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Reduction of CK and CK-MB indexes of infarct size by intravenous nitroglycerin
Insights
Intravenous nitroglycerin reduces infarct size in acute myocardial infarction patients by decreasing creatine kinase (CK) and CK-MB release. Early and late interventions showed significant benefits in reducing myocardial damage.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Acute myocardial infarction (AMI) is a leading cause of mortality.
- Accurate assessment of infarct size is crucial for prognosis and treatment evaluation.
- Creatine kinase (CK) and its isoenzyme CK-MB are key biomarkers for myocardial damage.
Purpose of the Study:
- To investigate the effect of intravenous nitroglycerin on infarct size in patients with AMI.
- To evaluate the efficacy of nitroglycerin in both early and late intervention strategies.
Main Methods:
- 31 patients with AMI received intravenous nitroglycerin.
- Infarct size was calculated using serial CK and CK-MB isoenzyme measurements.
- Patients were divided into early (<8 hours) and late (>8 hours) intervention subgroups.
- Hemodynamic parameters were monitored regularly.
Main Results:
- Nitroglycerin significantly reduced peak CK and CK-MB levels and the rate of release.
- Calculated infarct size was significantly smaller in nitroglycerin-treated patients compared to controls (p < 0.05).
- Both early and late interventions demonstrated a reduction in infarct size.
- Nitroglycerin improved hemodynamic parameters, including reduced left ventricular filling pressure and increased cardiac output.
Conclusions:
- Intravenous nitroglycerin effectively reduces infarct size in AMI patients.
- Therapeutic benefits are observed regardless of whether treatment is initiated early or late after symptom onset.
- Nitroglycerin administration improves cardiac function and hemodynamics during AMI.
Abstract:
The effect of i.v. nitroglycerin administration on indexes of infarct size was examined in 31 patients with acute myocardial infarction. Serial creatine kinase (CK) and CK-MB isoenzyme determinations were used to calculate infarct size. Twenty-nine patients served as controls. Two subgroups of the study group were formed to evaluate differences between early and late intervention. In the first group (n = 22), continuous infusion of nitroglycerin over 48 hours was initiated within 8 hours (mean 4.5 hours) after the onset of symptoms. Peak CK activity for the nitroglycerin-treated patients (n = 9) in this subgroup was 544 U/1 vs 871 U/1 for the controls (n = 13) (p less than 0.05). The rate of CK release was reduced from 79 to 33 U/1.hr (58%), as was total CK and CK-MB release (p less than 0.02). Calculated infarct size was 69 gEq in the controls and 48 gEq in patients receiving nitroglycerin (CK-MB: 69 vs 43 gEq, p less than 0.05). In the late intervention subgroup, nitroglycerin therapy was begun more than 8 hours (mean 12.8 hours) after the onset of symptoms. Here, too, use of the agent was associated with lower peak CK and CK-MB levels as well as a reduction in calculated infarct size (p less than 0.05). Hemodynamic measurements, recorded every 4 hours, showed that nitroglycerin also reduced left ventricular filling pressure significantly and cardiac output increased. Blood pressure fell slightly, and systemic vascular resistance declined. The results indicate that i.v. nitroglycerin reduces CK and CK-MB release and thus calculated infarct size in both early and late intervention.