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Afterload Mismatch Is Associated With Higher Cardiac Mortality After Heart Transplantation
Mattia Corianò1, Nicola Pradegan2, Andrea Golfetto1
1Cardiology Unit, Department of Cardiac, Thoracic, Vascular Sciences and Public Health University of Padua Italy.
Insights
After heart transplant (HT), afterload mismatch (AM) is identified as an independent predictor of cardiac mortality. This study defines AM phenotypes and their impact on long-term survival in HT recipients.
Area of Science:
- Cardiology
- Transplantation Medicine
- Cardiovascular Physiology
Background:
- Heart transplant (HT) recipients often exhibit altered ventricular-arterial interactions.
- The prognostic significance of these physiological changes, specifically afterload mismatch (AM), remains incompletely understood.
- This study investigates AM in HT patients to clarify its determinants and long-term cardiac mortality implications.
Purpose of the Study:
- To identify the presence and characteristics of afterload mismatch (AM) in heart transplant recipients.
- To determine the factors contributing to the development of AM post-transplantation.
- To assess the impact of AM on long-term cardiac mortality in this patient cohort.
Main Methods:
- An observational, single-center study analyzed a historical cohort of heart transplant (HT) recipients.
- Patients with preserved ejection fraction and minimal rejection/vasculopathy were included.
- Arterial and ventricular elastance were noninvasively calculated to classify patients into low afterload (LA), matched high afterload (MHA), and afterload mismatch (AM) groups.
Main Results:
- Afterload mismatch (AM) was associated with lower left ventricular ejection fraction and stroke volume compared to other groups.
- Predictors of AM included male recipient/male donor and male recipient/female donor combinations.
- AM was identified as an independent predictor of increased cardiac mortality, with significantly lower median survival (17.2 years) compared to LA and MHA groups.
Conclusions:
- Three distinct phenotypes were identified in heart transplant recipients based on ventricular-arterial interactions.
- Afterload mismatch (AM) emerged as a significant independent predictor of long-term cardiac mortality.
- These findings highlight the clinical importance of assessing ventricular-arterial coupling in heart transplant management.
Background:
Heart transplant (HT) recipients tend to develop unfavorable ventricular-arterial interactions, yet the prognostic implications of this altered physiology remain unclear. We aimed to identify the presence of afterload mismatch (AM) after heart transplantation, its determinants, and its impact on long-term cardiac mortality.
Methods:
An observational, single-center study was conducted on the historical cohort of patients who received HT at our institution. Patients survived the first year after HT with a LVEF ≥50%, cardiac allograft vasculopathy grades 0 to 1, and acute cellular rejection grades 0 to 1R. Arterial elastance and ventricular elastance were calculated noninvasively using blood pressure, end-systolic volume, and end-diastolic volume. Patients were grouped as follows: low afterload (LA- arterial elastance
Results:
Overall, 345 patients who received HT were enrolled. Left ventricular ejection fraction was lower in AM (57%) than in LA and MHA (63% and 64%, respectively; P<0.0001); stroke volume was lower in AM than in LA but comparable between AM and MHA (27, 35, and 26 mL/m2 for AM, LA, and MHA, respectively; P=0.0001). Predictors of AM were male recipient/male donor (β=0.15, P=0.0067) and male recipient/female donor (β=0.6, P=0.0078). After a median of 11.3 years, 59 recipients had died. Cardiac mortality was higher in the group with AM (AM median survival: 17.2, 27.8, and 24.1 years for AM, LA, and MHA, respectively; log-rank P=0.005). After adjusting for confounding variables, AM was associated with cardiac mortality (hazard ratio [HR], 2.26 [95% CI, 1.18-4.35]; P=0.0143)as were male recipient/female donor (HR, 2.94 [95% CI], 1.18-4.35; P=0.0358).
Conclusion:
Three phenotypes of patients who received HT were identified, and AM resulted as an independent predictor of cardiac mortality.
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