Misinterpretation About the Contribution of the Left Ventricular Long-Axis Shortening to the Stroke Volume

Wandt, Birger; Brodin, Lärs-Åke; Lundbäck, Stig

doi:10.1152/ajpheart.00530.2006

Cited by 5 publications

(4 citation statements)

References 4 publications

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“…This can be explained by the finding that the diameter of the mitral annulus was one-half of the diameter of the midventricular part of the ventricle. This has been commented by those authors in a recent reply (5) to a letter to the editor (43) in American Journal of Physiology-Heart and Circulatory Physiology. In Fig.…”

Section: Discussionmentioning

confidence: 96%

“…Longitudinal function. AVPD has been recognized as an important contributor to LV pumping (13,16,19,22,25) and used as a measure of global LV function (1,2,37), but the magnitude of the longitudinal contribution to SV has been unclear (4,5,9,43). The current study showing that 60% of the SV is derived from AVPD (SV AVPD% ) differs from earlier studies using echocardiography, suggesting the SV AVPD% to be as high as 82% (9) and from the volume generated by the mitral annular movement, which has been reported to be 19% (4).…”

Section: Discussionmentioning

confidence: 99%

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Atrioventricular plane displacement is the major contributor to left ventricular pumping in healthy adults, athletes, and patients with dilated cardiomyopathy

Carlsson

Ugander

Mosén

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

222

215

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Previous studies using echocardiography in healthy subjects have reported conflicting data regarding the percentage of the stroke volume (SV) of the left ventricle (LV) resulting from longitudinal and radial function, respectively. Therefore, the aim was to quantify the percentage of SV explained by longitudinal atrioventricular plane displacement (AVPD) in controls, athletes, and patients with decreased LV function due to dilated cardiomyopathy (DCM). Twelve healthy subjects, 12 elite triathletes, and 12 patients with DCM and ejection fraction below 30% were examined by cine magnetic resonance imaging. AVPD and SV were measured in long- and short-axis images, respectively. The percentage of the SV explained by longitudinal function (SV(AVPD%)) was calculated as the mean epicardial area of the largest short-axis slices in end diastole multiplied by the AVPD and divided by the SV. SV was higher in athletes [140 +/- 4 ml (mean +/- SE), P = 0.009] and lower in patients (72 +/- 7 ml, P < 0.001) when compared with controls (116 +/- 6 ml). AVPD was similar in athletes (17 +/- 1 mm, P = 0.45) and lower in patients (7 +/- 1 mm, P < 0.001) when compared with controls (16 +/- 0 mm). SV(AVPD%) was similar both in athletes (57 +/- 2%, P = 0.51) and in patients (67 +/- 4%, P = 0.24) when compared with controls (60 +/- 2%). In conclusion, longitudinal AVPD is the primary contributor to LV pumping and accounts for approximately 60% of the SV. Although AVPD is less than half in patients with DCM when compared with controls and athletes, the contribution of AVPD to LV function is maintained, which can be explained by the larger short-axis area in DCM.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Atrioventricular plane displacement is the major contributor to left ventricular pumping in healthy adults, athletes, and patients with dilated cardiomyopathy

Carlsson

Ugander

Mosén

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

222

215

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“…The portion of the LV stroke volume (LVSV) generated by the longitudinal function of the AVPD (LVSV AVPD ) has been studied by echocardiography (9,23,35). Recently, in this journal, there has been a debate regarding the LVSV AVPD (3,4,38). The measurements by Carlhall et al focused on the volume enclosed by the mitral annular movement during the cardiac cycle (3), and the authors conclude in their reply that this is not equal to the LVSV AVPD (4).…”

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confidence: 99%

The quantitative relationship between longitudinal and radial function in left, right, and total heart pumping in humans

Carlsson

Ugander²,

Heiberg³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

172

179

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The total heart volume variation (THVV) during systole has been proposed to be caused by radial function of the ventricles, but definitive data for both ventricles have not been presented. Furthermore, the right ventricle (RV) has been suggested to have a greater longitudinal pumping component than the left ventricle (LV). Therefore, we aimed to compare the stroke volume (SV) generated by radial function to the volume variation of the left, right, and total heart. To do this, we also needed to develop a new method for measuring the contribution of the longitudinal atrioventricular plane displacement (AVPD) to the RVSV (RVSV(AVPD)). For our study, 11 volunteers underwent cine MRI in the short- and long-axis planes and MRI flow measurement in all vessels leading to and from the heart. The left, right, and total heart showed correlations between volume variation from flow measurements and radial function calculated as SV minus the longitudinal function (r = 0.81, P < 0.01; r = 0.80, P < 0.01; and r = 0.92, P < 0.001, respectively). Compared with the LV, the RV had a greater AVPD (23.4 +/- 0.8 vs. 16.4 +/- 0.5 mm), center of volume movement (13.0 +/- 0.7 vs. 7.8 +/- 0.4 mm), and, RVSV(AVPD) (82 +/- 2% vs. 60 +/- 2%) (P < 0.001 for all). We found that THVV is predominantly caused by radial function of the ventricles. Longitudinal AVPD accounts for approximately 80% of the RVSV, compared with approximately 60% for the LVSV. This difference explains the larger portion of THVV found on the left side of the heart.

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“…The discrepancy with earlier reports suggesting lower values (3) mostly depends on the use of epicardial short-axis areas in the calculation of the stroke volume generated by AVPD. This approach takes into account that systolic longitudinal shortening, assuming myocardial incompressibility, leads to a redistribution of myocardial volume characterized by radial thickening, thus contributing to LV pumping (6).…”

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confidence: 99%

What is the actual contribution of atrioventricular plane displacement to left ventricular stroke volume?

Ballo¹,

Bocelli²,

Mondillo³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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TO THE EDITOR: In the recent article by Carlsson et al. (4), the authors found that left atrioventricular plane displacement (AVPD) accounted for 60% of left ventricular (LV) stroke volume. The discrepancy with earlier reports suggesting lower values (3) mostly depends on the use of epicardial short-axis areas in the calculation of the stroke volume generated by AVPD. This approach takes into account that systolic longitudinal shortening, assuming myocardial incompressibility, leads to a redistribution of myocardial volume characterized by radial thickening, thus contributing to LV pumping (6).A major issue in the interpretation of these findings is that the study included only subjects on opposite sides of the spectrum of LV systolic function, i.e., healthy individuals and athletes with normal systolic performance, and patients with advanced dilated cardiomyopathy and severely depressed systolic performance (ejection fraction, 22 Ϯ 2%). In these subjects, longitudinal and circumferential systolic functions were likely to be either both preserved or both markedly impaired, and this may partially explain the similarity between groups in terms of AVPD contribution to LV stroke volume. However, caution is required in extending the conclusions of the study to patients with intermediate degrees of systolic impairment. We have recently shown that a depression in systolic longitudinal function precedes that in circumferential function even when the latter is evaluated at the midwall, since both M-mode annular excursion and tissue Doppler-derived peak systolic annular velocity are related to midwall indexes by inverse exponential functions (1). Also, according to these relations, the relative decrease in longitudinal indexes over the range of mild to moderate systolic dysfunction is higher than that in circumferential indexes. As a consequence, many patients in the early and middle stages of systolic dysfunction may show even considerably reduced long-axis systolic annular excursion, despite a relative preservation of circumferential performance. For instance, based on our nonlinear models, a decrease in annular excursion from 15 to 10 mm (33.3% relative reduction) corresponded to a decrease in midwall shortening from 17.9% to 15.6% and in load-adjusted circumferential contractility from 96.3% to 83.3% (12.7% and 13.5% relative reduction, respectively). When we consider that systolic annular excursion is the primary determinant of LV long-axis excursion volume (5), a consistently lower contribution of AVPD to LV pumping is reasonably expectable in these subjects compared with normal individuals or patients with severe systolic impairment. Moreover, isolated longitudinal systolic dysfunction is often observed in the presence of normal LV diameters and wall thickness (2), so that the compensative mechanism due to increased short-axis epicardial area-allowing the maintenance of long-axis systolic excursion volume in advanced dilated cardiomyopathy-is not present in most of these patients.Based on these considerations, the ...

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Misinterpretation About the Contribution of the Left Ventricular Long-Axis Shortening to the Stroke Volume

Cited by 5 publications

References 4 publications

Atrioventricular plane displacement is the major contributor to left ventricular pumping in healthy adults, athletes, and patients with dilated cardiomyopathy

Atrioventricular plane displacement is the major contributor to left ventricular pumping in healthy adults, athletes, and patients with dilated cardiomyopathy

The quantitative relationship between longitudinal and radial function in left, right, and total heart pumping in humans

What is the actual contribution of atrioventricular plane displacement to left ventricular stroke volume?

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