![]() ![]() Today rapid point-of-care analyzers are generally available, enabling fast measurement of lactate levels. However, long transport times between blood sampling and analysis may have led to falsely high results. For patients with myocardial infarction, circulating venous lactate levels have been shown to be increased. In patients with ischemic heart disease, the amount of lactate released by the myocardium has been shown to be related to the severity of coronary artery disease. When tissue perfusion is impaired during acute myocardial infarction, decreased oxygen delivery can induce muscle cells to preferentially use glycolysis and produce lactate from pyruvate, rather than oxidize pyruvate for mitochondrial energy production. One of the most frequent causes of circulatory shock is acute myocardial infarction. In patients with cardiogenic shock, several studies document marked elevations in circulating lactate. Blood lactate measurements can be used as an indicator of hemodynamic impairment and as a predictor of outcome in various forms of shock. The clinical value of circulating lactate has been extensively demonstrated in critical care medicine. Point-of-care measurement of arterial lactate at admission in patients with STEMI has the potential to improve acute risk stratification. In particular, acute mortality was related to admission lactates ≥1.8 mmol/L. Higher lactate levels were independently related with 30-day mortality and an overall worse response to percutaneous coronary intervention (PCI). In STEMI patients, impaired hemodynamics, worse TIMI flow and non-smoking were related to increased arterial lactate levels. An intra aortic balloon pump (IABP) was used more frequently in patients with higher lactate levels (4.2%, 7.6% and 14.7%). The latter group also showed lower blush grades and greater enzymatic infarct sizes. Mortality at 30 days in the three groups was 2.0%, 1.5% and 6.5%. Resultsįactors independently associated with higher lactate levels were hypotension, heart rate, thrombolysis in myocardial infarction (TIMI) flow 0 to 1, diabetes and non-smoking. We compared both baseline characteristics and outcome measures of the three lactate groups. The study population (n= 1,176) was divided into tertiles with lactate levels ≤1.1 (n = 410), 1.2 to 1.7 (n = 398) and ≥1.8 mmol/l (n = 368). To assess the relation of systemic arterial lactate levels in STEMI patients with clinical correlates at presentation in the catheterization laboratory, we measured arterial lactate levels with a rapid point-of-care technique, immediately following femoral sheath insertion. Little is known at the moment concerning the clinical correlates of systemic lactate in patients with ST-segment elevation myocardial infarction (STEMI). Blood lactate measurements can be used as an indicator of hemodynamic impairment and relate to mortality in various forms of shock. ![]()
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