Predictors and Outcome of Sustained Improvement in Left Ventricular Function in Dilated Cardiomyopathy

Blechman, Ido; Arad, Michael; Nussbaum, Tamar; Goldenberg, Ilan; Freimark, Dov

doi:10.1002/clc.22331

Cited by 9 publications

(11 citation statements)

References 25 publications

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“…Left ventricular ejection fraction was lower in the re‐worsening group than in the improved group. This result is similar to those in previous studies 10,11 . De Groote et al 7,10 .…”

Section: Discussionsupporting

confidence: 94%

“…This result is similar to those in previous studies. 10,11 De Groote et al 7,10 revealed that patients with DCM with an increase of >5% in LVEF and achieving LVEF ≧45% after beta-blocker use had a favourable outcome, whereas the LVEF, after an initial increase, was lower in patients with subsequently declining LVEF during long-term observation than in those who maintained LVEF ≧45%. These observations suggest that the level of LVEF attained after the initial recovery may influence the subsequent trajectories of LVEF.…”

Section: Clinical Parameters At the Initial Left Ventricular Ejectionmentioning

confidence: 99%

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Late gadolinium enhancement for re‐worsening left ventricular ejection fraction in patients with dilated cardiomyopathy

et al. 2020

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Aims This study aimed to evaluate the clinical parameters including late gadolinium enhancement (LGE) of cardiovascular magnetic resonance to predict re-worsening of left ventricular ejection fraction (LVEF) in patients with dilated cardiomyopathy (DCM). Methods and results We included 138 patients with recent-onset DCM who had an LVEF <45% and underwent LGE of cardiovascular magnetic resonance imaging at diagnosis and echocardiography at the yearly follow-up [median 6 (4-8.3) years]. Initial LVEF recovery was defined as LVEF increase >10% from baseline, resulting in LVEF ≧45% after treatment. The patients were divided into three groups: (i) improved (n = 83, 60%), defined as those with sustained LVEF ≧45%; (ii) re-worsening (n = 39, 28%), those with >5% decrease and LVEF <45% after the initial LVEF recovery; and (iii) not-improved (n = 16, 12%), those without initial LVEF recovery. The primary endpoint was a composite of hospitalization for heart failure or sudden cardiac death. In baseline, LGE was observed in 70 patients. The LGE area was significantly larger in the re-worsening and not-improved groups than that in the improved group (P < 0.001). Loess curves of long-term LVEF trajectories showed that LVEF in the re-worsening group increased in the first 2 years and slowly declined thereafter. Multivariate logistic regression analysis demonstrated that LGE area [odds ratio (OR) 1.09, 95% confidence interval (CI) 1.03-1.16, P = 0.004], B-type natriuretic peptide (OR 1.49, 95% CI 1.05-2.21, P = 0.030) level at the initial recovery, and LVEF (OR 0.91, 95% CI 0.86-0.97, P = 0.004) at the initial LVEF recovery were independent predictors of re-worsening of LVEF. During a median follow-up of 2273 (interquartile range: 1634-3191) days, the primary endpoint was observed in 31 (22%) patients. Univariate Cox proportional hazards analysis demonstrated that the risk of experiencing the primary event in the re-worsening group was significantly higher (hazard ratio: 4.30, 95% CI 1.63-11.31, P = 0.003) than that in the improved group and was lower than that in the not-improved group (hazard ratio: 0.33, 95% CI 0.15-0.72, P = 0.006). Conclusions Re-worsening of LVEF was observed in 28% of patients with recent-onset DCM who showed an initial improvement in LVEF. High LGE burden, higher B-type natriuretic peptide level, and lower LVEF at the initial LVEF recovery were independent predictors of re-worsening of LVEF in patients with DCM. Careful observation is recommended for patients with a high risk for re-worsening of LVEF, even in those with an initial LVEF recovery.

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“…Left ventricular ejection fraction was lower in the re‐worsening group than in the improved group. This result is similar to those in previous studies 10,11 . De Groote et al 7,10 .…”

Section: Discussionsupporting

confidence: 94%

Section: Clinical Parameters At the Initial Left Ventricular Ejectionmentioning

confidence: 99%

Late gadolinium enhancement for re‐worsening left ventricular ejection fraction in patients with dilated cardiomyopathy

et al. 2020

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“…It has been hypothesized that the reason adult HF patients develop fibrosis is due to the length of disease duration which averages 5 years (48, 49). The average duration of disease (age of onset to time of transplant) in the patient population we studied was 1 year, with a range of 0.01 to 7.6 years.…”

Section: Discussionmentioning

confidence: 99%

Fibrosis and Fibrotic Gene Expression in Pediatric and Adult Patients With Idiopathic Dilated Cardiomyopathy

Woulfe

Siomos

Nguyen

et al. 2017

Journal of Cardiac Failure

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Background While fibrosis seems to be prognostic for adverse outcomes in adults with idiopathic dilated cardiomyopathy (IDC), little is known about the prevalence and development of fibrosis in pediatric IDC hearts. We hypothesize there is less activation of fibrosis at a molecular level in pediatric IDC hearts than in the failing adult heart. Methods and Results Pediatric hearts were analyzed histologically to determine the prevalence of fibrosis. Left ventricular tissue from adult and pediatric IDC hearts and adult and pediatric non-failing (NF) hearts were subjected to qRT-PCR to study the expression of important mRNAs that affect fibrosis. We found age-specific differences between IDC and NF hearts in regulation of non-coding galectin 3, Corin, MMP-2, MMP-9, TIMP-2, and TIMP-3. We also found markers that were similarly altered in both adult and pediatric IDC (ST2L, TIMP-1, and TIMP-4). Finally, microRNAs 29a-c were significantly decreased in the pediatric IDC patients. Conclusion Pediatric IDC patients demonstrate age-specific differences in the molecular pathways implicated in fibrosis in the adult heart. At the ultrastructural level the unique gene expression pattern appears to limit fibrosis in the failing pediatric heart.

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“…Furthermore, wall elasticity during diastolic filling is reduced [2]. An unbalanced muscular hypertrophy along with dysbalanced distribution of oxygen and nutrients leads to necrosis of individual cardiomyocytes, foci of scarring and a further reduction in both contractile performance and oxygen delivery [74,75]. Patients with LMNA and FLNC mutations present with a distinct clinical phenotype including sinoatrial and atrioventricular node dysfunction, atrial fibrillation and other supraventricular arrhythmias [73].…”

Section: Genetics Of Dcmmentioning

confidence: 99%

Dilated cardiomyopathy: from epidemiologic to genetic phenotypes

Reichart¹,

Magnussen²,

Zeller³

et al. 2019

J Intern Med

131

112

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Reichart D, Magnussen C, Zeller T, Blankenberg S (University Heart Center Hamburg, Hamburg, Germany). Dilated cardiomyopathy: from epidemiologic to genetic phenotypes. J Intern Med 2019; 286: 362-372.Dilated cardiomyopathy (DCM) is characterized by left ventricular dilatation and, consecutively, contractile dysfunction. The causes of DCM are heterogeneous. DCM often results from myocarditis, exposure to alcohol, drugs or other toxins and metabolic or endocrine disturbances. In about 35% of patients, genetic mutations can be identified that usually involve genes responsible for cytoskeletal, sarcomere and nuclear envelope proteins. Due to its heterogeneity, a detailed diagnostic work-up is necessary to identify the specific underlying cause and exclude other conditions with phenotype overlap. Patients with DCM show typical systolic heart failure symptoms, but, with progress of the disease, diastolic dysfunction is present as well. Depending on the underlying pathology, DCM patients also become apparent through arrhythmias, thromboembolic events or cardiogenic shock. Disease progression and prognosis are mostly driven by disease severity and reverse remodelling within the heart. The worst prognosis is seen in patients with lowest ejection fractions or severe diastolic dysfunction, leading to terminal heart failure with subsequent need for left ventricular assist device implantation or heart transplantation.Guideline-based heart failure medication and device therapy reduces the frequency of heart failure hospitalizations and improves survival.

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Predictors and Outcome of Sustained Improvement in Left Ventricular Function in Dilated Cardiomyopathy

Cited by 9 publications

References 25 publications

Late gadolinium enhancement for re‐worsening left ventricular ejection fraction in patients with dilated cardiomyopathy

Late gadolinium enhancement for re‐worsening left ventricular ejection fraction in patients with dilated cardiomyopathy

Fibrosis and Fibrotic Gene Expression in Pediatric and Adult Patients With Idiopathic Dilated Cardiomyopathy

Dilated cardiomyopathy: from epidemiologic to genetic phenotypes

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