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Does glutamate influence myocardial and peripheral tissue metabolism after aortic valve replacement for aortic stenosis?
Linköpings universitet, Institutionen för medicin och hälsa, Thoraxkirurgi. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för medicin och hälsa, Thoraxkirurgi. Linköpings universitet, Hälsouniversitetet.
Division of Clinical Physiology, Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden.
Linköpings universitet, Institutionen för medicin och hälsa, Thoraxkirurgi. Linköpings universitet, Hälsouniversitetet.
2006 (Engelska)Ingår i: Clinical Nutrition, ISSN 0261-5614, E-ISSN 1532-1983, Vol. 25, nr 6, s. 913-922Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background & aims

Glutamate plays an important role for myocardial metabolism in association with ischaemia. Patients with coronary artery disease characteristically demonstrate increased uptake of glutamate. Improved recovery of myocardial metabolism and haemodynamic state after coronary surgery has been reported in patients treated with glutamate infusion. However, the effect of glutamate has not been studied after other cardiac surgical procedures. In addition, the effects of glutamate on peripheral tissue metabolism remain to be described.

Methods

Twenty patients undergoing surgery for aortic stenosis were studied after randomisation to blinded infusion of glutamate or saline during 1 h immediately after skin closure. Myocardial and leg tissue metabolism were assessed with organ balance techniques.

Results

Postoperative glutamate infusion induced a marked increase in myocardial and leg tissue uptake of glutamate. This was associated with a significant uptake of lactate in the heart. The negative arterial–venous differences of amino acids and free fatty acids across the leg were significantly smaller in the glutamate group. Haemodynamic state remained stable and did not differ between groups.

Conclusion

The heart and peripheral tissues consumed the exogenously administered glutamate after surgery for aortic stenosis. Potentially favourable effects of glutamate on myocardial and peripheral tissue metabolism are suggested.

Ort, förlag, år, upplaga, sidor
2006. Vol. 25, nr 6, s. 913-922
Nyckelord [en]
Glutamate; Myocardial metabolism; Humans; Aortic stenosis; Surgery
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:liu:diva-14022DOI: 10.1016/j.clnu.2006.04.002OAI: oai:DiVA.org:liu-14022DiVA, id: diva2:22475
Tillgänglig från: 2006-09-28 Skapad: 2006-09-28 Senast uppdaterad: 2017-12-13
Ingår i avhandling
1. Surgery for aortic stenosis: with special reference to myocardial metabolism, postoperative heart failure and long-term outcome
Öppna denna publikation i ny flik eller fönster >>Surgery for aortic stenosis: with special reference to myocardial metabolism, postoperative heart failure and long-term outcome
2006 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Postoperative heart failure (PHF) remains a major determinant of the outcome after cardiac surgery. However, characteristics of and risk factors for PHF after valve surgery have received little attention.

Post-ischaemic disturbances of myocardial metabolism that may contribute to PHF and are amenable to metabolic treatment have been identified early after coronary surgery (CABG). Knowledge derived from these studies may not be applicable to other patient groups. We therefore studied myocardial energy metabolism in 20 elective patients undergoing aortic valve replacement (AVR) for isolated aortic stenosis (AS). The metabolic studies indicated that myocardial oxidative metabolism had not fully recovered when the procedure was completed. Free fatty acids were the only major substrates taken up by the heart. Signs of preoperative and postoperative metabolic adaptation with substantial uptake of glutamate, previously demonstrated in patients with coronary artery disease, were found. Postoperative infusion of glutamate, (2 mL/kg body weight and hour of 0.125 M solution) based on assessment of myocardial glutamate requirements in CABG patients, resulted in a two-fold increase in myocardial glutamate uptake and a seven-fold increase in AV differences across the leg. This was associated with a significant myocardial uptake of lactate and metabolic changes in the leg suggesting mitigation of net amino acid loss and peripheral tissue lipolysis.

Characteristics of and risk factors for PHF were evaluated in 398 patients undergoing isolated AVR for AS from 1 January 1995 to 31 December 2000. These were compared with 398 patients, matched for age and sex, undergoing on-pump isolated CABG. Forty-five AVR and 47 CABG patients fulfilled criteria for PHF and these were studied in detail. PHF usually presented at weaning from cardiopulmonary bypass. After CABG it was closely associated with preoperative ischaemic events and intraoperatively acquired myocardial infarction. Potential causes and eliciting events of PHF after AVR for AS were obvious only in one-third of the patients. Risk factors for PHF after AVR for AS indicated either pre-existing myocardial dysfunction, increased right or left ventricular after-load, or intraoperatively acquired myocardial injury. PHF was associated with high early mortality after CABG, whereas the consequences of PHF after AVR for AS became evident only with time, resulting in a 42% five-year mortality. Although PHF had a different temporal impact on late mortality after CABG and AVR for AS, it emerged as the statistically most significant risk factor for mortality occurring within 5 years from surgery both after AVR for AS and after CABG. Potential implications of our findings include needs for greater focus on preoperative surveillance of patients with AS for optimal timing of surgery, mitigation of intraoperatively acquired myocardial injury and tailoring of treatment for PHF. Furthermore, the findings have implications for long-term follow up of AS patients after surgery.

Ort, förlag, år, upplaga, sidor
Institutionen för medicin och vård, 2006
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 952
Nyckelord
Aortic stenosis, Surgery, Postoperative heart failure, Long-term outcome, Metabolism
Nationell ämneskategori
Klinisk vetenskap
Identifikatorer
urn:nbn:se:liu:diva-7471 (URN)91-85497-89-4 (ISBN)
Disputation
2006-06-09, Berzeliussalen, Campus US, Linköpings Universitet, Linköping, 13:00 (Engelska)
Opponent
Handledare
Tillgänglig från: 2006-09-28 Skapad: 2006-09-28 Senast uppdaterad: 2012-01-30

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Vánky, Farkas B.Håkansson, ErikSvedjeholm, Rolf

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