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Biomedical subjects

W J Kop

Publications and source records attributed to W J Kop.

32 records · Page 2Linked to original sources

Mental stress as a trigger of myocardial ischemia and infarction.

Recent research on the effects of behavioral activities on myocardial ischemia in coronary artery disease patients has provided a pathophysiologic model for understanding the mechanisms by which mental stress can trigger clinical cardiovascular events. This article reviews epidemiologic research implicating psychosocial stress as an acute trigger of myocardial infarction in patients with pre-existing coronary artery disease, and evidence for the pathophysiologic effects of acute mental stress in individuals with pre-existing coronary artery disease. Via its actions on the central and autonomic nervous systems, stress can produce a cascade of physiologic responses in vulnerable individuals that may lead to myocardial ischemia, ventricular fibrillation, plaque rupture, or coronary thrombosis. Also reviewed are field and laboratory studies that suggest important causal links between mental stress and myocardial ischemia, and evidence suggesting clinical significance for vulnerability to mental stress-induced ischemia.

Electrocardiography, Ambulatory↗

Defensive hostility: relationship to multiple markers of cardiac ischemia in patients with coronary disease.

Three studies assessed whether the combined traits of hostility and defensiveness identify a group of hostile individuals with functionally severe coronary artery disease (CAD). CAD patients completed the Cook-Medley Hostility Inventory (Ho) and the Marlowe-Crowne Social Desirability Scale (MC). Patients were classified into 4 groups: defensive hostile (DH: high Ho, high MC), low hostile (LH: low Ho, low MC), high hostile (HH: high Ho, low MC), and defensive (Def: low Ho, high MC). DH in comparison to HH, LH, and Def CAD patients demonstrate the greatest perfusion defects as measured by exercise thallium scintigraphy; DH patients exhibit the most frequent ischemic episodes during ambulatory electrocardiographic monitoring; and in a laboratory study, DH patients exhibit the most severe mental stress-induced ischemia assessed by echocardiography. Thus, the combination of high hostility and high defensiveness are associated with more functionally severe CAD and may predispose CAD patients to a more adverse prognosis.

Aged↗

Synthetic analogues of the antithrombin III-binding pentasaccharide sequence of heparin. Prediction of in vivo residence times.

The synthetic pentasaccharide Org 31540/SR 90107A represents the antithrombin III (ATIII) binding region of heparin and accelerates the ATIII-mediated inhibition of coagulation factor Xa. This compound and 15 structural analogues with ATIII binding constants (Kd) ranging from 2.7 to 2600 nmol/L were compared for their plasma elimination in rats as measured from their factor Xa inhibiting activity. After administration of a low dose (100 nmol/kg body wt IV), each pentasaccharide showed a characteristic plasma half-life varying from a minimum of 0.3 hour for pentasaccharides with low affinity for ATIII to 10.9 hours for pentasaccharides with high affinity for the protein. The latter value was close to the half-life measured for radioiodinated rat ATIII (11.8 hours). We hypothesized that the elimination half-life of pentasaccharides is markedly extended by ATIII binding, of which the extent is governed by the Kd of the complex. The following observations support this hypothesis. The low-dose, low-affinity pentasaccharides were almost fully recovered in the urine without having lost anti-factor Xa activity, whereas compounds with high ATIII binding affinity were only partly recovered in the urine. With a high dose (500 nmol/kg body wt), a rapid plasma clearance of pentasaccharide was observed until a concentration similar to that of endogenous ATIII was reached, in accordance with their expected 1:1 stoichiometric interaction. The elimination of half-life was similar to that of the low dose. The relation between Kd values and plasma half-lives could be explained by assuming rapid clearance of free and coclearance of ATIII-bound pentasaccharide with the protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Handedness, symptom reporting, and accident susceptibility.

A cross-sectional design was used to examine the relationship among handedness, self-reported symptoms, and accident susceptibility in a nonclinical sample (N = 285). Left-handedness was not found to be associated with elevated symptom reporting (and, consequently, health problems) and accident susceptibility. Thus, the present findings do not support the hypothesis that left-handedness is accompanied by reduced physical fitness or accident proneness.

Accident Proneness↗

The effect of successful coronary angioplasty on feelings of exhaustion.

Excess fatigue and exhaustion are among the most prevalent premonitory complaints of myocardial infarction and sudden cardiac death. These feelings may reflect subclinical heart disease, prolonged psychological tension, or both. The present study investigates to what extent coronary artery disease explains exhaustion. For this purpose, the relationship between the severity of coronary artery disease and exhaustion, and the relief of exhaustion after successful percutaneous transluminal coronary angioplasty (PTCA) is investigated. Patients who had a successful elective PTCA (N = 120) were evaluated on feelings of exhaustion on admission, 2 weeks after discharge and 6 months after discharge, making use of the Maastricht Questionnaire. Multiple regression analyses were used to investigate to what degree exhaustion on admission and after PTCA was determined by the extent of coronary artery disease and other patient characteristics. Severity of coronary artery disease before PTCA was positively associated with exhaustion and successful PTCA resulted in a significant decrease of exhaustion scores (P < 0.001). However, less than 5% of the variance of the exhaustion scores before PTCA could be explained by severity of coronary artery disease (R2 = 0.04, F = 5.1, P = 0.03). The majority of patients who were exhausted before PTCA remained exhausted after PTCA. Exhaustion was present in 75% of the patients before PTCA and in 65% 2 weeks after PTCA, which indicates that restoration of coronary perfusion by successful PTCA does not substantially reduce the number of exhausted patients. At 6 months, exhaustion was present in 60% of the patients, and there was no difference between patients with and without typical anginal complaints at that time.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗

Pentasaccharide and Orgaran arrest, whereas heparin delays thrombus formation in a rat arteriovenous shunt.

The mode of action of glycosaminoglycans (GAGs) towards thrombus formation in a rat arteriovenous shunt was studied by simultaneous examination of thrombus weight, platelet consumption and thrombin generation during 45 min of blood circulation. A comparison was made between the effects of heparin, the heparinoid Org 10172 (Orgaran), and the chemically synthesized methoxy derivative of the antithrombin III binding pentasaccharide fragment of heparin (Org 31540). All three compounds inhibited thrombus growth by 30% at a dose of 80 anti-Xa U/kg i. v. when assessed after 15 min of circulation through the shunt. In addition, a systemic decrease of 27% of platelet numbers in the placebo group was inhibited by heparin and Orgaran with 63% and by pentasaccharide with 48%. At a later stage, after 45 min of circulation, at comparable plasma anti-Xa levels, thrombi which had formed in the presence of Orgaran or pentasaccharide, but not in the presence of heparin, became less or non thrombogenic. This non-thrombogenicity was reflected by i) an inhibition of the local deposition of [51Cr]platelets of 75% with Orgaran and of 57% with pentasaccharide, and ii) an inhibition of ex-vivo thrombus-induced thrombin generation in pooled rat plasma of 67% with Orgaran and of 52% with pentasaccharide (inhibition compared to placebo). Although the mechanism of inducing non-thrombogenicity of a (developing) thrombus by Orgaran and pentasaccharide requires further investigation, the suppression of the local thrombin generation potency, measured by thrombus-induced thrombin generation in pooled plasma, is much more correlated with thrombus growth than systemic anticoagulant activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Is premenstrual syndrome an endocrine disorder?

To both patients and physicians it seems natural to attribute adverse premenstrual phenomena to cyclic fluctuations of hormones produced by the ovary. This seems so plausible that, although the endocrine mechanism that causes premenstrual syndrome remains unknown, the condition itself is often treated with hormonal substances. Psychosocial factors are thus considered to be of only secondary importance. They may play a role as a contributing factor, to the 'real' cause of premenstrual syndrome they are not an essential ingredient. The aim of this review article is to examine how strong the evidence is for the possible existence of an endocrine factor as the causative agent in premenstrual syndrome. Using an epidemiological approach we conclude that the continuing search for the responsible mechanism that causes premenstrual syndrome may very well be an endocrine 'Holy Grail'. Human behavior cannot be understood within a single (hormonal) frame of reference. Cyclical ovarian activity is only one of the etiological factors in premenstrual syndrome. Unravelling the pathogenesis of premenstrual syndrome requires a multidisciplinary approach.

Causality↗

A simple strategy to detect significant premenstrual changes.

The prevalence of the ten most prominent premenstrual symptoms (top-ten) was calculated in Dutch women (n = 202), who considered themselves to suffer from complaints related to menstruation. Premenstrual syndrome was diagnosed where the scores of 5 or more of the top-ten symptoms showed an increase of at least 2 points (on a visual analog scale rated from 1 to 10) from day 12 to day 26 during two consecutive cycles. This diagnosis was confirmed in almost all subjects using a 'gold standard' criterion of an increase of at least 30% in complaints from the follicular phase to the luteal phase. In contrast to the latter strategy the 'top-ten' method successfully excluded women who felt free from premenstrual complaints. It is concluded that the 'top-ten' method is a simple and valid strategy to detect significant premenstrual changes.

Analysis of Variance↗

Implicit learning in psychotic patients.

Implicit verbal learning of psychotic patients (n = 59) and non-psychotic control patients (n = 20) was studied using stem completion and association tasks in lexical and semantic priming paradigms. Performance on these tasks was contrasted with explicit memory on Rey's verbal learning test. Furthermore, correlations of these aspects of memory with positive and negative symptoms of psychosis were examined. Symptom ratings were based on an interview by a psychiatrist using the CPRS and SANS. As expected, the lexical and semantic priming effects in both patient groups were not significantly different, whereas the psychotic patients compared to the controls were impaired in explicit learning. None of the memory variables was significantly correlated with negative or positive symptoms. These findings are explained by the fact that priming effects, as opposed to explicit learning, depend on automatic memory processes, which do not require conscious effort. Moreover, the findings suggest the intactness of posterior cortical functions in psychotic patients.

Adult↗

Calcitonin gene-related peptide, the menstrual cycle and premenstrual syndrome.

Calcitonin gene-related peptide plasma levels were measured during four different phases of ovulatory menstrual cycles, in eight women suffering from the premenstrual syndrome and in eight controls. No significant fluctuations in calcitonin gene-related peptide levels occurred during the menstrual cycle. Neither were there significant differences in calcitonin gene-related peptide levels between the premenstrual syndrome and control groups.

Adult↗

Vital exhaustion predicts new cardiac events after successful coronary angioplasty.

Excessive tiredness is one of the most prevalent premonitory symptoms of myocardial infarction and sudden cardiac death. This state is labelled as vital exhaustion and consists of three components: fatigue, increased irritability, and demoralization. Vital exhaustion has been found to be an independent risk-indicator of myocardial infarction in one prospective study and several case-control studies. It is as yet unclear whether the association between vital exhaustion and future myocardial infarction can be explained by confounding of (subclinical) coronary artery disease. Therefore, the present study investigates the predictive value of vital exhaustion for the occurrence of new cardiac events after percutaneous transluminal coronary angioplasty (PTCA), while explicitly controlling for the severity of coronary artery disease. Patients with a successful PTCA were followed during 1.5 years. A new cardiac event was defined as present if one of the following end points occurred: cardiac death, myocardial infarction, coronary bypass surgery, repeat-PTCA, increase of coronary atherosclerosis, or new anginal complaints with documented ischemia. Vital exhaustion was assessed using the Maastricht Questionnaire two weeks after hospital discharge. Participants of the present study were 127 patients (mean age 55.6 +/- 9.1; 105 men, 22 women). Fifteen (35%) of the 43 exhausted patients experienced a new cardiac event, whereas 14 (17%) of the 84 not exhausted patients had a new cardiac event (OR = 2.7; CI = 1.1-6.3; p = .02). Multiple logistic regression analysis revealed that vital exhaustion continued to be of predictive value when other significant risk factors for new cardiac events were controlled for (i.e., severity of coronary artery disease and hypercholesterolemia).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

Relationship of blood coagulation and fibrinolysis to vital exhaustion.

OBJECTIVE: Acute physical and psychological stressors affect blood coagulation and fibrinolysis, but little is known about hemostatic factors associated with chronic psychological stress. Prolonged psychological stress may end in a state of vital exhaustion, which has been shown to be a risk factor for first myocardial infarction and recurrent events after coronary angioplasty. The present study tested the hypothesis that vital exhaustion resulting from chronic psychological stress is associated with impaired fibrinolytic capacity and increased coagulation factors. METHODS: On the basis of a validated questionnaire and subsequent structured interview, a well-defined group of otherwise healthy exhausted men was recruited (N = 15) and compared with age-matched not-exhausted controls (N = 15). Fibrinolytic measures included tissue plasminogen activator (TPA) antigen and plasminogen activator inhibitor (PAI-1) activity, and as coagulation factors we examined factors VIIc, factor VIIIc, and fibrinogen. Control variables were: blood pressure, smoking status, triglycerides, cholesterol, and standard hematological measures. Samples were collected twice to correct for intraindividual fluctuations. Statistical analyses were performed using 2 x 2 mixed model analysis of variance with subsequent univariate testing. RESULTS: Vital exhaustion was associated with significantly elevated levels of PAI-1 activity (p = .023). The higher PAI-1 activity in exhausted subjects (median = 13.0 U/ml vs. 6.0 U/ml) was not accounted for by smoking status or serum lipids. No significant differences were observed in TPA antigen, factor VIIc, factor VIIIc, and fibrinogen. The groups did not differ in blood pressure, smoking status, triglycerides, cholesterol, or standard hematological measures. CONCLUSION: These data suggest a reduced fibrinolytic capacity in exhausted individuals. Therefore, the relationship between vital exhaustion and risk of myocardial infarction may be mediated in part by an imbalance between blood coagulation and fibrinolysis.

Adult↗

Chronic and acute psychological risk factors for clinical manifestations of coronary artery disease.

Psychological factors are known to affect biological processes involved in the progression of coronary artery disease. This article focuses on psychological risk factors for progression of coronary artery disease and its clinical manifestations. Recent research on the adverse cardiovascular consequences of feelings of exhaustion and acute psychological arousal is reviewed, and a classification of psychological risk factors is presented distinguishing (1) chronic psychological risk factors, such as hostility; (2) episodic risk factors, such as exhaustion, with a duration ranging from several months to 2 years; and (3) acute psychological triggers, including mental activity and anger. The distinctive pathophysiological mechanisms by which these psychological risk factors promote coronary disease progression and cardiac ischemia are described, including hemodynamic reactivity, blood clotting, and inflammatory processes.

Acute Disease↗