Predictors of left ventricular reverse remodeling in patients with chronic heart failure

D'Auria, F; Polito, Maria Vincenza; Vitulano, Gennaro; Ciccarelli, Michele; Rosa, Roberta De; Gigantino, Alberto; Piscione, Federico; Galasso, Gennaro

doi:10.2459/jcm.0000000000000679

Cited by 7 publications

(9 citation statements)

References 24 publications

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“…Inflammation —Moreover, inflammation plays an important role in the pathophysiology of DCM [51,52,53]. Increased ROS in response to FFA and hyperglycemia activates NFκB, leading to an increased expression of cell adhesion molecules (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), an increased infiltration of macrophages and leucocytes and an increased expression of inflammatory cytokines (IL-1β, IL-6, IL-18, TNF-α and TGF-β1) [54,55,56,57].…”

Section: Pathophysiological Mechanisms Of Diabetic Cardiomyopathy:mentioning

confidence: 99%

Molecular Dysfunction and Phenotypic Derangement in Diabetic Cardiomyopathy

Evangelista

Nuti

Picchioni

et al. 2019

IJMS

105

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The high incidence and poor prognosis of heart failure (HF) patients affected with diabetes (DM) is in part related to a specific cardiac remodeling currently recognized as diabetic cardiomyopathy (DCM). This cardiac frame occurs regardless of the presence of coronary artery diseases (CAD) and it can account for 15–20% of the total diabetic population. The pathogenesis of DCM remains controversial, and several molecular and cellular alterations including myocardial hypertrophy, interstitial fibrosis, oxidative stress and vascular inflammation, have been postulated. The main cardio-vascular alterations associated with hyperglycemia comprise endothelial dysfunction, adverse effects of circulating free fatty acids (FFA) and increased systemic inflammation. High glucose concentrations lead to a loss of mitochondrial networks, increased reactive oxygen species (ROS), endothelial nitric oxide synthase (eNOS) activation and a reduction in cGMP production related to protein kinase G (PKG) activity. Current mechanisms enhance the collagen deposition with subsequent increased myocardial stiffness. Several concerns regarding the exact role of DCM in HF development such as having an appearance as either dilated or as a concentric phenotype and whether diabetes could be considered a causal factor or a comorbidity in HF, remain to be clarified. In this review, we sought to explain the different DCM subtypes and the underlying pathophysiological mechanisms. Therefore, the traditional and new molecular and signal alterations and their relationship with macroscopic structural abnormalities are described.

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Section: Pathophysiological Mechanisms Of Diabetic Cardiomyopathy:mentioning

confidence: 99%

Molecular Dysfunction and Phenotypic Derangement in Diabetic Cardiomyopathy

Evangelista

Nuti

Picchioni

et al. 2019

IJMS

105

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“…In a study of 927 HF patients (mean LVEF 35%, 48% with non‐ischaemic origin), followed up for 1 year, LVRR was more frequent among women [hazard ratio 1.54 (95% CI, 1.11 to 2.14), P = 0.011], regardless of the severity of left ventricular dysfunction 83 . Furthermore, non‐ischaemic aetiology was predicting LVRR as well—a consistent finding among many general HF populations 15,31,44,63,64,81,83,86 . Several other clinical parameters, such as a higher baseline systolic blood pressure, 5,15,79,80,85,87 shorter duration of HF symptoms, 79,83 and an absence of LBBB, 5,15,60,80,86,87 are associated with LVRR.…”

Section: Predictors Of Reverse Remodellingmentioning

confidence: 86%

“…Cardiac imaging is used not only for remodelling assessment, but different imaging modalities were also studied in the prognostication of successful LVRR. For example, baseline LVEF or chamber dimensions did not show a consistent association with LVRR 15,81,86,87 and perhaps should not be used routinely for this purpose. More advanced echocardiographic techniques, such as three‐dimensional echocardiography, speckle tracking, and estimation of wasted myocardial work using strain delay index across left ventricular segments, were studied in the prediction of LVRR mostly among patients with CRT 88,89 .…”

Section: Predictors Of Reverse Remodellingmentioning

confidence: 99%

“…The process of LVRR in patients with DCM and new‐onset HF may take up to 2 years after initiating treatment 68,78 . However, there is a significant portion of patients who do not improve despite optimal therapy, and based on previously published data, LVRR occurs only in about one‐third of cases, ranging from 19% to 45% 5,10,79–81 . This fact has serious clinical implications when considering treatment escalation towards more aggressive options, such as CRT, LVAD, or heart transplant.…”

Section: Predictors Of Reverse Remodellingmentioning

confidence: 99%

“… 68 , 78 However, there is a significant portion of patients who do not improve despite optimal therapy, and based on previously published data, LVRR occurs only in about one‐third of cases, ranging from 19% to 45%. 5 , 10 , 79 , 80 , 81 This fact has serious clinical implications when considering treatment escalation towards more aggressive options, such as CRT, LVAD, or heart transplant. Current guidelines recommend ICD implantation for primary prevention reasons if severe systolic dysfunction persists >3 months on optimal medical therapy 20 despite the fact that only one‐third of patients with DCM still fulfil these criteria 6 months after optimization of pharmacotherapy.…”

Section: Predictors Of Reverse Remodellingmentioning

confidence: 99%

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Left ventricular reverse remodelling and its predictors in non‐ischaemic cardiomyopathy

2022

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Adverse remodelling following an initial insult is the hallmark of heart failure (HF) development and progression. It is manifested as changes in size, shape, and function of the myocardium. While cardiac remodelling may be compensatory in the short term, further neurohumoral activation and haemodynamic overload drive this deleterious process that is associated with impaired prognosis. However, in some patients, the changes may be reversed. Left ventricular reverse remodelling (LVRR) is characterized as a decrease in chamber volume and normalization of shape associated with improvement in both systolic and diastolic function. LVRR might occur spontaneously or more often in response to therapeutic interventions that either remove the initial stressor or alleviate some of the mechanisms that contribute to further deterioration of the failing heart. Although the process of LVRR in patients with new-onset HF may take up to 2 years after initiating treatment, there is a significant portion of patients who do not improve despite optimal therapy, which has serious clinical implications when considering treatment escalation towards more aggressive options. On the contrary, in patients that achieve delayed improvement in cardiac function and architecture, waiting might avoid untimely implantable cardioverter-defibrillator implantation. Therefore, prognostication of successful LVRR based on clinical, imaging, and biomarker predictors is of utmost importance. LVRR has a positive impact on prognosis. However, reverse remodelled hearts continue to have abnormal features. In fact, most of the molecular, cellular, interstitial, and genome expression abnormalities remain and a susceptibility to dysfunction redevelopment under biomechanical stress persists in most patients. Hence, a distinction should be made between reverse remodelling and true myocardial recovery. In this comprehensive review, current evidence on LVRR, its predictors, and implications on prognostication, with a specific focus on HF patients with non-ischaemic cardiomyopathy, as well as on novel drugs, is presented.

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Clinical and echocardiographic benefit of Sacubitril/Valsartan in a real-world population with HF with reduced ejection fraction

Polito

Silverio

Rispoli

et al. 2020

Sci Rep

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The aim of this study was to evaluate the effects of Sacubitril/Valsartan (S/V) on clinical, laboratory and echocardiographic parameters and outcomes in a real-world population with heart failure with reduced ejection fraction (HFrEF). This was a prospective observational study enrolling patients with HFrEF undergoing treatment with S/V. The primary outcome was the composite of cardiac death and HF rehospitalization at 12 months follow-up; secondary outcomes were all-cause death, cardiac death and the occurrence of rehospitalization for worsening HF. The clinical outcome was compared with a retrospective cohort of 90 HFrEF patients treated with standard medical therapy. The study included 90 patients (66.1 ± 11.7 years) treated with S/V. The adjusted regression analysis showed a significantly lower risk for the primary outcome (HR:0.31; 95%CI, 0.11-0.83; p = 0.019) and for HF rehospitalization (HR:0.27; 95%CI, 0.08-0.94; p = 0.039) in S/V patients as compared to the control group. A significant improvement in NYHA class, left ventricular ejection fraction, left ventricular end systolic volume and systolic pulmonary arterial pressure was observed up to 6 months. S/V did not affect negatively renal function and was associated with a significantly lower dose of furosemide dose prescribed at 6-and 12-month follow-up. In this study, S/V reduced the risk of HF rehospitalization and cardiac death at 1 year in patients with HFrEF. S/V improved NYHA class, echocardiographic parameters and need of furosemide, and preserved renal function.Despite the improvements in clinical management and medical therapy of heart failure (HF), the outcome of patients with HF and reduced ejection fraction (HFrEF) remains poor 1 . If compared to the other HF entities, this category shows distinct demographic characteristics, comorbidities, response to therapy, and a substantially higher risk of mortality secondary to sudden cardiac death (SCD) and rehospitalization for worsening HF 2 . Many HFrEF patients are still undertreated and several drugs, such as beta-blockers and ACE inhibitors (ACEi), are under-dosed. This issue is also related to the incorrect risk evaluation by clinicians, who are likely to consider the absence or paucity of symptoms as an indicator of HF stability 3 . In fact, HFrEF is a progressive disorder that, despite the improvement of patient's clinical status achieved with conventional medications, may be associated with a high risk of adverse events at short and long-term follow-up 4 .Current European guidelines 5 recommend the use Sacubitril/Valsartan (S/V), an angiotensin receptorneprilysin inhibitor (ARNI), in replacement of the renin-angiotensin-aldosterone system (RAAS) inhibition in ambulatory HFrEF patients still symptomatic despite optimal medical therapy (OMT). This recommendation comes from a single randomized study named PARADIGM-HF trial 6 , which showed the superiority of S/V compared to Enalapril in reducing the incidence of cardiovascular death or hospitalizations for HF. Few studies have so far investigat...

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Predictors of left ventricular reverse remodeling in patients with chronic heart failure

Cited by 7 publications

References 24 publications

Molecular Dysfunction and Phenotypic Derangement in Diabetic Cardiomyopathy

Molecular Dysfunction and Phenotypic Derangement in Diabetic Cardiomyopathy

Left ventricular reverse remodelling and its predictors in non‐ischaemic cardiomyopathy

Clinical and echocardiographic benefit of Sacubitril/Valsartan in a real-world population with HF with reduced ejection fraction

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