Improved Fibrinolysis after one Year of Treatment with Enalapril in Men and Women with Uncomplicated Myocardial Infarction

Kurt O. A. Boman; Jan-Håkan Jansson; Katarina A. Nyhlén; Torbjörn K. Nilsson

doi:10.1055/s-0037-1612991

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 2002; 87(02): 311-316
DOI: 10.1055/s-0037-1612991

Letters to the Editor

Schattauer GmbH

Improved Fibrinolysis after one Year of Treatment with Enalapril in Men and Women with Uncomplicated Myocardial Infarction

Kurt O. A. Boman

¹Department of Medicine and Genetics, Skellefteå County Hospital, Skellefteå

,

Jan-Håkan Jansson

¹Department of Medicine and Genetics, Skellefteå County Hospital, Skellefteå

,

Katarina A. Nyhlén

¹Department of Medicine and Genetics, Skellefteå County Hospital, Skellefteå

,

Torbjörn K. Nilsson

²Department of Clinical Chemistry, Örebro University Hospital and Department of Biomedicine, Örebro University, Örebro, Sweden

› Institutsangaben

Abstract

Summary

Aims

To study long-term effects of enalapril on mass concentrations of tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1), tPA/PAI-1-complex and von Willebrand factor (vWF) in both genders with uncomplicated myocardial infarction.

Methods and results

More than three months after an uncomplicated myocardial infarction 82 survivors (46 males, 36 females) were randomised to enalapril/placebo. PAI-1, tPA, tPA/PAI-1-complex and vWF were measured after two weeks, six and 12 months following randomisation. PAI-1 decreased significantly in both genders in the enalapril-treated group after two weeks, with a maximum decrease at six months (mean reduction: 31% equal to 9.8 µg X L–1, CI: 5.2 to 14.5 µg X L–1, p = 0.0001) and remained significantly lower at 12 months. Mass concentration of tPA decreased significantly (mean reduction; 1.81 µg X L–1, CI: 0.903 to 2.708 µg X L–1, p <0.001) after two weeks treatment in both genders but returned to baseline values at 12 months. The tPA/PAI-1-complex decreased and was significantly lower (mean reduction 0.96 µg X L–1, CI: 0.36 to 1.56 µg X L–1, p = 0.003) in the enalapril group after two weeks and six months (p = 0.037). No decrease of vWF was seen in the enalapril group.

Conclusions

Enalapril treatment up to one year depressed mass concentrations of PAI-1 and transiently tPA and tPA/PAI-1 complex indicating an improvement of the fibrinolytic balance in both genders with uncomplicated myocardial infarction.

Keywords

Fibrinolysis - tissue plasminogen activator - plasminogen activator inhibitor - myocardial infarction - ACE-inhibitor

Volltext

Referenzen

References
1 Gram J, Jespersen J, Kluft C, Rijken CD. On the usefulness of fibrinolytic variables in the characterisation of a risk group for myocardial infarction. Acta Med Scand 1987; 221: 149-53.
2 Hamsten A. The hemostatic system and coronary heart disease. Throm Res 1993; 70: 1-38.
3 Munkvald S, Gram J, Jespersen J. A depression of active tissue plasminogen activator in plasma characterises patients with unstable angina pectoris who develop myocardial infarction. Eur Heart J 1990; 11: 525-8.
4 Jansson JH, Nilsson TK, Olofsson BO. Tissue plasminogen activator and other risk factors as predictors of cardiovascular events in patients with severe angina pectoris. Eur Heart J 1991; 12: 157-61.
5 Lijnen HR, Collen D. Impaired fibrinolysis and the risk for coronary heart disease. Circulation 1996; 94: 2052-4.
6 Thögersen AM, Jansson JH, Boman K. et al. High plasminogen activator inhibitor (PAI-1) and tissue plasminogen activator (tPA) levels in plasma precede a first acute myocardial infarction in both men and women: evidence for the fibrinolytic system as an independent primary risk factor. Circulation 1998; 98: 2241-7.
7 Juhan-Vague I, Pyke SDM, Alessi MC, Jespersen J, Haverkate F, Thompson SG. Fibrinolytic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. Circulation 1996; 94: 2057-63.
8 Folsom AR, Wu KK, Rosamond WD, Sharrett AR, Chambless LE. Prospective study of hemostatic factors and incidence of coronary heart disease. The ARIC Study. Circulation 1997; 96: 1102-8.
9 Smith FB, Lee AJ, Fowkes FGR, Price JF, Rumley A, Lowe GDO. Hemostatic factors as predictors of ischemic heart disease and stroke in the Edinburgh Artery Study. Arterioscler Thromb Vasc Biol 1997; 17: 3321-5.
10 Ridker PM, Gaboury CL, Conlin PR, Seely EW, Williams GH, Vaughan DE. Stimulation of plasminogen activator in vivo by infusion of angiotensin II. Evidence of a potential interaction between the renin-angiotensin system and fibrinolytic function. Circulation 1993; 87: 1969-73.
11 CONSENSUS. Effect of enalapril on mortality in severe congestive heart failure: result of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med 1987; 316: 1429-35.
12 SOLVD. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991; 325: 293-302.
13 Cohn JN, Johnson G, Ziesche S. et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med 1991; 325: 303-10.
14 Jansson JH, Boman K, Nilsson TK. Enalapril related changes in the fibrinolytic system in survivors of myocardial infarction. Eur J Clin Pharmacol 1993; 44: 485-8.
15 Wright RA, Flapan AD, Alberti KG, Ludlam CA, Fox KA. Effects of captopril therapy on endogenous fibrinolysis in men with recent, uncomplicated myocardial infarction. J Am Coll Cardiol 1994; 24: 67-73.
16 Vaughan DE, Rouleau JL, Ridker PM, Arnold JMO, Menapace FJ, Pfeffer MA. Effects of ramipril on plasma fibrinolytic balance in patients with acute anterior myocardial infarction. Circulation 1997; 96: 442-7.
17 Lottermoser K, Wostmann B, Weisser B. et al. Effects of captopril on fibrinolytic function in healthy humans. Eur J Med Res 1999; 26 4: 31-4.
18 Pedersen OD, Gram J, Jeunemaitre X, Billaud E, Jespersen J. Does long-term angiotensin converting enzyme inhibition affect the concentration of tissue-type plasminogen activator-plasminogen activator inhibitor-1 in the blood of patients with a previous myocardial infarction?. Coronary Artery Disease 1997; 08: 283-91.
19 Sundell IB, Nilsson TK, Rånby M, Hallmans G, Hellsten G. Fibrinolytic v ariables are related to age, sex, blood pressure and body build measurements: a cross-sectional study in Norsjö, Sweden. J Clin Epidemiol 1989; 42: 719-23.
20 Wiman B, Andersson T, Hallqvist J, Reuterwall C, Ahlbom A, deFaire U. Plasma levels of tissue plasminogen activator/plasminogen activator inhibitor-1 complex and von Willebrand factor are significant risk markers for recurrent myocardial infarction in the Stockholm Heart Epidemiology Program (SHEEP) study. Arterioscler Thromb Vasc Biol 2000; 20 (08) 2019-23.
21 Johansson L, Jansson JH, Boman K, Nilsson TK, Stegmayr B, Hallmans G. Tissue plasminogen activator, plasminogen activator inhibitor-1, and tissue plasminogen activator/plasminogen activator inhibitor-1 complex as risk factors for the development of a first stroke. Stroke 2000; 31 (01) 26-32.
22 Grimaudo V, Hauert J, Bachman F, Kruithof EKO. Diurnal variation of the fibrinolytic system. Thromb Haemost 1988; 59: 495-9.
23 Bergsdorf N, Nilsson T, Wallén P. An enzyme-linked immunosorbent assay for tissue plasminogen activator applied to patients with thromboembolic disease. Thromb Haemost 1983; 50: 740-4.
24 Cejka J. Enzyme immunoassay for factor VIII-related antigen. Clin Chem 1982; 28: 1356-8.
25 Chmielewska J, Wiman B. Determination of tissue plasminogen activator and its “fast” inhibitor from plasma. Clin Chem 1986; 32: 482-5.
26 Thorsen S, Philips M. Isolation of tissue-type plasminogen activatorinhibitor complexes from human plasma. Biochim Biophys Acta 1984; 802: 111-8.
27 Thompson SG, Kienast J, Pyke SDM, Haverkate F, van de Loo JCW. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. N Engl J Med 1995; 332: 635-41.
28 Hamsten A, Wiman B, de Faire U, Blombäck M. Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction. N Engl Med 1985; 313: 1557-63.
29 Olofsson BO, Dahlén G, Nilsson TK. Evidence for increased levels of plasminogen activator inhibitor and tissue plasminogen activator in plasma of patients with angiographically verified coronary artery disease. Eur Heart J 1989; 10: 77-82.
30 Hellsten G, Boman K, Bjerle P, Blom P, Nilsson TK. Increased plasminogen activator inhibitor and tissue plasminogen activator levels in subjects with electrocardiographic abnormality indicative of ischaemic heart disease: A cross-sectional study in Norsjö, Sweden. Eur Heart J 1992; 13: 57-60.
31 Nilsson TK, Olofsson BO, Jansson JH. Predictive value of tissue plasminogen activator massconcentration on long-term mortality in patients with angiographically verified coronary heart disease: a 7-year follow-up. Circulation 1992; 86 (Suppl Abstract No 2383): 1-598.
32 Nilsson TK, Boman K, Bjerle P, Hallmans G, Hellsten G. von Willebrand factor and fibrinolytic variables are differently affected in the insulin resistance syndrome. JIM 1994; 235: 419-23.
33 Pfeffer MA, Braunwald E, Moyé LA. et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the Survival and Ventricular Enlargement Trial. N Engl J Med 1992; 327: 669-77.
34 Brown NJ, Gainer JV, Murphey LJ, Vaughan DE. Bradykinin stimulates tissue plasminogen activator release from human forearm vasculature through B82) receptor-dependent, NO synthetase-independent, and cyclooxygenase-independent pathway. Circulation 2000; 102: 2190-6.
35 Labinjoh C, Newby DE, Dawson P, Johnston NR, Ludlam CA, Boon NA, Webb DJ. Fibrinolytic actions of intra-arterial angiotensin II and bradykinin in vivo in man. Cardiovasc Res 2000; 47: 707-14.
36 Minai K, Matsumoto T, Horie H. et al. Bradykinin stimulates the release of tissue plasminogen activator in human coronary circulation: effects of angiotensin-converting enzyme inhibitors. J AM Coll Cardiol 2001; 37: 1565-70.
37 Nagata K, Ishibashi T, Sakamoto T. et al. Effects of blockade of the renin-angiotensin system on tissue factor and plasminogen activator inhibitor-1 synthesis in human monocytes. J Hypertens 2001; 19: 775-83.
38 Hamdan AD, Quist WC, Gagne JB, Feener EP. Angiotensin-converting enzyme inhibition suppresses plasminogen activator inhibitor-1 expression in the neointima of balloon-injured rat aorta. Circulation 1996; 93: 1073-8.
39 Laursen JB, Rajagopalan S, Galis Z, Tarpey M, Freenan BA, Harrison DG. Role of superoxide in angiotensin II-induced but not catecholamine induced hypertension. Circulation 1997; 95: 588-93.
40 Katoh M, Egashira K, Mitsui T, Takeshita A, Narita H. Differential effects of imidapril and candesartan cilexetil on plasminogen activator inhibitor-1 expression induced by prolonged inhibition of nitric oxide synthesis in rat hearts. J Cardiovasc Pharmacol 2000; 35: 932-6.