Original Article
Platelet Hyperreactivity and Prognosis in Survivors of Myocardial Infarction
N Engl J Med 1990; 322:1549-1554May 31, 1990
- Abstract
- Abstract
We tested the hypothesis that an increase in spontaneous aggregability of platelets in vitro predicts mortality and coronary events in patients who have survived a recent myocardial infarction. A cohort of 149 survivors of infarction entered our study three months after the index infarction and was followed for five years. At entry and at intervals of six months, spontaneous platelet aggregation (SPA) was tested and graded as positive (aggregation within 10 minutes), intermediate (aggregation after 10 to 20 minutes), or negative (no aggregation within 20 minutes).
During follow-up, 6.4 percent (6 of 94) of the patients in the SPA-negative group died, as compared with 10.3 percent (3 of 29) in the SPA-intermediate group and 34.6 percent (9 of 26) in the SPA-positive group. As compared with the SPA-negative group, the SPA-intermediate group had a relative risk of death of 1.6 (95 percent confidence interval, 0.5 to 5.5) and the SPA-positive group had a risk of 5.4 (95 percent confidence interval, 2.2 to 13.4). At least one cardiac event (cardiac death or recurrent nonfatal myocardial infarction) occurred in 14.9 percent (14 of 94 patients) of the SPA-negative group, 24.1 percent (7 of 29) of the SPA-intermediate group, and 46.2 percent (12 of 26) of the SPA-positive group. A positive test result continued to have prognostic value throughout the five-year study.
We conclude that spontaneous platelet aggregation in vitro is a useful biologic marker for the prediction of coronary events and mortality in this low-risk group of survivors of a myocardial infarction. A causal relation is suggested but not proved by our study. (N Engl J Med 1990; 322:1549–54.)
Media in This Article
Figure 1
Event-free Survival during Five Years of Follow-up, According to SPA Status at Entry.Figure 2
Changes in SPA Status during Follow-up, According to SPA Status at Entry.Article Activity
- Article
PLATELETS have an important role in atherosclerosis and its complications, such as acute coronary ischemia.1 2 3 4 The pathophysiologic mechanism by which platelets contribute to the acute manifestations of coronary artery disease is not fully understood. A causal role of platelet hyperreactivity or of local platelet activation in an acute coronary event has been suggested but never proved.5 Platelet products in plasma (beta-thromboglobulin, thromboxane, and platelet factor 4) have been measured to determine platelet activation in patients with coronary artery disease.6 7 8 9 The results of these tests remain controversial and difficult to interpret. It has not yet been possible to select a platelet-function test that can be used to detect platelet activation in relation to the complications of atherosclerosis. Moreover, most of these studies have been done in the setting of an acute coronary event.
Tofler et al.10 have shown that increased platelet aggregability in the morning is concomitant with an increased frequency of myocardial infarction and sudden cardiac death, suggesting a causal relation. Several clinical studies have demonstrated that inhibition of platelet function by drugs such as aspirin exerts a beneficial effect on the course of coronary artery disease by reducing the risk of sudden death, myocardial infarction, and unstable angina.11 12 13 14 15
In two case reports, a syndrome characterized by peripheral ischemia of the fingers and toes has been described in patients with thrombocythemia and spontaneous platelet aggregation (SPA). Treatment with aspirin prevented the aggregation and the clinical signs of ischemia, both of which recurred after discontinuation of the treatment.16 , 17
Finding a platelet-function test that is relevant to the prognosis of patients with coronary artery disease could be a first step toward identifying patients who would benefit from treatment with antiplatelet drugs. Therefore, we tested the hypothesis that increased platelet aggregability, as measured by SPA in vitro in patients with a recent myocardial infarction, is related to future mortality and coronary events. To this end, we prospectively followed a cohort of survivors of myocardial infarction for five years.
Methods
Patients
The study cohort consisted of 149 survivors of myocardial infarction less than 71 years of age, who were referred to an outpatient unit of the Academic Hospital of the University of Amsterdam after completing their clinical rehabilitation period. All were in New York Heart Association (NYHA) functional class I or II.
Study Entry
Since platelet function may be affected by an acute ischemic event, the first aggregation study was performed three months after the index myocardial infarction. Base-line clinical characteristics relevant to prognosis were also recorded at that time.
Clinical Follow-up
All patients were evaluated at regular intervals during a five-year follow-up period. Since the use of aspirin affects thrombocyte aggregation and leads to a uniformly negative test result,18 , 19 the patients were encouraged at each visit not to use any platelet-inhibiting drug. Test results in the patients who admitted using such drugs in the week before testing for platelet aggregation were excluded.
During the first year after myocardial infarction, all patients participated in a secondary prevention study (the Amsterdam Metoprolol Trial)20 in which they received metoprolol (100 mg twice daily) or a placebo after randomization. Treatment for angina pectoris, cardiac pump failure, and hypertension was given according to a predetermined protocol.
End Points
The data were analyzed for two outcomes: death due to any cause and cardiac events. A cardiac event was defined as a nonfatal recurrent myocardial infarction or cardiac death; cardiac death was defined as death occurring in the hospital after a confirmed myocardial infarction, or as death occurring suddenly without previous symptoms or within 24 hours after the onset of new symptoms of heart disease. In the hierarchy of events, death superseded any earlier event. Likewise, only the first recurrent nonfatal myocardial infarction was considered to be an event in patients who were alive after completing five years of follow-up.
Platelet Aggregation
Aggregation studies were performed at entry and at six-month intervals. All venipunctures were performed between 9 and 10 a.m. Blood samples were drawn without stasis from an antecubital vein, with use of a 21-gauge needle. Nine volumes of blood were collected in one volume of 3.2 percent trisodium citrate in plastic tubes. The blood samples were left in capped plastic tubes for 15 minutes at room temperature and were centrifuged for 10 minutes at l00×g to obtain platelet-rich plasma. The remaining volume of blood was centrifuged further for 20 minutes at 900 ×g to obtain platelet-poor plasma. The platelet count of the platelet-rich plasma was determined. The plasma samples were left in capped plastic tubes at room temperature. Subsequently, aggregometry was performed at 37°C according to the method of Born21 with the use of a Payton Dual Channel Aggregometer (Payton Ltd., Scarborough, Ont., Canada). The aggregometer was adjusted before each test so that in each patient the value for light transmission for platelet-rich plasma was 0 percent and that for platelet-poor plasma was 100 percent. The occurrence of SPA in each sample was assessed one hour after venipuncture. After 0.4 ml of platelet-rich plasma was stirred in the aggregometer at 450 rpm for 20 minutes, aggregation was measured; an increase of 20 percent or more in the light transmission of the platelet-rich plasma was considered to indicate SPA. No correction for platelet count was made. The interval between the start of stirring and the deflection of the aggregation curve was expressed in minutes. In contrast to the current practice,18 , 19 according to which SPA is described as positive or negative, we categorized SPA as positive, intermediate, or negative. Three types of response were identified and defined: SPA negative — no aggregation occurred within 20 minutes of stirring; SPA intermediate — aggregation occurred between 10 and 20 minutes of stirring; and SPA positive — aggregation occurred within 10 minutes of stirring.
Statistical Analysis
Univariate analysis of the results of platelet-function tests and clinical variables was performed; the analysis concentrated on the risk ratios for mortality and the occurrence of cardiac events. Continuous variables were divided into three classes — low, medium, and high; the first class served as a reference category. The 95 percent confidence intervals for the respective risk ratios were calculated according to the method of Miettinen and Nurminen.22 If the 95 percent confidence interval of the risk ratio for mortality exceeded 1.0, the association of the respective variable with the risk of dying within five years was statistically significant at the 5 percent level.
Logistic multiple regression analysis was performed with the BMDP statistical package23 to select the base-line variables capable of being independently predictive. Indicator variables were used throughout; these variables have a value of 1 if the property under consideration is present, and 0 if it is not. The advantage of indicator variables is that each regression coefficient directly represents the log odds of death when all the other variables in the model are controlled. For continuous variables, the indicator variables for the categories of medium and high risk were considered for inclusion in the model. The BMDP program settings were such that variables were included in the model if they substantially improved the log likelihood (P<0.10); they were retained only if their removal substantially decreased the log likelihood (P<0.15). P values were two-tailed. Survival curves were constructed according to the method described by Peto et al.24
Results
Clinical End Points
The characteristics of the patients at the time of entry into the study are shown in Table 1Table 1
Characteristics of Patients at Entry.. All patients were followed for five years. The relation between the features of platelet aggregation at entry and the clinical outcome during five-year follow-up is shown in Table 2Table 2
Clinical Outcome According to SPA-Status Group.. Eighteen patients died (death was due to cardiac causes in 15 and to carcinoma in 3). When the two groups of patients with any SPA were compared with the group without SPA, the relative risk of dying was 1.6 (95 percent confidence interval, 0.5 to 5.5) in the group with intermediate SPA and 5.4 (95 percent confidence interval, 2.2 to 13.4) in the group with positive SPA. At least one cardiac event occurred in 33 patients. The relative risk of a cardiac event in the intermediate-SPA group was 1.6 (95 percent confidence interval, 0.7 to 3.5) and 3.1 in the SPA-positive group (95 percent confidence interval, 1.6 to 5.8), as compared with the SPA-negative group. For both outcomes (mortality and cardiac events), the relative risk increased with increasing aggregability.Table 3Table 3
Clinical Outcome According to Characteristics at Entry.* shows the clinical characteristics at study entry in relation to the total mortality and cardiac events. A significantly increased relative risk of death was observed in patients who had a peak creatine kinase MB fraction of ≥80 U per liter and in patients who were taking diuretics, digitalis, or metoprolol. The relative risk of cardiac events was increased in patients who had had an infarction or who were taking digitalis.The variables shown in Tables 2 and 3 were also used in logistic multiple regression analysis. For the risk of death within five years, a positive SPA status, digitalis therapy, and metoprolol treatment were the only independent predictive variables. Including metoprolol treatment in the regression analysis increased the log likelihood only marginally (P = 0.08). The influence of metoprolol — if any — was hard to explain, and we believed that the effect observed in this study was spurious. Therefore, we limited ourselves to including SPA positivity and digitalis therapy in the regression model (Table 4Table 4
Logistic Multiple Regression Analysis of Mortality during Five Years of Follow-up.). SPA positivity was the most powerful predictor; it increased the predicted five-year mortality rate from 6 percent to 29 percent among the patients who were not taking digitalis at entry and from 22 percent to 60 percent among those who were.The percentage of patients who had no end-point events (death or recurrent myocardial infarction) during the follow-up period after the myocardial infarction is shown in Figure 1Figure 1
Event-free Survival during Five Years of Follow-up, According to SPA Status at Entry.. Seventy-nine of the 94 patients in the SPA-negative group (84 percent), 22 of the 29 in the SPA-intermediate group (76 percent), and 12 of the 26 in the SPA-positive group (46 percent) were event-free at 60 months.Platelet-Aggregation Studies during Follow-up
Figure 2Figure 2
Changes in SPA Status during Follow-up, According to SPA Status at Entry. shows the results of platelet-aggregation studies performed at intervals of 6 or 12 months during the five-year follow-up period, according to the SPA index determined at entry. In the group of patients who were SPA-negative at entry, more than 90 percent of the tests performed during follow-up were negative. In the group of patients who were SPA-positive at entry, more than 50 percent of the tests were positive and less than 20 percent were negative during the first three years of follow-up. Patients in the SPA-intermediate group at entry occasionally had positive tests during follow-up; more often, their tests either continued to be SPA-intermediate or were SPA-negative.Table 5Table 5
Clinical Outcome According to SPA Status during Follow-up. shows the clinical outcomes in the groups in relation to the results of platelet-aggregation tests performed at different intervals after the index myocardial infarction. The platelet-aggregation tests performed during follow-up consistently showed the same relation to subsequent mortality and cardiac events as did the tests performed at entry. The rate of mortality and cardiac events was lowest in the SPA-negative group, highest in the SPA-positive group, and intermediate in the SPA-intermediate group.Discussion
This study found a positive association between platelet hyperreactivity in vitro and both mortality and cardiac events in survivors of myocardial infarction. During a follow-up period of five years, the relative risk of death was 5.4 times higher in the group with SPA within 10 minutes (the SPA-positive group) than in the group without this characteristic (the SPA-negative group). The 95 percent confidence interval lies between 2.2 and 13.4, indicating that the risk of death in the SPA-positive group was at least 2.2 but possibly even 13.4 times as high as in the SPA-negative group. The finding that 6.4 percent (6 of 94) of patients died in the SPA-negative group, 10.3 percent (3 of 29) in the SPA-intermediate group, and 34.6 percent (9 of 26) in the SPA-positive group illustrates the clinical relevance of this association.
Since the deaths of 15 of the 18 patients who died were due to cardiac causes, it is likely that platelet hyperaggregability is associated with the development of complications of atherosclerotic heart disease. This is corroborated by the finding that the relative risk of cardiac events (cardiac death or recurrent nonfatal myocardial infarction) was 3.1 times as high (95 percent confidence interval, 1.6 to 5.8) in the SPA-positive group as in the SPA-negative group.
The cumulative mortality of 12.1 percent over a period of five years in this cohort is low but not surprising. Evaluation of the patients' characteristics at entry showed a high prevalence of first myocardial infarctions, the absence of angina pectoris of NYHA classes III and IV, and a low prevalence of symptomatic heart failure as reflected by the low rate of the use of diuretics or digitalis. In fact, 82 percent of our patients were in NYHA functional class I at entry. Although none of our patients underwent coronary angiography or studies of left ventricular function at entry, we are confident that the clinical criteria mentioned above indicated that the patients were at low risk.25 26 27 This has two implications. First, the results of our study cannot be generalized to all survivors of myocardial infarction. Second, platelet aggregability as a risk factor apparently has an important role when the prevalence of other known risk factors for coronary events occurring after myocardial infarction is low. No conclusions can be drawn from this study about the role of platelet aggregability in patients with a high risk of dying after myocardial infarction. We do not know whether the effects of platelet aggregability would be fundamentally different in such patients. Univariate analysis of the clinical features at entry showed that only infarct size, the need for diuretics or digitalis, and the use of metoprolol increased the risk of death during follow-up (Table 3). The association between the use of metoprolol during the first year of the study (administered in double-blind fashion according to a concurrent research protocol) and an increased risk of death at the end of five years of follow-up is not clear. There is some controversy about the secondary preventive effect of metoprolol.28 , 29 It is highly unlikely that the adverse effects encountered in our study were due to a rebound effect30 when metoprolol was discontinued after one year at the end of the trial of secondary prevention. Of the 13 patients who took metoprolol at entry and died during follow-up, none died within three months after withdrawal of the drug.
It is of interest that smoking did not seem to influence the clinical outcomes in our cohort. This may be due to its small size. When the variables in the univariate analysis were used in multivariate analysis, SPA remained a powerful predictor of five-year mortality and cardiac events in this cohort at low risk. A positive SPA value, in combination with the use of digitalis as an indirect indicator of decreased cardiac function, increased the estimated mortality risk to 60 percent.
It is unlikely that our results are based on a chance finding made three months after infarction, as shown by the data in Table 5. Figure 2 also illustrates that this is not the case, because the patients with a negative test for platelet aggregation at entry had a very low chance of having positive tests (black bars) during follow-up. Also, the patients with positive tests at entry had a chance of more than 50 percent of continuing to have positive tests during the first three years of follow-up.
This study demonstrates that SPA is a useful biologic marker for predicting future coronary events and mortality in a subset of patients who have had a myocardial infarction. As yet, it cannot be concluded that this relation is causal. Also, the pathophysiologic importance of our results is uncertain. SPA may be the result of change in thrombocyte function, or it may be caused by a factor related to extensive atherosclerotic vascular damage or factors related to abnormal endothelial function. Our results, showing a strong association between a positive SPA status and an adverse prognosis, together with the presence of a biologic gradient,5 strongly suggest a relation between thrombocyte function and the complications of coronary artery disease. The results of other platelet-aggregation studies4 5 6 7 8 9 support this concept. Treatment with aspirin has been shown to have a beneficial effect in patients with unstable angina.11 12 13 14 Because spontaneous thrombocyte aggregation has not been measured in these studies, further studies of interventions in patients with atherosclerotic heart disease and spontaneous thrombocyte aggregation are needed to prove a causal relation. The results of our study provide a basis for further intervention studies with antiplatelet drugs in survivors of myocardial infarction.
We are indebted to Mr. P.T. Goedhart and Mrs. M. Buishand (Laboratory, Department of Internal Medicine, Academic Medical Center) for their expert technical assistance, and to Mrs. J. van Dam-Kremer for assistance in the preparation of the manuscript.
Source Information
From the Department of Cardiology (M.D.T.), the Department of Experimental Cardiology (F.J.L.v.C), and the Department of Internal Medicine (J.V.), Academic Medical Center, Amsterdam; and the Department of Cardiology, University Hospital, Leiden, the Netherlands (V.M.C.). Address reprint requests to Dr. Trip at the Academic Medical Center, Department of Cardiology — F4, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands.
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