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Rapid enzyme release from acutely infarcted myocardium after early thrombolytic therapy: washout or reperfusion
A van der Laarse1, E E van der Wall, R C van den Pol
1Department of Cardiology, University Hospital Leiden, The Netherlands.
Insights
Early thrombolytic therapy accelerates enzyme release in acute myocardial infarction (AMI) patients, indicating faster infarct development. This accelerated process, lasting 40-50 hours, is independent of infarct size in reperfused cases.
Area of Science:
- Cardiology
- Biochemistry
- Medical Research
Background:
- Acute myocardial infarction (AMI) management involves assessing infarct progression.
- Plasma enzyme activity, specifically alpha-hydroxybutyrate dehydrogenase (HBDH), is a marker for myocardial damage.
- Early intracoronary thrombolytic therapy is a treatment option for AMI.
Purpose of the Study:
- To analyze the rate of plasma enzyme appearance in patients with AMI.
- To correlate enzyme release kinetics with thrombolytic therapy, area at risk, and infarct size.
- To compare enzyme release patterns between thrombolytic and conventional therapy groups.
Main Methods:
- Randomized study of 448 patients with AMI.
- Serial measurement of plasma enzyme activities, focusing on HBDH.
- Calculation of cumulative HBDH activity over 24, 48, and 72 hours (Q24, Q48, Q72) to determine infarct size and enzyme appearance rate (Q24/Q72).
- Analysis based on "intention to treat" principle.
Main Results:
- The rate of HBDH appearance (Q24/Q72) was significantly higher in the thrombolysis group (0.653) compared to the conventional therapy group (0.504) (p < 0.001).
- In the thrombolysis group, Q24/Q72 was independent of infarct size, while in the control group, it was negatively correlated with infarct size (r = -0.26, p < 0.001).
- Mean Q72 values were larger in the control group than in the thrombolysis group, suggesting smaller infarcts with thrombolysis.
Conclusions:
- Reperfused myocardial infarctions exhibit an accelerated time course of infarct development compared to unreperfused ones.
- This accelerated necrosis process lasts approximately 40 to 50 hours and is minimally influenced by infarct size.
- The acceleration of enzyme release due to reperfusion mirrors enzyme release from anoxic hearts upon reoxygenation.
Abstract:
In a randomized study on early intracoronary thrombolytic therapy in patients with acute myocardial infarction (AMI), serial plasma enzyme activities were measured to analyze the rate of enzyme appearance in plasma with reference to treatment allocation, area at risk, and infarct size. Cumulative activities of alpha-hydroxybutyrate dehydrogenase (HBDH) appearing in plasma in the first 24 hours (Q24), 48 hours (Q48), and 72 hours (Q72) were calculated to obtain infarct size (= Q72) and rate of HBDH appearance in plasma (= Q24/Q72). Analyzed on the basis of "intention to treat" in 448 patients with AMI, the mean Q24/Q72 value (+/- SEM) was 0.653 +/- 0.011 in 230 patients receiving thrombolytic therapy; this value was significantly (p less than 0.001) higher than that observed in 218 patients receiving conventional therapy (0.504 +/- 0.012). In the thrombolysis group Q24/Q72 was independent of infarct size, whereas in the control group Q24/Q72 was negatively correlated with infarct size (r = -0.26; p less than 0.001). Plotted against the sum of ST segment elevations at admission (sigma ST) mean Q24 values were similar in both treatment groups, but mean Q48 and especially Q72 values were larger in the control group than in the thrombolysis group. We conclude that: (1) in reperfused infarctions the time course for development of infarct is accelerated in comparison to unreperfused infarcts; (2) this accelerated process of necrosis lasts about 40 to 50 hours, a duration that is hardly influenced by infarct size; and (3) the reperfusion-induced acceleration of enzyme release resembles the reoxygenation-induced enzyme release from anoxic hearts.(ABSTRACT TRUNCATED AT 250 WORDS)