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Published on: August 2, 2024
Cardiac allograft hypertrophy is associated with impaired exercise tolerance after heart transplantation
Eugenia Raichlin1, Malik A Al-Omari, Courtney L Hayes
1Division of Cardiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Insights
Concentric hypertrophy (CH) after heart transplantation (HTx) significantly impairs exercise capacity. Identifying CH early may improve functional outcomes in transplant recipients.
Area of Science:
- Cardiology
- Transplantation Medicine
- Exercise Physiology
Background:
- Exercise performance is crucial for quality of life but often limited post-heart transplantation (HTx).
- Cardiac allograft remodeling, specifically left ventricle mass and relative wall thickness, may influence functional capacity.
- Understanding these changes is vital for improving patient outcomes.
Purpose of the Study:
- To investigate the impact of cardiac allograft remodeling on functional capacity in heart transplant recipients.
- To determine the relationship between specific geometric patterns (normal geometry, concentric remodeling, concentric hypertrophy) and exercise tolerance.
- To identify potential mechanisms for exercise limitation after HTx.
Main Methods:
- Echocardiography was used to classify 117 heart transplant recipients into normal geometry (NG), concentric remodeling (CR), or concentric hypertrophy (CH) groups at 1 year post-transplant.
- Cardiopulmonary exercise testing was performed to assess exercise tolerance.
- Patients with acute rejection or graft vasculopathy were excluded.
Main Results:
- At 1 year post-HTx, 30% of patients exhibited CH, 55% CR, and 15% NG.
- The CH group showed significantly impaired exercise tolerance, including lower peak oxygen uptake (Vo2) and higher ventilatory equivalents for carbon dioxide (Ve/Vco2), compared to the NG group.
- A 1-year CH pattern was independently associated with reduced normalized peak Vo2 and elevated Ve/Vco2, increasing the risk for poor exercise capacity.
Conclusions:
- Concentric hypertrophy (CH) at 1 year post-heart transplantation is independently linked to decreased exercise capacity and altered ventilatory response.
- CH represents a potentially reversible factor contributing to exercise limitation in stable heart transplant recipients.
- Early identification of CH could have significant clinical implications for managing functional capacity after HTx.
Background:
Exercise performance, an important aspect of quality of life, remains limited after heart transplantation (HTx). This study examines the effect of cardiac allograft remodeling on functional capacity after HTx.
Methods:
The total cohort of 117 HTx recipients, based on echocardiographic determination of left ventricle mass and relative wall thickness at 1 year after HTx, was divided into 3 groups: (1) NG, normal geometry; (2) CR, concentric remodeling; and (3) CH, concentric hypertrophy. Cardiopulmonary exercise testing was performed 5.03 ± 3.08 years after HTx in all patients. Patients with acute rejection or significant graft vasculopathy were excluded.
Results:
At 1 year post-HTx, 30% of patients had CH, 55% had CR and 15% had NG. Exercise tolerance, measured by maximum achieved metabolic equivalents (4.62 ± 1.44 vs 5.52 ± 0.96 kcal/kg/h), normalized peak Vo(2) (52 ± 14% vs 63 ± 12%) and Ve/Vco(2) (41 ± 17 vs 34 ± 6), was impaired in the CH group compared with the NG group. A peak Vo(2) ≤14 ml/kg/min was found in 6%, 22% and 48% of patients in the NG, CR and CH groups, respectively (p = 0.01). The CH pattern was associated with a 7.4-fold increase in relative risk for a peak Vo(2) ≤14 ml/kg/min compared with NG patients (95% confidence interval 1.1 to 51.9, p = 0.001). After multivariate analysis, a 1-year CH pattern was independently associated with a reduced normalized peak Vo(2) (p = 0.018) and an elevated Ve/Vco(2) (p = 0.035).
Conclusions:
The presence of CH at 1 year after HTx is independently associated with decreased normalized peak Vo(2) and increased ventilatory response in stable heart transplant recipients. The identification of CH, a potentially reversible mechanism of impairment in exercise capacity after HTx, may have major clinical implications.
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