmed these findings [ 144 ]. According to Costanzo et al., patients who received phrenic nerve stimulation displayed an increase in the QOL and LVEF without a substantial change in end-systolic and end-diastolic volumes [ 141 ]. Large-scale clinical studies are necessary to determine the impact of phrenic nerve stimulation on mortality in individuals with HF and CSA syndrome [ 145 ].
Synchronized Diaphragmatic Therapy. Increased intrathoracic pressure exerts persistent stress on the heart muscle and may exacerbate heart failure (HF). The respiratory muscles have a substantial effect on intrathoracic pressure, and, thus, the implantation of a device coupled to an electrode that detects the heartbeat that activates the diaphragm was developed [ 145 ]. In the Stimulation of the Diaphragm in Patients with Severe Heart Failure Following Heart Surgery randomized trial including 33 subjects, an improvement in LVEF and HF symptoms, and an elevation in maximal power and oxygen consumption during exercise testing was noticed, with no considerable improvement in the six MWT, nor the BNP levels [ 146 ]. At the 1-year follow-up of the non-randomized VisOne Heart Failure trial, improvements in LVEF, QOL, and 6MWT were reported [ 147 ]. Although both trials included a limited number of patients, because of the encouraging outcomes, it might be beneficial to conduct additional research on a larger scale.
Although loop diuretics continue to represent the backbone of decongestive treatment in HF, the occurrence of drug resistance, particularly with prolonged usage, poses a therapeutic issue that requires the development of novel approaches [ 145 ].
TARGET-1 and TARGET-2 (A Study to Evaluate the Treatment of Patients with Acute Decompensated Heart Failure (ADHF) Using an Automated Fluid Management System) trials evaluated the safety and effectiveness of controlled decongestion using the Reprieve system, which is intended to detect urine output and administer a specific amount of substitute solution to reach the predefined fluid balance. In both trials, patients experienced an increase in urine output, a decrease in body weight, and a drop in central venous pressure (CVP), while the SBP remained constant and without renal dysfunction [ 148 ]. The first human trials of the Doraya catheter, a device designed to transiently lower renal venous pressure by generating a manageable gradient in the inferior vena cava just under the renal veins, have shown encouraging results [ 149 ]. The Doraya catheter appears to represent an innovative idea for the management of AHF patients with poor diuretic response, whereas the Reprieve device is intended for AHF patients responsive to diuretics [ 145 ].
The VENUS-HF (VENUS-Heart Failure Early Feasibility Study) regarding the preCARDIA system, a device implanted into the superior vena cava to induce transient blockage, resulting in a reduction in right ventricular preload, revealed a reduction in right atrial pressure and PCWP [ 150 ]. The WhiteSwell device, intended to produce a low-pressure zone in the outflow of the thoracic duct into the venous system, has been studied in both animal and human studies. In the animal experiment, WhiteSwell not only prevented the collection of more fluid but also stimulated its discharge [ 151 ]. The orthopnea and oedema improved when the device was applied to humans. The Aquapass system is a wearable device designed to raise the skin temperature of the lower body without affecting the body’s core temperature. Increasing sweat rate in HF patients appears to be a reasonable option for decongestive treatment; nevertheless, further research is required to determine the method’s particular usefulness and effectiveness [ 152 ].
In the ALLEVIATE-HF-1 (NCT04583527), ALLEVIATE-HF-2 (NCT04838353), and ALLEVIATE-HFrEF (NCT05133089) studies, patients with HFpEF, HFmEF, and HFrEF will be enrolled for treatment through a no-implant interatrial shunt, using clinical, echocardiographic, and invasive hemodynamic data. The transcatheter system is designed to lower left atrial pressure by developing a therapeutic interatrial shunt, without the need for a permanent cardiac implant or open-heart surgery.
RELIEVE-HF (Reducing Lung Congestion Symptoms in Advanced Heart Failure- NCT03499236), a randomized clinical trial, is evaluating the impact of the V-Wave Ventura Interatrial Shunt System on heart failure patients, including the ability to lower hospitalizations and improve symptoms, exercise capacity, and quality of life. This small, hourglass-shaped device facilitates blood to flow from the left to the right atrium, lowering the pressure on the left side during physical activity.
It is a certainty now that the technological advances from the last years have paved the way for the development of non-pharmacological approaches that may efficiently complement classical HF therapy. Although further experimental studies are required to elucidate the underlying mechanisms through which many of these therapies act, the promising and encouraging results reported to date compel us to extend the HF treatment beyond the classical view.
A late-breaking discovery presented at the European Society of Cardiology’s (ESC) Heart Failure 2022 congress was a voice analysis software that can be used by heart failure patients at home that can detect fluid in the lungs in up to 80% of cases, three weeks prior to an unexpected hospitalization or escalation in outpatient medication therapy [ 156 ]. As cardiovascular illnesses evolve, advances in therapeutic and diagnostic approaches are required, and artificial intelligence (AI) is now being rapidly integrated into the field of cardiovascular medicine. By analyzing colossal databases more effectively than the human brain, AI has the potential to improve medical diagnosis, treatment, risk prediction, clinical care, and drug development [ 157 ]. For healthcare providers, AI has the potential to reduce the risk of adverse events, patient waiting times, and per capita expenditures while boosting accessibility, productivity, and overall patient experience [ 158 ]. AI also has the potential to reduce workloads and margin of error for physicians, as well as to improve patient–doctor interactions and therapeutic decision making [ 159 , 160 ]. For patients, AI can improve their health and well-being by increasing their knowledge, shared decision making, and self-efficacy in disease management [ 160 ].
For accurate quantitative and qualitative evaluation of heart failure, AI has been incorporated into different cardiac imaging techniques, such as echocardiography, cardiac magnetic resonance imaging, and cardiac computed tomography. Machine learning algorithms have been found to deliver a near-instantaneous echocardiography evaluation. Knackstedt et al. showed that the LVEF and longitudinal strain could be determined in less than 8 s [ 161 ]. This quick and precise evaluation might also have applications outside the cardiology department, such as in the emergency room, where point-of-care ultrasound scans are becoming more popular [ 162 ]. AI has been also shown to be of crucial importance in cardiac magnetic resonance imaging, especially for ventricular segmentation [ 163 ]. Laser et al. compared knowledge-based reconstruction of right ventricular volumes to the gold standard of direct cardiac MRI, finding that knowledge-based reconstruction offers outstanding accuracy for right ventricular 3D volumetry [ 164 ]. AI-assisted 3D visualization and cardiac image reconstruction can aid in the identification of a range of disorders [ 165 , 166 ]. Similarly, completely automated AI systems have provided a considerably more accurate calculation of left ventricular mass, papillary muscle identification, common carotid artery, and descending aorta measurements [ 167 , 168 ]. AI has been increasingly used for cardiac computed tomography, particularly for the assessment of coronary artery calcification scoring and risk stratification of future events [ 169 ]. Interestingly, AI uses various risk calculation scoring systems to estimate cardiovascular mortality and predictive models to predict the risk of future hospitalization so that proper monitoring and control may be carried out to avoid such harmful results [ 140 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 , 162 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 , 172 , 173 , 174 , 175 ].
Current HF healthcare services are insufficient to satisfy the demands of an ageing population with rising comorbidities and disease complexity, as well as the disparity in medical care distribution between rural and urban areas. As a result of these factors, an urgent need to develop alternative healthcare treatments has arisen. eHealth apps have the ability to relieve a large amount of the strain on healthcare services while also improving patient care. The PASSION-HF (Patient Self-Care using eHealth in Chronic Heart Failure) project intends to create a virtual doctor, a digital decision support system that offers options based on current clinical standards. Patient independence is enhanced by providing tailored HF management 24 h a day, 7 days a week. In addition, the program establishes processes and decision points at which medical experts must be involved [ 176 ].
Although AI has the potential to solve many of the fundamental challenges faced by the current HF pandemic, it is still a fast-growing field, and therefore some caution is advised. Transparency in data quality, population representativeness, and performance evaluation will be critical. Clinicians, patients, caregivers, and IT professionals should all be included in discussions about legal, technological, and regulatory problems, with ethics and equity being prioritized [ 177 ].
Heart failure is becoming an irrefutably significant disease entity as the population ages. Thus, various mechanisms contributing to the development and progression of HF have been discovered and targeted with novel medications and non-pharmacological approaches throughout the last three decades. This has improved the clinical outcome of millions of people worldwide with HF in terms of mortality, quality of life, and survival. Researchers are aiming to identify subgroups in which specific drugs and/or devices may be most successful, innovative methods for enhanced diagnosis and prediction of prognosis in HF patients, and novel tools for treating HF. New therapies will hopefully bring more benefits and extend these results to the treatment of HFpEF also, as well as other causes and phenotypes of HF.
This research received no external funding.
Conceptualization: I.P.P., M.Ș.C.H. and I.T.; methodology, resources: I.P.P.; writing—original draft preparation: I.P.P., M.Ș.C.H. and I.T.; writing—review and editing: D.M.T., M.A.M., D.N.Ș., L.I.Ș. and R.I; visualization and supervision: D.N.Ș., L.I.Ș. and R.I.; project administration: I.P.P. and I.T. All authors have read and agreed to the published version of the manuscript.
Informed consent statement, data availability statement, conflicts of interest.
The authors declare no conflict of interest.
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It is important to note that hypertension is a cardiovascular disease that refers to elevated blood pressure. The given analysis will focus on the case of Dr. Ally, who is a 49-year-old professor with several underlying conditions. Due to not taking his medications, the patient experiences a range of issues, which are linked with hypertension, and it is contributing to a left-sided form of congestive heart failure.
The patient’s problems include essential hypertension, fatigue, dyspnea, epistaxis, dizziness, and blurred vision. In his eyes, hypertension can cause damage to the small blood vessels in the retina, leading to a condition called hypertensive retinopathy. This can cause vision changes such as blurriness, floaters, and even blindness (“Hypertension,” n.d.). In his heart, hypertension can lead to left ventricular hypertrophy and increased workload on the heart. This can lead to heart failure, which can cause rales or crackles on chest auscultation, as well as fatigue, dyspnea, and other symptoms. The doctor suggests that the patient might have developed congestive heart failure, but it is likely to be left-sided since it is the most common starting site and causes breathing issues (“Respiratory depression,” n.d.; Chopra et al., 2021). Common antihypertensive drugs that may have been used include diuretics, digitalis, calcium channel blockers, and beta blockers. Cardiac glycosides, such as digitalis, “increase the contractibility of the heart muscle, reduce the heart rate” (“Digitalis,” n.d., para. 2). Diuretics work by increasing urine output, which reduces blood volume and pressure.
In conclusion, the patient experiences a range of issues related to hypertension, which is likely to cause left-sided congestive heart failure since it is the most common in the population. It is important to note that Dr. Ally’s condition highlights the importance of regular checkups and adherence to medication regimes. It is essential to keep hypertension under control to prevent long-term complications such as heart failure, kidney disease, and retinal damage.
Chopra, H. K., Nanda, N. C., Narula, J., Wander, G. S., Manjunath, C. N., & Chandra, P. (2021). Hypertension: New frontiers — A textbook of cardiology . Jaypee Brothers Medical Pub.
Digitalis [PDF document]. (n.d.).
Hypertension [PDF document]. (n.d.).
Respiratory depression [PDF document]. (n.d.).
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1. IvyPanda . "Hypertension and Congestive Heart Failure." January 28, 2024. https://ivypanda.com/essays/hypertension-and-congestive-heart-failure/.
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IvyPanda . "Hypertension and Congestive Heart Failure." January 28, 2024. https://ivypanda.com/essays/hypertension-and-congestive-heart-failure/.
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Congestive Heart Failure in Older Adults Essay. Congestive heart failure (CHF) is one of the common health challenges in aging persons. The health condition is one of the major causes of deaths and health complications for individuals that above sixty-five years. Congestive heart failure is not only a major cause of health complication and ...
Congestive heart failure (CHF), as defined by the American College of Cardiology (ACC) and the American Heart Association (AHA), is "a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood." Ischemic heart disease is the leading cause of death worldwide and also the leading cause of CHF. CHF is a common disorder ...
Over time, stage B heart failure can progress to symptomatic heart failure (stages C and D). In a study of preclinical heart failure involving 413 people with stage B heart failure, 6% progressed to symptomatic heart failure over four years. A 2007 study found a 95.7% five-year survival rate for stage B heart failure.
Heart failure is a condition that occurs when the heart can't pump as well as it should. This may happen when the heart muscle becomes weak or stiff. As a result, it doesn't deliver enough blood to the rest of the body. When the body doesn't get enough blood, it doesn't get enough oxygen and nutrients. Heart failure can become life ...
Congestive or chronic heart failure (CHF) is a widespread issue among a number of groups, but it is especially prominent among older populations. Although there are an array of quantitative studies regarding the given problem, one might not find plentiful data on the qualitative aspect of the matter. Breathlessness is among the most common ...
Congestive heart failure (CHF) is a "progressive and debilitating disease" that is characterized by the congestion of body tissues (Nair & Peate, 2013, p. 237). Five percent of all medical admissions in hospitals are due to CHF. When an individual has this disease, his or her heart is not able to pump adequate blood for circulation ...
Request an Appointment. 410-955-5000 Maryland. 855-695-4872 Outside of Maryland. +1-410-502-7683 International. Find a Doctor. Congestive heart failure (also called heart failure) is a serious condition in which the heart doesn't pump blood as efficiently as it should.
Heart failure is a term used to describe a heart that cannot keep up with its workload. The body may not get the oxygen it needs. Heart failure is a serious condition, and usually there's no cure. But many people with heart failure lead a full, enjoyable life when the condition is managed with heart failure medications and a healthy lifestyle.
INTRODUCTION. Heart failure (HF) is one of the major public health problems with a prevalence of 1-2% in developed countries (varies by definition and region), and it increases with age (rising to over 10% in people over 70 years of age)[].Approximately 33% of men and 28% of women at the age of 55 have a lifetime risk of developing HF[].The pathophysiology of HF is complex and it is therefore ...
As the heart weakens, blood begins to back up and force liquid through the capillary walls. The term "congestive" refers to the resulting buildup of fluid in the ankles and feet, arms, lungs, and/or other organs. Almost 6 million Americans have congestive heart failure. However, with the correct treatment, patients can recover to good health.
High-output failure is an uncommon disorder characterized by an elevated resting cardiac index of greater than 2.5-4.0 L/min/m 2 and low systemic vascular resistance. The common causes of high output failure are severe anemia, vascular shunting, hyperthyroidism and vitamin B1 deficiency.
The study of congestive heart failure (CHF) has significant ramifications for registered nurses' day-to-day work, influencing how they provide patient care and advance their careers. ... In conclusion, this essay thoroughly examines Congestive Heart Failure (CHF), delving into its historical context, contemporary treatment modalities, a ...
Congestive heart failure (CHF), as defined by the American College of Cardiology (ACC) and the American Heart Association (AHA), is "a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood.". Ischemic heart disease is the leading cause of death worldwide and also the ...
Essay On Congestive Heart Failure. Good Essays. 1589 Words; 7 Pages; Open Document. Congestive Heart Failure Congestive Heart Failure is a condition in which the heart cannot pump enough blood to meet the needs of the rest of the body (Department of Health & Human Services, 2012). The failure can occur in on either side of the heart.
Right-sided heart failure is a type of heart failure that occurs when fluid gets stuck into the abdomen, legs, and feet, which can cause swelling. This heart failure can vary in treatment options, but achievable approaches can come into play when trying to maintain a healthy heart as soon as symptoms are present.
Congestive heart failure is a common condition that increases in prevalence with increasing age. In 2003, guidance from the National Institute for Health and Clinical Excellence acknowledged that the "rising epidemic of heart failure" is partly the result of people living longer and the more effective treatments for coronary heart disease now available.
Congestive heart failure (CHF) is a chronic disease when the heart does not pump blood as well as it should. It is commonly caused by high levels of cholesterol that causes coronary artery disease. Some of the symptoms of CHF include shortness of breath, rapid heartbeat, swollen legs, and fatigue. It is important for a person suffering from ...
Evidenced-Based Practice Assignment. Introduction The prevalence of Congestive Heart Failure (CHF) has been increasing globally because of the aging population and the increased risk factors such as lung disease, diabetes mellitus, hyperlipidemia, and hypertension. It is estimated that over 6.5 million Americans over 20 years have heart failure ...
1. Introduction. Heart failure (HF) is a progressively deteriorating medical condition that is associated with a high risk of hospitalization and unscheduled hospital visits and significantly reduces the patients' life expectancy and quality of life [].Although epidemiological studies report that heart failure affects about 1 to 2% of the general adult population, the true prevalence of HF ...
Congestive Heart Failure Essay. Decent Essays. 642 Words; 3 Pages; Open Document. Congestive Heart Failure Congestive heart failure is an older name for heart failure. Congestive heart failure takes place when the heart is unable to maintain an adequate circulation of blood in the bodily tissues or to pump out the venous blood returned to it by ...
One leading expert on CHF states that: "Congestive heart failure is a sequel to various heart diseases and is often the end stage of cardiac disease," (Little 2002) a demonstration of a multifaceted cause and effect disease that often ends with morbidity in its victims. In the same work Little also sites and older study that indicates that ...
Extensive prior studies have led to the development of guidelines and clinical scores to stratify stroke risk related to AF in the general population. 3 Clinical scores, such as congestive heart failure, hypertension, age ≥75 (doubled), diabetes, stroke (doubled), vascular disease, age 65 to 74 and sex category (female) (CHA 2 DS 2 ‐VASc), help medical providers determine when to initiate ...
Get a custom essay on Hypertension and Congestive Heart Failure. The patient's problems include essential hypertension, fatigue, dyspnea, epistaxis, dizziness, and blurred vision. In his eyes, hypertension can cause damage to the small blood vessels in the retina, leading to a condition called hypertensive retinopathy.