Current Advances in Optimal Medical Therapy for Heart Failure

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Cardiology".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2277

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Guest Editor
Second Department of Internal Medicine, University of Toyama, Toyama 9300194, Japan
Interests: heart failure; heart transplantation; cardiology; cardiothoracic surgery
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Special Issue Information

Dear Colleagues,

We are currently in the era of the heart failure pandemic. The number of heart failures is increasing and the severity of heart failure is advancing. However, novel medications have been introduced, including the “fantastic four”. Nevertheless, therapeutic strategies regarding how to appropriately use these medications in real-world clinical practice remain unestablished. We often encounter elderly heart failure patients with multiple comorbidities. Large-scale randomized control trials do not necessarily provide us with appropriate answers regarding how to manage such patients. Now is the time to establish therapeutic strategies using novel medications to treat heart failure patients in real-world clinical practice. All original articles or systemic reviews on this topic related to current advances in heart disease are welcome and highly encouraged for submission.

Dr. Teruhiko Imamura
Guest Editor

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Keywords

  • heart failure
  • hemodynamics
  • hypertension
  • cardiac function
  • heart disease

Published Papers (3 papers)

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Research

11 pages, 1020 KiB  
Article
Differential Prognostic Impact of Risk-Prediction Models for Heart Failure in Acute Myocardial Infarction: The Original and Revised Heart Failure Time-Points
by Kazunari Asada, Yuichi Saito, Hiroki Goto, Hiroaki Yaginuma, Takanori Sato, Osamu Hashimoto, Hideki Kitahara and Yoshio Kobayashi
J. Clin. Med. 2024, 13(9), 2501; https://doi.org/10.3390/jcm13092501 - 24 Apr 2024
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Abstract
Background: We previously developed a risk-scoring system for heart failure (HF) in patients with acute myocardial infarction (MI), namely “HF time-points (HFTPs)”. In the original HFTPs, the presence of HF on admission, during hospitalization, and at short-term follow-up was individually scored. This study [...] Read more.
Background: We previously developed a risk-scoring system for heart failure (HF) in patients with acute myocardial infarction (MI), namely “HF time-points (HFTPs)”. In the original HFTPs, the presence of HF on admission, during hospitalization, and at short-term follow-up was individually scored. This study examined whether the revised HFTPs, with additional scoring of previous HF, provide better predictivity. Methods: This multicenter registry included a total of 1331 patients with acute MI undergoing percutaneous coronary intervention. HF was evaluated at four time-points before and after acute MI onset: (1) a history of HF; (2) elevated natriuretic peptide levels on admission; (3) in-hospital HF events; and (4) elevated natriuretic peptide levels at a median of 31 days after the onset. When HF was present at each time-point, one point was assigned to a risk scoring system, namely the original and revised HFTPs, ranging from 0 to 3 and from 0 to 4. The primary endpoint was a composite of cardiovascular death and HF rehospitalization after discharge. Results: Of the 1331 patients, 65 (4.9%) had the primary outcome events during a median follow-up period of 507 (interquartile range, 335–1106) days. The increase in both original and revised HFTPs was associated with an increased risk of the primary outcomes in a stepwise fashion with similar diagnostic ability. Conclusions: The original and revised HFTPs were both predictive of long-term HF-related outcomes in patients with acute MI undergoing percutaneous coronary intervention. Yet, the original HFTPs may be sufficient to estimate HF risks after MI. Full article
(This article belongs to the Special Issue Current Advances in Optimal Medical Therapy for Heart Failure)
13 pages, 2506 KiB  
Article
Sodium-Glucose Cotransporter-2 Inhibitors in Heart Failure with Malnutrition, Frailty, Sarcopenia, or Cachexia
by Yu Horiuchi, Masahiko Asami, Kazuyuki Yahagi, Asahi Oshima, Yuki Gonda, Daiki Yoshiura, Kota Komiyama, Hitomi Yuzawa, Jun Tanaka, Jiro Aoki and Kengo Tanabe
J. Clin. Med. 2024, 13(6), 1670; https://doi.org/10.3390/jcm13061670 - 14 Mar 2024
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Abstract
(1) Background: In patients with heart failure (HF) and impaired nutritional status or decreased muscle mass, sodium-glucose cotransporter-2 inhibitors (SGLT2is) may worsen these conditions and result in poor prognosis, especially worsening of frailty. We aimed to investigate the relationship between SGLT2is and [...] Read more.
(1) Background: In patients with heart failure (HF) and impaired nutritional status or decreased muscle mass, sodium-glucose cotransporter-2 inhibitors (SGLT2is) may worsen these conditions and result in poor prognosis, especially worsening of frailty. We aimed to investigate the relationship between SGLT2is and clinical outcomes, including frailty-related events, in patients with HF and malnutrition, frailty, sarcopenia, or cachexia. (2) Methods: In this retrospective observational cohort study, a global federated health research network provided data on patients with HF and malnutrition, frailty, sarcopenia, or cachexia from January 2016 to December 2021. We investigated the incidence of the composite endpoint of death or frailty-related events within one year. (3) Results: Among 214,778 patients included in the analysis, 4715 were treated with SGLT2is. After propensity score matching, 4697 patients in the SGLT2is group were matched with 4697 patients in the non-SGLT2is groups. The incidence of the composite endpoint, mortality, and frailty-related events was lower in the SGLT2is group than in the non-SGLT2is group (composite endpoint, 65.6% versus 77.6%, p < 0.001; mortality, 17.4% vs. 35.5%, p < 0.001; frailty-related events, 59.4% vs. 64.3%, p < 0.001). (4) Conclusions: Patients with HF and malnutrition, frailty, sarcopenia, or cachexia had a high incidence of death and frailty-related events. SGLT2is were associated with a lower incidence of these events. Full article
(This article belongs to the Special Issue Current Advances in Optimal Medical Therapy for Heart Failure)
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14 pages, 2474 KiB  
Article
PR Interval as a Novel Therapeutic Target of Ivabradine Therapy—Prognostic Impact of Ivabradine-Induced PR Prolongation in Heart Failure Patients
by Riona Yamamoto, Naoya Kataoka, Teruhiko Imamura, Toshihide Izumida and Koichiro Kinugawa
J. Clin. Med. 2024, 13(2), 510; https://doi.org/10.3390/jcm13020510 - 16 Jan 2024
Viewed by 702
Abstract
Background: Ivabradine reduces heart rate by inhibiting the “funny current” expressed on the sinoatrial node and improves mortality and morbidity in patients with systolic heart failure and sinus tachycardia. The funny current is known to be expressed also on the atrioventricular node according [...] Read more.
Background: Ivabradine reduces heart rate by inhibiting the “funny current” expressed on the sinoatrial node and improves mortality and morbidity in patients with systolic heart failure and sinus tachycardia. The funny current is known to be expressed also on the atrioventricular node according to experimental studies. However, the impact of ivabradine on PR interval remained unknown. Methods: Patients with a left ventricular ejection fraction of less than 50% who received 1 month of ivabradine were screened. Electrocardiographic and echocardiographic data, particularly concerning heart rate, the PR interval, and trans-mitral flow pattern, were collected at baseline and 1-month follow-up. The primary endpoint was defined as the composite of cardiovascular death and hospital readmission for worsening heart failure following ivabradine administration. Results: In the cohort of 29 enrolled patients (median age: 66 years, 62% male), the median baseline heart rate was 86 beats per minute and the median PR interval was 168 milliseconds. Following ivabradine administration, a significant decrease of 20 beats per minute in the heart rate and a significant increase of 24 milliseconds in the PR interval were observed. The truncated interval of the A-wave, detected in the trans-mitral flow, consistently demonstrated a negative correlation with the PR interval both before and after the administration of ivabradine. During a median of 1.8 years of follow-up, six patients reached the primary endpoint. A combination of heart rate reduction and PR prolongation following ivabradine administration, both of which were independent factors associated with the primary endpoint (p < 0.05 for both), was associated with greater freedom from the primary endpoint compared with either/neither of them (p = 0.002). Conclusions: Ivabradine seems to prolong PR interval, which is a novel surrogate marker of favorable clinical outcomes in patients with systolic heart failure. This effect may be associated with the dynamics of the trans-mitral flow pattern, in conjunction with heart rate and the PR interval. Clinical implications of PR interval-guided ivabradine therapy remains the future concern. Full article
(This article belongs to the Special Issue Current Advances in Optimal Medical Therapy for Heart Failure)
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