J Thorac Cardiovasc Surg 1998;116:368
© 1998 Mosby, Inc.
Impact of coronary venous pressure elevation on left ventricular function: Implications for the Fontan circulation
Uwe Mehlhorn, MD
To the Editor:
I read with great interest the article by Klautz and associates
1 on the effects of coronary venous pressure elevation on left ventricular function. They are to be congratulated on their data collection and analysis. However, in my opinion their model to mimic the clinical setting of the Fontan circulation suffers from a major flaw. In their model, coronary venous return into the right atrium and right ventricle was drained into the venous side of the right heart bypass circuit via a height-adjustable reservoir, and both caval veins were cannulated, snared, and drained directly into the venous side of the right heart bypass circuit. 1 Thus only the right atrium and right ventricle were subjected to elevated pressures, but neither superior nor inferior vena caval pressure (i.e., central venous pressure) was elevated. 1 In the Fontan circulation, however, not only is right atrial pressure elevated but also central venous pressure is substantially increased. This is important for the following reasons. Elevated right atrial or coronary sinus pressure increases myocardial microvascular pressure, thus increasing fluid filtration into the myocardial interstitium. 2,3 As a result, fluid removal from the cardiac interstitium via myocardial lymphatics increases to minimize myocardial edema formation. 2,3 Because the myocardial lymphatics ultimately drain into the central venous system via the thoracic duct, central venous pressure elevation impedes myocardial lymph drainage, resulting in substantial myocardial edema formation associated with left ventricular dysfunction. 2 These mechanisms have been demonstrated by Laine and Allen, 2 who determined the impact of simultaneous coronary sinus and central venous pressure elevation on myocardial lymph flow rate, myocardial edema formation, and left ventricular performance in dogs. In addition, Davis and coworkers 4 showed in a dog model that elevation of right heart and central venous pressure induced by only 3 hours of pulmonary artery banding resulted in an increase in left ventricular myocardial water content associated with both systolic and diastolic left ventricular dysfunction. These data suggest that the model used by Klautz and colleagues 1 may be of limited value for determining the impact of the Fontan circulation on left ventricular function because central venous pressure was not elevated.
My second comment concerns the study protocol. The authors state: "After reaching a new level of coronary venous pressure, we waited for 15 minutes before taking new measurements." 1 Fifteen minutes were probably not sufficient to reach a new steady state, and thus the authors might have missed subsequent left ventricular dysfunction induced by coronary venous pressure elevation. In a recent, meticulously conducted study that was not cited by the authors, Pratt and coworkers 5 demonstrated that 1 hour of isolated coronary sinus pressure elevation to 25 mm Hg did not result in left ventricular dysfunction. However, extending the period of coronary sinus pressure hypertension to 3 hours resulted in myocardial edema associated with decreased left ventricular end-systolic elastance and preload-recruitable stroke work, as well as prolonged time constant of active relaxation. 5 These data suggest that factors other than potential coronary blood flow impairment may be responsible for left ventricular dysfunction resulting from coronary sinus hypertension, such as compromised myocardial fluid balance, as demonstrated by previous work. 2-5 Specifically, these data do not support the implications by Klautz and associates 1 that diverting the coronary sinus to the left atrium during Fontan-type operations is not desirable.
Department of Cardiothoracic SurgeryUniversity of Cologne,
Joseph-Stelzmann-Str. 9,
50924 Cologne, Germany
References
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Klautz RJM, van Rijk-Zwikker GL, Steendijk P, Wilde J, Teitel DF, Baan J. Acute elevation of coronary venous pressure does not affect left ventricular contractility in the normal and stressed swine heart: implications for the Fontan operation. J Thorac Cardiovasc Surg 1997;114:560-7.[Abstract/Free Full Text]
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Laine GA, Allen SJ. Left ventricular myocardial edema: lymph flow, interstitial fibrosis, and cardiac function. Circ Res 1991;68:1713-21.[Abstract/Free Full Text]
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Mehlhorn U, Davis KL, Laine GA, Geissler HJ, Allen SJ. Myocardial fluid balance in acute hypertension. Microcirculation 1996;3:371-8.[Medline]
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Davis KL, Mehlhorn U, Laine GA, Allen SJ. Myocardial edema, left ventricular function, and pulmonary hypertension. J Appl Physiol 1995;78:132-7.[Abstract/Free Full Text]
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Pratt JW, Schertel ER, Schaefer SL, et al. Acute transient coronary sinus hypertension impairs left ventricular function and induces myocardial edema. Am J Physiol 1996;271:H834-41.[Abstract/Free Full Text]
