scholarly journals Incidence of sudden cardiac death after heart transplantation

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
G Bonnet ◽  
G Coutance ◽  
V Waldmann ◽  
O Aubert ◽  
A Asselin ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Heart Transplantation ◽  
Cardiac Death ◽  
Graft Failure ◽  
Causes Of Death ◽  
First Year ◽  
Transplant Recipients ◽  
Graft Dysfunction ◽  
Heart Transplant Recipients ◽  
Causes Of Deaths

Abstract Background Sudden cardiac death (SCD) is a major contributor to the rate of mortality after heart transplantation. However, little is known about the incidence of SCD in heart recipients. Objective To assess the incidence of SCD after heart transplantation. Methods We enrolled consecutive patients transplanted between 2004 and 2017 in two French referral centers. We defined 7 main groups of causes of deaths: SCD, cardiovascular (including Cardiac allograft vasculopathy), infection, primary graft dysfunction, graft failure (including late graft dysfunction, rejection), malignancy and others. Causes of deaths were independently adjudicated by two senior cardiologists based on the analysis of death certificates and medical records. Discrepancies were resolved by discussion until a consensus was made. SCD was defined as an unexpected out-of-hospital cardiac arrest without obvious non-cardiac cause, in the first hour after initiation of symptoms. Results A total of 1,363 patients were included. The median follow-up post-transplant was 3.99 years (IQR=0.49–7.49). 450 patients (33%) deceased during the first year. The leading cumulative causes of death in the first year after transplantation were infection, primary graft failure, multiple organ failure during the period in intensiv car unit. Beyond the post-operativ high-risk period of the first year, the leading cumulative cause of death was SCD: among the 213 deaths that occurred beyond the first year, 44 patients (21%) died from SCD. In this period, the incidence rate of SCD reached 0,82 per 100 person-year (95% CI: 0.51–2.05). Conclusion In a large multicentric and highly phenotyped cohort of heart transplant recipients, the leading cumulative cause of death beyond the first-year post transplant was sudden cardiac death. Our results open discussion on management of heart recipient, such as the implementation of cardioverter-defibrillators. Figure 1. Cumulative incidence of causes of death in heart transplant recipients beyond the first year (n=913). Funding Acknowledgement Type of funding source: None

scholarly journals Determinants of sudden cardiac death after heart transplantation

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
G Bonnet ◽  
G Coutance ◽  
V Waldmann ◽  
O Aubert ◽  
A Asselin ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Sudden Death ◽  
Incidence Rate ◽  
Heart Transplant ◽  
Cardiac Death ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
First Year ◽  
Transplant Recipients ◽  
Heart Transplant Recipients

Abstract Background Heart transplant recipients are at high-risk of sudden cardiac death (SCD). However, risk factors of SCD in heart recipients remained poorly described. Objective To assess the predictors of SCD beyond the first-year post-transplant. Methods We enrolled consecutive patients transplanted between 2004 and 2017 in two French referral centers. We excluded patients deceased during the first year. Patients underwent an evaluation at the day of transplantation and during the first year, comprising clinical, biological, histological, immunological (circulating anti-HLA DSA) and interventional (cardiac allograft vasculopathy assessment) parameters. Echocardiographies were routinely performed in all included patients according to a prespecified protocol. According to the last consensus, SCD was defined as an unexpected out-of-hospital cardiac arrest without obvious non-cardiac cause, in the first hour after initiation of symptoms. Cox model analysis was used to determine the parameters associated with sudden death risk. Results A total of 913 patients were included. The median follow-up post-HT was 5.9 years (IQR=2.9–8.5). Among the 213 deaths after one year, 44 patients (21%) died from SCD. In this population, the incidence rate of SCD was 0,82 per 100 person-year (95% CI: 0,51–2,05). Among the 60 parameters tested in univariate analysis, we identified 2 independent factors of sudden death after 1 year post-HT: left ventricular ejection fraction (LVEF) ≤55% any time after transplantation ( HR 4.07, 95% CI 1.94–8.53, p<0.001) and the presence of circulating anti-HLA DSA at the time of transplantation (HR 2.79, 95% CI 1.37–5.68, p=0.005). The incidence rate of SCD was 2.17 per 100 person-year (95% CI: 1.42; 4.60) and 1.21 per 100 person-year (95% CI: 0.80; 2.58) in patients with FEVG<55% (n=73) and in patients with pre-formed DSA (n=260), respectively. Conclusion In a large multicentric and highly phenotyped cohort of heart transplant recipients, we identified two independent factors associated with SCD beyond the first year. This study provides fresh evidence of SCD assessment for improving risk stratification of HT recipients. Funding Acknowledgement Type of funding source: None

QT Dispersion Is Not associated with Sudden Cardiac Death or Mortality in Heart Transplant Recipients

2008 ◽  
Vol 11 (5) ◽  
pp. E281-E284
Author(s):  
Gregory M. Marcus ◽  
Khanh L. Hoang ◽  
Sharon A. Hunt ◽  
Sung H. Chun ◽  
Byron K. Lee
Keyword(s):  
Sudden Cardiac Death ◽  
Heart Transplant ◽  
Cardiac Death ◽  
Qt Dispersion ◽  
Transplant Recipients ◽  
Heart Transplant Recipients

scholarly journals Determinants of sudden cardiac death after heart transplantation

2021 ◽  
Vol 13 (1) ◽  
pp. 83-84
Author(s):  
G. Bonnet ◽  
G. Coutance ◽  
V. Waldmann ◽  
O. Aubert ◽  
A. Asselin ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Heart Transplantation ◽  
Cardiac Death

Abstract 18139: Myocardial Fibrosis Quantified by Cardiovascular Magnetic Resonance is Associated with Histology and Graft Function After Pediatric Heart Transplantation

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Brian Feingold ◽  
Cláudia M Salgado ◽  
Miguel Reyes-Múgica ◽  
Stacey Drant ◽  
Susan A Miller ◽  
...  
Keyword(s):  
Cardiovascular Magnetic Resonance ◽  
Magnetic Resonance ◽  
Heart Transplantation ◽  
Myocardial Fibrosis ◽  
Graft Failure ◽  
Extracellular Volume ◽  
Graft Function ◽  
Automated Image Analysis ◽  
Graft Dysfunction ◽  
Pediatric Heart Transplantation

Background: Late survival after pediatric heart transplantation (HTx) remains poor. Many late deaths are due to “graft failure,” typically in the presence of vasculopathy and diffuse myocardial fibrosis (DMF) - a process associated with ventricular remodeling and heart failure (HF). Cardiovascular magnetic resonance (CMR)-derived extracellular volume (ECV) is a validated measure of DMF in the absence of edema or infiltrative disease, and predicts outcomes of HF and mortality in adults. We hypothesize that ECV is a meaningful biomarker of graft dysfunction following pediatric HTx. Objective: To test the association of ECV with histologic myocardial fibrosis after pediatric HTx. We also explored associations of ECV with hemodynamic, echocardiographic, and serum measures of graft function. Methods: We prospectively enrolled consecutive HTx recipients who were ≥13 years old and ≥9 months post HTx for ECV quantification at the time of surveillance endomyocardial biopsy (EMB). Fibrosis was quantified on EMB by automated image analysis after picrosirius staining and digital scanning. CMR measures of blood and myocardial T1 from basal and mid short axis slices, along with contemporaneous hematocrit, quantified ECV. Results: Nineteen pts (12 male) underwent CMR at a mean age of 18.4 ± 2.8 yrs (range 14.9 - 24.4 yrs) and a mean time after HTx of 10.4 ± 6.6 yrs (1.0 - 20.7 yrs). Four pts were excluded from analysis due to acute rejection (ISHLT grade ≥2R) on concurrent EMB (n=2) or poor quality imaging (n=2). Mean ECV was 27.1 ± 3.8 (20.9 - 32.1). Late gadolinium enhancement was observed in 1 pt. ECV showed moderate correlations with histologic myocardial fibrosis (r=0.61; p=0.02) and serum b-type natriuretic peptide (r=0.66; p=0.008). There was a trend to correlation with pulmonary capillary wedge pressure (r=0.51; p=0.06). We found no associations of ECV with systolic or diastolic function, time after HTx, or graft age. Conclusions: We demonstrate a novel association of ECV with histologic myocardial fibrosis and serum and hemodynamic markers of HF after pediatric HTx. Given prior observations of myocardial fibrosis in chronic graft failure, these findings suggest that ECV may be a relevant, noninvasive marker of graft dysfunction and a potential therapeutic target.

Primary Graft Dysfunction in Heart Transplant Recipients—Risk Factors and Longitudinal Outcomes

ASAIO Journal ◽  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Nicholas F. Smith ◽  
Sina Salehi Omran ◽  
Michael V. Genuardi ◽  
Edward T. Horn ◽  
Arman Kilic ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Transplant ◽  
Transplant Recipients ◽  
Primary Graft Dysfunction ◽  
Graft Dysfunction ◽  
Longitudinal Outcomes ◽  
Heart Transplant Recipients

Enhanced brain natriuretic peptide response to peak exercise in heart transplant recipients

1998 ◽  
Vol 85 (6) ◽  
pp. 2270-2276 ◽  
Author(s):  
Bernard Geny ◽  
Anne Charloux ◽  
Eliane Lampert ◽  
Jean Lonsdorfer ◽  
Pascal Haberey ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Transplantation ◽  
Left Ventricular Mass ◽  
Heart Transplant ◽  
Left Ventricular Mass Index ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Transplant Recipients ◽  
Heart Transplant Recipients

We investigated the atrial (ANP) and brain natriuretic peptides (BNP), catecholamines, heart rate, and blood pressure responses to graded upright maximal cycling exercise of eight matched healthy subjects and cardiac-denervated heart transplant recipients (HTR). Baseline heart rate and diastolic blood pressure, together with ANP (15.2 ± 3.7 vs. 4.4 ± 0.8 pmol/l; P < 0.01) and BNP (14.3 ± 2.6 vs. 7.4 ± 0.6 pmol/l; P< 0.01), were elevated in HTR, but catecholamine levels were similar in both groups. Peak exercise O2uptake and heart rate were lower in HTR. Exercise-induced maximal ANP increase was similar in both groups (167 ± 34 vs. 216 ± 47%). Enhanced BNP increase was significant only in HTR (37 ± 8 vs. 16 ± 8%; P < 0.05). Similar norepinephrine but lower peak epinephrine levels were observed in HTR. ANP and heart rate changes from rest to 75% peak exercise were negatively correlated ( r = −0.76, P < 0.05), and BNP increase was correlated with left ventricular mass index ( r = 0.83, P < 0.01) after heart transplantation. Although ANP increase was not exaggerated, these data support the idea that the chronotropic limitation secondary to sinus node denervation might stimulate ANP release during early exercise in HTR. Furthermore, the BNP response to maximal exercise, which is related to the left ventricular mass index of HTR, is enhanced after heart transplantation.

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