Longitudinal shortening remains the principal component of left ventricular pumping in patients with chronic myocardial infarction even when the absolute atrioventricular plane displacement is decreased

Abstract

Background: The majority (60%) of left ventricular (LV) stroke volume (SV) is generated by longitudinal shortening causing apical atrioventricular plane displacement (AVPD) in systole. The remaining SV is caused by radial inward motion of the epicardium both in the septal and the lateral wall. We aimed to determine if these longitudinal, septal and lateral contributions to LVSV are changed in patients with chronic myocardial infarction (MI).

Methods: Patients with a chronic (>3 months) ST-elevation MI in the left anterior descending (LAD, n = 20) or right coronary artery (RCA, n = 16) and healthy controls (n = 20) were examined with cardiovascular magnetic resonance (CMR). AVPD was quantified in long axis cine CMR images and LV volumes and dimensions in short axis cine images.

Results: AVPD was decreased both in patients with LAD-MI (11 ± 1 mm, p < 0.001) and RCA-MI (13 ± 1 mm, p < 0.05) compared to controls (15 ± 0 mm). However, the longitudinal contribution to SV was unchanged for both LAD-MI (58 ± 3%, p = 0.08) and RCA-MI (59 ± 3%, p = 0.09) compared to controls (64 ± 2%). The preserved longitudinal contribution despite decreased absolute AVPD was a results of increased epicardial dimensions (p < 0.01 for LAD-MI and p = 0.06 for RCA-MI). In LAD-MI the septal contribution to LVSV was decreased (5 ± 1%) compared to both controls (10 ± 1%, p < 0.01) and patients with RCA-MIs (10 ± 1%, p < 0.01). The lateral contribution was increased in LAD-MI patients (44 ± 3%) compared to both RCA-MI (35 ± 2%, p < 0.05) and controls (29 ± 2%, p < 0.001).

Conclusion: Longitudinal shortening remains the principal component of left ventricular pumping in patients with chronic MI even when the absolute AVPD is decreased.

Keywords: Cardiac output; Cardiac pumping; Heart failure; Late gadolinium enhancement; Mitral annular plane systolic excursion; Regional function.

Fig. 1

Illustration of the method for quantifying atrioventricular plane displacement (AVPD), septal and lateral contribution to left ventricular stroke volume (LVSV). Short-axis (SA) and four-chamber (4Ch), three-chamber (3Ch) and 2-chamber (2Ch) images are shown in end-diastole (ED) and end-systole (ES). The epicardial border of the SA is shown as a solid line in ED and broken line in ES. The ED epicardial contour is transposed on the ES image for comparison. The difference between the epicardial contours in the SA images are defined as the radial pumping and is subdivided into the septal (black arrows) and lateral (white arrows) contributions as defined by the right ventricular septal insertion points (marked with circles). The AVPD was calculated by marking the most basal part of the muscular wall in ED and ES as denoted by the white circles. The position of the AV-plane in ED is transposed to the ES image for comparison and the AVPD is marked by the double-headed arrows

Fig. 2

Mean extent of myocardial infarction for the two vessel territories LAD (left) and RCA (right). Extent is normalized to the population size of each group for comparison between territories, and 0–100% indicate the number of patients having myocardial infarction in a certain area. Overlaid is the standard 17-segment AHA model

Fig. 3

Comparison of the longitudinal contribution to LV stroke volume for patients with MI in the LAD and RCA vessel territories and controls. There was no significant difference between the groups. Solid line indicates the mean

Fig. 4

Comparison of the septal contribution to LV stroke volume for patients with MI in the LAD and RCA vessel territories and controls. Septal contribution to SV was significantly lower for the LAD-MI compared to both RCA-MI and controls. There was, however, no significant difference between RCA-MI and controls. Negative values of septal contribution are explained by dyskinesia of the septum, i.e. septal movement toward the RV in systole. Solid line indicates the mean. *P < 0.05, **P < 0.01 NS non-significant

Fig. 5

Comparison of the lateral contribution to LV stroke volume for patients with MI in the LAD and RCA vessel territories and controls. Lateral contribution to SV was lower for the RCA-MI compared to LAD-MI. Solid line indicates the mean. *P < 0.05, *** P < 0.001

Fig. 6

Illustration of differences in longitudinal, septal and lateral contributions to left ventricular pumping in a patient with LAD-MI (top row) and RCA-MI (bottom row). Cine images in the left-ventricular outflow tract view are shown in end diastole (left column) and end systole (middle column) and the corresponding late gadolinium enhancement (LGE) images (right column, c and f) show the extent of the infarcted area (arrows). The solid white outline of the LV in end diastole (a and d) is superimposed on the images in end systole (b and e) where the ventricles in end systole have been outlined with a dashed line. The AV-plane displacement (AVPD) is the difference of the horizontal white line at base of LV in end-diastole and end-systole and marked by double arrow at the base of ventricle in e. Longitudinal pumping is the difference in the basal contours at end diastole and end systole. Radial pumping is caused by the displacement of the epicardial border from end diastole and end systole. Note in b that the lateral component of radial pumping is increased (arrow at lateral wall in b) and compensates for the decreased longitudinal and septal contributions to LV pumping. As a contrast, the RCA-MI patient shown in the lower panels has a normal AVPD despite the MI. This may be compensatory to the decreased lateral contribution to LVSV in this patient due to the MI

Fig. 7

An example of a patient who has developed a very large apical aneurysm secondary to a myocardial infarction within the LAD territory. The upper row is in end diastole while the lower row is in end systole. In this case most of the stroke volume is generated by longitudinal AVPD (≈ 90%) of the viable myocardium at the base of the LV