A metabolic protective strategy could improve long-term survival in patients with LV-dysfunction undergoing CABG.
OBJECTIVE
Adverse outcome after CABG is closely related to postoperative heart failure precipitated by ischemia and myocardial infarction. Restrictive use of inotropes is therefore desirable. Patients with preoperative left ventricular dysfunction are a high-risk group in this respect. To reduce myocardial oxygen expenditure we evolved a metabolic strategy for perioperative care.


METHODS
Observational study on 104 consecutive patients with severe left ventricular dysfunction undergoing CABG. The metabolic strategy implied physiological measures to minimize myocardial oxygen expenditure including restrictive use of inotropes and specific measures such as extended CPB and metabolic support to facilitate myocardial recovery. Hemodynamic state was primarily assessed by mixed venous oxygen saturation (SvO(2)). Follow-up averaged 9.7+/-1.4 years.


RESULTS
LVEF was 0.30+/-0.05 (range 0.20-0.37) and 3.5+/-1.3 vessels were bypassed. Inotropes were used in 6.7% for weaning from CPB. Increase of s-creatinine by > or =50% compared to preoperative values was observed in 2.9%. Logistic EuroSCORE was 8.3% whereas observed 30-day mortality was 1.0%. Crude 5-year survival was 89.4%.


CONCLUSIONS
The metabolic strategy allowed restrictive use of inotropes and was associated with encouraging long-term survival. Renal function was well preserved suggesting that SvO(2) served as an adequate marker of circulation. Randomized trials with metabolic support are warranted.
Departments of Cardiothoracic Surgery and Cardiothoracic Anesthesia, Linköping Heart Center, Linköping University Hospital, Linköping University, Linköping, Sweden. rolf.svedjeholm@lio.se
Rolf
R
Svedjeholm
Mårten
M
Vidlund
Ingemar
I
Vanhanen
Erik
E
Håkanson
D000368:Aged; D002314:Cardioplegic Solutions / Q000627:therapeutic use*; D002315:Cardiopulmonary Bypass; D002316:Cardiotonic Agents / Q000627:therapeutic use; D001026:Coronary Artery Bypass / Q000009:adverse effects / Q000401:mortality; D004734:Energy Metabolism; D005260:Female; D005947:Glucose / Q000627:therapeutic use; D018698:Glutamic Acid / Q000008:administration & dosage; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D006801:Humans; D007328:Insulin / Q000627:therapeutic use; D053208:Kaplan-Meier Estimate; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000150:complications / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology / Q000601:surgery*; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D011188:Potassium / Q000627:therapeutic use; D020127:Recovery of Function; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D013318:Stroke Volume; D013548:Sweden; D013997:Time Factors; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology; D016277:Ventricular Function, Left
D002314:Cardioplegic Solutions; D002316:Cardiotonic Agents; D007328:Insulin; C030396:glucose-insulin-potassium cardioplegic solution; D018698:Glutamic Acid; D005947:Glucose; D011188:Potassium