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R Mitusch

Publications and source records attributed to R Mitusch.

At least 19 recordsLinked to original sources

Angina intensity is not different in diabetic and non-diabetic patients with acute myocardial infarction.

BACKGROUND: Diabetic patients with acute myocardial infarction (AMI) may have diminished pain or a higher frequency of asymptomatic infarctions. This appears to be a common clinical perception. METHODS: Data from two registries of AMI patients presenting in hospital (MITRA PLUS with 18786 patients; North German Registry, NGR, 1042 patients with detailed symptom interviews) were analyzed concerning symptoms of acute myocardial infarction in patients with diabetes mellitus (DM) and without diabetes (non-DM). RESULTS: DM patients were significantly older and more often female than non-DM. There were no differences in the frequency of pre-infarction angina between DM and non-DM (Mitra Plus). In NGR, severe angina during AMI occurred in 49.8% of DM and 46.3% of non-DM (n. s.). No chest pain was reported in 16.9% of DM and 15.0% of non-DM (n. s.). Extra-thoracic pain, dizziness, nausea, sweating, palpitations, radiation of angina and localization of radiating pain was not different between DM and non-DM patients. Severe dyspnea occurred in 29.5% of DM and 19.5% of non-DM patients (p = 0.003). CONCLUSIONS: Apart from a higher frequency of severe dyspnea in diabetics, there appears to be no difference in the clinical symptoms of AMI patients with and without diabetes mellitus. AMI with little or no angina was also frequently found in non-diabetics. In the hospital, diabetics with suspected AMI do not appear to need a special judgement of symptoms. This could accelerate access of diabetics to standard therapeutic procedures.

Aged↗

[Day-night variability of the prehospital phase of acute myocardial infarct].

While a circadian rhythm in the onset of acute myocardial infarction (AMI) is well established, little is known about the variability of prehospital delay and decision processes. Seven hundred and thirty-nine consecutive AMI patients (median age 65.3 years; 30.2% women) with a median decision time of 60 min and a total prehospital delay of 180 min were studied. In 30.9% of patients onset of AMI symptoms was at night (10.00 p.m.-06.00 a.m.). At night patient decision time was significantly longer than during daytime (120 vs 45 min, difference 75 min; p < 0.001), total prehospital delay was prolonged accordingly (240 vs 170 min, difference 70 min; p < 0.001). The relative risk (RR; 95% confidence interval, CI) for a late decision (> 1 h) to seek medical care at night was significantly increased in females (RR 1.96; CI 1.07-3.61, p = 0.028), non-smokers (RR 2.49; CI 1.42-4.39, p = 0.001) and patients with radiation of anginal pain (RR 2.34; CI 1.32-4.15; p = 0.003). Of all patients with a late decision to seek medical care at night, 95.6% belonged to one of these groups. These variables were not significant for early or late decisions during daytime. Decision processes of AMI patients may be different during daytime and at night. In conclusion, in AMI patients, decision time to seek medical help is prolonged at night. Simple clinical variables (female sex, non-smokers, radiation of anginal pain) identify patients at high risk for a late decision at night. This information should be included into public and individualized education campaigns.

Aged↗

Emotional attitudes toward symptoms and inadequate coping strategies are major determinants of patient delay in acute myocardial infarction.

BACKGROUND: Early reperfusion treatment in acute myocardial infarction (AMI) preserves ventricular function and saves lives. After onset of AMI symptoms, patients often delay for hours until the decision to seek medical help. AIM: Of the MI-heart (Myocardial Infarction--HElp seeking And ReacTions) study was to identify factors determining patient decision delay. METHODS: 739 consecutive patients with confirmed AMI (median age 65.3 years, 30.2% females) were studied after transfer from the intensive care unit. A standardized interview covered AMI symptoms, attitudes toward symptoms, coping strategies, and clinical and sociodemographic variables. RESULTS: Of patients, 93.3% knew an AMI could be deadly. 43.9% of the patients who suspected an AMI, and knew it could be deadly, decided late (> 1 hour) to seek medical help. In univariate analyses, attitudes toward symptoms and coping strategies had the highest impact on a late decision. Stepwise logistic regression identified the following independent contributors to a late decision to seek medical help (relative risk, 95% confidence interval): wanting to wait and see (3.53; 2.32-5.39), not taking symptoms seriously (2.47; 1.64-3.72), not wanting to bother anybody (2.14; 1.29-3.57), symptoms improving at first (2.33; 1.52-3.56), asking others for advice (0.46; 0.30-0.71), taking pain medication (2.01; 1.01-4.03), age > 65 years (1.69; 1.17-2.44), very strong intensity of angina (0.60; 0.42-0.87). CONCLUSIONS: Emotional attitudes to AMI symptoms and inadequate coping strategies are the major determinants of patient decision delay. They should be considered as a key factor in patient and public education. Modification of these emotional factors might best be achieved by an individualized approach.

Adaptation, Psychological↗

[Bradycardia despite hyperthyroidism].

Hyperthyroidism is usually associated with tachycardia, hypothyroidism with bradycardia. After observing clinically inapparent hyperthyroidism in patients requiring pacemaker implantation, we studied the occurrence of hyperthyroidism in patients receiving a first permanent pacemaker. Of 237 patients (age 71.4 +/- 8.9 years; 54.9% females), 16 (6.75%) had subclinical (TSH < 0.1 mE/l and fT3 < or = 9.0 pmol/l) and 4 (1.69%) overt hyperthyroidism (TSH < 0.1 mE/l and fT3 > 9.0 pmol/l). Prevalence of hyperthyroidism was similar to that in the general population. Compared to euthyroid patients, in the patients with subclinical or overt hyperthyroidism there were significantly more females (n = 16) than males (n = 4; p = 0.018). Hyperthyroid patients were older (75.0 +/- 9.6 vs. 70.7 +/- 8.9 years; p = 0.015). At follow-up, all patients had a relevant proportion of pacemacer-induced beats. Clinical signs of hyperthyroidism or cardiac symptoms were not different between groups. In conclusion, bradycardia does not exclude the presence of hyperthyroidism. Temporary pacing is recommended in thyreotoxicosis with bradycardia. In contrast, primary implantation of a permanent pacemaker appears to be adequate in patients with bradycardia, cardiovascular disease and an additional diagnosis of hyperthyroidism.

Age Factors↗

Evaluation of a sensitive immunoluminometric assay for the determination of C-reactive protein (CRP) in serum and plasma and the establishment of reference ranges for different groups of subjects.

A sensitive immunoluminometric assay originally designed to measure C-reactive protein (CRP) in neonates and minimal serum volumes was adapted to measure this protein in a routine method without prior sample dilution. The concentration range covered without prior dilution was 10 micrograms/l to 20 mg/l using a sample volume of 5 microliters serum and a total assay time of less than 2 h. Serum samples were assayed from participants in a community medicine programme (SHIP--Study of Health in Pomerania) of the University of Greifswald, Germany (n = 414), as well as from mother-child pairs at birth (n = 30) and women attending the infertility clinic (n = 36). The validation of the assay was compared with a commercial latex-enhanced turbidimetric immunoassay (Roche Diagnostics--Integra 700) using routine serum samples (n = 60) from hospital patients. Comparison was made with the routine assay used in the SHIP study (Roche Diagnostics--Hitachi 717/Tina Quant). From 414 SHIP samples measured in the immunoluminometric assay, 289 were below the detection level in the turbidimetric (Tina Quant) assay. A significant positive correlation (p < 0.01) between log C-reactive protein concentration with age was found, both in the non-screened (all CRP values) (n = 414, r = 0.222) and selected (CRP < 5.00 mg/l = 90th percentile) (n = 370, r = 0.242) SHIP participants. Women were found to have significantly higher CRP levels than men (women: median age 47 a, median CRP 1.29 mg/l; men: median age 55 a, median CRP 1.00 mg/l--p = 0.016) in the non-selected SHIP participants. The situation was different in the selected group, (median age: men 54 a, women 48 a) where no significant difference in median CRP values between the sexes was seen (men: 0.874 mg/l, women 0.951 mg/l, p = 0.206). The distribution of CRP values in a "Normal Healthy Population" is skewed (mean/median--SHIP: all--2.08; selected--1.49). From the 414 SHIP samples measured in the immunoluminometric assay, 289 were below the detection level (2.5 mg/l) in the turbidimetric (Tina Quant) assay. From the 125 remaining samples the correlation between both methods was acceptable (r = 0.813), the regression line y = a + bx being: CRP (ILMA) = 1.83 + 0.842*CRP (Tina Quant). The Tina Quant assay gave values significantly higher than the ILMA in the range 2.5-25 mg/l CRP (p < 0.001). The total information loss in 289/414 subjects with a CRP < 2.5 mg/l with the Tina Quant assay makes it no longer suitable for epidemiological studies in which CRP is to be studied as a risk factor for cardiovascular events. The comparison between the immunoluminometric assay and the latex-enhanced immunoturbidimetric assay (Roche Integra) was much better. The latter measured down to less than 0.3 mg/l, thus being more suitable for epidemiological studies than the Tina Quant assay from the same producer. The correlation and regression data between the ILMA (x) and the Roche Integra assay (y) were: r = 0.971; CRP (Roche Integra) = 0.635 + 0.984*CRP (ILMA); n = 50.10 sera with CRP levels between 25 and 460 mg/l showed no high-dose hook effect in either assay. The remaining 50 sera were measurable in both assays. The turbidimetric assay gave rise to marginally but significantly higher values than the immunoluminometric assay (p = 0.004). The mothers at birth had a median CRP of 3.64 mg/l (range 1.49-12.6 mg/l), the neonates a median CRP of 34 micrograms/l (range 4-288 micrograms/l). All births were without complications, with gestational periods between 38 and 42 weeks. There was no correlation between maternal and neonatal CRP at birth. Mothers at birth had significantly higher CRP levels than healthy non-pregnant women (p < 0.001). Women attending the infertility clinic had CRP-values similar to age-matched healthy non-pregnant women (median 0.698 mg/l, range 0.05-9.97 mg/l). Interassay coefficients of variation at CRP concentrations of 0.85 and 7.9 mg/l were 8.99 and 7.93%, respectively, for the immunoluminometric

Adolescent↗

Prothrombin fragments F1+2, thrombin-antithrombin III complexes, fibrin monomers and fibrinogen in patients with coronary atherosclerosis.

We determined the plasma levels of prothrombin fragment F1+2, thrombin-antithrombin III complexes (TAT), fibrin monomers (FM), D-dimers (DD) and fibrinogen in 57 patients with angiographically verified graded coronary artery disease (CAD) free of concomitant peripheral atherosclerosis, cerebrovascular disease or diabetes mellitus and a group of 21 apparently healthy controls. Blood was collected from the antecubital vein through atraumatic venipuncture prior to the angiographic procedure. Plasma levels of hemostatic markers were related to the presence and graded severity of CAD. The levels of prothrombin fragment F1+2 (1.74+/-0.11 vs. 1.0+/-0.07 nmol/l, P<0.001), FM (41.6+/-5.5 vs. 7.42+/-3.05 nmol/l, P<0.001), TAT (15.6+/-2.7 vs. 2.96+/-0.32 microg/l, P<0.001) and fibrinogen (3.64+/-1.3 vs. 3.08+/-0.33 g/l, P<0.01) were significantly higher in patients with CAD compared to controls, while there was no difference regarding the fibrinolytic system represented by DD (441.6+/-58.9 vs. 337.4+/-42.05 microg/l, n.s.). Within the CAD group, patients with extensive coronary atherosclerosis (> or =2 vessel disease) had significantly higher values for prothrombin fragment F1+2 (1.89 vs. 1.57 nmol/l, P = 0.04), FM (50.7 vs. 29.8 nmol/l, P = 0.03), and a trend to significance was noted for fibrinogen (3.9 vs. 3.3 g/l, P = 0.07) suggesting that blood coagulability was related to the severity of the disease and that hemostatic markers of thrombin activity represent a useful tool to identify patients with a latent hypercoagulable state with a higher susceptibility to sustain coronary thrombosis.

Antithrombin III↗

Relation between QT dispersion and the extent of myocardial ischemia in patients with three-vessel coronary artery disease.

The aim of the study was to examine the relation between the extent of myocardial ischemia and changes in QT interval dispersion in patients with obstructive coronary artery disease and in patients with normal coronary arteries. QT interval dispersion reflects regional variations in ventricular repolarization and cardiac electrical instability. Previous studies showed QT interval dispersion changes during episodes of myocardial ischemia in patients with coronary artery disease, but no data on the relation between extent of myocardial ischemia and degree of QT interval dispersion changes are available. To assess the effects of myocardial ischemia on myocardial repolarization by analyzing the change in QT dispersion during incremental atrial pacing, we studied 33 patients (7 women and 26 men, mean age 60.1 +/- 5.1 years, 18 patients with normal coronary arteries, 15 patients with coronary 3-vessel disease). QT dispersion was measured at baseline, after each pacing period, within 30 seconds after cessation of pacing ("peak ischemic stress"), and at 1-minute intervals for up to 5 minutes. Paired blood samples for determination of serum lactate were withdrawn from the coronary sinus and radial artery to determine the cardiac lactate extraction ratio at each point of electrocardiographic registration. In patients with coronary artery disease, QT dispersion increased from a baseline value of 39 +/- 7 ms to a peak ischemic stress value of 63 +/- 10 ms (p <0.0001). Patients with normal coronary arteries showed almost unchanged values of QT dispersion (41 +/- 9 vs 42 +/- 7 ms). There was a significant relation between the pacing-induced change in QT dispersion and the induced change in myocardial lactate extraction ratio (r = 0.76, p <0.0001). The change in QT dispersion (baseline vs peak pacing stress) was related to the extent of the cardiac lactate extraction ratio (r = -0.79, p <0.0001). These data indicate that the severity or extent of induced myocardial ischemia was related to the degree of induced changes of the variability in the timing of the ventricular recovery pattern.

Aged↗

[Atherosclerosis of the aorta as a source of arterial embolisms].

Aortic atherosclerosis has early been recognized as a potential source of embolism. The histological finding of cholesterol clefts in small end-arteries characterized the entity of cholesterol embolism. The clinical picture was extremely variable and the diagnosis was frequently established post-mortem or by means of invasive although insensitive procedures including biopsy and angiography. Therefore, cholesterol embolism was thought to be rare. With the routine use of transesophageal echocardiography for the diagnostic workup of arterial embolism, aortic atherosclerosis was shown to be the source of otherwise unexplainable embolism. Cross-sectional studies demonstrated an independent association between prominent plaques of more than 4 to 5 mm of thickness or plaques with mobile components in the aortic arch. In follow-up studies, the risk of embolic events in patients with this kind of lesions exceeded 10% per patient-year. The results of pathological studies were consistent with these findings showing that ulcerated complex plaques carry an independent risk for embolic events. Apart from spontaneous embolism, atherosclerosis of the proximal aorta was shown to be a cause of embolic complications during cardiac surgery and catheterization procedures which involve the aorta. Medical treatment for the prevention of embolism in atherosclerotic disease of the aorta has not been studied systematically. In a variant form of aortic atherosclerosis consisting of mobile pedunculated thrombi inserting on relatively small plaques, anticoagulant therapy has proved to be useful in small numbers of patients. Recurrent embolic events could be prevented and regression of the thrombotic masses has been observed.

Aortic Diseases↗

Low frequency of clinically silent circulating emboli in patients with mitral valve prolapse or patent foramen ovale detected by bigated transcranial Doppler ultrasound.

Patent foramen ovale (PFO), but not uncomplicated mitral valve prolapse (MVP), is a possible source of cardiac embolism to the brain. There are only a few reports on the frequency of clinically silent circulating microemboli in these two conditions. We performed 1-hour recordings of one middle cerebral artery in 4 patients with MVP and 14 patients with PFO to detect circulating microemboli. For the identification of microembolic signals we used blinded off-line evaluation and bigated transcranial Doppler sonography (sampling from two different depths in the vessel). Microembolic signals were detected conventionally in 3 out of 14 patients with PFO (3, 8, and 14 microemboli/h), and in none out of the 4 patients with MVP. The absence of microembolic signals in patients with MVP and the low frequency of microemboli in patients with PFO reflect the different embolic potential of these two cardiac abnormalities.

Adult↗

An optimized AV delay algorithm for patients with intermittent atrioventricular conduction.

Detection and promotion of an intermittent atrioventricular (AV) conduction is the objective of an AV delay hysteresis algorithm in dual chamber pacemaker (DDD) pacing. The AV delay following an atrial event is automatically extended by a programmable interval (AV hysteresis interval) if the previous cycle showed spontaneous AV conduction, i.e., a ventricular event was detected within the previous AV delay. An automatic search mode scans for spontaneous ventricular events during the hysteresis interval: a single AV delay extension (equal to the programmed AV delay hysteresis) will occur after a successive, programmable number of AV cycles with ventricular pacing. If a spontaneous AV conduction is present, the AV delay will remain extended by the hysteresis interval. Our first results in 17 patients with intermittent AV block disclosed a satisfactorily working algorithm with effective reduction of ventricular stimuli. In relation to the underlying conduction disturbance and pacemaker settings, the majority of our patients showed a reduction of ventricular pacing events up to 90% without any adverse hemodynamic or electrophysiological changes. Based on clinical (promotion of a physiological activation and contraction sequence) and technical (reduction of power consumption) advantages, the AV hysteresis principle could be of incremental value for future dual chamber pacing in patients with intermittent complete heart block.

Aged↗

Priming of neutrophils after elective percutaneous transluminal coronary angioplasty is unrelated to accompanying brief myocardial ischemia.

OBJECTIVE: The purpose of this study was to investigate the effect of brief myocardial ischemia and vascular trauma induced by elective percutaneous transluminal coronary angioplasty on in vivo 'priming' and activation of neutrophils. PATIENTS AND METHODS: We studied 16 patients undergoing elective coronary angioplasty for symptomatic coronary artery disease and a control group of seven patients undergoing diagnostic cardiac catheterization. Free radical production from purified neutrophils (Ficoll-Hypaque density gradient method) was measured indirectly by the chemiluminescence method. Myocardial ischemia during balloon inflation was assessed by serial lactate determinations from coronary sinus and arterial blood. The degree of transient angioplasty-related myocardial ischemia was related to the oxidative response of activated neutrophils. RESULTS: Mean (+/-S.E.M.) oxidative response, i.e. the lucigenin- and luminol-enhanced-chemiluminescence (counts per minute) of neutrophils sampled from the coronary sinus increased significantly after percutaneous transluminal coronary angioplasty (Lucigenin-chemiluminescence: pre-angioplasty 3.69+/-0.64x10(5) vs. post-angioplasty 7.08+/-1.2x10(5), P<0.01; Luminol-chemiluminescence: pre-angioplasty 2.81+/-0.67x10(6) vs. post-angioplasty 5.2+/-0.92x10(6), P<0.01). Twelve of 16 patients developed transient cardiac lactate production (mean coronary sinus lactate excess: +0.12 mmol/l) and three disclosed a lactate extraction ratio <10%, both suggestive of myocardial ischemia. However, there was no correlation between the cardiac lactate production and the increased oxidative response after coronary angioplasty (r2 (Lucigenin-chemiluminescence)=0.02, n.s.; r2 (Luminol-chemiluminescence)=0.06, n.s.). CONCLUSION: 'Priming' of neutrophils, as reflected by increased oxidative response, is likely to occur after coronary angioplasty, but not after the angiographic procedure itself. However, 'priming' seems to be unrelated to the transient brief period of myocardial ischemia and rather depends on an alternative mechanism.

Adult↗

Vascular events during follow-up in patients with aortic arch atherosclerosis.

BACKGROUND AND PURPOSE: An association between aortic arch atherosclerosis and vascular events has been demonstrated. However, few data exist regarding follow-up evaluation of this disease. METHODS: In this study, 183 patients with the diagnosis of aortic arch atherosclerosis were prospectively followed up. This diagnosis was made during an echocardiographic cross-sectional study. In 136 patients, raised plaques with thickness < 5 mm had been shown to exist, and in 47 patients complex plaques with thickness > or = 5 mm or plaques with mobile components had been demonstrated on the initial transesophageal echocardiography. RESULTS: During a mean follow-up period of 16 +/- 7 months, vascular events with a presumed embolic origin occurred in 15 patients. The incidence was 4.1 per 100 person-years in patients with raised plaques compared with 13.7 per 100 person-years in the group with complex plaques. The Kaplan-Meier survival analysis revealed a significantly higher rate of vascular events in patients who were found to have complex plaques (P < .01). In the Cox proportional hazards analysis, the finding of complex plaques (relative risk [RR], 4.3; 95% confidence interval [CI], 1.5 to 12.0; P = .006), coronary artery disease (RR, 4.0; 95% CI, 1.2 to 13.1; P = .02), and a history of previous embolism (RR, 4.0; 95% CI, 1.1 to 14.4; P = .03) were independent predictors of vascular events. CONCLUSIONS: Patients with the finding of protruding plaques or plaques with mobile components have a high risk of subsequent vascular events.

Adult↗

Embolism from the aortic arch in patients with cerebral ischemia.

The pathogenic role of aortic arch atherosclerosis (AAA) in embolic stroke is not well understood. We investigated, prospectively, the prevalence and severity of AAA in patients with embolic stroke to ascertain its role as a risk factor for cerebral ischemia. We examined 100 consecutive patients who had experienced acute symptoms due to cerebral ischemia. Clinical examination, electrocardiogram, x-ray, ultrasound examination of craniocervical arteries, transesophageal echocardiography (TEE), cranial computerized tomography, and magnetic resonance imaging were undertaken. Seventy-five patients showed evidence of AAA; 34 patients had moderate to severe (> 5 mm thickening) AAA. Age was positively related to the severity of AAA, as were smoking, coronary heart disease, diabetes mellitus, internal carotid artery (ICA) occlusive disease, and embologenic heart disease. Hypertension, which was evident in 52 patients, did not distinguish those cases showing AAA. Twelve patients showed evidence of high-degree ICA stenosis on the symptomatic side, although the extent of ICA stenosis and AAA were unrelated. A cardiac source of emboli was found in 28 patients. AAA was found to be the probable source for embolic stroke in 14 patients. These data indicate that aortic arch atherosclerosis is an important source of cerebral emboli which may increase the risk for ischemic stroke. Furthermore, we suggest that TEE examination of the aortic arch may be important for the diagnosis of AAA and ultimately for the prophylactic treatment of severe cerebral ischemia.

Adult↗

Aortic atherosclerotic plaques as a source of systemic embolism.

OBJECTIVES: Our study was designed to determined the significance of aortogenic embolism in an unselected autopsy collective. BACKGROUND: Although embolism arising from atherosclerotic plaques in the aorta has been acknowledged, the role of aortic atheromatosis among other well known sources of embolism remains to be further clarified. METHODS: We examined the proximal part of the arterial system with regard to the presence of atherosclerotic lesions as well as cardiac changes in 120 consecutive necropsy studies. Pathologic evidence of embolic events was recorded. Clinical and neuropathologic data were also surveyed in all patients. RESULTS: Among atherosclerotic lesions, fibrous plaques (p < 0.05) and calcified (p < 0.0001) and ulcerated lesions (p < 0.0001) as well as thrombi (p < 0.005) were observed significantly more frequently in the aortic arch and in the descending aorta than in the ascending aorta, whereas fatty streaks were distributed uniformly. In 40 (33%) of the 120 patients, we found pathologic evidence of arterial embolization. Multiple logistic regression analysis revealed a significant correlation between embolism and complicated atherosclerotic plaques in the aortic arch (odds ratio [OR] 5.8, 95% confidence interval [CI] 1.1 to 31.7, p < 0.05), severe ipsilateral carotid artery disease (OR 3.1, 95% CI 3.1 to 45.3, p < 0.001) and atrial fibrillation (OR 3.5, 95% CI 1.1 to 9.9, p < 0.05). CONCLUSIONS: Complicated atherosclerotic plaques in the aortic arch represent an independent risk factor for systemic embolism similar to atrial fibrillation and severe atherosclerosis of the carotid arteries.

Adult↗

Detection of a hypercoagulable state in nonvalvular atrial fibrillation and the effect of anticoagulant therapy.

The purpose of the study was to evaluate alterations of the hemostatic system and the effect of anticoagulant therapy in nonvalvular atrial fibrillation. A set of molecular hematologic markers was measured prospectively in 69 patients with atrial fibrillation and 28 age-matched patients in sinus rhythm. Significantly elevated levels of thrombin-antithrombin III complex (8.5 +/- 1.6 vs. 2.5 +/- 0.3 micrograms/l; p < 0.001), fibrin monomers (27.1 +/- 3.2 vs. 13.4 +/- 3.7 nM; p < 0.001), D-dimers (788 +/- 76 vs. 405 +/- 46 micrograms/l; p < 0.005), and tissue-type plasminogen activator (9.6 +/- 0.5 vs. 7.2 +/- 0.5 micrograms/l; p < 0.05) were observed in patients with atrial fibrillation compared to those in sinus rhythm. In a subgroup of patients in whom anticoagulant therapy with oral coumadin or standard intravenous heparin was established after the initial study, hemostatic activation decreased significantly. In conclusion, molecular hematologic markers indicate a hypercoagulable state in atrial fibrillation which may characterized a group of patients at elevated risk of thromboembolic disease.

Aged↗

[Arteriosclerosis of the thoracic aorta as a source of systemic emboli. A clinico-pathologic study].

The significance of the thoracic aorta as a source of systemic emboli in addition to other sources of embolism remains unexplained. A study of 120 consecutive necropsies (65 men, 55 women; mean age 71 [29-94] years) analysed the possible correlation of the severity of arteriosclerosis of the aorta, the carotid arteries and the arteries at the base of the brain as well as cardiac changes, with potential sources of emboli and with proven emboli (n = 39). Complex and fibrous plaques in the arch of the aorta, ipsilateral carotid artery stenoses, a history of atrial fibrillation and heart weight correlated significantly with emboli on both uni- and multivariant analysis. But the presence of calcified and complex plaques in the descending aorta, as well as moderate and severe arteriosclerosis in the arteries at the base of the brain, correlated significantly only on univariant analysis. Ischaemic brain lesions had been clinically silent in twelve of 32 cases, while visceral emboli had been silent in nine out of ten cases. -It is concluded from these data that, in addition to the cardiac chambers and arteriosclerosis of the arteries at the base of the brain, advanced arteriosclerosis of the aortic arch is an important source of systemic emboli. As many of the emboli remain silent, their incidence is probably underestimated clinically.

Adult↗

Transesophageal echocardiographic determinants of embolism in nonrheumatic atrial fibrillation.

The purpose of the study was to determine the relation of transesophageal echocardiographic findings to symptoms of systemic embolism in patients with nonrheumatic atrial fibrillation. Transthoracic and transesophageal echocardiography were used to study 107 patients with atrial fibrillation including 49 patients without embolic complications and 58 patients who had suffered from previous cerebral or peripheral embolism. A multiple logistic regression analysis revealed that left atrial thrombi (odds ratio 9.0, 95% CI 2.4-33.6, p < 0.005) and the presence of dense left atrial spontaneous contrast (odds ratio 8.4, 95% CI 1.3-53.1, p < 0.05) were independently related to embolic symptoms. Intensive left atrial spontaneous contrast was associated with an increased left atrial diameter (odds ratio 2.0, 95% CI 1.1-3.6, p < 0.05), the presence of chronic atrial fibrillation (odds ratio 6.9, 95% CI 1.6-29.8, p < 0.01) and aortic atherosclerosis (odds ratio 2.6, 95% CI 1.2-5.5, p < 0.05). It was further negatively correlated to mitral regurgitation (odds ratio 0.4, 95% CI 0.2-0.9, p < 0.05). In conclusion, dense spontaneous echo contrast and left atrial thrombi are associated to thromboembolic complications in patients with nonrheumatic atrial fibrillation. Classifying of spontaneous contrast seems to be useful when estimating the thromboembolic risk in atrial fibrillation.

Adult↗