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R Mitusch

Publications and source records attributed to R Mitusch.

At least 19 recordsLinked to original sources
PubMed1999

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↗
PubMed1998

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↗
PubMed1998

[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↗
PubMed1998

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↗
PubMed1998

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↗
PubMed1997

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↗
PubMed1997

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↗
PubMed1996

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↗
PubMed1996

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↗
PubMed1996

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↗
PubMed1995

[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↗
PubMed1995

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↗
PubMed1995

Adverse pacemaker hemodynamics evaluated by pulmonary venous flow monitoring.

The pacemaker syndrome refers to symptoms and signs in the pacemaker patient caused by an inadequate timing of atrial and ventricular contractions. The lack of normal atrioventricular synchrony may result in a decreased cardiac output and venous cannon A waves. The objective of this study was to define the left atrial and pulmonary venous flow response to ventricular pacing in a group of 14 unselected consecutive patients with total heart block and sinus rhythm. Pulmonary venous flow was assessed by transesophageal pulsed Doppler echocardiography in the VVI and DDD pacing modes. An inappropriate atrial timing caused a marked augmentation of the normally small pulmonary venous z wave in all patients ("negative atrial kick," peak z wave in DDD pacing 14.5 +/- 4.6 cm/s, VVI pacing 51.8 +/- 15.0 cm/s). Restoration of AV synchrony (DDD pacing, AV interval 100 ms) abolished these "cannon z waves" in all patients, and a normal pattern of pulmonary venous flow was achieved. Abnormal pulmonary venous flow characteristics were observed in 2 of 14 patients during DDD pacing with short AV intervals (100 ms). The Doppler pattern was similar to the findings seen in VVI pacing. Assessment of pulmonary venous flow by transesophageal pulsed Doppler echocardiography may provide a simple, sensitive, and relatively noninvasive technique to evaluate patients with suspected pacing induced adverse hemodynamics.

Aged↗
PubMed1995

[Spontaneous remission of a vascularized left atrial space-occupying lesion].

We report on a 73-year-old woman with mitral stenosis and an echocardiographically and angiocardiographically proven vascularized mass at the superior part of the left atrium. The patient was put on anticoagulation with phenprocoumon. An echocardiographical follow up 10 months later revealed the disappearance of this mass; only a stalklike structure was present at the site of the former mass. Clinical presentation, echocardiographic and angiocardiographic findings are consistent with a vascularized atrial thrombus. Nevertheless, currently available imaging procedures cannot definitely discriminate vascularized thrombus, myxoma and hemangioma.

Aged↗
PubMed1995

[Noninvasive diagnosis of coronary heart disease with cardiokymography: use of signal averaging technique].

Regional wall motion abnormality is the best indicator for coronary ischemia. Myocardial wall motion is registrated by cardiokymography (CKG), a mechanocardiographic method. Because of the high incidence of artefacts, echocardiography and nuclear imaging technique have been preferred. Computer-assisted signal averaging CKG improves practicability and allows measurements during exercise testing. Exercise testing was performed in 54 patients with suspected ischemic heart disease without mitral or aortic valve dysfunction, myocardial infarction or prior cardiac surgery. The results of simultaneously recorded ECG and CKG were compared with coronary angiographic results. CKG sensitivity and specificity were higher than that of ECG (76 and 80% vs 71 and 52%). If diagnosis was based on pathological or nonpathological results of both CKG and ECG, sensitivity and negative predictive value increased to 87 and 83%, respectively. Sensitivity reached 93% when only one pathological result was required. CKG combined with signal-averaging techniques has advanced to become a specific and sensitive tool in the non-invasive diagnostic approach to ischemic heart disease.

Adult↗
PubMed1995

[Determinants of arterial embolism with special reference to atheromatous changes of the thoracic aorta].

Potential sources of arterial embolism were evaluated with special emphasis on aortic atheromatosis in patients who underwent transesophageal echocardiography for various clinical reasons. Among 375 patients, 166 had suffered from cerebrovascular disease or peripheral embolism and 209 were free from symptoms of embolism. Univariate analysis revealed that atheromatosis of the aortic arch and descending aorta as well as cardiac thrombi, aneurysms of the interatrial septum and arterial hypertension were significantly more common in patients who had a history of embolism or ischemic stroke. In a stepwise multiple regression analysis, aortic arch atheromatosis (odds ratio 1.7, 95% CI 1.1-2.6), cardiac thrombi (odds ratio 4.1, 95% CI 1.7-9.8), atrial septal aneurysm (odds ratio 3.0, 95% CI 1.2-7.8) and arterial hypertension (odds ratio 1.8, 95% CI 1.1-3.0) were determined as independent predictors of embolic symptoms. We conclude that atheromatous lesions of the aortic arch are an independent risk factor for arterial embolism and ischemic stroke among other well known sources of embolism.

Aged↗
PubMed1994

Systemic embolism in aortic arch atheromatosis.

The role of aortic atheromatosis as a risk factor for systemic embolism and its relationship to other potential sources of embolism was examined in 335 patients undergoing transoesophageal echocardiography for various clinical reasons. Multiple logistic regression analysis revealed a significant correlation between embolism and moderate (atheroma protruding less than 5 mm into the aortic lumen, grade 2) to complex (atheroma protruding at least 5 mm into the vessel lumen with or without mobile components, grade 3) atherosclerosis of the aortic arch. Odds ratios were 4.0 for grade 2 atheromatosis (95% CI 1.1-14.4; P < 0.05) and 9.7 for grade 3 atheromatosis (95% CI 1.5-61.0; P < 0.05). Other significant associations were found with cardiac thrombi (odds ratio 4.0, 95% CI 1.7-9.3; P < 0.005) and hypertension (odds ratio 1.8, 95% CI 1.0-3.3; P < 0.05). In a subset of 163 patients in whom results of an ultrasound examination were available, atherosclerosis of the carotid arteries was another significant marker of embolism (odds ratio 2.0, 95% CI 1.2-3.3; P < 0.01). In conclusion, aortic arch atheromatosis, which was predominantly recognized in patients with cerebrovascular events of undetermined cause, seems to carry a risk of embolism that is comparable to cardiac and carotid atherosclerosis.

Aorta, Thoracic↗