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Troponin-I release after cardiac surgery with different surgical techniques and post-operative neurological outcomes
Norzeihan Jan Bappu1, Panangipalli Venugopal, Akhshay Kumar Bisoi
1Department of Cardiothoracic Surgery, The Royal Infirmary of Edinburgh, Little France, Crescent, Old Dalkeith Road, Edinburgh, Scotland, United Kingdom. jan.bappu@luht.scot.nhs.uk
Insights
This study found no significant short-term neurological or cognitive deficits after coronary artery bypass graft (CABG) surgery, regardless of surgical technique. Troponin-I release correlated with graft number, not surgical approach, and did not predict short-term outcomes.
Area of Science:
- Cardiology
- Neurology
- Cardiac Surgery
Background:
- Cerebral hypoperfusion during cardiopulmonary bypass (CPB) surgery is linked to post-operative neurological deficits.
- Cardiac biomarkers like troponin-I are used to predict myocardial injury.
Purpose of the Study:
- To investigate troponin-I release in off-pump vs. on-pump coronary artery bypass graft (CABG) surgery.
- To determine the relationship between troponin-I release and post-operative neurological/cognitive outcomes.
Main Methods:
- Prospective study of 44 adult patients undergoing CABG, divided into on-pump (n=22) and off-pump (n=22) groups.
- Troponin-I levels measured using a 1-step enzyme immunoassay.
- Neurological assessment via NIH Stroke Scale; cognitive function assessed using modified Weschler Memory Scale.
Main Results:
- Troponin-I levels rose significantly post-operatively in both groups, with no significant difference between on-pump and off-pump techniques (p=0.124).
- Troponin-I release showed a significant correlation with the number of grafts used, irrespective of surgical technique.
- No patients exhibited neurological or cognitive deficits at 3 or 7 days post-operatively.
Conclusions:
- No significant short-term neurological or cognitive dysfunction was observed post-CABG surgery.
- Troponin-I release, while correlated with graft number, did not predict short-term neurological outcomes in this study.
Abstract:
Cerebral hypoperfusion during cardiopulmonary bypass surgery has been thought to be a factor in the aetiology of brain damage with evidence of post-operative neurological deficits. Cardiac-specific biomarkers such as troponin-I, troponin-T and CK-MB have been used extensively to predict myocardial injury and ischaemia. This prospective study investigated the level of troponin-I release in both off-pump and CPB-technique CABG surgery, as well as postulated a relationship of troponin release and post-operative neurological outcome. A total of 44 adult patients undergoing coronary artery bypass graft (CABG) were enrolled into either an off-pump or on-pump groups, with 22 patients participating in each. Group A (on-pump) underwent myocardial revascularisation with CPB and cardioplegic arrest, while Group B (off pump) underwent beating heart surgery. The measurement of troponin-I is a 1-step enzyme immunoassay method, with specificity and sensitivity set at 0.4 ug/mL. Neurological assessment was done using the NIH Stroke Scale, and neuropsychologic assessment was assessed on cognitive function using modified Weschler Memory Scale, for which scores were standardized to achieve a composite measure of concentration. A set of statistical analysis was done to correlate troponin-I release with different surgical techniques of CPB and OPCAB. Although each independent technique showed a marked rise of troponin-I from baseline to 6 hours post-operatively, the difference in troponin release was not significant between the 2 groups at specified time intervals (p=0.124). There was however a significant correlation of troponin-I release with the number of grafts used in the surgery, irrespective of the type of grafts or surgical technique. None of the patients in either group showed any neurological or cognitive deficits presenting at day 3 and day 7 post-operatively. The findings of this study demonstrate that there is no significant short-term cognitive or neurological dysfunctions post-operatively, as indicated by troponin-I release in assessing the severity of myocardial injury.
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