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Biomedical subjects

J E Muller

Publications and source records attributed to J E Muller.

At least 55 records · Page 3Linked to original sources
PubMed1997

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.

Adult↗
PubMed1997

Hypobetalipoproteinemia is associated with low levels of hemostatic risk factors in the Framingham offspring population.

BACKGROUND: Given the importance of thrombosis in causation of acute coronary syndromes, it is possible that the beneficial effect of low lipid levels on the risk of coronary events is achieved by lowering thrombotic potential of the blood. Hypobetalipoproteinemia is characterized by plasma concentrations of apolipoprotein B and LDL cholesterol that are one third of those observed in the general population. The aim of this study was to utilize subjects with hypobetalipoproteinemia to examine the relation between thrombotic potential and low levels of LDL cholesterol. METHODS AND RESULTS: Hemostatic risk factors were measured in 1878 individuals (1003 women and 875 men) participating in cycle 5 of the Framingham Offspring Study. The subjects were divided into five groups on the basis of LDL cholesterol level. Subjects with hypobetalipoproteinemia (LDL cholesterol < 70 mg/dL) had the lowest levels of fibrinogen, plasminogen activator inhibitor-1 antigen, and tissue plasminogen activator antigen. As LDL cholesterol increased, there was a significant increase in the levels of the hemostatic risk factors, with the exception of von Willebrand factor antigen. Adjustment with multivariate regression analyses for the covariates age, sex, body mass index, diabetes mellitus, smoking, alcohol intake, triglyceride level, and use of antihypertensive medication did not materially alter the results. CONCLUSIONS: Decreasing levels of LDL cholesterol are associated with decreasing levels of hemostatic risk factors. Subjects with hypobetalipoproteinemia have the lowest levels of hemostatic risk factors and may be protected against thrombotic complications of atherosclerotic cardiovascular disease because of reduced thrombotic potential. One mechanism by which lipid-lowering therapy may decrease clinical cardiac events is through a reduction in thrombotic tendency.

Apolipoproteins B↗
PubMed1997

Circadian variation in the onset of unstable angina and non-Q-wave acute myocardial infarction (the TIMI III Registry and TIMI IIIB).

Circadian variation has been demonstrated in several types of acute cardiovascular disease, including acute myocardial infarction (AMI), sudden cardiac death, silent ambulatory ischemia, and thrombotic stroke. In contrast, no diurnal variation was observed in 1 study of non-Q-wave AMI, and limited data are available for unstable angina. To assess whether circadian variation is present in unstable angina and non-Q-wave AMI, we examined the time of onset of ischemic pain in 7,731 patients who were prospectively identified in the Thrombolysis in Myocardial Ischemia (TIMI) III Registry, 3,318 of whom were enrolled in the prospective study, and in 1,473 patients enrolled in the TIMI IIIB trial. A circadian variation in the onset of pain was observed, with an increase in the number of patients experiencing the onset of pain in the morning hours between 6 A.M. and 12 noon (p <0.001). This circadian variation was observed both in patients with unstable angina and in those with evolving non-Q-wave AMI. A similar circadian pattern was observed in all subgroups tested. These findings were confirmed in the TIMI IIIB trial and complement previous studies suggesting that circadian variation exists in the onset of the full spectrum of myocardial ischemic syndromes.

Aged↗
PubMed1996

Angioscopic predictors of early adverse outcome after coronary angioplasty in patients with unstable angina and non-Q-wave myocardial infarction.

BACKGROUND: Clinical and angiographic criteria have a limited ability to predict adverse outcome in patients with unstable angina who are undergoing percutaneous transluminal coronary angioplasty (PTCA). We investigated whether the use of angioscopy can improve prediction of early adverse outcome after PTCA. METHODS AND RESULTS: Angioscopic characterization of the culprit lesion was performed before PTCA in 32 patients with unstable angina and 10 with non-Q-wave infarction. Seven patients (17%) had an adverse outcome (myocardial infarction, repeat PTCA, or need for coronary artery bypass graft surgery) within 24 hours after PTCA. Six of 18 patients with a yellow culprit lesion had an adverse outcome compared with 1 of 24 in whom the culprit lesion was white (P = .03). Six of 20 patients with plaque disruption suffered an adverse outcome compared with 1 of 22 with nondisrupted plaques (P = .04). Six of 17 patients with intraluminal thrombus had an adverse outcome, whereas only 1 of 25 patients without thrombus suffered an adverse outcome (P = .01). Yellow color, disruption, and thrombus at the culprit lesion site were associated with an eightfold increase in risk of adverse outcome after PTCA. The prediction of PTCA outcome based on characteristics of the plaque that were identifiable by angioscopy was superior to that estimated by the use of angiographic variables. CONCLUSIONS: In patients with unstable angina and non-Q-wave infarction, angioscopic features of disruption, yellow color, or thrombus at the culprit lesion site can identify patients at high risk of early adverse outcome after PTCA. Angioscopy was superior to angiography for prediction of PTCA outcome.

Adult↗
PubMed1996

Triggering myocardial infarction by sexual activity. Low absolute risk and prevention by regular physical exertion. Determinants of Myocardial Infarction Onset Study Investigators.

OBJECTIVE: To determine the relative risks of nonfatal myocardial infarction (MI) triggered by sexual activity among the general population and in patients with prior coronary heart disease. DESIGN: Relative risks and effect modification were calculated by the case-crossover method, a new epidemiologic technique designed to quantify the transient change in risk following exposure to a potential disease trigger. SETTING/PARTICIPANTS: A total of 1774 patients with MI were interviewed in 45 hospitals throughout the United States. Data were gathered on potential triggers of MI occurring immediately prior to the event and during the previous year. Results are presented for the 858 patients who were sexually active in the year prior to the MI, with attention to the 273 patients who had coronary artery disease prior to their index MI, and the effect of regular exertion on risk. MAIN OUTCOME MEASURE: The relative risk of nonfatal MI following sexual activity. RESULTS: Of the 858 patients, 79(9%) reported sexual activity in the 24 hours preceding MI, and 27(3%) reported sexual activity in the 2 hours preceding onset of symptoms of MI. The relative risk of MI occurring in the 2 hours after sexual activity was 2.5(95% confidence interval [CI], 1.7-3.7). The relative risk of triggering onset of MI among patients with a history of prior angina (2.1 [95% CI, 0.8-5.8]) or prior MI (2.9 [95% CI, 1.3-6.5]) was not greater than that observed in those without prior cardiac disease. Sexual activity was a likely contributor to the onset of MI in only 0.9% of cases and regular exertion was associated with decreasing risk. CONCLUSIONS: Sexual activity can trigger the onset of MI. However, the relative risk is low, and since the absolute hourly risk of MI is extremely low, the absolute risk increase caused by sexual activity also is extremely low (1 chance in a million for a healthy individual). Moreover, the relative risk is not increased in patients with a prior history of cardiac disease and regular exercise appears to prevent triggering. These findings should be useful for counseling patients and decreasing the fear of sexual activity that often prevents complete rehabilitation from cardiovascular disease.

Adult↗
PubMed1996

A patent infarct-related artery is associated with reduced long-term mortality after percutaneous transluminal coronary angioplasty for postinfarction ischemia and an ejection fraction <50%.

BACKGROUND: Prognosis after myocardial infarction (MI) is influenced by the presence of post-MI ischemia and possibly the patency of the infarct-related artery. The purpose of this study was to compare long-term outcome (reinfarction and death) in patients with open versus closed coronary arteries after percutaneous transluminal coronary angioplasty performed for MI complicated by persistent ischemia. METHODS AND RESULTS: Between 1981 and 1989, 505 patients underwent percutaneous transluminal coronary angioplasty for post-MI ischemia at the Deaconess Hospital. Long-term incidence (mean follow-up, 34 months) of death, nonfatal reinfarction, repeated coronary angioplasty, and coronary bypass surgery was determined for 479 patients and then compared on the basis of the status of the artery, open versus closed, at the end of angioplasty. The 5-year Kaplan-Meier actuarial mortality rate was 4.9% for 456 patients with open infarct-related arteries and 19.4% for 23 patients with closed infarct-related arteries (P=.0008). Multivariate Cox proportional hazards analyses controlling for age, sex, number of diseased vessels, type and location of MI, and year of coronary angioplasty revealed a hazard ratio for death for closed compared with open arteries of 6.1 (95% CI, 1.8 to 20.0). Among patients with ejection fractions <50%, a closed artery was associated with a higher mortality (p=.0014) compared with patients with open arteries. The status of the artery was not associated with a difference in mortality in patients with ejection fractions > or = 50%. CONCLUSIONS: As open artery after coronary angioplasty for post-MI ischemia is associated with significantly lower long-term mortality, particularly in patients with ejection fractions <50%.

Adult↗
PubMed1996

Stress-induced hemodynamic and hemostatic changes in patients with systemic hypertension: effect of verapamil.

Stress-induced hemodynamic and hemostatic responses may acutely trigger atherosclerotic plaque disruption and thrombosis leading to myocardial infarction. This study was designed to evaluate the responses to three stressors and to determine if once-daily sustained release verapamil (Verelan) modified these responses. We studied 13 patients with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 4 weeks of therapy, patients were evaluated following assumption of the upright posture, mental stress, and cold pressor test. During placebo, the stressors produced an increase in systolic pressure (144 +/- 2 to 167 +/- 3 mmHg, p < 0.001), heart rate (70 +/- 2 to 77 +/- 2 beats/ min, p < 0.001), and platelet aggregability to adenosine diphosphate (threshold concentration fell from 2.8 +/- 0.4 to 1.9 +/- 0.1 microM, p = 0.05) and epinephrine (3.4 +/- 0.9 to 1.6 +/- 0.6 microM, p < 0.001). Verapamil lowered systolic pressure at baseline (144 +/- 2 to 134 +/- 2 mmHg, p < 0.001), and after stress (167 +/- 3 to 154 +/- 3 mmHg, p < 0.001), but did not alter the absolute increase with stress. During verapamil, platelet reactivity did not increase with stress, and the post-stress response to epinephrine was reduced (higher threshold concentration) compared with placebo (3.9 +/- 1.3 vs. 1.5 +/- 0.3 microM, p = 0.05). Verapamil also reduced the response to collagen (increased lag time) at baseline and after stress (111 +/- 9 vs. 91 +/- 3 s, p < 0.01). We conclude that verapamil blunted potentially harmful stress-induced hemodynamic and hemostatic changes. Further studies are required to determine whether these effects translate into a lower incidence of acute cardiovascular events.

Adenosine Diphosphate↗
PubMed1996

The pathophysiology of the onset of morning cardiovascular events.

Evidence obtained over the past decade indicates that myocardial infarction (MI) and sudden death are not random events but rather, in many cases, may be triggered by the daily activities of the subject. The importance of physical or mental stresses as triggers is suggested by the parallel morning increased onsets of MI, sudden cardiac death, and stroke. Unstable angina and MI are usually precipitated by thrombus formation over a disrupted plaque that causes partial or complete obstruction of coronary artery blood flow. This process may be caused by physiologic factors that lead to rupture of a vulnerable plaque and subsequent thrombosis. Beta-blockers and aspirin, which can diminish these physiologic processes, have been shown to blunt or abolish the morning peak of onset of acute MI. It is hypothesized that occlusive coronary thrombosis occurs when an atherosclerotic plaque becomes vulnerable to rupture, and mental or physical stress causes the plaque to rupture. Increases in coagulability or vasoconstriction triggered by daily activities may also contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation of the onset of acute cardiovascular disease suggests the need for pharmacologic protection of patients during the vulnerable periods and provides clues to the mechanism of disease onset, the investigation of which may lead to improved methods of prevention.

Angina Pectoris↗
PubMed1996

Prevention and practical aspects of triggering of cardiovascular events.

The recognition of the peak morning incidence of cardiovascular events and the role of triggering mechanisms can lead to some practical suggestions. For instance, adequate pharmacologic coverage over the full 24-hour period, in particular during the morning period of increased risk, is desirable among individuals taking antihypertensive and anti-ischemic medication. Although the absolute risk of an event occurring following a single exposure to a potential trigger is in general too low to recommend avoidance of the stressor, further research in this area may result in the design of pharmacologic and nonpharmacologic means to prevent the trigger from precipitating disease onset.

Coronary Disease↗
PubMed1995

Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators.

BACKGROUND: Many anecdotes and several uncontrolled case series have suggested that emotionally stressful events, and more specifically, anger, immediately precede and appear to trigger the onset of acute myocardial infarction. However, controlled studies to determine the relative risk of myocardial infarction after episodes of anger have not been reported. METHODS AND RESULTS: We interviewed 1623 patients (501 women) an average of 4 days after myocardial infarction. The interview identified the time, place, and quality of myocardial infarction pain and other symptoms, the estimated usual frequency of anger during the previous year, and the intensity and timing of anger and other potentially triggering factors during the 26 hours before the onset of myocardial infarction. Anger was assessed by the onset anger scale, a single-item, seven-level, self-report scale, and the state anger subscale of the State-Trait Personality Inventory. Occurrence of anger in the 2 hours preceding the onset of myocardial infarction was compared with its expected frequency using two types of self-matched control data based on the case-crossover study design. The onset anger scale identified 39 patients with episodes of anger in the 2 hours before the onset of myocardial infarction. The relative risk of myocardial infarction in the 2 hours after an episode of anger was 2.3 (95% confidence interval, 1.7 to 3.2). The state anger subscale corroborated these findings with a relative risk of 1.9 (95% confidence interval, 1.3 to 2.7). Regular users of aspirin had a significantly lower relative risk (1.4; 95% confidence interval, 0.8 to 2.6) than nonusers (2.9; 95% confidence interval, 2.0 to 4.1) (P < .05). CONCLUSIONS: Episodes of anger are capable of triggering the onset of acute myocardial infarction, but aspirin may reduce this risk. A better understanding of the manner in which external events trigger the onset of acute cardiovascular events may lead to innovative preventive strategies aimed at severing the link between these external stressors and their pathological consequences.

Adrenergic beta-Antagonists↗
PubMed1995

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)

Adult↗
PubMed1995

Morning peak in ventricular tachyarrhythmias detected by time of implantable cardioverter/defibrillator therapy. The CPI Investigators.

BACKGROUND: A morning peak in occurrence of sudden cardiac death has been identified in epidemiological studies, but the studies are subject to selection bias, with the exclusion of unwitnessed deaths, which are more likely to occur at night. The recent availability of implantable cardioverter/defibrillators that record the time of ventricular tachyarrhythmias requiring either pacing or shock therapy provides an opportunity to clarify the timing of ventricular tachyarrhythmias predisposing to sudden cardiac death. Analysis of the timing of arrhythmias in different patient subgroups, such as patients with poor left ventricular function, may provide further insight into the mechanism of onset of sudden cardiac death. METHODS AND RESULTS: We studied patients in whom a cardioverter/defibrillator (Ventak PRx) was implanted between September 1990 and September 1993 in US centers. Events that could be timed occurred in 483 patients. With an RR cycle length of 240 ms as a cutoff, corresponding to a heart rate of 250 beats per minute, episodes were categorized as rapid (n = 1217) or less rapid (n = 9266) ventricular tachyarrhythmias. A higher proportion of both rapid and less rapid ventricular tachyarrhythmias began in the late morning compared with other times of the day. The subgroup of patients with ejection fraction < 20% at the time of implantation demonstrated a more uniform 24-hour distribution of tachycardias < or = 250 beats per minute than patients with higher left ventricular ejection fraction. CONCLUSIONS: Further investigation of the late morning peak and of precipitants of ventricular tachyarrhythmias by use of data from the implantable cardioverter/defibrillator may provide insight into the pathophysiological mechanisms causing sudden cardiac death.

Circadian Rhythm↗
PubMed1995

Association between increased estrogen status and increased fibrinolytic potential in the Framingham Offspring Study.

BACKGROUND: Although extensive evidence indicates that estrogen is responsible for the markedly decreased cardiovascular risk of premenopausal women, the mechanism through which estrogen might exert its protective effect has not been adequately explained. Since thrombosis is now recognized to play an important role in the onset of cardiovascular disease, we investigated the relation between estrogen status and fibrinolytic potential, a determinant of thrombotic risk. METHODS AND RESULTS: We determined levels of plasminogen activator inhibitor (PAI-1) antigen and tissue plasminogen activator (TPA) antigen in 1431 subjects from the Framingham Offspring Study. Fibrinolytic potential was compared between subjects with high estrogen status (premenopausal women and postmenopausal women receiving hormone replacement therapy) and low estrogen status (men and postmenopausal women not receiving hormone replacement therapy). In all comparisons, subjects with high estrogen status had greater fibrinolytic potential (lower PAI-1 levels) than subjects with low estrogen status. First, postmenopausal women receiving estrogen replacement therapy had lower levels of PAI-1 than those not receiving therapy (13.0 +/- 0.5 versus 19.5 +/- 1.0 ng/mL, P < .001). Second, premenopausal women had lower levels of PAI-1 than men of a similar age (14.8 +/- 0.6 versus 20.3 +/- 0.8 ng/mL, P < .001); this sex difference diminished when postmenopausal women not receiving hormone replacement therapy were compared with men of a similar age (19.6 +/- 0.7 versus 21.1 +/- 0.7 ng/mL, P = .089). Third, premenopausal women had markedly lower levels of PAI-1 antigen than postmenopausal women not receiving estrogen therapy (14.8 +/- 0.6 versus 19.5 +/- 1.0 ng/mL, P < .001). The between-group differences observed for TPA antigen were similar to those for PAI-1 antigen. CONCLUSIONS: Each of these comparisons indicates that the cardioprotective effect of estrogen may be mediated, in part, by an increase in fibrinolytic potential. These findings might provide at least a partial explanation for the protection against cardiovascular disease experienced by premenopausal women, and the loss of that protection following menopause.

Coronary Disease↗
PubMed1995

Triggering of plaque disruption and arterial thrombosis in an atherosclerotic rabbit model.

BACKGROUND: It is now recognized that plaque disruption and thrombosis, a process often triggered by activities of the patient, is generally the cause of the onset of acute coronary syndromes. Understanding of disease onset could be greatly enhanced by the availability of a suitable animal model of plaque disruption and thrombosis. The aim of this study was to replicate and further characterize an atherosclerotic rabbit model of triggering of arterial thrombosis that was introduced by Constantinides and Chakravarti more than 30 years ago but not subsequently used. Aortic plaques were induced by a high-cholesterol diet, by mechanical balloon injury of the artery, or by a combination of the two. Triggering was attempted by injection of Russell's viper venom (RVV), which is a proteolytic procoagulant, and histamine. METHODS AND RESULTS: A total of 53 New Zealand White rabbits were exposed to one of four preparatory regimens: rabbits in group I (n = 9) were fed a regular diet for 8 months; rabbits in group II (n = 13) were fed a diet of 1% cholesterol for 2 months alternated with 2 months of a regular diet for a total of 8 months; rabbits in group III (n = 5) underwent balloon-induced arterial wall injury, then were given a regular diet for 8 months; and rabbits in group IV (n = 14) underwent balloon-induced arterial wall injury, then were given a diet of 1% cholesterol for 2 months followed by a regular diet for 2 months for a total of 4 months. After completion of the preparatory regimen, triggering of plaque disruption and thrombosis was attempted by injection of RVV (0.15 mg/kg IP) and histamine (0.02 mg/kg IV). In group I, normal control rabbits without atherosclerosis, only one small thrombus was noted in 1 of 9 rabbits. In group II, cholesterol-fed rabbits, thrombosis occurred in 3 of 13 rabbits. Thrombus occurred in all rabbits in group III (5 of 5) and in 10 of 14 rabbits in group IV. Although the frequency of thrombosis was not significantly different between groups I and II, possibly due to a small sample size, it was significantly different among all four groups (P < .001). Also, the frequency and amount of thrombus formation were significantly different among all four groups (P < .001; P < .0001) but not between groups I and II. Rabbits with atherosclerosis (those in groups II and IV) demonstrated plaque disruption and overlying platelet-rich thrombus formation similar to that observed in patients with acute coronary syndromes. The surface area covered by thrombus was 2 mm2 in group I, 15.3 +/- 19.2 mm2 in group II, 223 +/- 119 mm2 in group III, and 263 +/- 222 mm2 in group IV. Rabbits in groups III and IV had the greatest amount of thrombus, and this amount was significantly greater than in rabbits in groups I and II (P < .001 and P < .03, respectively). CONCLUSIONS: A suitable animal model is available for the study of plaque disruption and arterial thrombosis. Hypercholesterolemia and mechanical arterial wall injury seemed to produce plaques vulnerable to triggering of disruption and thrombosis, whereas normal arteries were relatively resistant to triggering. This model provides a method to evaluate agents that might decrease the occurrence of vulnerable plaques or the amount of thrombus formed after triggering. Most important, the model can be used to identify the features of vulnerable plaques and the pharmacological stressors that trigger plaque disruption and thrombus formation.

Animals↗