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Eur J Cardiothorac Surg 2006;30:689
© 2006 Elsevier Science NL
Letters to the Editor |
Department of Anaesthesiology and Intensive Care, University of Muenster, Albert-Schweitzer-Str. 33, 48149 Muenster, Germany
Received 16 May 2006; accepted 19 July 2006.
* Corresponding author. Tel.: +49 251 8347255; fax: +49 251 8348667. (Email: lange-m{at}anit.uni-muenster.de).
Key Words: Vasopressin Norepinephrine Off-pump coronary bypass Milrinone
Jeon et al. [1] report that both norepinephrine and vasopressin restored the milrinone-induced decrease in systemic vascular resistance in patients undergoing off-pump coronary artery bypass surgery. Interestingly, only low-dose vasopressin decreased the pulmonary vascular resistance/systemic vascular resistance ratio. The conclusion that vasopressin is superior to norepinephrine in restoring arterial blood pressure in patients with pulmonary hypertension and right heart failure [1] may not be entirely correct and should be reconsidered due to three important aspects:
Firstly, the vasopressin doses used in the presented study (up to 0.16 U/min) [1] markedly exceeded the doses (0.010.04 U/min) currently recommended for the treatment of patients with septic shock related to relative vasopressin deficiency [2,3].
In addition, the increase in mean arterial pressure (MAP) in the norepinephrine group was stronger than in the vasopressin group (+29% vs +20%). This difference in goal-MAP indicates that the doses of norepinephrine and vasopressin were not equivalent [1].
Finally, previous experimental [4] and clinical trials [5] demonstrated that conventional vasopressors, such as norepinephrine, should not be replaced by vasopressin [3]. In this context it is noteworthy that pharmacological vasopressin doses needed to restore MAP to the same extent as norepinephrine were associated with increased gastric-arterial
gradients [4,5], most likely due to impaired splanchnic mucosal microcirculation.
In summary, it remains unclear if vasopressin is superior to norepinephrine in reversing milrinone-induced hypotension, especially because outcome variables were not determined in the study by Jeon et al. [1].
Footnotes
The authors of the original paper [1] were invited to reply to this Letter to the Editor but they did not respond.
References
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