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. 2020 Sep;7(2):e001243.
doi: 10.1136/openhrt-2020-001243.

Left ventricular longitudinal shortening: relation to stroke volume and ejection fraction in ageing, blood pressure, body size and gender in the HUNT3 study

Affiliations

Left ventricular longitudinal shortening: relation to stroke volume and ejection fraction in ageing, blood pressure, body size and gender in the HUNT3 study

Asbjørn Støylen et al. Open Heart. 2020 Sep.

Abstract

Background: Aims of this cross-sectional study were to assess: the relative contribution of left ventricular (LV) systolic long-axis shortening (mean mitral annular plane systolic excursion, MAPSE) to stroke volume (SV), the mechanisms for preserved ejection fraction (EF) despite reduced MAPSE, the age dependency of myocardial volume and myocardial systolic compression.

Methods: Linear dimensions and longitudinal and cross-sectional M-modes were acquired in 1266 individuals without history of heart disease, diabetes or known hypertension from the third wave of the Nord-Trøndelag Health Study. Measurements were entered into a half-ellipsoid LV model for volume calculations, and volumes were related to age, body size (body surface area, BSA), sex and blood pressure (BP).

Results: Mean BP and proportion with hypertensive values increased with increasing age. MAPSE contributed to 75% of SV, with no relation to age or BSA as both MAPSE and SV decreased with increasing age. LV end-diastolic volume (LVEDV) and SV increased with BSA and decreased with higher age; EF was not related to age or BSA. Myocardial volume increased with higher age and BSA, with an additional gender dependency. The association of age with myocardial volume was not significant when corrected for BP, while both systolic and diastolic BP were significant associated with myocardial volume. Myocardial compression was less than 3%.

Conclusions: MAPSE contributes approximately 75% and short axis shortening 25% to SV. Both decline with age, but their percentage contributions to SV are unchanged. EF is preserved by the simultaneous decrease in LVEDV and SV. Myocardial volume is positively associated with age, but this is only related to higher BP, which may have implications for BP treatment in ageing. The myocardium is near incompressible.

Keywords: cardiac function; echocardiography; hypertension.

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Conflict of interest statement

Competing interests: None declared.

Figures

Figure 1
Figure 1
Schematic diagram of the systolic deformation of the left ventricle. Systolic contours are shown by the broken lines, diastolic by the unbroken. (A) Outer, or total volumes. total volume=myocardial vol+cavity vol. The ventricle reduces both length and outer diameter, and the total volume decreases as a function of both deformations (orange and light red). if the myocardium is incompressible, the myocardial volume is the same in both diastole and systole. thus, diastolic cavity volume=total diastolic volume – myocardial volume and systolic cavity volume=total systolic volume – myocardial volume. Stroke volume=diastolic cavity volume – systolic cavity volume, which then must be diastolic total volume – systolic total volume. The systolic decrease of the outer volume must then equal the stroke volume (SV), irrespective of the internal configuration changes of the cavity and myocardium, which are irrelevant. The longitudinal shortening (MAPSE) X the cross-sectional mitral annular area makes up the fraction of the SV due to long axis shortening (light red cylinder). The remaining systolic outer volume reduction must be due to outer diameter shortening (orange). (B)Cavity and myocardial volumes. both total and cavity volumes can be measured by diameter and length in systole and diastole as detailed in the online supplemental appendix. Myocardial volume is total volume – cavity volume in end-diastole and end-systole, respectively. myocardial systolic compression is myocardial diastolic – systolic volume. Stroke volume = end-diastolic – end systolic cavity volume. The cavity decreases due to decrease of both diameter and length (dark and light violet), but the inner diameter decrease (endocardial fractional shortening) is due to both outer diameter shortening, and myocardial thickening, the latter being mainly a function of myocardial longitudinal shortening. MAPSE, mean mitral annular plane systolic excursion.
Figure 2
Figure 2
Measurements for the volume calculations. Top left: wall length (WL) measurements taken as a straight line from the epicardial apex to the mitral annulus, shown for the septal and lateral WL measurements in the four-chamber view. Top right, the reconstructed M-modes from the same mitral annular points, showing the apical motion (MAPSE) equal to the left ventricular shortening. In the study, the mean of four walls from four-chamber to two-chamber views were used. MAPSE: mean mitral annular plane systolic excursion; IVSd: diastolic septum thickness; IVSs: systolic septum thickness; LVPWd: diastolic posterior wall; LVPWs: systolic posterior wall; LVIDd: internal diastolic (cavity) diameter; LVIDs: internal systolic (cavity) diameter.
Figure 3
Figure 3
(A) Blood pressure in the study population. Upper limits of high normal blood pressure (130/80 mm Hg) and lower limit for hypertension (140/90 mm Hg) are indicated by the dotted lines. The study shows both increasing mean BP with increasing age, as well as increasing proportions with hypertensive values. (B) Myocardial volume in relation to SBP and DBP and age. Here, cut-off values of 130/80 mm Hg (high normal) was used, but as seen in the text, the volumes differed only 2–4 mL for a cut-off of 140/90 mm Hg. There was no significant correlation of myocardial volume with age within BP groups. BP, blood pressure; DBP, diastolic blood pressure; SBP, systolic blood pressure.
Figure 4
Figure 4
Distribution of the model derived volumes. The distribution is skewed, while the basic measures were not, so the skewness may be due to the model. LV, left ventricular; LVEDV; left ventricular end-diastolic (cavity) volume; MVd; end-diastolic myocardial volume; SV; stroke volume.

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