Thromb Haemost 2003; 89(05): 892-903
DOI: 10.1055/s-0037-1613477
Vascular Development and Vessel Remodelling
Schattauer GmbH

Evidence of prolonged disturbances in the haemostatic, hemorheologic and inflammatory profiles in transmural myocardial infarction survivors

A 12-month follow-up study
Luis Sargento
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
,
Carlota Saldanha
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
,
José Monteiro
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
,
Carlos Perdigão
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
,
João Martins eSilva
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
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Publikationsverlauf

Received 14. November 2002

Accepted after revision 27. Januar 2003

Publikationsdatum:
09. Dezember 2017 (online)

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Summary

Haemostatic, hemorheologic and inflammatory disturbances have been associated with acute coronary syndromes. Most knowledge is reported in cross sectional studies and are without time dependent evolution of these profiles.

The aim of this study was to evaluate, during the first year, the evolution of the haemostatic, hemorheologic and inflammatory profiles determined at hospital discharge in survivors with transmural myocardial infarction (MI).

Eighty eight (79 male; 9 female) mean age of 58 ± 11 years, survivors of a transmural MI were prospectively studied at discharge, 6 months and one year after the event. Haemostatic (protein C, antithrombin III and plasminogen activator inhibitor 1), hemorheologic (blood fluidity and components) and inflammatory profiles (polymorphonuclear elastase and leukocyte count) were determined using standard methodology.

The results of the study can be summarized as follows: (1) Protein C decreased (p < 0.05) over time while PAI-1 only varied significantly until 6th month. (2) Plasma viscosity and fibrinogen (p < 0.001) decrease over time, while erythrocyte aggregation (p < 0.001) and haematocrit increased. Whole blood viscosity did not vary. (3) Leukocyte decreased (p < 0.001) and elastase did not (4). Those patients with cardiovascular events (n = 7) had higher PAI-1 concentration (p<0.05) and leukocyte count (p < 0.01), at discharge (5) Left ventricle ejection fraction correlated significantly with plasma viscosity (r = 0.35 p < 0.05). The results of this longitudinal study show dynamic modifications of the haemostatic, hemorheologic and inflammatory profiles during the first year of a transmural myocardial infarction. In addition, there are interrelations between them and the clinical profile that could help to explain the clinical evolution of this group of patients.