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Predictive value of hemostatic factors for sudden death in patients with stable angina pectoris
D Benchimol1, J F Dartigues, H Benchimol
1Service de Cardiologie et Maladies Vasculaires, Hôpital Cardiologique, Pessac, France.
Insights
Sudden cardiac death risk in stable angina patients is predicted by left ventricular hypertrophy, reduced ejection fraction, and faster euglobulin clot lysis time. These hemostatic factors offer valuable insights for risk assessment.
Area of Science:
- Cardiology
- Hemostasis
- Sudden Cardiac Death
Background:
- Stable angina patients face risks of sudden cardiac death.
- Identifying hemostatic risk factors is crucial for risk stratification.
Purpose of the Study:
- To identify hemostatic and clinical risk factors for sudden death in stable angina patients.
- To determine independent predictors of sudden cardiac death in this cohort.
Main Methods:
- Prospective study of 323 stable angina patients, excluding those with heart failure or recent myocardial infarction.
- Clinical, angiographic, lipid, and extensive hemostatic variables were assessed.
- Cox univariate and multivariate models were used to identify predictors of sudden death.
Main Results:
- Independent predictors of sudden death included left ventricular hypertrophy, lower left ventricular ejection fraction, and shorter euglobulin clot lysis time.
- Fibrinogen and Jenkins' score showed borderline significance.
- The study identified specific hemostatic markers associated with increased sudden death risk.
Conclusions:
- Left ventricular hypertrophy, reduced ejection fraction, and impaired fibrinolysis (shorter euglobulin clot lysis time) are key predictors of sudden death in stable angina.
- Hemostatic variables, particularly those related to dynamic fibrinolysis, are valuable for assessing sudden death risk.
- These findings can aid in refining risk assessment strategies for patients with stable angina.
Abstract:
To assess hemostatic risk factors for sudden death in patients with stable angina, 323 consecutive patients were recruited prospectively. Patients with clinical heart failure or recent myocardial infarction were excluded. The following clinical variables were recorded: age, gender, smoking habits, hypertension, previous myocardial infarction, left ventricular hypertrophy, and severe ventricular arrhythmia. Angiographic variables included coronary extent, assessed from Jenkins' and mean atherosclerotic scores, and left ventricular ejection fraction. Lipid variables included total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and apolipoproteins A-I and B. Hemostatic factors included fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2 antiplasmin, euglobulin clot lysis time, tissue plasminogen activator before and after venous occlusion, and plasminogen activator inhibitor. There were 34 deaths, 19 of which were sudden during the follow-up period (60 +/- 17 months). The association between each variable and the risk of sudden death was assessed by calculating the relative risk with the Cox univariate model. All significant predictors from the univariate analysis were then incorporated in a Cox multivariate model to select the independent predictors of sudden death. The independent predictors of sudden death were left ventricular hypertrophy (p < 0.04), lower left ventricular ejection fraction (p < 0.04), and shorter euglobulin clot lysis time after venous occlusion (p < 0.02), whereas fibrinogen (p < 0.07) and Jenkins' score (p < 0.08) were borderline. Determination of hemostatic variables, especially those pertaining to dynamic fibrinolysis, may thus be of value in assessing risk of sudden death.