The effect of rest days on injury rates.

Despite the importance of recuperation, few have studied the impact of rest periods on injury prevention. We determined the effect of rest days (breaks) on injury rates and treatments using electronic injury records from an acrobatic circus company that employs former world-class athletes as acrobats. To account for accumulated fatigue, we considered breaks across SD3 (third consecutive week of 1-day rest) to SD6 as a single exposure level (SD3-6), and vacation and DD (2-day rest) as a single exposure level. Medical attention injury rates were increased post- vs pre-break {rate ratio 1.45 [95% confidence intervals (95% CI): 1.22-1.73]} with less of an effect for 1-day time loss [1.25 (95% CI: 0.58-2.67)] and 15-day time loss [1.10 (95% CI: 0.26-4.56)]. However, the increase in injury rate post break for SD3-6 was similar to that of DD-Vacation (P=0.48, 0.53, and 0.65) for medical attention, and both ≥1 day and ≥15 days time loss, respectively. The increase in the number of treatments post-break was less for SD3-6 vs DD-vacation. Our findings suggest that 2-day breaks every four to 6 weeks may be sufficient to avoid an increasing injury rate due to cumulative fatigue in professional acrobatic circus artists.

Circulating adhesion molecules after short-term exposure to particulate matter among welders.

BACKGROUND: Studies from several countries indicate that welders experience increased risk of mortality and morbidity from ischaemic heart disease. Although the underlying mechanisms are unclear, vascular responses to particulate matter contained in welding fumes may play a role. To investigate this, we studied the acute effects of welding fume exposure on the endothelial component of vascular function, as measured by circulating adhesion molecules involved in leukocyte adhesion (sICAM-1 and sVCAM-1) and coagulation (vWF). METHODS: A panel of 26 male welders was studied repeatedly across a 6 h work-shift on a high exposure welding day and/or a low exposure non-welding day. Personal PM(2.5) exposure was measured throughout the work-shift. Blood samples were collected in the morning (baseline) prior to the exposure period, immediately after the exposure period, and the following morning. To account for the repeated measurements, we used linear mixed models to evaluate the effects of welding (binary) and PM(2.5) (continuous) exposure on each blood marker, adjusting for baseline blood marker concentration, smoking, age and time of day. RESULTS: Welding and PM(2.5) exposure were significantly associated with a decrease in sVCAM-1 in the afternoon and the following morning and an increase in vWF in the afternoon. CONCLUSIONS: The data suggest that welding and short-term occupational exposure to PM(2.5) may acutely affect the endothelial component of vascular function.

A retrospective study of the relationship between biomarkers of atherosclerosis and erectile dysfunction in 988 men.

Erectile dysfunction (ED) is associated with clinical atherosclerosis and several atherosclerotic risk factors including smoking, hypertension, dyslipidemia, diabetes mellitus, obesity and sedentary lifestyle. Clinical atherosclerosis is also associated with these same risk factors and with biomarkers of inflammation, thrombosis, endothelial cell activation. We evaluated the cross-sectional association between the degree of ED and levels of atherosclerotic biomarkers. A subcohort of 988 US male health professionals between the ages 46 and 81 years as part of an ongoing epidemiologic study had atherosclerotic biomarkers measured from blood collected in 1994-1995. These same men had in 2000, been retrospectively asked about erectile function in 1995 and in 2000. Biennial questionnaires since 1986 assessed medical conditions, medications, smoking, physical activity, body mass index, alcohol intake. The retrospective assessment of erectile function in 2000 for 1995 in these 988 men ranged from very good - 28.2%, good - 25.1%, fair - 19.2%, poor - 13.6%, to very poor - 13.9%. Men with poor to very poor erectile function compared to men with good and very good erectile function had 2.9 the odds of having elevated Factor VII levels (P=0.03), 1.9 times the odds of having elevated vascular cell adhesion molecule (P=0.13) and 2.0 times the odds of having elevated intracellular adhesion molecule (P=0.06) and 2.1 times the odds of having elevated total cholesterol/high-density lipoprotein ratio (P=0.02) comparing the top to bottom quintiles for each atherosclerotic biomarker after multivariate adjustment. Lipoprotein(a), homocysteine, interleukin-6 and tumor necrosis factor receptor, C-reactive protein and fibrinogen were not associated with the degree of erectile function after adjustment. We conclude that selected biomarkers for endothelial function, thrombosis and dyslipidemia but not inflammation are associated with the degree of ED in this cross-sectional analysis. Future studies evaluating the prospective association of ED, endothelial function and cardiovascular disease appear warranted.

Association of ventricular arrhythmias detected by implantable cardioverter defibrillator and ambient air pollutants in the St Louis, Missouri metropolitan area.

BACKGROUND: It has previously been reported that the risk of ventricular arrhythmias is positively associated with ambient air pollution among patients with implantable cardioverter defibrillators (ICD) in Boston. AIMS: To assess the association of community exposures to air pollution with ventricular arrhythmias in a cohort of ICD patients in metropolitan St Louis, Missouri. METHODS: ICD detected episodes reported during clinical follow up were abstracted and reviewed by an electrophysiologist to identify ventricular arrhythmias. A total of 139 ventricular arrhythmias were identified among 56 patients. A case-crossover design was used with control periods matched on weekday and hour of the day within the same calendar month. Conditional logistic regression models were adjusted for temperature, barometric pressure, and relative humidity in the 24 hours preceding the event. RESULTS: There was a significant (24%, 95% CI 7% to 44%) increase in risk of ventricular arrhythmias associated with each 5 ppb increase in mean sulphur dioxide and non-significantly increased risk (22%, 95% CI -6% to 60%; and 18%, 95% CI -7% to 50%) associated with increases in nitrogen dioxide (6 ppb) and elemental carbon (0.5 microg/m3), respectively in the 24 hours before the arrhythmia. CONCLUSIONS: These results provide evidence of an association between ventricular arrhythmias and ambient air pollutants in St Louis. This is consistent with previous results from Boston, although the pollutants responsible for the increased risk are different.

Increased particulate air pollution and the triggering of myocardial infarction.

BACKGROUND: Elevated concentrations of ambient particulate air pollution have been associated with increased hospital admissions for cardiovascular disease. Whether high concentrations of ambient particles can trigger the onset of acute myocardial infarction (MI), however, remains unknown. METHODS AND RESULTS: We interviewed 772 patients with MI in the greater Boston area between January 1995 and May 1996 as part of the Determinants of Myocardial Infarction Onset Study. Hourly concentrations of particle mass <2.5 microm (PM(2.5)), carbon black, and gaseous air pollutants were measured. A case-crossover approach was used to analyze the data for evidence of triggering. The risk of MI onset increased in association with elevated concentrations of fine particles in the previous 2-hour period. In addition, a delayed response associated with 24-hour average exposure 1 day before the onset of symptoms was observed. Multivariate analyses considering both time windows jointly revealed an estimated odds ratio of 1.48 associated with an increase of 25 microg/m(3) PM(2.5) during a 2-hour period before the onset and an odds ratio of 1.69 for an increase of 20 microg/m(3) PM(2.5) in the 24-hour period 1 day before the onset (95% CIs 1.09, 2.02 and 1.13, 2.34, respectively). CONCLUSIONS: The present study suggests that elevated concentrations of fine particles in the air may transiently elevate the risk of MIs within a few hours and 1 day after exposure. Further studies in other locations are needed to clarify the importance of this potentially preventable trigger of MI.

Triggering myocardial infarction by marijuana.

BACKGROUND: Marijuana use in the age group prone to coronary artery disease is higher than it was in the past. Smoking marijuana is known to have hemodynamic consequences, including a dose-dependent increase in heart rate, supine hypertension, and postural hypotension; however, whether it can trigger the onset of myocardial infarction is unknown. METHODS AND RESULTS: In the Determinants of Myocardial Infarction Onset Study, we interviewed 3882 patients (1258 women) with acute myocardial infarction an average of 4 days after infarction onset. We used the case-crossover study design to compare the reported use of marijuana in the hour preceding symptoms of myocardial infarction onset to its expected frequency using self-matched control data. Of the 3882 patients, 124 (3.2%) reported smoking marijuana in the prior year, 37 within 24 hours and 9 within 1 hour of myocardial infarction symptoms. Compared with nonusers, marijuana users were more likely to be men (94% versus 67%, P<0.001), current cigarette smokers (68% versus 32%, P<0.001), and obese (43% versus 32%, P=0.008). They were less likely to have a history of angina (12% versus 25%, P<0.001) or hypertension (30% versus 44%, P=0.002). The risk of myocardial infarction onset was elevated 4.8 times over baseline (95% confidence interval, 2.4 to 9.5) in the 60 minutes after marijuana use. The elevated risk rapidly decreased thereafter. CONCLUSIONS: Smoking marijuana is a rare trigger of acute myocardial infarction. Understanding the mechanism through which marijuana causes infarction may provide insight into the triggering of myocardial infarction by this and other, more common stressors.

Triggering of myocardial infarction by cocaine.

BACKGROUND: Cocaine has been implicated as a trigger of acute myocardial infarction in patients with and those without underlying coronary atherosclerosis. However, the magnitude of the increase in risk of acute myocardial infarction immediately after cocaine use remains unknown. METHODS AND RESULTS: In the Determinants of Myocardial Infarction Onset Study, we interviewed 3946 patients (1282 women) with acute myocardial infarction an average of 4 days after infarction onset. Data were collected on the use of cocaine and other potential triggers of myocardial infarction. We compared the reported use of cocaine in the hour preceding the onset of myocardial infarction symptoms with its expected frequency by using self-matched control data based on the case-crossover study design. Of the 3946 patients interviewed, 38 (1%) reported cocaine use in the prior year and 9 reported use within the 60 minutes preceding the onset of infarction symptoms. Compared with nonusers, cocaine users were more likely to be male (87% vs 67%, P=0.01), current cigarette smokers (84% vs 32%, P<0.001), younger (44+/-8 vs 61+/-13 years, P<0.001), and minority group members (63% vs 11%, P<0.001). The risk of myocardial infarction onset was elevated 23.7 times over baseline (95% CI 8.5 to 66.3) in the 60 minutes after cocaine use. The elevated risk rapidly decreased thereafter. CONCLUSIONS: Cocaine use is associated with a large abrupt and transient increase in the risk of acute myocardial infarction in patients who are otherwise at relatively low risk. This finding suggests that studying the pathophysiological changes produced by cocaine may provide insights into the mechanisms by which myocardial infarction is triggered by other stressors.

Association of blood pressure with fibrinolytic potential in the Framingham offspring population.

BACKGROUND: Hypertension is an established risk factor for acute coronary events. Because fibrinolytic and hemostatic factors are also associated with cardiovascular disease, we examined the relations of systolic and diastolic blood pressures (SBP and DBP) to levels of plasminogen activator inhibitor antigen, tissue plasminogen activator antigen, fibrinogen, factor VII, von Willebrand factor, fibrinogen, and plasma viscosity in subjects of the Framingham Offspring Study. METHODS AND RESULTS: We studied 1193 men and 1459 women after the exclusion of subjects with known cardiovascular disease and those receiving anticoagulant or antihypertensive therapy. Linear regression models were used to evaluate SBP and DBP as predictors of fibrinolytic and hemostatic factor levels in separate sex models, with adjustment for age, body mass index, smoking, diabetes, total cholesterol, HDL, triglycerides, alcohol intake, and estrogen use (in women). In both sexes, levels of plasminogen activator inhibitor and tissue plasminogen activator antigen were positively related to SBP and DBP (P<0.001). Plasma viscosity was positively related to SBP (P=0.008) and DBP (P=0.001) in women only. There was no association between SBP or DBP and fibrinogen, factor VII, or von Willebrand factor in either sex. CONCLUSIONS: These data suggest that impaired fibrinolysis may play an important role in the pathogenesis of cardiovascular disease in hypertensive patients.

Alcohol consumption and hemostatic factors: analysis of the Framingham Offspring cohort.

BACKGROUND: Moderate alcohol consumers have lower rates of cardiovascular disease than abstainers. One proposed mechanism is a beneficial effect on hemostatic parameters, but previous studies have provided conflicting results. METHODS AND RESULTS: We measured levels of fibrinogen, plasma viscosity, von Willebrand factor, factor VII, plasminogen activator inhibitor antigen-1, and tissue plasminogen activator antigen in a cross-sectional analysis of 3223 adults free of cardiovascular disease enrolled in the Framingham Offspring Study. We assessed their alcohol consumption with a standardized questionnaire. Light-to-moderate alcohol consumption was associated with lower levels of fibrinogen, plasma viscosity, von Willebrand factor, and factor VII. This association was most pronounced for consumers of 3 to 7 drinks weekly for viscosity and 7 to 21 drinks weekly for the other hemostatic measures. Alcohol intake of 7 to 21 drinks weekly or more was associated with impaired fibrinolytic potential, reflected by higher levels of plasminogen activator inhibitor antigen-1 and tissue plasminogen activator antigen. Wine drinkers had lower plasminogen activator inhibitor antigen-1 levels than other drinkers, particularly at 3 to 21 drinks weekly, but beverage type did not otherwise consistently affect the results. CONCLUSIONS: Light-to-moderate alcohol consumption is associated with lower levels of coagulatory factors, but higher intake is associated with impaired fibrinolytic potential. These findings are consistent with the hypothesis that a balance between hemostatic and fibrinolytic activity may contribute to the complex relation of alcohol use with coronary heart disease.

Similar results of percutaneous transluminal coronary angioplasty for women and men with postmyocardial infarction ischemia.

OBJECTIVES: The purpose of this study was to determine whether there are gender differences in the outcome of percutaneous transluminal coronary angioplasty performed for postmyocardial infarction ischemia. BACKGROUND: Although women have a higher mortality rate after myocardial infarction than that of men, they are less frequently referred for coronary angioplasty (and coronary artery bypass graft surgery) than are men, possibly because of expectations of a worse procedural outcome. METHODS: We analyzed the morbidity and mortality at coronary angioplasty and during a mean follow-up period of 34.4 months for women and 34.2 months for men in 505 consecutive patients (164 women and 341 men) with postmyocardial infarction ischemia between 1981 and 1989. RESULTS: Compared with men, women had similar procedural success rates (89.6% and 91.2%, respectively), need for coronary artery bypass surgery (3.7% and 2.6%) and mortality rates at coronary angioplasty (0.6% and 0.9%). During the follow-up period, there were no significant gender differences in the requirement for coronary artery bypass surgery (3.6% and 4%), repeat angioplasty (18.7% and 17.3%), reinfarction (5.8% and 6%) and death (3.6% and 3.7%) or the combined end points of all four events (26.6% and 26.6%). Women had significantly more recurrent angina than did men (54% vs. 42.5%, p < 0.01), even though the extent of coronary artery disease and frequency of incomplete revascularization were similar in men and women. CONCLUSIONS: The procedural outcome of coronary angioplasty for postmyocardial infarction ischemia is similar in women and men. Long-term follow-up is also similar except that women experience an increased incidence of recurrent angina, an outcome also reported after bypass surgery. Therefore, concerns over the safety of coronary angioplasty in women should not adversely influence decisions concerning referral of women for coronary angioplasty after myocardial infarction complicated by ischemia.

Educational attainment, anger, and the risk of triggering myocardial infarction onset. The Determinants of Myocardial Infarction Onset Study Investigators.

BACKGROUND: While it has recently been shown that anger may trigger the onset of acute myocardial infarction, there has been no study of the role of socioeconomic factors in such triggering. Socioeconomic factors, such as educational attainment, may modulate the risk of triggering because of their influence on individual reactivity to external stressors and on the prevalence of traditional cardiac risk factors. OBJECTIVE: To evaluate the influence of educational attainment on the relative risk of myocardial infarction onset following episodes of anger. METHODS: We interviewed 1623 patients (501 women) an average of 4 days following a myocardial infarction. Data were collected on standard demographic variables as well as risk factors for coronary artery disease. Educational attainment was categorized into 3 levels: less than high school, completed high school, and at least some college. Anger was assessed by the Onset Anger Scale, a single-item, 7-level, self-report scale. Occurrence of anger in the 2 hours preceding the onset of myocardial infarction was compared with its expected frequency using self-matched control data based on the case-crossover study design. RESULTS: The risk of having a myocardial infarction triggered by isolated episodes of anger declined consistently and significantly with increasing levels of educational attainment (P = .03). The relative risk was twice as high among those with less than high school education (relative risk, 3.3; 95% confidence interval, 2.0-5.4) compared with patients with at least some college education (relative risk, 1.6; 95% confidence interval, 0.9-2.9). CONCLUSIONS: These findings indicate that socioeconomic factors are potent modulators of the risk of triggering acute cardiovascular disease onset. A better understanding of the physiological mechanisms underlying this association may lead to novel approaches to prevent acute cardiovascular events.

Education and the metabolic syndrome in women.

OBJECTIVE: The main objective was to examine the association between the metabolic syndrome and socioeconomic position (as indicated by education) among women. RESEARCH DESIGN AND METHODS: The study sample comprised healthy women (aged 30-65 years) in Sweden who were representative of the general population in a metropolitan area. Socioeconomic position was measured by educational level (mandatory [< or = 9 years], high school, or college/university). The metabolic syndrome was defined as the presence of two or more of the following components: 1) fasting plasma glucose level > or = 7.0 mmol/l; 2) arterial blood pressure > or = 160/90 mmHg; 3) fasting plasma triglycerides > or = 1.7 mmol/l and/or HDL cholesterol < 1.0 mmol/l; and 4) central obesity (waist-to-hip ratio > 0.85 and/or BMI > 30 kg/m2). RESULTS: After adjustment for age, the risk ratio for the presence of the metabolic syndrome comparing the lowest (< or = 9 years) with the highest (college/university) education was 2.7 (95% CI 1.1-6.8). This association persisted after controlling for menopausal status, family history of diabetes, and behavioral risk factors. CONCLUSIONS: Low education is associated with increased risk for metabolic syndrome in middle-aged women. These findings show that not only are women with low socioeconomic position at increased risk for individual risk factors that are associated with cardiovascular disease and type 2 diabetes, they are also at increased risk for the metabolic clustering of risk factors.

Routine perioperative dipyridamole 201Tl imaging in diabetic patients undergoing vascular surgery.

OBJECTIVE: To assess the utility of dipyridamole thallium testing in symptomatic and asymptomatic patients with diabetes undergoing vascular surgery. RESEARCH DESIGN AND METHODS: Dipyridamole 201Tl myocardial scintigraphy was performed preoperatively in 93 consecutive patients with diabetes undergoing peripheral vascular procedures. The utility of clinical and thallium variables in predicting cardiovascular complications was assessed. RESULTS: Two groups of patients were identified: group A (36 patients) without clinical evidence of cardiac disease and group B (57 patients) with clinical evidence of cardiac disease. Dipyridamole thallium scans were abnormal in 21 of 36 (58%) of group A patients compared with 53 of 57 (93%) of group B patients (P < 0.0001). Compared with group B patients with perfusion defects, group A patients with perfusion abnormalities tended to have fewer defects per scan (2.7 +/- 1.5 vs. 3.6 +/- 1.9, P = 0.05). No perioperative cardiac complications occurred in group A patients while perioperative cardiac complications occurred in 9 of 57 (16%, 95% CI 7-28%) group B patients (P = 0.01). For the entire study population, the complication rate was 10%. CONCLUSIONS: Diabetic individuals without clinical markers for coronary artery disease appear to be at low risk for adverse postoperative cardiac events after vascular surgery. Preoperative myocardial perfusion imaging may add little to cardiovascular risk assessment in this subgroup of patients with diabetes.

Impact of diabetes on long-term survival after acute myocardial infarction: comparability of risk with prior myocardial infarction.

OBJECTIVE: To determine the effect of diabetes on long-term survival after acute myocardial infarction and to compare its effect with that of a previous myocardial infarction. RESEARCH DESIGN AND METHODS: In a prospective cohort study, we followed 1,935 patients hospitalized with a confirmed acute myocardial infarction at 45 U.S. medical centers between 1989 and 1993, as part of the Determinants of Myocardial Infarction Onset Study. Trained interviewers performed chart reviews and face-to-face interviews with all patients. We analyzed survival using Cox proportional hazards regression to control for potentially confounding factors. RESULTS: Of the 1,935 patients, 320 (17%) died during a mean follow-up of 3.7 years. A total of 399 patients (21%) had previously diagnosed diabetes. Diabetes was associated with markedly higher total mortality in unadjusted (hazard ratio [HR] 2.4; 95% CI 1.9-3.0) and adjusted (1.7; 1.3-2.1) analyses. The magnitude of the effect of diabetes was identical to that of a previous myocardial infarction. The effect of diabetes was not significantly modified by age, smoking, household income, use of thrombolytic therapy, type of hypoglycemic treatment, or duration of diabetes, but the risk associated with diabetes was higher among women than men (adjusted HRs 2.7 vs. 1.3, P = 0.01). CONCLUSIONS: Diabetes is associated with markedly increased mortality after acute myocardial infarction, particularly in women. The increase in risk is of the same magnitude as a previous myocardial infarction and provides further support for aggressive treatment of coronary risk factors among diabetic patients.

Alcohol consumption and subclinical findings on magnetic resonance imaging of the brain in older adults: the cardiovascular health study.

BACKGROUND AND PURPOSE: Subclinical findings on MRI of the brain are associated with poorer cognitive and neurological function among older adults. We sought to determine how alcohol consumption is related to these findings. METHODS: As part of the Cardiovascular Health Study, 3660 adults aged 65 years and older underwent MRI of the brain from 1992 to 1994. We excluded 284 participants with a confirmed history of cerebrovascular disease. We assessed self-reported intake of beer, wine, and liquor at the annual clinic visit closest to the date of the MRI and grouped participants into 6 categories: abstainers, former drinkers, <1 drink weekly, 1 to <7 drinks weekly, 7 to <15 drinks weekly, and >/=15 drinks weekly. Neuroradiologists assessed white matter grade, infarcts, ventricular size, and sulcal size in a standardized and blinded manner. We used multivariate regression to control for sociodemographic and clinical characteristics. RESULTS: We found a U-shaped relationship between alcohol consumption and white matter abnormalities. Compared with abstainers, individuals consuming 1 to <7 drinks had an OR of 0.68, and those consuming >/=15 drinks weekly had an OR of 0.95 (p for quadratic term=0.01). Heavier alcohol consumption was associated with a lower prevalence of infarcts (OR for >/=15 drinks weekly relative to abstainers 0.59; P for trend=0.004), but larger ventricular size (OR for >/=15 drinks weekly relative to abstainers 1.32; P for trend=0.006) and sulcal size (OR for >/=15 drinks weekly relative to abstainers 1.53; P for trend=0.007). CONCLUSIONS: Moderate alcohol consumption is associated with a lower prevalence of white matter abnormalities and infarcts, thought to be of vascular origin, but with a dose-dependent higher prevalence of brain atrophy on MRI among older adults. The extent to which these competing associations influence overall brain function will require further study.

Height is not associated with long-term survival after acute myocardial infarction.

BACKGROUND: Studies show an inverse association between height and risk of myocardial infarction. How height affects survival after acute myocardial infarction is uncertain. METHODS: In the Determinants of Myocardial Infarction Onset Study, trained interviewers performed chart reviews and face-to-face interviews with 1935 patients hospitalized with acute myocardial infarction in 45 US medical centers between 1989 and 1993. We excluded 15 patients with missing information on height. After a search of the National Death Index for patients who died before 1996, we analyzed the relationship of height and survival with Cox proportional hazards regression. RESULTS: Of the 1920 eligible patients, 317 (17%) died during a median follow-up of 3.8 years. Height was positively associated with younger age, greater educational attainment, and a lower likelihood of being sedentary among both men and women. Height was not associated with long-term survival among women in unadjusted or adjusted analyses. Among men, height was associated with survival only in unadjusted analyses; adjustment for age eliminated this association. We found no relationship between height and survival in any individual age group among men or women. CONCLUSIONS: Although stature may be associated with the risk of acute myocardial infarction, it is not associated with long-term survival after such an event.

Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death.

To evaluate the impact of elimination of the morning peak of cardiovascular events, we performed a meta-analysis of studies of circadian variation of myocardial infarction and sudden cardiac death. The impact would be significant because approximately 1 of every 11 acute myocardial infarctions and 1 of every 15 sudden cardiac deaths are attributable to the morning excess incidence.

Long-term prognostic value of preoperative dipyridamole thallium imaging and clinical indexes in patients with diabetes mellitus undergoing peripheral vascular surgery.

The objective of this study is to assess the prognostic impact of preoperative dipyridamole thallium imaging and clinical variables on the long-term outcome of diabetic patients undergoing peripheral vascular surgery. Complete follow-up was obtained in 101 consecutive patients with diabetes mellitus undergoing routine dipyridamole thallium scintigraphy before vascular surgery (mean 4.2 +/- 3.2 years, range 1 month to 11 years). Low risk was defined by diabetes alone with a normal resting electrocardiogram. High risk was defined as a history of angina, myocardial infarction, congestive heart failure, or resting electrocardiogram abnormalities. There were 71 deaths in 98 patients discharged alive from the hospital (median survival 4.4 years). Age, the presence of resting electrocardiogram abnormalities, and an abnormal thallium scan were independent predictors of late death. After adjusting for age >70 years and thallium abnormalities, high-risk patients had a death rate 4.8 times (95% confidence interval 1.7 to 13.4, p <0.002) greater than low-risk patients. The presence of >2 reversible thallium defects was useful in further risk stratification of both low- and high-risk patients. Low-risk patients with >2 reversible defects had a median survival of 4.0 years compared with 9.4 years in those with < or =2 reversible defects (p <0.001). Similarly, high-risk patients with < or =2 reversible defects had an intermediate median survival rate of 4.7 years compared with 1.8 years in the group with >2 reversible defects (p <0.001). Therefore, advanced age and the presence of resting electrocardiographic or thallium abnormalities identifies a subset of diabetic patients with a poor long-term outcome after vascular surgery. Combined clinical and thallium variables may identify a population in whom intensive medical or surgical interventions may be warranted to reduce both perioperative and late cardiac events.

Significance of location (anterior versus inferior) and type (Q-wave versus non-Q-wave) of acute myocardial infarction in patients undergoing percutaneous transluminal coronary angioplasty for postinfarction ischemia.

Predictors of increased risk for recurrent cardiac events and death after acute myocardial infarction include postinfarction myocardial ischemia, anterior location of the infarct, and non-Q-wave versus Q-wave infarction. Although coronary angioplasty is performed in patients with postinfarction ischemia to alleviate symptoms, the outcome according to location and type of infarction and the effect on prevention of subsequent myocardial infarction and death are not known. To determine if location and type of myocardial infarction provide prognostic information in patients with postinfarction ischemia, we analyzed morbidity and mortality during and after coronary angioplasty according to the location (anterior vs inferior) and type (Q-wave vs non-Q-wave) of myocardial infarction in 505 consecutive patients. The incidence of recurrent angina, repeat coronary angioplasty, coronary bypass surgery, reinfarction, and death during long-term follow-up after hospital discharge (mean 34 +/- 19 months) for the 440 patients with an initial successful angioplasty was also compared. During the procedure, there was no difference in the primary success rate or mortality among the different groups; however, more patients with anterior non-Q-wave myocardial infarction underwent emergent bypass grafting after unsuccessful coronary angioplasty (p = 0.001). Multivariate Cox proportional-hazards analyses controlling for age, gender, number of diseased vessels, location, type of infarction, and year of coronary angioplasty revealed that more patients with anterior infarction had > or = 1 cardiac event (repeat angioplasty, coronary artery bypass grafting, reinfarction, or death) than did those with inferior infarction (RR 1.80, 95% confidence interval [Ci] 1.22 to 2.65, p = 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of aspirin dosage and enteric coating on platelet reactivity.

Although aspirin is effective in the prevention and treatment of cardiovascular diseases, the optimal dose remains uncertain. The purpose of this study was to compare the platelet inhibitory and prostacyclin-sparing effects of 2 doses (81 and 325 mg) and forms (enteric-coated and regular) of aspirin. Since platelet reactivity has been reported to increase after strenuous exercise, a known trigger of myocardial infarction, subjects were studied following maximal treadmill exercise as well as at rest. Forty male healthy subjects were evaluated using a randomized, double-blind, parallel study design. Blood samples were obtained before and after maximal treadmill exercise at baseline and after 7 days on aspirin therapy. Both enteric and regular aspirin in 81- and 325-mg dosages markedly inhibited adenosine diphosphate and epinephrine-induced aggregation at rest and after exercise. Aspirin also inhibited the platelet response to collagen as assessed by a longer lag time to aggregation. The prolongation of lag time was greater for 325 mg than for 81 mg (100 +/- 7 vs 91 +/- 7; p = 0.04, after exercise). There were no significant dose-related differences in plasma 6-keto-prostaglandin F1alpha level; however, enteric-coated aspirin inhibited the exercise-induced increase in 6-keto-prostaglandin F1alpha to a lesser extent than regular aspirin. Although both doses (81 and 325 mg) and types (regular and enteric-coated) of aspirin inhibited adenosine diphosphate and epinephrine-induced aggregation equally, the 325-mg dose inhibited collagen-induced aggregation to a greater extent than 81 mg. The greater platelet inhibition observed with 325 mg may be clinically relevant in acute coronary syndromes characterized by plaque rupture with extensive collagen exposure and platelet activation.