Influence of atrioventricular interaction on mitral valve closure and left ventricular isovolumic contraction measured by tissue Doppler imaging.

This paper focuses on investigating how the atrioventricular (AV) interaction influences mitral valve closure (MVC) and left ventricular (LV) isovolumic contraction in the heart. The research demonstrated that depending upon the AV delay, the mitral valve closure can be caused either directly by the atrial relaxation (atriogenic) or by LV contraction (ventriculogenic), bringing about significant changes in the velocity and acceleration of the LV isovolumic contraction.

Study Method

• The research employed a horse model due to its low heart rate and naturally long AV delay which makes it an ideal candidate for the study. The model was used to explore the relationship between AV delay, MVC, and LV isovolumic contraction.
• Six horses were evaluated across three heart rhythm scenarios – during normal sinus rhythm, during right ventricular pacing without preceding atrial contraction, and dual-chamber pacing at AV delays varying from 150 to 350 ms, maintained at a constant rate.
• Data was gathered through the right parasternal 4-chamber views. Measurement of MVC was performed using anatomic M-mode while radial tissue Doppler was used for measuring LV pre-ejection velocity and isovolumic acceleration.

Findings From the Study

• Two positive peaks in pre-ejection velocity were observed during sinus rhythm and when AV delays were long (≥300 ms). The first peak, identified as LV recoil, happened during atrial relaxation and typically occurred before MVC. The second peak, coinciding with LV isovolumic contraction, took place after MVC.
• The presence of these two peaks implied that initially, MVC was caused by atrial relaxation and this event was then followed by true isovolumic contraction.
• In contrast, when AV delays were short (<300 ms) and during right ventricular pacing, MVC occurred considerably late with only one observable pre-ejection peak. In this scenario, the research inferred that MVC was coinciding with the end of this single peak, suggesting that MVC was caused due to LV contraction.
• Significant increase in the peak velocity and isovolumic acceleration was observed because the mitral valve was in an open state at the commencement of LV contraction.

Conclusion

• The research concluded that the cause of MVC—atriogenic or ventriculogenic—depends on the AV delay. This difference in the onset mechanism of MVC leads to significant alterations in the peak pre-ejection velocity and isovolumic acceleration of the left ventricle.