Key result
Atriopulmonary bridge opening restores cardiac output by ~1 L/min after right coronary occlusion.
Why the study?
Recent research determined that cardiac suction occurs between systole and diastole, prompting analysis of left ventricular suction capacity after right ventricular exclusion via an atriopulmonary bridge.
Does excluding the dysfunctional right ventricle via an atriopulmonary bridge restore normal hemodynamic parameters through left ventricular suction in a canine model of ischemic right ventricular dysfunction?
Does excluding the dysfunctional right ventricle via an atriopulmonary bridge restore normal hemodynamic parameters through left ventricular suction in a canine model of ischemic right ventricular dysfunction?
Answers are grounded in this paper and cite their sources.
In a canine model of ischemic right ventricular dysfunction, bypassing the right ventricle via an atriopulmonary bridge restores normal hemodynamic parameters, demonstrating that active left ventricular suction can maintain right-sided circulation when pulmonary vascular resistance is low.
Introduction and Objective:Recent research has determined that the "cardiac suction" phase occurs between systole and diastole.The aim of this work was to analyze the suction capacity of the left ventricle after excluding the right ventricle through an atriopulmonary bridge.Methods: An atriopulmonary bridge was performed on six dogs, followed by right coronary artery occlusion to generate right ventricular dysfunction.Cardiac output (CO), cardiac index (CI), systolic index (SI), left ventricular stroke work index (LVSWI), right ventricular stroke work index (RVSWI), systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were evaluated using a Swan Ganz catheter.Recordings were acquired at baseline before any procedure, 60 minutes after right coronary occlusion with the atriopulmonary bridge connection closed and 60 minutes after opening the atriopulmonary connection.At the end of the experiment, coronary angiography and histological examination were performed to verify the right coronary occlusion.Results: Sixty minutes of coronary occlusion produced decreased CO (3.43 to 2.25 l/min), CI (5.22 to 3.39 l/m 2 ), SI (41.5 to 20.8 ml/beat/m2), LVSWI (53.3 to 14.4 g × m/beat/m 2 ), and RVSWI (1.61 to -1.97 g × m/beat/m 2 ).When the atriopulmonary bridge was opened, CO increased to 3.39 l/min (p<0.05),CI to 4.95 l/m 2 (p<0.05),SI to 45.1 ml/beat/m 2 (p<0.05),LVSWI to 40.8 g × m/beat/ m 2 (p<0.05) and RVSWI to 1.57 g × m/beat/m 2 (p<0.05), and right atrial pressure decreased from 10.6 to 3 mmHg (p<0.05) and PVR from 109 to 48.9 dyn/s/cm -5 (ns). Conclusion:As demonstrated by means of an atriopulmonary bridge, right ventricular dysfunction experimentally induced by ischemia is compensated by a left ventricular suction mechanism, restoring normal circulatory parameters.
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Trainini Jorge C (2019) studied Experimentally induced right ventricular dysfunction via right coronary artery occlusion (n=6). Atriopulmonary bridge connection opening (excluding the right ventricle) vs. Closed atriopulmonary bridge connection after 60 minutes of right coronary artery occlusion was evaluated on Cardiac output (l/min) at 60 minutes after opening the atriopulmonary connection (p=<0.05). Atriopulmonary bridge opening after right coronary occlusion restored cardiac output from 2.25 to 3.29 l/min (p<0.05) and reduced right atrial pressure from 10.16 to 3.00 mmHg (p<0.05).
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