PubMed HealthSearch

Biomedical subjects

U Stierle

Publications and source records attributed to U Stierle.

At least 19 recordsLinked to original sources

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

Cardiac release and kinetics of endothelin after severe short-lasting myocardial ischemia.

OBJECTIVES: The aim of this study was to investigate the release kinetics of endothelin after induced short-lasting myocardial ischemia. BACKGROUND: Endothelin is an endothelium-derived vasoactive peptide. Unequivocal proof of its cardiac release in ischemic syndromes has not yet been demonstrated. METHODS: A coronary sinus study with atrial pacing was performed in 23 patients with coronary artery disease. Endothelin (ET), cardiac troponin-T (TnT), myoglobin (Mb) and creatine kinase (CK) samples were withdrawn from the coronary sinus and a peripheral vein before and 1, 5, 10, 30 and 45 min and 1, 2, 3 and 6 h after pacing. The appearance of angina pectoris, abnormal cardiac lactate metabolism and ST segment depression were further criteria for myocardial ischemia. RESULTS: In the study group, pacing stress induced severe ischemia (mean duration +/- SD 6.1 +/- 1.2 min), with a maximum of 0.34 +/- 0.12-mV ST segment depression in 21 of 23 patients and angina pectoris in 22 of 23. The maximal cardiac lactate production was 42.8 +/- 17.3% (p < 0.03). TnT and CK levels in the total group were normal; in 14 of 23 patients a transient elevation of Mb with a maximum after 3 h was detected (86.4 +/- 27.1 micrograms/liter, p < 0.03). The ET concentrations increased significantly (p < 0.001) in the coronary sinus (from 4.6 +/- 0.8 [baseline] to 12.9 +/- 2.7 pg/ml at 1 min after cessation of pacing) and the peripheral vein, respectively (from 4.7 +/- 0.7 [baseline] to 8.3 +/- 2.1 pg/ml at 1 min). ET further remained elevated for 1 h with persisting higher coronary sinus than peripheral venous concentrations, indicating cardiac ET release. In a control group of 18 patients without heart disease, all variables were unchanged. CONCLUSIONS: Short-lasting severe myocardial ischemia was associated with significant ET release of cardiac origin that lasted up to 1 h.

Cardiac Pacing, Artificial

Impact of early accelerated dose tissue plasminogen activator on in-hospital patency of the infarcted vessel in patients with acute right ventricular infarction.

OBJECTIVE: To assess the efficacy of early accelerated dose tissue plasminogen activator on in-hospital patency of the infarct related artery in patients with inferior myocardial infarction with and without right ventricular involvement. DESIGN: Single centre prospective assessment before discharge of infarct related vessel patency after early thrombolysis. SETTING: Tertiary cardiac referral centre at a university hospital. PATIENTS AND METHODS: 90 consecutive unselected patients with acute myocardial infarction, of whom 35 (39%) had electro-cardiographic evidence of right ventricular involvement (ST segment elevation greater than 0.1 mV in right precordial lead V4R), were studied. All patients received accelerated dose tissue plasminogen activator 100 mg within six hours from the onset of symptoms and had control angiography before discharge. MAIN OUTCOME MEASURES: Infarct related coronary artery patency using the Thrombolysis in Myocardial Infarction (TIMI) grading system before discharge. Incidence of prolonged systemic hypotension, sinus bradycardia, complete atrioventricular block, and ventricular tachyarrhythmia during early hospitalisation. RESULTS: Despite aspirin and bolus heparinisation before thrombolysis and high dose heparinisation thereafter for at least 48 hours the infarct related artery was more likely to be occluded (TIMI 0 or 1 flow) in patients with right ventricular involvement than in those without (69 v 29%, P < 0.001), as shown by control angiography performed a mean of 12.8 days after thrombolysis. These findings may be explained, at least in part, by predominant involvement of the proximal right coronary artery (66 v 31%, P < 0.05) and a low cardiac output syndrome, being indirectly reflected by a high incidence of prolonged hypotension (26 v 7%, P = 0.02), bradycardia (34 v 14%, P = 0.03), and complete atrioventricular block (37 v 5%, P = 0.0001). CONCLUSION: Primary angioplasty should be considered as the treatment of choice in patients with acute inferior infarction with right ventricular involvement because of the high failure rate of thrombolysis.

Coronary Angiography

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

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

Accelerated ST-segment reduction after thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) compared to urokinase.

Effects of therapy with urokinase (UK) and with recombinant tissue plasminogen activator (rtPA) were compared in patients with acute myocardial infarction (AMI). To achieve homogenous therapeutic conditions the comparison was restricted to patients having their first AMI and to cases of clinically successful thrombolytic therapy (defined by non-invasive criteria, such as a 50% decrease in elevated ST-segment in the worst load of a 12 lead ECG within 300 min after onset of thrombolytic therapy, complete pain resolution during thrombolytic therapy, and later confirmed by angiography 10 days after AMI). Effects of UK and rtPA on continuous multilead ST-segment analysis and cardiac proteins (creatine kinase and its isoenzyme CK-MB, aspartate transaminase and hydroxybutyrate dehydrogenase) were analyzed during 24 hours following onset of therapy. Continuous ST analysis showed a faster resolution of the elevated ST-segments after thrombolytic therapy with rtPA than with UK(p < 0.01). Accelerated idioventricular rhythms (p < 0.05) occurred sooner following rtPA than UK treatment. The wash-out of creatine kinase was increased (p < 0.01) after rtPA. Although both drugs induced comparable, angiographically controlled reperfusion, the results suggest that the process of reperfusion was accelerated during thrombolysis with rtPA compared to UK. Thrombolytic therapy of AMI with rtPA may hence improve myocardial salvage.

Adult

[Detection of stress-induced myocardial ischemia in isolated coronary ectasia and aneurysm (dilatative coronaropathy)].

Forty eight patients with bilateral isolated non-stenotic coronary artery ectasia or aneurysm without associated cardiac defects ("dilated coronaropathy") were identified in consecutive diagnostic cardiac catheterizations between 1986-6/1994 (angiographic incidence 0.44%). Ectasia was defined as a luminal dilatation of the 1.5-2-fold, aneurysm of more than double the normal limits. In 16 patients a myocardial infarction (5 non-q-infarctions/11 q-wave-infarctions) was the indication for coronary angiography, a thrombotic occlusion of the infarct vessel was documented in 8/16 patients. In patients without myocardial infarction (study group) an evaluation of exercise-induced myocardial ischemia was performed by means of a coronary sinus lactate study, treadmill ergometry and Thallium-201-scintigraphy. A corresponding coronary insufficiency was objective in all tests in the study group. An exercise-induced myocardial ischemia was found in 21/31 in the coronary sinus study, 19/29 in the treadmill ergometry and 13/26 patients in the scintigraphy; significant differences were found in comparison to the results of a control group of patients without heart disease (n = 29, p < 0.001). After administration of 0.8 mg nitroglycerin (NTG) a further significant deterioration of myocardial ischemia was measured in the 21 patients with pathologic lactate metabolism developing a frank cardiac lactate production (p < 0.03). The extent of myocardial ischemia in the coronary sinus study was significantly correlated to the coronary diameters of the proximal and middle segments of the Ramus interventricularis anterior and the middle segment of the Ramus circumflexus (r = 0.87, p < 0.02). A differentiation between ectasia and aneurysm therefore seems to be of functional relevance. Angiographic stigmata of an impaired coronary blood flow such as a segmental to and from movement and a local deposition of dye were found significantly more often with increasing coronary diameters (p < 0.04). "Dilated coronaropathy" is an entity of non-stenotic, ischemic coronary artery disease. NTG was of no therapeutic benefit or led to an aggravation of the exercise-induced myocardial ischemia. Because of this potential adverse effect the administration of NTG should be avoided in "dilated coronaropathy".

Adult

[Effect of lowered cholesterol on the course of coronary heart disease. An analysis of the results of controlled, angiographically documented intervention studies].

AIM: To find out from published reports whether the tendency of coronary heart disease (CHD) to progress can be retarded by lowering total and LDL cholesterol concentrations. METHODS: After a data-base search a meta-analysis was undertaken of all those randomized, controlled and angiographically documented studies which contained informations about the effect of cholesterol reduction on the course of CHD over a period of at least 2 years. A total of 12 studies covering 3781 patients met the stated criteria. RESULTS: The different lipid-lowering measures (usually drugs) achieved a statistically significant reduction of the number of patients with progression of the coronary angiographic findings and a significant increase in the number of those with actual regression. The number of coronary incidents, such as myocardial infarction, unstable angina, sudden cardiac death, necessary aortocoronary bypass operations or percutaneous transluminal coronary angioplasty was lower by 34% in the groups with measures to influence cholesterol metabolism than in the untreated groups. In the studies in which coronary arteriograms were evaluated quantitatively there was an annual increase in the mean degree of stenosis of 1.01% in the untreated and 0.37% in the treated groups. CONCLUSIONS: The difference in the increase of the mean degree of stenosis is probably not only important because of the resulting haemodynamic changes in myocardial perfusion. The quantitatively only slightly increased trend towards progression in the untreated groups can be interpreted as a marker for an active process of atherogenesis with a tendency of plaques to break off and of plaque thromboses.

Anticholesteremic Agents

[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

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

[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

[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

[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

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

Primary angiosarcoma of the heart. Report of a case and review of the literature.

We report on a 44-year-old male with primary cardiac angiosarcoma who died 11 months after onset of nonspecific symptoms (thoracic pain and general fatigue) of intracerebral metastases. A right atrial tumor mass and a pericardial effusion could be demonstrated by transthoracic and transesophageal echocardiography. Cardiac angiography showed a right atrial hemangioma, fed by the right coronary artery. In a review of 108 cases of primary cardiac angiosarcoma we summarize clinical features, diagnostic means, therapeutic approaches and life expectancy of this rare disease.

Adult