心力衰竭有什么新进展?2025年9月

IF 10.8 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Julian Hoevelmann, Philipp Markwirth, Mert Tokcan, Bernhard Haring
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Key topics of this issue include novel insights into arrhythmia-induced cardiomyopathy (AIC), profiling of hypotension in HF, the association between clonal haematopoiesis and incident HF, as well as the phenotype-specific relationship between blood pressure (BP) and cardiovascular outcomes in different HF subtypes.</p><p>Arrhythmia-induced cardiomyopathy is a reversible cause of left ventricular systolic dysfunction (LVSD) associated with atrial fibrillation (AF).<span><sup>1</sup></span> In current practice, AIC remains poorly defined and insufficiently characterized, and it is most often identified retrospectively, once left ventricular function improves following adequate rhythm control with antiarrhythmic drugs or AF ablation. Catheter ablation has been shown to improve outcomes in patients with AF and HF.<span><sup>2-4</sup></span> However, distinguishing AIC from other primary cardiomyopathies causing LVSD remains a major challenge, as its diagnosis typically depends on retrospective confirmation following recovery of left ventricular ejection fraction (LVEF). In a post-hoc analysis of the DECAAF II trial, Assaf <i>et al</i>.<span><sup>5</sup></span> aimed to evaluate the prevalence and predictors of AIC in patients with persistent AF and LVSD utilizing late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging.</p><p>Among 815 patients undergoing ablation, 119 with LVSD were analysed. At baseline the cohort had a mean LVEF of 39%. Close to two thirds of patients (60.5%) fulfilled criteria for AIC, defined as LVEF recovery to ≥50% with ≥10% absolute improvement or an absolute improvement (≥15%) after ablation. Patients with AIC showed significantly greater LVEF improvement of 19.9 ± 7.6% compared to 4.8 ± 7.5% in non-AIC patients (<i>p</i> &lt; 0.001). Lower AF burden at 12 months post-ablation correlated with higher LVEF at 3 months post-ablation (r = −0.23, <i>p</i> = 0.02). Using the Youden index, an AF burden of &lt;3.8% was identified as the optimal predictor of AIC status (area under the curve 0.706, <i>p</i> = 0.024). LGE-CMR revealed that AIC patients had significantly less atrial septal fibrosis (12.2% vs. 20.7%, <i>p</i> &lt; 0.001), while global left atrial fibrosis burden was not predictive.</p><p>In conclusion, the findings of the study provide evidence that in the majority patients with persistent AF the tachyarrhythmic condition plays a pivotal role in the development of LVSD. A low AF burden as well as atrial septal regional fibrosis were identified as predictors of AIC in these patients.</p><p>Hypotension remains a key concern in the management of HF with reduced ejection fraction (HFrEF), often limiting the optimization of guideline-directed medical therapy (GDMT). Indeed, hypotension remains the most frequently perceived clinical barrier to implementation of GDMT before creatinine increase and hyperkalaemia.<span><sup>6</sup></span> Contrary to this perception, the prevalence of low systolic BP &lt;90 mmHg was shown to be very low (1.8% of HF patients) in a real-world cohort.<span><sup>7</sup></span> This discrepancy raises the question of whether conventional office BP measurements truly reflect the burden of hypotension in daily life.</p><p>In a recent research letter, Soloveva <i>et al</i>.<span><sup>8</sup></span> profiled hypotension in 79 well-treated HFrEF patients using office, orthostatic, and ambulatory BP monitoring (ABPM). Strikingly, office systolic BP &lt;90 mmHg was observed in only 3.8% of patients, while nearly half experienced postprandial hypotension and 46% had daytime episodes of systolic BP &lt;90 mmHg on ABPM. Importantly, only a quarter of patients were free of any hypotensive episodes. Symptoms such as dizziness and fatigue were common, but did not consistently align with BP drops, suggesting that patient complaints may reflect the underlying HF itself rather than hypotension <i>per se</i>.</p><p>Clinically, these findings underscore the limitations of relying on office BP alone when titrating HF therapy. ABPM appears critical for uncovering ‘hidden’ hypotension, yet the presence of low BP should not automatically prompt down-titration. Registry data from more than 42 000 patients show that low systolic BP is less detrimental when patients are on optimized doses of HF medications, emphasizing that low BP alone should not derail medication optimization.<span><sup>9</sup></span> Instead, clinicians should focus on maintaining GDMT, while addressing triggers such as meals, dehydration, or prolonged standing.</p><p>Clonal hematopoiesis of indeterminate potential (CHIP) is caused by acquired mutations in haematopoietic stem cells that yield clonal progeny of mutant leucocytes.<span><sup>10</sup></span> Although CHIP carriers typically display normal haematological indices and remain clinically inapparent,<span><sup>11</sup></span> CHIP is strongly linked with age-related chronic diseases and haematologic malignancies. However, evidence linking CHIP with HF yielded conflicting findings.<span><sup>12-14</sup></span> To this purpose, Karakasis and colleagues conducted a systematic review and meta-analysis to evaluate the association of CHIP with the incidence and clinical outcomes of HF.<span><sup>15</sup></span></p><p>The authors evaluated a total of 13 studies based on five cohorts encompassing 57 755 individuals. Regardless of prior history of coronary artery disease, participants with CHIP had significantly greater risk of new-onset HF compared to the non-CHIP group (hazard ratio [HR] 1.23, 95% confidence interval [CI] 1.12–1.35, <i>p</i> &lt; 0.0001). No significant subgroup differences for incident HF were observed based on LVEF or age. A subgroup analysis of gene-specific CHIP subtypes revealed significant differences among ASXL1, DNMT3A, TET2, and JAK2 regarding the risk of incident HF (<i>p</i> subgroup = 0.03). While ASXL1, TET2, and JAK2 were associated with a significantly increased risk of incident HF, DNMT3A demonstrated a non-significant effect (HR 1.13, 95% CI 0.99–1.28). However, it should be noted that the studies included in the meta-analysis utilized different sequencing methodologies, which may influence the detection of these mutations. Interestingly, a total of four cohorts, including 362 participants, also investigated the association of CHIP with the composite outcome of all-cause mortality and hospitalization for HF in patients with preexisting baseline HF. Participants with CHIP had a significantly higher risk of the composite outcome compared to the non-CHIP group (HR 1.84, 95% CI 1.25–2.70, <i>p</i> = 0.002).</p><p>Therapeutic targeting of CHIP is a new area of research with several promising strategies. One approach involves the inhibition of overactive inflammatory pathways related to the presence of CHIP.<span><sup>16</sup></span> While this method does not directly target CHIP, it alleviates the adverse effects caused by inflammation. Another approach attempts to eliminate the mutated blood cells through selective targeting.<span><sup>17</sup></span> This strategy hinges on the accurate identification of cell surface antigens unique to CHIP cells. In conclusion, the study by Karakasis <i>et al</i>.<span><sup>15</sup></span> highlights the emerging importance of CHIP for HF risk stratification and its potential role as a biomarker for more personalized approaches.</p><p>Management of BP in patients with HF remains controversial, with conflicting evidence regarding optimal BP targets across HF phenotypes.<span><sup>18, 19</sup></span> Li <i>et al</i>.<span><sup>20</sup></span> conducted a large individual patient data meta-analysis pooling 28 406 participants from eight landmark randomized clinical trials, encompassing the full spectrum of LVEF. Using time-dependent Cox regression models, the study examined the association between longitudinal systolic and diastolic BP and key outcomes, including cardiovascular death and HF hospitalization.</p><p>The analysis revealed a non-linear, phenotype-specific relationship between BP and outcomes. In patients with HFrEF, low systolic BP (&lt;120 mmHg) was consistently associated with increased risk of cardiovascular death and HF hospitalization (HR 1.71, 95% CI 1.60–1.82, <i>p</i> &lt; 0.001), whereas higher systolic BP (&gt;140 mmHg) was not linked to worse outcomes. Conversely, in HF with mildly reduced or preserved ejection fraction (HFmrEF/HFpEF), both low and high systolic BP were associated with adverse outcomes (HR 1.74, 95% CI 1.47–2.07, <i>p</i> &lt; 0.001 and HR 1.77, 95% CI 1.45–2.17, <i>p</i> &lt; 0.001; respectively), producing a U-shaped risk curve. Similar trends were observed for diastolic BP.</p><p>These findings underscore the limitations of uniform BP targets in HF patients and highlight LVEF as a key modifier of BP–outcome relationships. For HFrEF, low BP likely reflects advanced disease and impaired cardiac output, whereas in HFmrEF/HFpEF, both hypotension and uncontrolled hypertension contribute to risk. The authors suggest that dynamic, phenotype-tailored BP management strategies may improve outcomes, but emphasize the need for prospective trials to define optimal BP targets in contemporary HF populations.</p>","PeriodicalId":164,"journal":{"name":"European Journal of Heart Failure","volume":"27 9","pages":"1603-1605"},"PeriodicalIF":10.8000,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ejhf.70054","citationCount":"0","resultStr":"{\"title\":\"What's new in heart failure? 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Key topics of this issue include novel insights into arrhythmia-induced cardiomyopathy (AIC), profiling of hypotension in HF, the association between clonal haematopoiesis and incident HF, as well as the phenotype-specific relationship between blood pressure (BP) and cardiovascular outcomes in different HF subtypes.</p><p>Arrhythmia-induced cardiomyopathy is a reversible cause of left ventricular systolic dysfunction (LVSD) associated with atrial fibrillation (AF).<span><sup>1</sup></span> In current practice, AIC remains poorly defined and insufficiently characterized, and it is most often identified retrospectively, once left ventricular function improves following adequate rhythm control with antiarrhythmic drugs or AF ablation. Catheter ablation has been shown to improve outcomes in patients with AF and HF.<span><sup>2-4</sup></span> However, distinguishing AIC from other primary cardiomyopathies causing LVSD remains a major challenge, as its diagnosis typically depends on retrospective confirmation following recovery of left ventricular ejection fraction (LVEF). In a post-hoc analysis of the DECAAF II trial, Assaf <i>et al</i>.<span><sup>5</sup></span> aimed to evaluate the prevalence and predictors of AIC in patients with persistent AF and LVSD utilizing late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging.</p><p>Among 815 patients undergoing ablation, 119 with LVSD were analysed. At baseline the cohort had a mean LVEF of 39%. Close to two thirds of patients (60.5%) fulfilled criteria for AIC, defined as LVEF recovery to ≥50% with ≥10% absolute improvement or an absolute improvement (≥15%) after ablation. Patients with AIC showed significantly greater LVEF improvement of 19.9 ± 7.6% compared to 4.8 ± 7.5% in non-AIC patients (<i>p</i> &lt; 0.001). Lower AF burden at 12 months post-ablation correlated with higher LVEF at 3 months post-ablation (r = −0.23, <i>p</i> = 0.02). Using the Youden index, an AF burden of &lt;3.8% was identified as the optimal predictor of AIC status (area under the curve 0.706, <i>p</i> = 0.024). LGE-CMR revealed that AIC patients had significantly less atrial septal fibrosis (12.2% vs. 20.7%, <i>p</i> &lt; 0.001), while global left atrial fibrosis burden was not predictive.</p><p>In conclusion, the findings of the study provide evidence that in the majority patients with persistent AF the tachyarrhythmic condition plays a pivotal role in the development of LVSD. A low AF burden as well as atrial septal regional fibrosis were identified as predictors of AIC in these patients.</p><p>Hypotension remains a key concern in the management of HF with reduced ejection fraction (HFrEF), often limiting the optimization of guideline-directed medical therapy (GDMT). Indeed, hypotension remains the most frequently perceived clinical barrier to implementation of GDMT before creatinine increase and hyperkalaemia.<span><sup>6</sup></span> Contrary to this perception, the prevalence of low systolic BP &lt;90 mmHg was shown to be very low (1.8% of HF patients) in a real-world cohort.<span><sup>7</sup></span> This discrepancy raises the question of whether conventional office BP measurements truly reflect the burden of hypotension in daily life.</p><p>In a recent research letter, Soloveva <i>et al</i>.<span><sup>8</sup></span> profiled hypotension in 79 well-treated HFrEF patients using office, orthostatic, and ambulatory BP monitoring (ABPM). Strikingly, office systolic BP &lt;90 mmHg was observed in only 3.8% of patients, while nearly half experienced postprandial hypotension and 46% had daytime episodes of systolic BP &lt;90 mmHg on ABPM. Importantly, only a quarter of patients were free of any hypotensive episodes. Symptoms such as dizziness and fatigue were common, but did not consistently align with BP drops, suggesting that patient complaints may reflect the underlying HF itself rather than hypotension <i>per se</i>.</p><p>Clinically, these findings underscore the limitations of relying on office BP alone when titrating HF therapy. ABPM appears critical for uncovering ‘hidden’ hypotension, yet the presence of low BP should not automatically prompt down-titration. Registry data from more than 42 000 patients show that low systolic BP is less detrimental when patients are on optimized doses of HF medications, emphasizing that low BP alone should not derail medication optimization.<span><sup>9</sup></span> Instead, clinicians should focus on maintaining GDMT, while addressing triggers such as meals, dehydration, or prolonged standing.</p><p>Clonal hematopoiesis of indeterminate potential (CHIP) is caused by acquired mutations in haematopoietic stem cells that yield clonal progeny of mutant leucocytes.<span><sup>10</sup></span> Although CHIP carriers typically display normal haematological indices and remain clinically inapparent,<span><sup>11</sup></span> CHIP is strongly linked with age-related chronic diseases and haematologic malignancies. However, evidence linking CHIP with HF yielded conflicting findings.<span><sup>12-14</sup></span> To this purpose, Karakasis and colleagues conducted a systematic review and meta-analysis to evaluate the association of CHIP with the incidence and clinical outcomes of HF.<span><sup>15</sup></span></p><p>The authors evaluated a total of 13 studies based on five cohorts encompassing 57 755 individuals. Regardless of prior history of coronary artery disease, participants with CHIP had significantly greater risk of new-onset HF compared to the non-CHIP group (hazard ratio [HR] 1.23, 95% confidence interval [CI] 1.12–1.35, <i>p</i> &lt; 0.0001). No significant subgroup differences for incident HF were observed based on LVEF or age. A subgroup analysis of gene-specific CHIP subtypes revealed significant differences among ASXL1, DNMT3A, TET2, and JAK2 regarding the risk of incident HF (<i>p</i> subgroup = 0.03). While ASXL1, TET2, and JAK2 were associated with a significantly increased risk of incident HF, DNMT3A demonstrated a non-significant effect (HR 1.13, 95% CI 0.99–1.28). However, it should be noted that the studies included in the meta-analysis utilized different sequencing methodologies, which may influence the detection of these mutations. Interestingly, a total of four cohorts, including 362 participants, also investigated the association of CHIP with the composite outcome of all-cause mortality and hospitalization for HF in patients with preexisting baseline HF. Participants with CHIP had a significantly higher risk of the composite outcome compared to the non-CHIP group (HR 1.84, 95% CI 1.25–2.70, <i>p</i> = 0.002).</p><p>Therapeutic targeting of CHIP is a new area of research with several promising strategies. One approach involves the inhibition of overactive inflammatory pathways related to the presence of CHIP.<span><sup>16</sup></span> While this method does not directly target CHIP, it alleviates the adverse effects caused by inflammation. Another approach attempts to eliminate the mutated blood cells through selective targeting.<span><sup>17</sup></span> This strategy hinges on the accurate identification of cell surface antigens unique to CHIP cells. In conclusion, the study by Karakasis <i>et al</i>.<span><sup>15</sup></span> highlights the emerging importance of CHIP for HF risk stratification and its potential role as a biomarker for more personalized approaches.</p><p>Management of BP in patients with HF remains controversial, with conflicting evidence regarding optimal BP targets across HF phenotypes.<span><sup>18, 19</sup></span> Li <i>et al</i>.<span><sup>20</sup></span> conducted a large individual patient data meta-analysis pooling 28 406 participants from eight landmark randomized clinical trials, encompassing the full spectrum of LVEF. Using time-dependent Cox regression models, the study examined the association between longitudinal systolic and diastolic BP and key outcomes, including cardiovascular death and HF hospitalization.</p><p>The analysis revealed a non-linear, phenotype-specific relationship between BP and outcomes. 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引用次数: 0

摘要

为此,Karakasis及其同事进行了一项系统综述和荟萃分析,以评估CHIP与hf发病率和临床结局的关系。作者基于5个队列共评估了13项研究,共包含57755人。无论既往是否有冠状动脉疾病史,CHIP患者发生新发HF的风险显著高于非CHIP组(风险比[HR] 1.23, 95%可信区间[CI] 1.12-1.35, p &lt; 0.0001)。基于LVEF或年龄,未观察到发生HF的亚组差异。基因特异性CHIP亚型的亚组分析显示,ASXL1、DNMT3A、TET2和JAK2在HF发生风险方面存在显著差异(p亚组= 0.03)。ASXL1、TET2和JAK2与HF发生风险显著增加相关,而DNMT3A则无显著影响(HR 1.13, 95% CI 0.99-1.28)。然而,应该指出的是,meta分析中包含的研究使用了不同的测序方法,这可能会影响这些突变的检测。有趣的是,共有四个队列,包括362名参与者,也调查了CHIP与既往基线HF患者全因死亡率和HF住院的综合结局的关系。与非CHIP组相比,CHIP患者发生综合结局的风险明显更高(HR 1.84, 95% CI 1.25-2.70, p = 0.002)。CHIP的靶向治疗是一个新的研究领域,有几种很有前景的策略。一种方法涉及抑制与CHIP存在相关的过度活跃的炎症途径。16虽然这种方法不直接针对CHIP,但它减轻了炎症引起的不良反应。另一种方法试图通过选择性靶向来消除突变的血细胞这一策略取决于对CHIP细胞独特的细胞表面抗原的准确鉴定。总之,Karakasis等人的研究强调了CHIP对HF风险分层的重要性及其作为更个性化方法的生物标志物的潜在作用。HF患者的血压管理仍然存在争议,关于各种HF表型的最佳血压目标的证据相互矛盾。[18,19] Li等人20进行了一项大型个体患者数据荟萃分析,纳入了来自8项具有里程碑意义的随机临床试验的28406名参与者,涵盖了LVEF的全谱。使用时间依赖的Cox回归模型,该研究检查了纵向收缩压和舒张压与主要结局(包括心血管死亡和心衰住院)之间的关系。分析揭示了BP与预后之间的非线性、表型特异性关系。在HFrEF患者中,低收缩压(&lt;120 mmHg)始终与心血管死亡和HF住院风险增加相关(HR 1.71, 95% CI 1.60-1.82, p &lt; 0.001),而高收缩压(&gt;140 mmHg)与较差的结果无关。相反,在射血分数轻度降低或保留的HF (HFmrEF/HFpEF)中,低和高收缩压均与不良结局相关(HR分别为1.74,95% CI 1.47-2.07, p &lt; 0.001和HR 1.77, 95% CI 1.45-2.17, p &lt; 0.001),形成u型风险曲线。舒张压也有类似的变化趋势。这些发现强调了在心衰患者中统一血压目标的局限性,并强调了LVEF是血压-结局关系的关键调节因素。对于HFrEF,低血压可能反映疾病晚期和心输出量受损,而在HFmrEF/HFpEF中,低血压和未控制的高血压都是风险因素。作者认为,动态的、针对表型的血压管理策略可能会改善结果,但强调需要前瞻性试验来确定当代心衰人群的最佳血压目标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

What's new in heart failure? September 2025

What's new in heart failure? September 2025

In this column, we want to provide clinicians and researchers with short and concise summaries of recently published articles in the European Journal of Heart Failure that we think may be of particular relevance to heart failure (HF) specialists (Figure 1). Key topics of this issue include novel insights into arrhythmia-induced cardiomyopathy (AIC), profiling of hypotension in HF, the association between clonal haematopoiesis and incident HF, as well as the phenotype-specific relationship between blood pressure (BP) and cardiovascular outcomes in different HF subtypes.

Arrhythmia-induced cardiomyopathy is a reversible cause of left ventricular systolic dysfunction (LVSD) associated with atrial fibrillation (AF).1 In current practice, AIC remains poorly defined and insufficiently characterized, and it is most often identified retrospectively, once left ventricular function improves following adequate rhythm control with antiarrhythmic drugs or AF ablation. Catheter ablation has been shown to improve outcomes in patients with AF and HF.2-4 However, distinguishing AIC from other primary cardiomyopathies causing LVSD remains a major challenge, as its diagnosis typically depends on retrospective confirmation following recovery of left ventricular ejection fraction (LVEF). In a post-hoc analysis of the DECAAF II trial, Assaf et al.5 aimed to evaluate the prevalence and predictors of AIC in patients with persistent AF and LVSD utilizing late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging.

Among 815 patients undergoing ablation, 119 with LVSD were analysed. At baseline the cohort had a mean LVEF of 39%. Close to two thirds of patients (60.5%) fulfilled criteria for AIC, defined as LVEF recovery to ≥50% with ≥10% absolute improvement or an absolute improvement (≥15%) after ablation. Patients with AIC showed significantly greater LVEF improvement of 19.9 ± 7.6% compared to 4.8 ± 7.5% in non-AIC patients (p < 0.001). Lower AF burden at 12 months post-ablation correlated with higher LVEF at 3 months post-ablation (r = −0.23, p = 0.02). Using the Youden index, an AF burden of <3.8% was identified as the optimal predictor of AIC status (area under the curve 0.706, p = 0.024). LGE-CMR revealed that AIC patients had significantly less atrial septal fibrosis (12.2% vs. 20.7%, p < 0.001), while global left atrial fibrosis burden was not predictive.

In conclusion, the findings of the study provide evidence that in the majority patients with persistent AF the tachyarrhythmic condition plays a pivotal role in the development of LVSD. A low AF burden as well as atrial septal regional fibrosis were identified as predictors of AIC in these patients.

Hypotension remains a key concern in the management of HF with reduced ejection fraction (HFrEF), often limiting the optimization of guideline-directed medical therapy (GDMT). Indeed, hypotension remains the most frequently perceived clinical barrier to implementation of GDMT before creatinine increase and hyperkalaemia.6 Contrary to this perception, the prevalence of low systolic BP <90 mmHg was shown to be very low (1.8% of HF patients) in a real-world cohort.7 This discrepancy raises the question of whether conventional office BP measurements truly reflect the burden of hypotension in daily life.

In a recent research letter, Soloveva et al.8 profiled hypotension in 79 well-treated HFrEF patients using office, orthostatic, and ambulatory BP monitoring (ABPM). Strikingly, office systolic BP <90 mmHg was observed in only 3.8% of patients, while nearly half experienced postprandial hypotension and 46% had daytime episodes of systolic BP <90 mmHg on ABPM. Importantly, only a quarter of patients were free of any hypotensive episodes. Symptoms such as dizziness and fatigue were common, but did not consistently align with BP drops, suggesting that patient complaints may reflect the underlying HF itself rather than hypotension per se.

Clinically, these findings underscore the limitations of relying on office BP alone when titrating HF therapy. ABPM appears critical for uncovering ‘hidden’ hypotension, yet the presence of low BP should not automatically prompt down-titration. Registry data from more than 42 000 patients show that low systolic BP is less detrimental when patients are on optimized doses of HF medications, emphasizing that low BP alone should not derail medication optimization.9 Instead, clinicians should focus on maintaining GDMT, while addressing triggers such as meals, dehydration, or prolonged standing.

Clonal hematopoiesis of indeterminate potential (CHIP) is caused by acquired mutations in haematopoietic stem cells that yield clonal progeny of mutant leucocytes.10 Although CHIP carriers typically display normal haematological indices and remain clinically inapparent,11 CHIP is strongly linked with age-related chronic diseases and haematologic malignancies. However, evidence linking CHIP with HF yielded conflicting findings.12-14 To this purpose, Karakasis and colleagues conducted a systematic review and meta-analysis to evaluate the association of CHIP with the incidence and clinical outcomes of HF.15

The authors evaluated a total of 13 studies based on five cohorts encompassing 57 755 individuals. Regardless of prior history of coronary artery disease, participants with CHIP had significantly greater risk of new-onset HF compared to the non-CHIP group (hazard ratio [HR] 1.23, 95% confidence interval [CI] 1.12–1.35, p < 0.0001). No significant subgroup differences for incident HF were observed based on LVEF or age. A subgroup analysis of gene-specific CHIP subtypes revealed significant differences among ASXL1, DNMT3A, TET2, and JAK2 regarding the risk of incident HF (p subgroup = 0.03). While ASXL1, TET2, and JAK2 were associated with a significantly increased risk of incident HF, DNMT3A demonstrated a non-significant effect (HR 1.13, 95% CI 0.99–1.28). However, it should be noted that the studies included in the meta-analysis utilized different sequencing methodologies, which may influence the detection of these mutations. Interestingly, a total of four cohorts, including 362 participants, also investigated the association of CHIP with the composite outcome of all-cause mortality and hospitalization for HF in patients with preexisting baseline HF. Participants with CHIP had a significantly higher risk of the composite outcome compared to the non-CHIP group (HR 1.84, 95% CI 1.25–2.70, p = 0.002).

Therapeutic targeting of CHIP is a new area of research with several promising strategies. One approach involves the inhibition of overactive inflammatory pathways related to the presence of CHIP.16 While this method does not directly target CHIP, it alleviates the adverse effects caused by inflammation. Another approach attempts to eliminate the mutated blood cells through selective targeting.17 This strategy hinges on the accurate identification of cell surface antigens unique to CHIP cells. In conclusion, the study by Karakasis et al.15 highlights the emerging importance of CHIP for HF risk stratification and its potential role as a biomarker for more personalized approaches.

Management of BP in patients with HF remains controversial, with conflicting evidence regarding optimal BP targets across HF phenotypes.18, 19 Li et al.20 conducted a large individual patient data meta-analysis pooling 28 406 participants from eight landmark randomized clinical trials, encompassing the full spectrum of LVEF. Using time-dependent Cox regression models, the study examined the association between longitudinal systolic and diastolic BP and key outcomes, including cardiovascular death and HF hospitalization.

The analysis revealed a non-linear, phenotype-specific relationship between BP and outcomes. In patients with HFrEF, low systolic BP (<120 mmHg) was consistently associated with increased risk of cardiovascular death and HF hospitalization (HR 1.71, 95% CI 1.60–1.82, p < 0.001), whereas higher systolic BP (>140 mmHg) was not linked to worse outcomes. Conversely, in HF with mildly reduced or preserved ejection fraction (HFmrEF/HFpEF), both low and high systolic BP were associated with adverse outcomes (HR 1.74, 95% CI 1.47–2.07, p < 0.001 and HR 1.77, 95% CI 1.45–2.17, p < 0.001; respectively), producing a U-shaped risk curve. Similar trends were observed for diastolic BP.

These findings underscore the limitations of uniform BP targets in HF patients and highlight LVEF as a key modifier of BP–outcome relationships. For HFrEF, low BP likely reflects advanced disease and impaired cardiac output, whereas in HFmrEF/HFpEF, both hypotension and uncontrolled hypertension contribute to risk. The authors suggest that dynamic, phenotype-tailored BP management strategies may improve outcomes, but emphasize the need for prospective trials to define optimal BP targets in contemporary HF populations.

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来源期刊
European Journal of Heart Failure
European Journal of Heart Failure 医学-心血管系统
CiteScore
27.30
自引率
11.50%
发文量
365
审稿时长
1 months
期刊介绍: European Journal of Heart Failure is an international journal dedicated to advancing knowledge in the field of heart failure management. The journal publishes reviews and editorials aimed at improving understanding, prevention, investigation, and treatment of heart failure. It covers various disciplines such as molecular and cellular biology, pathology, physiology, electrophysiology, pharmacology, clinical sciences, social sciences, and population sciences. The journal welcomes submissions of manuscripts on basic, clinical, and population sciences, as well as original contributions on nursing, care of the elderly, primary care, health economics, and other related specialist fields. It is published monthly and has a readership that includes cardiologists, emergency room physicians, intensivists, internists, general physicians, cardiac nurses, diabetologists, epidemiologists, basic scientists focusing on cardiovascular research, and those working in rehabilitation. The journal is abstracted and indexed in various databases such as Academic Search, Embase, MEDLINE/PubMed, and Science Citation Index.
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