scholarly journals Family History of Dilated Cardiomyopathy among Patients with Heart Failure from the HF-ACTION Genetic Ancillary Study

2013 ◽  
Vol 6 (3) ◽  
pp. 179-183 ◽  
Author(s):  
Laura Hudson ◽  
Ana Morales ◽  
Ana Clara Mauro ◽  
David Whellan ◽  
Kirkwood F. Adams ◽  
...  
Keyword(s):  
Heart Failure ◽  
Family History ◽  
Dilated Cardiomyopathy ◽  
Ancillary Study ◽  
Patients With Heart Failure ◽  
History Of

scholarly journals Clinical and Genetic Investigations of 109 Index Patients With Dilated Cardiomyopathy and 445 of Their Relatives

2020 ◽  
Vol 13 (10) ◽  
Author(s):  
Thomas M. Hey ◽  
Torsten B. Rasmussen ◽  
Trine Madsen ◽  
Mads Malik Aagaard ◽  
Maria Harbo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Family History ◽  
Dilated Cardiomyopathy ◽  
Prognostic Information ◽  
Tertiary Referral Center ◽  
Pathogenic Variants ◽  
Clinical Investigations ◽  
History Of ◽  
Sporadic Cases ◽  
Firm Basis

Background: It was the aim to investigate the frequency and genetic basis of dilated cardiomyopathy (DCM) among relatives of index patients with unexplained heart failure at a tertiary referral center. Methods: Clinical investigations were performed in 109 DCM index patients and 445 of their relatives. All index patients underwent genetic investigations of 76 disease-associated DCM genes. A family history of DCM occurred in 11% (n=12) while clinical investigations identified familial DCM in a total of 32% (n=35). One-fifth of all relatives (n=95) had DCM of whom 60% (n=57) had symptoms of heart failure at diagnosis, whereas 40% (n=38) were asymptomatic. Symptomatic relatives had a shorter event-free survival than asymptomatic DCM relatives ( P <0.001). Results: Genetic investigations identified 43 pathogenic (n=27) or likely pathogenic (n=16) variants according to the American College of Medical Genetics and Genomics and the Association for Molecular Pathology criteria. Forty-four percent (n=48/109) of index patients carried a pathogenic/likely pathogenic variant of whom 36% (n=27/74) had sporadic DCM, whereas 60% (21/35) were familial cases. Thirteen of the pathogenic/likely pathogenic variants were also present in ≥7 affected individuals and thereby considered to be of sufficient high confidence for use in predictive genetic testing. Conclusions: A family history of DCM identified only 34% (n=12/35) of hereditary DCM, whereas systematic clinical screening identified the remaining 66% (n=23) of DCM families. This emphasized the importance of clinical investigations to identify familial DCM. The high number of pathogenic/likely pathogenic variants identified in familial DCM provides a firm basis for offering genetic investigations in affected families. This should also be considered in sporadic cases since adequate family evaluation may not always be possible and the results of the genetic investigations may carry prognostic information with an impact on individual management.

scholarly journals Rate of Heart Failure Following Atrial Fibrillation According to Presence of Family History of Dilated Cardiomyopathy or Heart Failure: A Nationwide Study

2021 ◽  
Author(s):  
Magnus N. Ebbesen ◽  
Maria D’Souza ◽  
Charlotte Andersson ◽  
Jawad H. Butt ◽  
Christian Madelaire ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Heart Disease ◽  
Family History ◽  
Ischemic Heart Disease ◽  
Dilated Cardiomyopathy ◽  
Family Member ◽  
Ischemic Heart ◽  
Degree Relative ◽  
History Of

Background It is poorly understood why some patients with atrial fibrillation develop heart failure (HF) and others do not. We examined the rate of developing HF in patients with atrial fibrillation with and without first‐degree family members with HF or dilated cardiomyopathy (DCM). Methods and Results Using Danish nationwide registries, patients born after 1942 diagnosed with atrial fibrillation in the period 2005 to 2015 were identified and followed for up to 5 years. Patients with pre‐existing HF, DCM, and/or ischemic heart disease diagnoses were excluded. Exposure was defined as a first‐degree relative with HF or DCM. The rate of developing the composite end point of HF or death, and the components, was estimated with multivariable Cox proportional hazard regression models. We included 10 605 patients. A total of 17% had a family member with DCM/HF. Having a family member with HF/DCM was associated with an increased 5‐year risk of the composite of HF/death (cumulative incidence, 9.2% [95% CI, 7.8–10.7] versus 5.6% [95% CI, 5.0–6.1]; adjusted hazard ratio [HR] 1.36 [95% CI, 1.13–1.64]). (HF 8.4% [95% CI, 7.0–9.8] versus 4.5% [95% CI, 4.1–5.0]); (adjusted HR, 1.49 [95% CI, 1.22–1.82]). However, familial HF/DCM was not significantly associated with an increased 5‐year risk and rate of death (0.8% [95% CI, 0.4–1.2] versus 1.1% [95% CI, 0.8–1.3]); (adjusted HR, 0.80 [95% CI, 0.46–1.39]). Conclusions In patients with incident atrial fibrillation without prior ischemic heart disease or HF diagnoses, 1 of 6 had a first‐degree relative with HF, and having such a family history of HF/DCM was associated with an 87% increase in 5‐year incidence of HF compared with those without.

P990Assessment of clinical risk factors for all-cause mortality among hypertrophic cardiomyopathy patients with ICDs

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Mielczarek ◽  
P Syska ◽  
M Lewandowski ◽  
A Przybylski ◽  
M Sterlinski ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Family History ◽  
Secondary Prevention ◽  
Positive Family History ◽  
Left Ventricular ◽  
Icd Implantation ◽  
All Cause Mortality ◽  
History Of ◽  
End Stage

Abstract Introduction According to the literature, the annual mortality rate of hypertrophic cardiomyopathy (HCM) patients is estimated to 1–2%. Sudden cardiac death (SCD), heart failure and thromboembolism are the main causes of death among this population. Patients at high risk for SCD, identified using HCM risk score, are qualified for ICD implantation. Unfortunately for clinicians, there is no validated model or statistical tool for assessment of the risk of mortality within the HCM patients with ICDs. Purpose The aim of this study was to determine the main risk factors of all- cause mortality in HCM patients with ICDs. Methods The long-term follow-up of group of 104 consecutive patients with HCM, who had the ICD implanted between 1996 and 2006 in tertiary reference clinical unit was performed. Twenty patients who died during observation were the subject of the current analysis. ICD was implanted for primary (n=16) and secondary (n=4) prevention of SCD within this subpopulation. Analysis were performed for mentioned below potential risk factors: age at the time of implantation, syncopes, family history of SCD, atrial fibrillation/supraventricular tachycardia, decreased left ventricular ejection fraction (LVEF), non-sustained ventricular tachycardia (nsVT), maximum left ventricular wall thickness, abnormal exercise blood pressure response, left ventricular outflow tract obstruction. Results The average time of survival since ICD implantation was 8,5±4,6 years. Decreased LVEF (Wald chi2 4,57; p=0,033), secondary prevention (Wald chi2 8,57; p=0,003), family history of SCD (Wald chi2 4,93; p=0,026) and episodes of nsVT (Wald chi2 3,49; p=0,062) are the clinical risk factors that significantly affect the time of survival. The probability of death, expressed as Hazard Ratio, was 27-fold higher in secondary prevention group (HR=27,18), almost 10-fold higher in patients with positive family history of SCD (HR=9,74) and 3,7-fold higher when nsVT was detected. The cause of death was established in 16/20 patients. In 15 cases, these were deaths from cardiovascular causes: end-stage heart failure (8), complications of heart transplantation or circulatory support (4), SCD (1) and other cardiovascular (2). Conclusion Secondary prevention, positive family history of SCD, nsVT and decreased LVEF seem to be the most significant risk factors associated with all- cause mortality in HCM patients with ICDs. Despite the ICD implantation, subpopulation studied had poor prognosis with high incidence of progression to end-stage heart failure. Further studies to create validated model for assessment of death risk in long-term observation of patients with HCM after ICD implantation are required.

Effects of metoprolol CR/XL on mortality and hospitalizations in patients with heart failure and history of hypertension

2002 ◽  
Vol 8 (1) ◽  
pp. 8-14 ◽  
Author(s):  
Johan Herlitz ◽  
John Wikstrand ◽  
Marty Denny ◽  
Paul Fenster ◽  
Thomas Heywood ◽  
...  
Keyword(s):  
Heart Failure ◽  
Patients With Heart Failure ◽  
History Of

scholarly journals The influence of atrial fibrillation on the levels of NT-proBNP versus GDF-15 in patients with heart failure

2019 ◽  
Vol 109 (3) ◽  
pp. 331-338 ◽  
Author(s):  
Bernadet T. Santema ◽  
Michelle M. Y. Chan ◽  
Jasper Tromp ◽  
Martin Dokter ◽  
Haye H. van der Wal ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Sinus Rhythm ◽  
Plasma Levels ◽  
Validation Cohort ◽  
Post Hoc Analysis ◽  
Patients With Heart Failure ◽  
History Of ◽  
Post Hoc ◽  
Multivariable Adjustment

Abstract Background In heart failure (HF), levels of NT-proBNP are influenced by the presence of concomitant atrial fibrillation (AF), making it difficult to distinguish between HF versus AF in patients with raised NT-proBNP. It is unknown whether levels of GDF-15 are also influenced by AF in patients with HF. In this study we compared the plasma levels of NT-proBNP versus GDF-15 in patients with HF in AF versus sinus rhythm (SR). Methods In a post hoc analysis of the index cohort of BIOSTAT-CHF (n = 2516), we studied patients with HF categorized into three groups: (1) AF at baseline (n = 733), (2) SR at baseline with a history of AF (n = 183), and (3) SR at baseline and no history of AF (n = 1025). The findings were validated in the validation cohort of BIOSTAT-CHF (n = 1738). Results Plasma NT-proBNP levels of patients who had AF at baseline were higher than those of patients in SR (both with and without a history of AF), even after multivariable adjustment (3417 [25th–75th percentile 1897–6486] versus 1788 [682–3870], adjusted p < 0.001, versus 2231 pg/mL [902–5270], adjusted p < 0.001). In contrast, after adjusting for clinical confounders, the levels of GDF-15 were comparable between the three groups (3179 [2062–5253] versus 2545 [1686–4337], adjusted p = 0.36, versus 2294 [1471–3855] pg/mL, adjusted p = 0.08). Similar patterns of both NT-proBNP and GDF-15 were found in the validation cohort. Conclusion These data show that in patients with HF, NT-proBNP is significantly influenced by underlying AF at time of measurement and not by previous episodes of AF, whereas the levels of GDF-15 are not influenced by the presence of AF. Therefore, GDF-15 might have additive value combined with NT-proBNP in the assessment of patients with HF and concomitant AF. Graphic abstract

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