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Plasminogen activator inhibitor: a risk factor for myocardial infarction in diabetic patients
R P Gray1, J S Yudkin, D L Patterson
1Department of Medicine, University College and Middlesex School of Medicine, Whittington Hospital, London.
Insights
Diabetic patients admitted for acute myocardial infarction exhibit significantly higher plasminogen activator inhibitor activity. This impaired fibrinolytic activity may contribute to poor outcomes in diabetic individuals.
Area of Science:
- Cardiology
- Diabetology
- Thrombosis
Background:
- Diabetes mellitus is a known risk factor for cardiovascular disease.
- Diabetic patients often experience poorer outcomes following acute myocardial infarction (AMI).
- Fibrinolytic system dysfunction may play a role in the pathophysiology of AMI in diabetics.
Purpose of the Study:
- To compare fibrinolytic activity, specifically plasminogen activator inhibitor (PAI) levels, between diabetic and non-diabetic patients admitted with AMI.
- To investigate the correlation between PAI levels and glycemic control, insulin levels, and heart failure severity in AMI patients.
Main Methods:
- A comparative study was conducted at a district general hospital.
- Included 90 non-diabetic and 38 diabetic patients admitted with acute myocardial infarction.
- Measured plasminogen activator inhibitor (PAI) activity and antigen levels, correlating them with clinical parameters and glycemic markers.
Main Results:
- Diabetic patients showed significantly higher PAI activity and antigen levels compared to non-diabetic patients (p < 0.0001).
- PAI levels correlated positively with admission plasma glucose, glycated hemoglobin, insulin levels, and Killip heart failure grade.
- Elevated PAI levels persisted in diabetic patients at 6-12 months follow-up.
Conclusions:
- Diabetic patients have elevated PAI activity, suggesting impaired fibrinolysis.
- Raised PAI activity may predispose diabetics to AMI and hinder reperfusion, contributing to worse clinical outcomes.
- Further research is warranted to explore therapeutic strategies targeting PAI in diabetic AMI patients.
Objective:
To determine whether diabetic patients admitted with acute myocardial infarction have impaired fibrinolytic activity due to raised plasminogen activator inhibitor compared with non-diabetic patients.
Setting:
A district general hospital.
Patients:
90 non-diabetic and 38 diabetic patients admitted with acute myocardial infarction.
Results:
Both plasminogen activator inhibitor activity and antigen were significantly higher in diabetic than in non-diabetic patients (24.7 (6.8) v 18.5 (6.8) AU/ml; p = 0.0001 and 64.2 (range 13.1 to 328.8) v 38.5 (range 10.9 to 173.7 ng/ml; z = 3.3; p = 0.0008) with a positive correlation between activity and antigen (rs = 0.51; p = 0.0001). In both groups, activity and antigen concentrations were significantly higher than in diabetic and non-diabetic subjects without coronary artery disease (p = 0.002 to 0.0001 for each comparison). Plasminogen activator inhibitor activity correlated significantly with admission plasma glucose (r = 0.32; p = 0.0001), glycated haemoglobin (r = 0.32; p = 0.0001), admission plasma insulin (rs = 0.48; p = 0.001), and Killip grade of heart failure both on admission (rs = 0.27; p = 0.001) and on discharge (rs = 0.22; p = 0.006), but not with cumulative creatine kinase MB isoenzyme release (rs = -0.08). There were similar but weaker correlations between tissue plasminogen activator antigen and admission plasma glucose, glycated haemoglobin, and insulin. In 18 patients (12 non-diabetic and six diabetic) plasminogen activator inhibitor activity was measured between six and 12 months (8.3 (1.6)) after the acute infarct and remained similar to activity on admission (24.8 (1.9) AU/ml (NS) for diabetic and 17.9 (6.9) AU/ml (NS) for non-diabetic patients) and was still significantly higher in diabetic than in non-diabetic patients (p = 0.007).
Conclusion:
These results show that diabetic patients have higher plasminogen activator inhibitor activity than non-diabetic patients both on admission with acute myocardial infarction and at follow up six to 12 months later. Raised plasminogen activator inhibitor activity may predispose diabetic patients to myocardial infarction and may also impair pharmacological and spontaneous reperfusion after acute myocardial infarction thus contributing to the poor outcome in these subjects.