Miscellaneous
Erik Hedström, MD, PhD
Associate professor, consultant
Lund University, Skåne University Hospital, Lund, Sweden
Lund, Sweden
Katarina Steding-Ehrenborg, PhD
Associate Professor
Lund University, Skane University Hospital
Lund, Skane Lan, Sweden
Anders Nelsson, MD
MD, PhD student
Lund University, Skåne University Hospital, Sweden
Henrik Engblom, MD, PhD
Professor
Lund University
Lund, Skane Lan, Sweden
Oscar Braun, MD, PhD
Associate Professor
Skåne University Hospital, Sweden
Håkan Arheden, MD, PhD
Professor
Lund University
Lund, Sweden
Previous studies have shown that when the atrial short-axis area is smaller than the ventricular short axis area, a hydraulic force contributes to the longitudinal motion of the atrioventricular plane (1, 2). This atrio-ventricular area difference (AVAD) is easily obtained using cardiac magnetic resonance (CMR) imaging. In short, diastolic filling is augmented when the left ventricular short-axis area is larger than the left atrial short-axis area (1). In patients with heart failure with preserved ejection fraction (HFpEF) the left atrium is often enlarged which could potentially change AVAD resulting in impaired diastolic function (2). The left atrium is enlarged also in patients after heart transplantation when it is re-created during the transplantation by suturing the back wall containing the lung veins from the recipient’s atrium to the atrium of the donor heart. We hypothesized that this surgical technique affects the geometrical relationship between the ventricle and atrium, and thus diastolic filling. Therefore, the aim of this study was to assess diastolic function determined as AVAD in patients after heart transplantation, and to assess if AVAD differs when comparing patients after heart transplantation, and patients with heart failure with reduced (HFrEF) or preserved (HFpEF) ejection fraction, to healthy controls.
Methods:
22 patients after heart transplantation (53 [35-66] years), 15 with HFrEF (63 [60-69] years), 15 with HFpEF (74 [64-80] years), and 15 controls (64 [61-66] years) underwent CMR. Short-axis images of the left ventricle and atrium were acquired. Ventricular, atrial, and total heart volumes were manually delineated. Atrio-ventricular area difference was calculated as the largest ventricular short-axis area minus the largest atrial short-axis area at end-diastole and end-systole. Groups were compared using Kruskal-Wallis non-parametric test and values are presented as median [interquartile range].
Results:
Figure 1 shows left atrial volume normalized for total heart volume (LA/THV), which was larger in all patient groups compared to controls, with the largest difference in patients after heart transplantation (0.13 [0.1-0.14] vs controls 0.05 [0.04-0.06], p< 0.0001).
At end diastole, when AVAD reaches its largest positive value in healthy controls, 9 patients after transplantation (41%) instead had a negative AVAD (Figure 2, Panel A). This was also seen in 2 HFpEF patients. At end systole, 11 HFrEF patients (73%) had positive AVAD already at diastolic onset (Figure 2, Panel B).
Conclusion:
Negative AVAD in diastole in heart transplantation patients may contribute to impaired diastolic filling. In contrast, positive AVAD in patients with HFrEF likely aids diastolic filling. Further understanding of AVAD’s role in diastolic filling may have future implications for the transplant surgeon by taking the geometrical relationship between atrium and ventricle into account.