Long-Term Anticoagulant Therapy After Acute Myocardial Infarction

Kühn, P; Ness, AR; Jones, Richard J.; Bay, Emmet B.

doi:10.1001/archinte.1961.03620120068010

Cited by 15 publications

(7 citation statements)

References 16 publications

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“…Indeed, some authors have identified 'high-risk groups' with a strikingly high relapse rate which include patients who were on long-term anticoagulation for > 2 years (Keyes et al, 1956;Van Cleve, 1965;Kamath & Thorne, 1969), patients in whom anticoagulation was stopped because of bleeding (Sharland, 1966;Sise et al, 1961;Thomes et al, 1960), patients with advanced atherosclerosis in general (Kuhn et al, 1961) and more than one myocardial infarction in their history (Nichol et al, 1958;Van Cleve, 1966) or patients with angina in the month preceeding cessation (Michaels, 1970). Indeed, some authors have identified 'high-risk groups' with a strikingly high relapse rate which include patients who were on long-term anticoagulation for > 2 years (Keyes et al, 1956;Van Cleve, 1965;Kamath & Thorne, 1969), patients in whom anticoagulation was stopped because of bleeding (Sharland, 1966;Sise et al, 1961;Thomes et al, 1960), patients with advanced atherosclerosis in general (Kuhn et al, 1961) and more than one myocardial infarction in their history (Nichol et al, 1958;Van Cleve, 1966) or patients with angina in the month preceeding cessation (Michaels, 1970).…”

Section: Discussionmentioning

confidence: 99%

“…The controversy over the presence or absence of a rebound phenomenon after cessation of oral anticoagulant therapy now extends over more than three decades (Marshall, 1963;Liebermann & Lindner, 1965;Dinon & Vander Veer, 1969;Kuhn et al, 1961;Evans & O'Rourke, 1970;Hart & Coull, 1983;Carter et al, 1958;Sharland, 1966;Sise et al, 1961;Thomas et al, 1960;Keyes et al, 1956;Nichol et al, 1958;Michaels & Beamish, 1967;Beer & Schlup, 1986;Grip et al, 1991;Michaels, 1970;Côté et al, 1977;Van Cleve, 1965Kamath & Thorne, 1969;Wright, 1960Wright, , 1961Pickering et al, 1964) and it is still unclear whether or not the phenomenon is real. Recent reports on rebound angina pectoris and rebound coagulation after cessation of heparin (Theroux et al, 1992) or of thrombin inhibitors (Gold et al, 1993;Willerson & Casscells, 1993) have again focused on the topic.…”

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confidence: 99%

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Rebound after cessation of oral anticoagulant therapy: the biochemical evidence

et al. 1996

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The existence of a phenomenon of rebound hypercoagulability after cessation of oral anticoagulant therapy is controversial. The sensitive procoagulant markers for in vivo thrombin and fibrin formation are potential tools for the reassessment of the presence of each a phenomenon. We examined 19 patients anticoagulated for 6 +/- 2 months (SD, range 3-12) because of venous thromboembolism or myocardial infarction as follows: twice during stable, oral anticoagulation (INR 3.1-3.7) and then on days 1, 2, 3, 4, 5, 7, 9, 11, 13, 15, and > 30 after cessation of oral anticoagulation. Thrombin-antithrombin III complexes (TAT) and fibrinopeptide A (FPA) were measured in addition to the prothrombin times and factors II, V, VII, and X. None of the 19 patients developed clinically manifest thromboembolism within the following 9-18 months. However, the patients' TAT levels increased transiently: rising from 1.5 +/- 0.1 ng/ml (SEM) to 3.0 +/- 0.2 ng/ml on day 4 (P < 0.001), and returned to 1.7 +/- 0.1 ng/ml after day 30 (normals 1.8 +/- 0.33). 17/19 patients showed TAT peak levels above the upper limit of normal between days 3 and 11 (average: day 4), which normalized again after 30 d. 8/19 patients also had transient FPA levels above the upper normal limits ( < 1.81). We conclude that our patients increased their thrombin and fibrin formation transiently and that a subpopulation reached values consistent with a prethrombotic state.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Rebound after cessation of oral anticoagulant therapy: the biochemical evidence

et al. 1996

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“…Although there is a large variation between positive and negative results (e.g. Macmillan et al, 1960;Kuhn et al, 1961;Harvald et al, 1962;Aspenstrom and Korsan-Bengtsen, 1964;Conrad et al, 1964;Ebert et al, 1969;Manchester, 1964;Seaman et al, 1969\Menwissen et al, 1969Loeliger et al, 1967;Ritland and Lyngren, 1969;Veterans Adminis tration Hospital investigators, 1965, a reduction in the recurrence of secondary myocardial infarction was observed more clearly than a reduction in total mor tality or coronary death. If total mortality or coronary death were reduced during anticoagulant treatment, this effect was usually most pronounced during the first year of treatment and less evident during the following years.…”

Section: Discussionmentioning

confidence: 99%

Secondary Prevention of Myocardial Infarction: a Comparison of Acetylsalicylic Acid, Placebo and Phenprocoumon

Breddin¹,

Loew²,

Lechner³

et al. 1980

Pathophysiol Haemos Thromb

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A multicenter clinical trial on the prevention of recurrent myocardial infarction was started in 1970 and continued until March 1977. 946 patients who had survived a myocardial infarction for 30–42 days were randomly allocated in equal proportions to acetylsalicylic acid (ASA, 1.5 g/day) (317 patients), placebo (309 patients) or phenprocoumon treatment (320 patients) and followed to determine the incidence of total mortality, coronary death and nonfatal recurrent myocardial infarction. The ASA and placebo groups were treated double-blind. The observation period for each patient was 2 years. The outcome at 24 months has been established for 231 patients on ASA, for 215 on placebo and for 233 on phenprocoumon treatment. Total mortality was lower in the ASA group (27 patients) than in the placebo (32 patients) and phenprocoumon group (39 patients). These differences are not statistically significant. Coronary deaths (fatal myocardial infarction and sudden death) were 13 in the ASA, 22 in the placebo- and 26 in the phenprocoumon group. This represents a reduction rate of 42.3% in the ASA group compared with placebo (p > 0.1) and of 46.3% in the ASA group compared with phenprocoumon (p < 0.07). Considering male patients alone, the difference regarding coronary death is significant between ASA versus placebo (p < 0.05) and ASA versus phenprocoumon (p < 0.05). Coronary events (coronary death and non-fatal recurrent myocardial infarction) were lower in the ASA group (24 patients) than in the placebo (37 patients) (p < 0.06) or phenprocoumon groups (32 patients). Gastrointestinal discomfort, with or without hermorrhage, was more frequent in the ASA group than in the placebo or phenprocoumon groups. These results, in combination with similar trends reported in other clinical trials with ASA, suggest that ASA treatment is beneficial in patients who have survived a myocardial infarct.

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“…J., 1966, 2, 392-393 While fierce arguments have raged round the place of anticoagulants in the management of ischaemic heart disease, evidence has been brought forward that, such treatment having been started, cessation may be hazardous (B.M.7., 1962). A number of reviews suggesting that the stopping of anticoagulant therapy may be followed by an increased thrombotic tendency have been published (Dinon and Vander Veer, 1960;Kuhn et al, 1961 ;Sise et al, 1961) and a possible theoretical basis has been suggested by Poller and Thomson (1964). Dinon and Vander Veer (1960) reported a series of 20 patients who sustained a myocardial infarction (the first infarction in 18 cases) and reinfarcted within one month of stopping anticoagulant therapy.…”

Section: Effect Of Cessation Of Anticoagulant Therapy On the Course Omentioning

confidence: 99%

“…Anticoagulants had been given for an average period of 40 days (range 24 to 82 days) and in most cases, therefore, the new infarction occurred at a time when the chances of such a relapse were still high. Kuhn et al (1961), in a study of long-term anticoagulants in patients who had suffered myocardial infarction, noted a reinfarction rate of 5 % in the month following cessation of anticoagulants-this was higher than in any other month. However, the numbers involved-five reinfarctions (four of which were fatal)-were rather small and could be regarded only as suggestive.…”

mentioning

confidence: 91%

Effect of cessation of anticoagulant therapy on the course of ischaemic heart disease.

Sharland¹

1966

BMJ

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While fierce arguments have raged round the place of anticoagulants in the management of ischaemic heart disease, evidence has been brought forward that, such treatment having been started, cessation may be hazardous (B.M.7., 1962). A number of reviews suggesting that the stopping of anticoagulant therapy may be followed by an increased thrombotic tendency have been published (Dinon and Vander Veer, 1960;Kuhn et al., 1961 ;Sise et al., 1961) and a possible theoretical basis has been suggested by Poller and Thomson (1964). Dinon and Vander Veer (1960) reported a series of 20 patients who sustained a myocardial infarction (the first infarction in 18 cases) and reinfarcted within one month of stopping anticoagulant therapy. Anticoagulants had been given for an average period of 40 days (range 24 to 82 days) and in most cases, therefore, the new infarction occurred at a time when the chances of such a relapse were still high. Kuhn et al. (1961), in a study of long-term anticoagulants in patients who had suffered myocardial infarction, noted a reinfarction rate of 5 % in the month following cessation of anticoagulants-this was higher than in any other month. However, the numbers involved-five reinfarctions (four of which were fatal)-were rather small and could be regarded only as suggestive.Sise et al. (1961), in a study of a large series of patients who had stopped anticoagulants, noted that among 45 instances where anticoagulants were stopped because of bleeding (and the patient was given vitamin K or a blood transfusion) there were 20 " relapses " (10 fatal and 10 non-fatal) in the following year, the largest proportion occurring in the first month. By contrast, in 53 instances when anticoagulants were given up because of difficulties in cooperating, because of the necessity for operation and for other non-urgent reasons, there were 15 " relapses " (seven fatal and eight non-fatal) in the subsequent year, and these appeared to be fairly evenly spread.The difference in the mortality rate in the first month was at the 5% level of significance, while if all relapses were considered the difference was at the 1 % level.These observations show that stopping of anticoagulants is associated with an increased thrombotic tendency only when cessation is because of haemorrhage. ObservationsThe present data were obtained during the course of a study of the effects of a low-fat diet compared with an ordinary diet on the progress of ischaemic heart disease. A consecutive series of men were used for the trial. They were all under the age of 65, had sustained one episode of cardiac infarction, and were subsequently free from serious complications such as persistent heart failure. Cases where the cardiac infarction was thought to be a complication of an existing disease-for example, diabetes or severe hypertension-were likewise excluded. Many of the men received up to 14 weeks' anticoagulant treatment but none were on long-term anticoagulants.

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Long-Term Anticoagulant Therapy After Acute Myocardial Infarction

Cited by 15 publications

References 16 publications

Rebound after cessation of oral anticoagulant therapy: the biochemical evidence

Rebound after cessation of oral anticoagulant therapy: the biochemical evidence

Secondary Prevention of Myocardial Infarction: a Comparison of Acetylsalicylic Acid, Placebo and Phenprocoumon

Effect of cessation of anticoagulant therapy on the course of ischaemic heart disease.

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