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Effects of arterial distensibility on left ventricular ejection in the depressed contractile state
Y Maruyama1, O Nishioka, E Nozaki
1First Department of Internal Medicine, Fukushima Medical College, Japan.
Insights
Reduced arterial distensibility worsens cardiac output, especially when cardiac dysfunction is present. This effect is more pronounced in states of depressed cardiac function, impacting stroke work and overall cardiac output.
Area of Science:
- Cardiovascular Physiology
- Hemodynamics
- Cardiac Mechanics
Background:
- Arterial distensibility is a key determinant of ventricular afterload and cardiac performance.
- Understanding its impact across different contractile states is crucial for managing cardiovascular diseases.
Purpose of the Study:
- To investigate the influence of altered arterial distensibility on ventricular ejection dynamics.
- To assess these effects under conditions of normal, regionally depressed, globally depressed, and globally augmented ventricular contractility.
Main Methods:
- Utilized excised, perfused, and paced canine hearts.
- Manipulated arterial compliance (arterial distensibility) to low (0.4 x 10(-4) dyne-1.cm5) and high (2.3 x 10(-4) dyne-1.cm5) values.
- Introduced different contractile states: control, left circumflex coronary artery ligation, lignocaine administration, and dobutamine infusion.
Main Results:
- Decreased arterial distensibility significantly reduced cardiac output, particularly in the ligation (75% of control) and lignocaine (82% of control) groups.
- Stroke work decreased substantially (63-70%) with reduced arterial distensibility in the ligation and lignocaine groups.
- The deleterious effect on cardiac output was most pronounced when cardiac dysfunction was present.
Conclusions:
- Reduced arterial distensibility exacerbates the decline in cardiac output in the presence of cardiac dysfunction.
- This phenomenon is linked to increased end-ejection pressure and diminished ventricular ejection dynamics, particularly with afterload dependency.
Objective:
The aim was to evaluate the effects of arterial distensibility on ventricular ejection in various ventricular contractile states: (1) control; (2) a regionally depressed contractile state due to left circumflex coronary artery occlusion (ligation); (3) a globally depressed contractile state induced by lignocaine (lignocaine); and (4) a globally augmented contractile state due to dobutamine infusion (dobutamine).
Methods:
Arterial compliance was decreased from 2.3 x 10(-4) dyne-1.cm5 (C2.3) to 0.4 x 10(-4) dyne-1.cm5 (C0.4), maintaining other afterload components and left ventricular end diastolic pressure constant. Nine excised perfused and paced canine hearts, supported from donor dogs, were used.
Results:
In control, ligation, lignocaine, and dobutamine groups, the difference in cardiac output between the compliance values of C0.4 and C2.3 was 124(SEM 32), 204(36), 163(33), and 130(24) ml, respectively. Thus cardiac output at C0.4, as a percentage of that at C2.3, was 88(2.8)% (control), 75(2.9)% (ligation), 82(2.9)% (lignocaine), and 88(2.4)% (dobutamine), respectively: control v ligation, and lignocaine v ligation, p < 0.001; control v lignocaine, and dobutamine v ligation, p < 0.01. Stroke work at C0.4 decreased in the ligation group (63%, p < 0.001) and in the lignocaine group (70%, p < 0.001).
Conclusions:
When cardiac dysfunction is already present, decreased arterial distensibility has a further deleterious effect on cardiac output. This may be due to the fact that the pressure at the end of ejection is higher and as a result the change in dimension during ejection is considerably reduced, especially in cases with depressed cardiac function caused by afterload dependency.