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Biomedical subjects

M Sitzer

Publications and source records attributed to M Sitzer.

At least 37 records · Page 2Linked to original sources

Survival and quality of life outcome after mechanical ventilation in elderly stroke patients.

OBJECTIVES: Mortality is high and functional outcome poor in mechanically ventilated stroke patients. In addition, age >65 years is an independent predictor of death at 2 months among these patients. Our objective was to determine survival rates, functional outcome, and quality of life (QoL) in stroke patients older than 65 years requiring mechanical ventilation. METHODS: A prospective cohort study with an additional cross-sectional survey in 65 patients aged 65 years and older (mean age (SD): 75.6 (6.0) years) with ischaemic or haemorrhagic stroke who underwent mechanical ventilation. Main outcome measures were survival rate at 6 months, and Barthel Index (BI), modified Rankin Scale, and QoL at 15.8 (SD 8.0) months. RESULTS: Survival rate at 6 months was 40%. Elective intubation (odds ratio (OR) 13.6; p = 0.002) was the only independent positive predictor for survival, while age >77.5 years (OR 0.1; p = 0.004) and white blood count >10/nl at admission (OR 0.31; p = 0.032) were independent negative predictors for survival at 6 months. At the time of the cross-sectional survey, BI was >70 in five out of 22 patients, 35-70 in three and <35 in the remaining 14 patients. QoL was impaired primarily in the physical domain, whereas the psychosocial domain was less affected. CONCLUSIONS: Although only 40% of elderly patients intubated in the acute phase of stroke survived at least 6 months, one in four survivors recovered to a good functional outcome with a reasonable QoL. Elderly stroke patients need to be selected carefully for intensive care treatment, but elective intubation to allow diagnostic procedures should not be withheld primarily based on their age.

Age Factors↗

Posterior encephalopathy with vasospasm: MRI and angiography.

Posterior encephalopathy is characterised by headache, impairment of consciousness, seizures and progressive visual loss. MRI shows bilateral, predominantly posterior, cortical and subcortical lesions with a distribution. Our aim was to analyse the MRI lesion pattern and angiographic findings because the pathophysiology of posterior encephalopathy is incompletely understood. We report three patients with clinical and imaging findings consistent with posterior encephalopathy who underwent serial MRI including diffusion-weighted imaging (DWI) and construction of apparent diffusion coefficient (ADC) maps, and four-vessel digital subtraction angiography (DSA). DWI revealed symmetrical subcortical and cortical parieto-occipital high signal. High and also low ADCs indicated probable vasogenic and cytotoxic oedema. On follow-up there was focal cortical laminar necrosis, while the white-matter lesions resolved almost completely, except in the arterial border zones. DSA revealed diffuse arterial narrowing, slightly more marked in the posterior circulation. These findings suggest that posterior encephalopathy may in some cases be due to diffuse, severe vasospasm affecting especially in the parieto-occipital grey matter, with its higher vulnerability to ischemia. Cerebral vasospasm due to digitoxin intoxication, resulting in posterior encephalopathy, has not yet been described previously.

Adult↗

[Brain infarctions caused by paradoxical embolism during long-distance flights].

HISTORY AND ADMISSION FINDINGS: Over the period of one year three long-distance airline passengers (aged 21, 63, and 64 years) were admitted to our department because of a first-time acute neurological deficit having occurred during their long-distance flights. INVESTIGATIONS: In all three cases acute stroke MRI showed embolic cerebral ischemia, and transesophageal echocardiography revealed a persistent foramen ovale (PFO). Venous duplex and compression ultrasonography of the legs showed no signs of thrombosis. Extra- and transcranial Doppler, Holter ECG recording, routine blood analysis and additional tests for thrombophilia (incl. lupus anticoagulans, APC resistance, protein C, S, and AT III) revealed no signs of cardiovascular disease or other stroke causes. Only in case 3 the prothrombin gene G 20210A was found. DIAGNOSIS, TREATMENT AND COURSE: Ischemic stroke due to paradoxical embolism through a PFO was diagnosed in all three patients. One patient recovered fully within 2 days, one was discharged with a persistent motor deficit and the third patient died subsequently as a result of multiple cerebral infarctions accompanied by massive pulmonary embolism. CONCLUSION: These three cases illustrate that paradoxical embolic stroke is a possible severe complication of long-distance air travel in passengers with a PFO and this should be taken into account when deciding upon individual risk-adjusted prophylactic measures.

Adult↗

[Poststroke depression: risk factors and effects on the course of the stroke].

The incidence of poststroke depression (PSD) varies between 20% and 25% as a major variant and an additional 10% and 20% as a minor variant. Its prevalence peaks 3-6 months after stroke onset. In nearly a quarter of all PSD patients, depressive symptoms persist over at least 2 years.Several longitudinal studies have identified different factors which may increase the risk of PSD. Most probably, the severity of the neurological deficit, female gender, history of previous psychiatric disorders, and bad social living conditions increase the risk of PSD. It is uncertain whether lesion location or size modulate PSD risk. Increasing age is not associated with a higher PSD incidence. In contrast, it is obvious that PSD is associated with less favorable outcome and higher mortality. The degree of disability and quality of life are significantly reduced in PSD patients. In conclusion, PSD is presently a not predictable complication of ischemic stroke which is significantly associated with less favorable outcome.Early diagnosis and adequate therapy are still necessary in stroke rehabilitation.

Brain↗

S100B as a surrogate marker for successful clot lysis in hyperacute middle cerebral artery occlusion.

OBJECTIVES: The astroglial protein S100B is a marker of cerebral tissue damage. This study investigated whether the serum kinetic of S100B may serve as a surrogate marker of successful clot lysis and early recanalisation (<6 hours) in hyperacute proximal middle cerebral artery (MCA/M1) occlusion. METHODS: The authors prospectively included 23 patients (mean (SD) age, 70.2 (11.0) years) presenting with MCA/M1 occlusion on magnetic resonance angiography (n=18), intra-arterial angiography (IA; n=2), or transcranial Doppler sonography (TCD; n=3) within five hours after symptom onset. Rates of recanalisation and their point of time were determined using TCD or IA. Individual S100B values were determined at hospital admission, every eight hours within the first three days, and at 12 hour intervals from day 4 to day 6. Additionally, the S100B area under the curve (AUC) and the S100B peak value were obtained. RESULTS: Early recanalisation (<6 hours after symptom onset, n=7) was associated with a significantly lower mean S100B AUC compared with no recanalisation (22.2 (40.1) versus 406.8 (284.4) micro g/l per hour; p<0.001). Using receiver operating calculations, a single S100B value obtained 48-96 hours after stroke onset of less than 0.4 micro g/l (cut off point) provided a 86% sensitivity and 100% specificity for sufficient MCA/M1 clot lysis <6 hours. The overall accuracy for a single S100B value obtained in the 48-96 hours time window was as high as for the AUC (95.7%). CONCLUSION: A single S100B value <0.4 micro g/l obtained 48-96 hours after stroke onset indicates successful clot lysis <6 hours in MCA/M1 occlusion with a high degree of accuracy. Thus, determination of a single S100B value may serve as a surrogate marker of early and sufficient MCA/M1 recanalisation in large scale thrombolytic studies.

Acute Disease↗

[Recanalizing therapies in acute stroke].

Systemic thrombolysis with rt-PA within 3 hours after symptom onset has developed into a standard therapy for acute stroke patients. Recombinant t-PA is now licensed in Europe for this indication. Within 3 to 6 hours, no general therapeutic standard has been established yet. Currently, the available data are in favor of intra-arterial thrombolysis for patients with proximal occlusions of the middle cerebral artery. Systemic thrombolysis is not generally recommended in this time window, but is used in some centers for selected patients. In addition to thrombolysis and new strategies to improve thrombolysis (including patient selection with MRI), several interventional and surgical recanalization techniques are discussed.

Acute Disease↗

[The unstable carotid stenosis: definition and biological processes].

The occurrence of cerebral or retinal ischemic symptoms ipsilateral to high-grade internal carotid artery (ICA) stenosis indicates a status of instability with a substantial risk for future major stroke. Additionally, the detection of microembolic signals downstream of ICA stenosis is predictive for future cerebral ischemia in asymptomatic and symptomatic patients. There is substantial evidence that in unstable ICA stenosis plaque rupture and thrombus formation are the most frequent pathoanatomic findings. In contrast, in nearly the half of unstable carotid plaques the lumen surface appears to be intact. Within plaque tissue, the unstable plaque is mainly characterized by a substantial amount of inflammatory cell (i. e. macrophages, T-cells) infiltration. These cells are mainly localized in the fibrous cap near the necrotic core. Produced by macrophages, matrix degrading enzymes (e. g. MMP-9) are overexpressed in the unstable ICA stenosis. Thrombogenicity is mainly determined by the local concentration of activated tissue factor, also expressed by inflammatory cells. Furthermore, a significantly higher rate of apoptotic smooth muscle cells can be found within the fibrous cap of instable carotid stenoses. Whether infection with Chlamydia pneumoniae contribute to instability is unlikely, because a positive association to clinical instability has not been shown up to now. The exact and detailed characterization of the unstable ICA plaque and the correlation of different biological mechanisms to clinical instability may offer the possibility to use it as a human model of unstable atherosclerosis in general and to test the efficacy of new developed anti-atherosclerotic pharmaceutical agents.

Carotid Stenosis↗

Pravastatin improves cerebral vasomotor reactivity in patients with subcortical small-vessel disease.

BACKGROUND AND PURPOSE: Recent investigations have suggested an important role of statins in the prevention of stroke and dementia independent of their lipid-lowering properties. Using transcranial Doppler sonography (TCD), we examined acetazolamide reactivity as a marker of cerebral vasoreactivity in patients with subcortical small-vessel disease before and after pravastatin treatment. METHODS: In 16 patients (mean age 68+/-10 years) with subcortical small-vessel disease, cerebral vasomotor reactivity was tested using TCD insonating the middle cerebral artery. Cerebral blood flow velocity (CBFV) increase after bolus injection of 1 g acetazolamide was determined before and after 2-month treatment with pravastatin sodium 20 mg daily. RESULTS: Relative CBFV increase was significantly greater after pravastatin treatment (41.9+/-23.7% versus 55.7+/-18.3%, P=0.004). Comparison of CBFV at rest before and after treatment with pravastatin did not show significant differences. There was a strong negative correlation between the pravastatin-induced enhancement of vasomotor reactivity and the pretreatment CBFV increase (beta=-0.64, P=0.019). No associations were found between the effect of pravastatin on vasomotor reactivity and pretreatment levels or changes of LDL cholesterol. CONCLUSIONS: This pilot study provides the first evidence for a significant improvement of cerebral vasomotor reactivity by statin therapy in patients with cerebral small-vessel disease. The results may help to elucidate the preventive effect of statins and provide insights into the pathophysiology of cerebral small-vessel disease.

Acetazolamide↗

[Post-stroke depression: diagnosis and therapy].

Depression occurs at least temporarily in up to 30 - 40 % of all patients that have experienced a stroke. In the literature the term of a "Poststroke Depression" (PSD) has already been established. However standardised criteria for this diagnoses do not exist to this day. In most cases the DSM or ICD classification system is applied. Other investigators used various psychiatric rating scales. Even though it is generally acknowledged that there is a high prevalence, the occurrence of depression in combination with a stroke fails in most cases to be diagnosed or is left untreated. The need for treatment is even more pronounced by studies showing that a combination of stroke and depression will result in a less favourable outcome, particularly pertaining to that of functional treatment (motor skills, independent participation in activities of daily life). This difference in impairment between a depressed stroke patient and a not depressed stroke patient could be proven in studies that have been conducted over years. Despite the necessity of treatment that can be concluded from such a finding, the recent literature does not offer consistent information as to the ideal point of time for intervention nor the kind and intensity necessitated. According to singular studies, that have rarely been conducted under controlled conditions, there have been positive outcomes after early treatment. Along with psychostimulants that were most predominantly applied in the USA, as well as conventional tricyclic antidepressants, the group of the "Selective Serotonin Reuptake Inhibitors, SSRIs" have resulted in particularly favourable clinical outcomes.

Animals↗

Expression of tissue factor in high-grade carotid artery stenosis: association with plaque destabilization.

BACKGROUND AND PURPOSE: The procoagulant protein tissue factor (TF) has been implicated in thromboembolic complications associated with advanced atherosclerosis. In this study, we investigated whether TF expression in high-grade stenoses of the internal carotid artery (ICA) is associated with clinical features of plaque destabilization and addressed the relationship between TF expression and plaque inflammation. METHODS: In 36 consecutive patients undergoing surgery for high-grade ICA stenosis, clinical evidence of plaque instability was provided by the recent occurrence of ischemic symptoms attributable to the stenosis and the detection of cerebral microembolism by means of transcranial Doppler ultrasound monitoring of the ipsilateral middle cerebral artery. Endarterectomy specimens were stained immunocytochemically for TF expression as well as macrophage (CD68) and T cell (CD3) infiltration. RESULTS: Morphologically, TF immunoreactivity was codistributed with plaque inflammation and predominantly localized to CD68+ macrophages. Accordingly, statistical analysis revealed a significant association of TF expression with plaque infiltration by macrophages (P<0.0001) and T cells (P=0.013). Plaques extensively stained for TF (median of TF+ total section area >40% in semiquantitative assessment) were more frequent in symptomatic (12/27) than in asymptomatic patients (1/9). Conversely, plaques exhibiting little TF expression (median of TF+ section area <20%) were more frequent in asymptomatic (3/9) than in symptomatic (1/27) patients (P=0.016). Likewise, we found a highly significant association of TF expression with the occurrence of cerebral microembolism (P=0.008). CONCLUSIONS: Induction of TF at sites of plaque inflammation may play an important role in the destabilization of high-grade ICA stenosis.

Carotid Artery, Internal↗

Endovascular treatment of symptomatic carotid stenosis using stent placement: long-term follow-up of patients with a balanced surgical risk/benefit ratio.

BACKGROUND AND PURPOSE: Carotid endarterectomy (CEA) is not necessarily beneficial in all patients with symptomatic high-grade (>/=70%) internal carotid artery (ICA) stenosis. Independent risk factors modulate both the individual stroke risk under medical treatment and the combined stroke and death risk after CEA. Endovascular stenting of symptomatic ICA stenosis may be an alternative to CEA in patients with a balanced surgical risk/benefit ratio. METHODS: We included 43 patients (71% men; median age, 67 years) with a recently symptomatic ICA stenosis with >/=70% luminal narrowing in whom the individual sum of medical and surgical risk factors suggested a balanced surgical risk/benefit ratio (risk-modeling appraisal derived from the European Carotid Surgery Trial). After stenting of the stenosed ICA with distal balloon protection, the mean+/-SD follow-up, including clinical and ultrasonographic examinations, was 20+/-11.8 months, with a median number of examinations of 5 per patient. RESULTS: Recanalization of ICA stenoses was technically successful in 40 of 43 procedures (93%). Within the 30-day postinterventional period 1 death occurred (2.5%), and the combined stroke and death rate within follow-up was 5%. Except for 1 asymptomatic ICA occlusion, no restenosis >/=70% occurred during follow-up. CONCLUSIONS: ICA stenting in symptomatic patients with a balanced surgical risk/benefit ratio is technically feasible, with a low periprocedural risk of stroke or death. Furthermore, the risk of future stroke and rate of significant restenosis during long-term follow-up appears to be low, suggesting that ICA stenting may be useful in carotid revascularization and stroke prevention.

Aged↗

[Unstable carotid stenosis--an inflammatory disease?].

Arterioarterial thromboembolism from extracranial internal carotid artery (ICA) stenosis is an important pathogenic mechanism of ischemic stroke. However, even a high-grade ICA stenosis carries a greatly variable annual risk of stroke, as high as 13% following a recent occurrence of transient or minor cerebral ischemia or as low as 1-2% in clinically asymptomatic patients. There is increasing evidence that inflammatory processes play a central role in atherosclerosis and particularly in plaque destabilization converting chronic atherosclerosis into an acute neurological disorder. In thromboendarterectomy specimens from patients with high-grade ICA stenoses, the extent of inflammatory infiltration and the expression of matrixmetalloproteinase-9 correlated to clinical and ultrasonic features of plaque destabilization such as cerebral microembolism. Inflammation might become a new therapeutic target in symptomatic carotid artery disease.

Carotid Artery, Internal↗

Chlamydia pneumoniae infection and early asymptomatic carotid atherosclerosis.

BACKGROUND: Chronic Chlamydia pneumoniae infection has been implicated in the pathogenesis of atherosclerosis but whether it plays a role at an early stage in the disease is uncertain. An early estimate of atherosclerosis can be obtained by ultrasonic imaging of the carotid artery to determine intima-media thickness (IMT) and the thickness of any atheroma plaques. METHODS AND RESULTS: In 983 normal population individuals aged 30 to 70 years, we measured common carotid artery (CCA) and carotid bulb IMT, and also carotid plaque thickness and the degree of internal carotid artery (ICA) stenosis. C. pneumoniae IgA titers of >/=16 and IgG titers of >/=64 were taken as positive. There was no association between C. pneumoniae IgA or IgG seropositivity with right, left, or mean CCA or bulb IMT, or with the presence of carotid plaques. There was a significant association between IgA seropositivity and >50% mean carotid stenosis with an odds ratio of 5.24 (95% CI 1.24 to 22.21, P=0.0245) after controlling for age and sex; after controlling for other cardiovascular risk factors, this was not significant 3.96 (95% CI 0. 84 to 18.78, P=0.082). No association was found between IgA or IgG seropositivity and markers of fibrinogen, log C-reactive protein, or leukocyte count. CONCLUSIONS: We found no evidence that serological evidence of C. pneumoniae infection is associated with early atherosclerosis. It is possible that IgA seropositivity is associated with more advanced disease but this hypothesis needs to be examined in a population with a higher prevalence of advanced atherosclerosis. We found no evidence that C. pneumoniae results in a chronic systemic inflammatory state.

Adult↗

Cerebral microembolism, a disease marker for ischemic cerebrovascular events in the antiphospholipid syndrome of systemic lupus erythematosus?

OBJECTIVES: We investigated whether the detectability of microembolic Doppler signals (MES) in the intracranial circulation may help to define the individual cerebrovascular risk in systemic lupus erythematosus (SLE) with antiphospholipid syndrome (APS). MATERIAL AND METHODS: Retrospective cross-sectional study of 70 patients with SLE with or without APS, and 30 controls with a history of cerebral ischemia of unknown cause. Of all patients, 38 had a clinical history of APS and 32 did not. RESULTS: 15 patients with APS (39%) showed MES. In contrast, all patients without APS and 29 of 30 controls were microemboli-negative. MES were more strongly associated with cerebrovascular symptoms than with APS, antiphospholipid antibodies, or cardiac pathology. The time elapsed since the last ischemic cerebrovascular symptom was significantly shorter in microemboli-positive patients than in microemboli-negative patients (P<0.001). CONCLUSION: MES may be related to disease activity in patients with SLE and APS. Their detection may help to assess individual cerebrovascular risk and contribute to therapeutic decision making and therapeutic monitoring.

Adolescent↗

Reliability and validity of noninvasive imaging of internal carotid artery pseudo-occlusion.

BACKGROUND AND PURPOSE: Our study evaluated noninvasive tests for the diagnosis of atheromatous internal carotid artery (ICA) pseudo-occlusion. METHODS: Twenty patients (17 men, 3 women; mean age +/-SD, 64.3+/-11.6 years) with angiographically proven atheromatous ICA pseudo-occlusion (20 vessels) were prospectively examined with MR angiography (MRA; 2D and 3D time-of-flight techniques), color Doppler-assisted duplex imaging (CDDI) and power-flow imaging (PFI) with and without an intravenous ultrasonic contrast agent. As a control group, 13 patients (13 men; mean+/-SD age, 63.0+/-9.0 years) with angiographically proven ICA occlusion (13 vessels) were studied with the same techniques. For the determination of interobserver agreement (kappa statistics), the findings of each diagnostic technique were read by 2 blinded and independent observers who were not involved in patient recruitment and initial data acquisition. Specificity and sensitivity were calculated for all noninvasive techniques (observer consensus) in comparison to the standard of reference (intra-arterial angiography). RESULTS: Interobserver reliabilities were kappa=0.86 for intra-arterial angiography, kappa=0.90 for unenhanced CDDI, kappa=0. 93 for enhanced CDDI, kappa=0.93 for unenhanced PFI, kappa=1.0 for enhanced PFI, kappa=0.93 for 2D MRA, and kappa=0.77 for 3D MRA, respectively (P<0.0001). Specificities and sensitivities were 0.92 and 0.70 for unenhanced CDDI, 0.92 and 0.83 for enhanced CDDI, 0.92 and 0.95 for unenhanced PFI, 1.0 and 0.94 for enhanced PFI, 1.0 and 0.65 for 2D MRA, and 0.89 and 0.47 for 3D MRA, respectively. CONCLUSIONS: Advanced ultrasonographic techniques, especially PFI (with only 1 false-positive diagnosis of occlusion in the present series), can provide reliable and valid data to differentiate between ICA pseudo-occlusion and complete occlusion. In contrast, time-of-flight MRA at its present state is not capable of predicting minimal residual flow within a nearly occluded ICA.

Aged↗