Heart Failure, Introduction

Shah, Tina; Palaskas, Nicolas; Bozkurt, Biykem

doi:10.1007/978-3-319-15961-4_1

Cited by 9 publications

(8 citation statements)

References 36 publications

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“…Treatment with digoxin inhibits the sodium-potassium ATPase pump, resulting in positive cardiac inotropy in addition to a reduced effect from the sympathetic nervous system and responses from RAAS. The drug is used in cases of atrial fibrillation, atrial flutter, and HF [29].…”

Section: Digoxinmentioning

confidence: 99%

A Systematic Review of the Effect of Vericiguat on Patients with Heart Failure

Sahana,

Wehland,

Simonsen

et al. 2023

IJMS

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Despite recent advances in heart failure (HF) therapy, the risk of cardiovascular (CV) mortality, morbidity, and HF hospitalization (HFH) are major challenges in HF treatment. We aimed to review the potential of vericiguat as a treatment option for HF. A systematic literature review was performed using the PubMed database and ClinicalTrials.gov. Four randomized controlled trials were identified, which study the safety and efficacy of vericiguat in HF patients. Vericiguat activates soluble guanylate cyclase (sGC) by binding to the beta-subunit, bypassing the requirement for NO-induced activation. The nitric oxide (NO)–sGC–cyclic guanosine monophosphate (cGMP) pathway plays an essential role in cardiovascular (CV) regulation and the protection of healthy cardiac function but is impaired in HF. Vericiguat reduced the risk of CV death and HFH in HF patients with reduced ejection fraction (HFrEF) but showed no therapeutic effect on HF with preserved ejection fraction (HFpEF). The trials demonstrated a favorable safety profile with most common adverse events such as hypotension, syncope, and anemia. Therefore, vericiguat is recommended for patients with HFrEF and a minimum systolic blood pressure of 100 mmHg. Treatment with vericiguat is considered when the individual patient experiences decompensation despite being on guideline-recommended medication, e.g., angiotensin-converting inhibitor/AT1 receptor antagonist, beta-adrenoceptor antagonist, spironolactone, and sodium-glucose transporter 2 inhibitors. Furthermore, larger studies are required to investigate any potential effect of vericiguat in HFpEF patients. Despite the limitations, vericiguat can be recommended for patients with HFrEF, where standard-of-care is insufficient, and the disease worsens.

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Section: Digoxinmentioning

confidence: 99%

A Systematic Review of the Effect of Vericiguat on Patients with Heart Failure

Sahana,

Wehland,

Simonsen

et al. 2023

IJMS

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“…Standard heart failure therapies, including angiotensin-converting enzyme inhibitors, beta-blockers, and diuretics, might be considered in patients with significant ventricular dysfunction. These medications aim to alleviate symptoms, stabilise hemodynamics, and enhance cardiac function [89].…”

Section: Current Management Strategies For Tcmmentioning

confidence: 99%

Unveiling the Enigma: Exploring the Intricate Link Between Coronary Microvascular Dysfunction and Takotsubo Cardiomyopathy

Datta,

Nath,

Pathade

et al. 2023

Cureus

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This review article delves into the intricate and evolving relationship between coronary microvascular dysfunction (CMD) and takotsubo cardiomyopathy (TCM), two intriguing cardiovascular conditions increasingly recognised for their potential interplay. We examine their characteristics, shared pathophysiological mechanisms, diagnostic challenges, and management strategies. Emerging evidence suggests a link between microvascular dysfunction and the development of TCM, leading to a deeper exploration of their connection. Accurate diagnosis of both conditions becomes essential, as microvascular dysfunction may modify TCM outcomes. We underscore the significance of understanding this connection for improved patient care, emphasising the need for tailored interventions when CMD and TCM coexist. Collaborative research and heightened clinical awareness are advocated to advance our comprehension of this relationship. Through interdisciplinary efforts, we aim to refine diagnostic precision, develop targeted therapies, and enhance patient outcomes in cardiovascular medicine.

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“…Even in a disease preluded by autosomal missense mutations, such as non-ischaemic dilated cardiomyopathy (DCM), pathological dilation and systolic dysfunction may occur in both ventricles, or specifically the left ventricle, due to the different physiology of systemic and pulmonary output influencing the aetiology of the disease [14][15][16][17] . However, the approach to managing acute right ventricular dysfunction often differs to left ventricular dysfunction due to the RV's inability to adapt to increased afterload pressure whereas the LV is less capable adapting to volume overload [18][19][20][21][22] . Furthermore, right ventricular involvement can exacerbate LV-dominant cardiomyopathies and has been used as a measure of survivability for patients with heart failure (HF) 18,23,24 .…”

Section: Introductionmentioning

confidence: 99%

Ventricle-specific myocardial protein and metabolite characterisation in healthy humans, with differential regulation in end-stage cardiomyopathies

Hunter,

Li,

Parker

et al. 2024

Preprint

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Background: The left and right ventricles of the human heart are functionally and developmentally distinct such that genetic or acquired insults can cause dysfunction in one or both ventricles resulting in heart failure. The left ventricle is most clinically relevant in research as its dysfunction is the most dominant cause of heart failure whereby right ventricular involvement can exacerbate the condition. However, the molecular composition of the left ventricular adult human myocardium relative to the right ventricle in health and in heart failure has yet to be thoroughly explored. Methods: We performed unbiased quantitative mass spectrometry analyses on the myocardium of pre-mortem cryopreserved non-diseased human hearts to compare the proteome (n = 27) and metabolome (n = 25) between the normal left and right ventricles. We then characterised the proteome and metabolome of the left and right ventricles within end-stage dilated cardiomyopathy (n = 14 and 13) and ischaemic cardiomyopathy (n = 19-17), respectively. All analyses featured a mix of paired and unpaired samples. Intra-condition comparative analyses were performed to identify differences of molecular abundance between the ventricles, and intra-ventricular analyses were performed between sexes of non-diseased hearts. Novel and innovative techniques were used to merge datasets, increasing the sample size and statistical power. KEGG and Gene Ontology databases were used to perform enrichment analyses and inform metabolic trends. Results: Constituents of gluconeogenesis, glycolysis, lipogenesis, lipolysis, fatty acid catabolism, the citrate cycle and oxidative phosphorylation were down-regulated in the non-diseased left ventricle, while glycogenesis, pyruvate and ketone metabolism were up-regulated. Inter-ventricular significance of these metabolic pathways was then found to be diminished within end-stage dilated cardiomyopathy and ischaemic cardiomyopathy, while heart failure-associated pathways were increased in the left ventricle relative to the right within ischaemic cardiomyopathy, such as fluid sheer-stress, increased glutamine to glutamate ratio, and down-regulation of contractile proteins, indicating a left ventricular pathological bias. Conclusions: The inter-ventricular molecular analyses within this study aides to fill a critical gap in our understanding of the metabolic differences between the human left and right ventricular myocardium and may be used to inform future therapeutic targets for heart failure processes in one or both the ventricles.

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Heart Failure, Introduction

Cited by 9 publications

References 36 publications

A Systematic Review of the Effect of Vericiguat on Patients with Heart Failure

A Systematic Review of the Effect of Vericiguat on Patients with Heart Failure

Unveiling the Enigma: Exploring the Intricate Link Between Coronary Microvascular Dysfunction and Takotsubo Cardiomyopathy

Ventricle-specific myocardial protein and metabolite characterisation in healthy humans, with differential regulation in end-stage cardiomyopathies

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