Evaluation of intracoronary blood from obstructive vessel in patients of ST-elevation myocardial infarction undergoing PPCI()

OBJECTIVE: Information available on acid–base imbalance in ST-elevation myocardial infarction (STEMI) submitted to primary percutaneous intervention is limited and no data were present on intracoronary blood analysis, extracted from obstructed artery. METHODS: This was a prospective study conducted over 12 months in which STEMI patients presenting in emergency and undergoing primary percutaneous coronary intervention were included. Blood gas analysis of intracoronary arterial blood from obstructed vessel and peripheral arterial blood was performed. Patients in whom adequate intracoronary sample could not be obtained were excluded. Intracoronary and peripheral arterial blood gas measurements were correlated and relationship of intracoronary parameters were compared with clinical parameters, investigational markers and short-term outcome. RESULTS: The mean age of study population was 54.8 years and average symptom onset to door time was 162 min. On comparing intracoronary blood with peripheral blood arterial obtained, pH (95% confidence interval [CI] −0.01 to 0.02;p = 0.44), lactate (95% CI 0.03–0.1;p = 0.28), bicarbonate (95% CI 0.6–1.5;p = 0.64), pCO(2) (95% CI 1.1–2.4;p = 0.79) and pO(2) (95% CI 3.2–47.5; p = 0.06) were all found to be statistically insignificant. Intracoronary hyperlactatemia was present in patients presenting with higher symptom onset to door time (p = 0.025). Systolic blood pressure (SBP) (p = 0.03) was also significantly lower in patients who had high intracoronary lactate levels. CONCLUSION: The evaluation of intracoronary blood provides no additional information regarding the prognosis and short-term (30-day) outcome of the patients when compared with peripheral blood. However, there was a significant intracoronary hyperlactatemia in patients presenting late after symptom onset. SBP was also significantly less in patients with high intracoronary lactate, which signifies that predominant cause of hyperlactatemia was systemic hypoperfusion rather than local increase in lactate levels.