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Left Ventricular Systolic‐Diastolic Coupling: Insight from Magnetic Resonance Dobutamine Stress

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Left ventricular systolic and diastolic function are intrinsically linked, such that diastolic relaxation is influenced by the preceding systolic contraction – similar to how a springs recoil to its original shape is influenced by the degree of compression. Several clinical investigations have proposed quantifying the ratio between diastolic and systolic function to assess the coupling efficiency between the two, however, these cross‐sectional comparisons may be influenced by additional confounding factors, such as differences in tissue characteristics. Therefore, to extend our understanding, and directly examine the relationship between left ventricular systolic and diastolic coupling, we performed cardiac magnetic resonance imaging in six healthy volunteers (4F/2M, 22 ± 3 years, 24.4 ± 3.0 kg/m2) at rest and during low‐dose intravenous dobutamine infusion (2 µg/kg/min) to increase cardiac inotropy without affecting other, potentially confounding, regulators of diastolic function. Systolic and diastolic function was measured using gold‐standard tissue tagging, from three evenly spaced short axis images spanning the left ventricle from base to apex. As expected, dobutamine infusion increased peak circumferential strain (‐19.8 ± 1.6 % vs ‐21.3 ± 2.0 %, p = 0.002), systolic circumferential strain rate (CSRs: ‐96 ± 2 %/s vs ‐117 ± 7 %/s, p = 0.001), peak twist (8.2 ± 0.9 ° vs 10.7 ± 1.1 °, p = 0.002) and peak rate of systolic twist (TR: 40 ± 7 °/s vs 58 ± 8 °/s, p = 0.004). Independent of any changes in heart rate (59 ± 9 bpm vs 58 ± 9 bpm, p = 0.303) or end‐diastolic volume (171 ± 26 mL vs 170 ± 24 mL, p = 0.882), early diastolic circumferential strain rate (CSRd: 141 ± 15 %/s vs 163 ± 9 %/s, p = 0.019) and peak untwisting rate (UTR: ‐67 ± 24 °/s vs ‐88 ± 16 °/s, p = 0.018) subsequently increased. As a result, the ratio between diastolic and systolic measurements remained unchanged (CSRd/CSRs: 1.47 ± 0.14 vs 1.40 ± 0.15, p = 0.266; UTR/TR: 1.69 ± 0.54 vs 1.57 ± 0.37, p = 0.190). Taken together, these data support a growing body of evidence linking left ventricular systolic function with subsequent early diastolic relaxation and suggest that future investigations examining diastolic function should consider the influence of preceding systolic contractions.
Title: Left Ventricular Systolic‐Diastolic Coupling: Insight from Magnetic Resonance Dobutamine Stress
Description:
Left ventricular systolic and diastolic function are intrinsically linked, such that diastolic relaxation is influenced by the preceding systolic contraction – similar to how a springs recoil to its original shape is influenced by the degree of compression.
Several clinical investigations have proposed quantifying the ratio between diastolic and systolic function to assess the coupling efficiency between the two, however, these cross‐sectional comparisons may be influenced by additional confounding factors, such as differences in tissue characteristics.
Therefore, to extend our understanding, and directly examine the relationship between left ventricular systolic and diastolic coupling, we performed cardiac magnetic resonance imaging in six healthy volunteers (4F/2M, 22 ± 3 years, 24.
4 ± 3.
0 kg/m2) at rest and during low‐dose intravenous dobutamine infusion (2 µg/kg/min) to increase cardiac inotropy without affecting other, potentially confounding, regulators of diastolic function.
Systolic and diastolic function was measured using gold‐standard tissue tagging, from three evenly spaced short axis images spanning the left ventricle from base to apex.
As expected, dobutamine infusion increased peak circumferential strain (‐19.
8 ± 1.
6 % vs ‐21.
3 ± 2.
0 %, p = 0.
002), systolic circumferential strain rate (CSRs: ‐96 ± 2 %/s vs ‐117 ± 7 %/s, p = 0.
001), peak twist (8.
2 ± 0.
9 ° vs 10.
7 ± 1.
1 °, p = 0.
002) and peak rate of systolic twist (TR: 40 ± 7 °/s vs 58 ± 8 °/s, p = 0.
004).
Independent of any changes in heart rate (59 ± 9 bpm vs 58 ± 9 bpm, p = 0.
303) or end‐diastolic volume (171 ± 26 mL vs 170 ± 24 mL, p = 0.
882), early diastolic circumferential strain rate (CSRd: 141 ± 15 %/s vs 163 ± 9 %/s, p = 0.
019) and peak untwisting rate (UTR: ‐67 ± 24 °/s vs ‐88 ± 16 °/s, p = 0.
018) subsequently increased.
As a result, the ratio between diastolic and systolic measurements remained unchanged (CSRd/CSRs: 1.
47 ± 0.
14 vs 1.
40 ± 0.
15, p = 0.
266; UTR/TR: 1.
69 ± 0.
54 vs 1.
57 ± 0.
37, p = 0.
190).
Taken together, these data support a growing body of evidence linking left ventricular systolic function with subsequent early diastolic relaxation and suggest that future investigations examining diastolic function should consider the influence of preceding systolic contractions.

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