Clinical prediction of large vessel occlusion in anterior circulation stroke: mission impossible?

Simple clinical scores to predict large vessel occlusion (LVO) in acute ischemic stroke would be helpful to triage patients in the prehospital phase. We assessed the ability of various combinations of National Institutes of Health Stroke Scale (NIHSS) subitems and published stroke scales (i.e., RACE scale, 3I-SS, sNIHSS-8, sNIHSS-5, sNIHSS-1, mNIHSS, a-NIHSS items profiles A-E, CPSS1, CPSS2, and CPSSS) to predict LVO on CT or MR arteriography in 1085 consecutive patients (39.4 % women, mean age 67.7 years) with anterior circulation strokes within 6 h of symptom onset. 657 patients (61 %) had an occlusion of the internal carotid artery or the M1/M2 segment of the middle cerebral artery. Best cut-off value of the total NIHSS score to predict LVO was 7 (PPV 84.2 %, sensitivity 81.0 %, specificity 76.6 %, NPV 72.4 %, ACC 79.3 %). Receiver operating characteristic curves of various combinations of NIHSS subitems and published scores were equally or less predictive to show LVO than the total NIHSS score. At intersection of sensitivity and specificity curves in all scores, at least 1/5 of patients with LVO were missed. Best odds ratios for LVO among NIHSS subitems were best gaze (9.6, 95 %-CI 6.765-13.632), visual fields (7.0, 95 %-CI 3.981-12.370), motor arms (7.6, 95 %-CI 5.589-10.204), and aphasia/neglect (7.1, 95 %-CI 5.352-9.492). There is a significant correlation between clinical scores based on the NIHSS score and LVO on arteriography. However, if clinically relevant thresholds are applied to the scores, a sizable number of LVOs are missed. Therefore, clinical scores cannot replace vessel imaging.

Occlusion of the superior mesenteric artery

Mode of access: Internet.

Microsurgical Aneurysm Model in Rats and Mice: Development of Endovascular Treatment and Optimization of Magnetic Resonance Imaging

The rupture of a cerebral artery aneurysm causes a devastating subarachnoid hemorrhage (SAH), with a mortality of almost 50% during the first month. Each year, 8-11/100 000 people suffer from aneurysmal SAH in Western countries, but the number is twice as high in Finland and Japan. The disease is most common among those of working age, the mean age at rupture being 50-55 years. Unruptured cerebral aneurysms are found in 2-6% of the population, but knowledge about the true risk of rupture is limited. The vast majority of aneurysms should be considered rupture-prone, and treatment for these patients is warranted. Both unruptured and ruptured aneurysms can be treated by either microsurgical clipping or endovascular embolization. In a standard microsurgical procedure, the neck of the aneurysm is closed by a metal clip, sealing off the aneurysm from the circulation. Endovascular embolization is performed by packing the aneurysm from the inside of the vessel lumen with detachable platinum coils. Coiling is associated with slightly lower morbidity and mortality than microsurgery, but the long-term results of microsurgically treated aneurysms are better. Endovascular treatment methods are constantly being developed further in order to achieve better long-term results. New coils and novel embolic agents need to be tested in a variety of animal models before they can be used in humans. In this study, we developed an experimental rat aneurysm model and showed its suitability for testing endovascular devices. We optimized noninvasive MRI sequences at 4.7 Tesla for follow-up of coiled experimental aneurysms and for volumetric measurement of aneurysm neck remnants. We used this model to compare platinum coils with polyglycolic-polylactic acid (PGLA) -coated coils, and showed the benefits of the latter in this model. The experimental aneurysm model and the imaging methods also gave insight into the mechanisms involved in aneurysm formation, and the model can be used in the development of novel imaging techniques. This model is affordable, easily reproducible, reliable, and suitable for MRI follow-up. It is also suitable for endovascular treatment, and it evades spontaneous occlusion.

Cerebral hemodynamics during graded Valsalva maneuvers

The Valsalva maneuver (VM) produces large and abrupt changes in mean arterial pressure (MAP) that challenge cerebral blood flow and oxygenation. We examined the effect of VM intensity on middle cerebral artery blood velocity (MCAv) and cortical oxygenation responses during (phases I-III) and following (phase IV) a VM. Healthy participants (n = 20 mean +/- SD: 27 +/- 7 years) completed 30 and 90% of their maximal VM mouth pressure for 10 s (order randomized) whilst standing. Beat-to-beat MCAv, cerebral oxygenation (NIRS) and MAP across the different phases of the VM are reported as the difference from standing baseline. There were significant interaction (phase * intensity) effects for MCAv, total oxygenation index (TOI) and MAP (all P < 0.01). MCAv decreased during phases II and III (P < 0.01), with the greatest decrease during phase III (-5 +/- 8 and -19 +/- 15 cm.s(-1) for 30 and 90% VM, respectively). This pattern was also evident in TOI (phase III: -1 +/- 1 and -5 +/- 4%, both P < 0.05). Phase IV increased MCAv (22 +/- 15 and 34 +/- 23 cm.s(-1)), MAP (15 +/- 14 and 24 +/- 17 mm Hg) and TOI (5 +/- 6 and 7 +/- 5%) relative to baseline (all P < 0.05). Cerebral autoregulation, indexed, as the % MCAv/%MAP ratio, showed a phase effect only (P < 0.001), with the least regulation during phase IV (2.4 +/- 3.0 and 3.2 +/- 2.9). These data illustrate that an intense VM profoundly affects cerebral hemodynamics, with a reactive hyperemia occurring during phase IV following modest ischemia during phases II and III.

Acurácia da avaliação doppler velocimétrica da velocidade máxima do pico sistólico da artéria cerebral média na detecção da anemia fetal na doença hemolítica perinatal: uma revisão sistemática

O contexto do estudo é a predição da anemia fetal em gestantes portadoras da doença hemolítica perinatal e tem como objetivo avaliar a acurácia da medida doppler velocimétrica da velocidade máxima do pico sistólico da artéria cerebral média na detecção da anemia fetal na doença hemolítica perinatal. A identificação dos estudos foi realizada com a adoção de bancos de dados gerais (MEDLINE e LILACS) e a partir de referências bibliográficas de outros autores. Os estudos selecionados tinham como critérios serem do tipo observacionais, com gestantes apresentando coombs indireto maior do que 1:8, técnica de insonação do vaso adequada, Vmax-ACM ≥ 1,5MOM, presença obrigatória de comparação com o padrão-ouro (hemoglobina fetal e/ou neonatal), e nível de evidência diagnóstica acima ou igual a 4. Os dados dos estudos selecionados foram alocados em tabelas 2x2 comparando o resultado do teste com o padrão-ouro. A acurácia diagnóstica foi expressa principalmente através da razão de verossimilhança. A revisão incluiu onze estudos, com uma amostra total de 688. Três estudos apresentaram delineamento do tipo prospectivo e nível de evidência diagnóstica categoria 1. A performance do teste em questão apresentou variação razoável. O estudo de Mari et al (2000) foi considerado o de melhor qualidade metodológica, apresentando uma RV(+) de 8,45 e uma RV(-) de 0,02. A medida do doppler da Vmax da ACM como preditor da anemia fetal na doença hemolítica perinatal está consolidada. Porém, alguns pontos precisam ser melhor esclarecidos, como o intervalo ideal dos exames em casos graves e a validade do método em fetos que já foram submetidos a transfusões intra-uterinas.

Escala de Fisher como factor predictor de hidrocefalia en hemorragia subaracnoidea espontanea

Objetivo. Determinar si la cantidad de sangre y su localización es el espacio subaracnoideo, medible con la escala de Fisher en las primeras 24 horas de ocurrido el ictus hemorrágico, es un factor predictor para el desarrollo de hidrocefalia en pacientes con diagnóstico de hemorragia subaracnoidea (HSA) espontánea, vistos en el Hospital Universitario Clínica San Rafael (HUCSR) con seguimiento de 12 meses. Métodos. 251 pacientes fueron incluidos en una cohorte retrospectiva. La asociación entre la escala de Fisher y el desarrollo de hidrocefalia en pacientes con HSA espontánea fue analizada a través de un análisis bivariado y multivariado. Resultados. La edad promedio de los pacientes fue de 55,5 ± 15 años; con predominancia en el sexo femenino 65,7%. La prevalencia de hidrocefalia fue de 27,1% en la cohorte y la etiología de la HSA fue en su mayoría por ruptura de aneurismas de arterias cerebrales; 78,5%. La sobrevida a 12 meses fue de 65,7%. Tanto el grado 4 en la escala de Fisher como Hunt-Hess III se asocian con el desarrollo de hidrocefalia: ORA; 2.93 IC 95%: 1.51-5.65, P <0.001, ORA 2.83 IC 95%: 1.31-6.17 P=0.008 respectivamente. Conclusión. La presencia de sangrado Intraventricular o intraparenquimatoso ( Fisher 4) en las primeras 24 horas, asociado a un deterioro neurológico al ingreso Hunt-Hess III están asociados con el desarrollo de hidrocefalia en los 251 pacientes evaluados con diagnóstico de HSA espontánea; hallazgos consistentes con lo reportado en la literatura mundial.

Índice de pulsatilidad de arteria cerebral media como predictor para desenlaces desfavorables en fetos pequeños para la edad gestacional

Introducción: La aparición de vasodilatación aislada de la arteria cerebral media en fetos pequeños para la edad gestacional sin otros cambios en el doppler puede interpretarse como fisiológica o podría ser la manifestación inicial de una restricción de crecimiento intrauterino de inicio tardío. Se pretende evaluar la asociación de la disminución del índice de pulsatibilidad de la arteria cerebral media, como predictor de desenlaces perinatales adversos, en fetos con bajo peso para edad gestacional. Metodología: Se realizó un estudio de cohorte analítica de temporalidad histórica para determinar si el hallazgo de disminución de la pulsatibilidad en el doppler de arteria cerebral media se asocia con el pronóstico perinatal adverso, en fetos pequeños para edad gestacional mediante un muestreo no probabilístico. Resultados: Se recolectaron un total de 325 flujometría doppler de fetos pequeños para edad gestacional. El riesgo de parto pretérmino fue RR 2.6 IC95% 1.6-4.1, de hospitalización fue RR 1.4 IC95%1.1-1.9 y de muerte fue 2.1 IC95%1.5-3.2 cuando hay índice de pulsatilidad alterada en la arteria cerebral media. La regresión logística mostró que el riesgo de desenlaces desfavorables con alteraciones en la arteria cerebral media fue de RR 4.2 IC95% 2.5-7.1 ajustado por edad materna, edad gestacional y bajo peso al nacer. Discusión Los pacientes expuestos presentan mayor riesgo de desenlaces desfavorables con diferencias significativas, no así en otros estudios publicados. El presente estudio muestra asociaciones significativas que debe ser evaluada con estudios más amplios.

Nitric oxide suppresses cerebral vasomotion by sGC-independent effects on ryanodine receptors and voltage-gated calcium channels

Background/Aims: In cerebral arteries, nitric oxide (NO) release plays a key role in suppressing vasomotion. Our aim was to establish the pathways affected by NO in rat middle cerebral arteries. Methods: In isolated segments of artery, isometric tension and simultaneous measurements of either smooth muscle membrane potential or intracellular [Ca 2+ ] ([Ca 2+ ] SMC ) changes were recorded. Results: In the absence of L -NAME, asynchronous propagating Ca 2+ waves were recorded that were sensitive to block with ryanodine, but not nifedipine. L -NAME stimulated pronounced vasomotion and synchronous Ca 2+ oscillations with close temporal coupling between membrane potential, tone and [Ca 2+ ] SMC . If nifedipine was applied together with L -NAME, [Ca 2+ ] SMC decreased and synchronous Ca 2+ oscillations were lost, but asynchronous propagating Ca 2+ waves persisted. Vasomotion was similarly evoked by either iberiotoxin, or by ryanodine, and to a lesser extent by ODQ. Exogenous application of NONOate stimulated endothelium-independent hyperpolarization and relaxation of either L -NAME-induced or spontaneous arterial tone. NO-evoked hyperpolarization involved activation of BK Ca channels via ryanodine receptors (RYRs), with little involvement of sGC. Further, in whole cell mode, NO inhibited current through L-type voltage-gated Ca 2+ channels (VGCC), which was independent of both voltage and sGC. Conclusion: NO exerts sGC-independent actions at RYRs and at VGCC, both of which normally suppress cerebral artery myogenic tone.

EFFECT OF TESTOSTERONE ON THE PRESSOR-RESPONSE TO COMMON CAROTID OCCLUSION IN GONADECTOMIZED CONSCIOUS MALE-RATS WITH LESION OF THE MEDIAN-EMINENCE

The influence of testosterone on the development of the pressor response to common carotid occlusion was investigated in control and median eminence-lesioned male rats. In control rats (N = 9), gonadectomy performed 21 days before the experiments reduced by 22% (from 51 +/- 2 to 40 +/- 2 mmHg) and treatment with testosterone (300-mu-g for 4 days before the measurements) increased the initial peak pressor response (from 51 +/- 2 to 57 +/- 2 mmHg) which depends on carotid innervation. The maintained response which is of central origin (probably ischemic) was less affected. In nongonadectomized rats (N = 6), lesions of the median eminence (6 days) decreased the initial peak by 19% (from 52 +/- 2 to 42 +/- 3 mmHg) and the maintained response by 56% (from 32 +/- 2 to 14 +/- 1 mmHg). Sham-operated rats served as controls. In gonadectomized animals (N = 6) the lesion reduced only the maintained response (from 23 +/- 2 to 11 +/- 1 mmHg). Testosterone supplementation restored the maintained response but did not alter the initial peak. These results indicate that the pressor response to common carotid occlusion in male rats is modulated by testosterone and that the depression in the maintained response caused by median eminence lesion can be reversed by steroid supplementation.

SEX-RELATED DIFFERENCES IN CARDIOVASCULAR-RESPONSES TO COMMON CAROTID OCCLUSION IN CONSCIOUS RATS

Mean arterial pressure and heart rate were determined in conscious, unrestrained groups of 10 male, female and androgenized female Wistar rats 20 s (early pressor response) and 1 min (late sustained response) after bilateral carotid artery occlusion. The early pressor response, which is of carotid reflex origin, was 40% greater in female than in male rats (45 +/- 2 vs 63 +/- 3 mmHg, respectively). The late sustained response, which is of central origin (probably ischemic), did not differ between male and female rats (32 +/- 2 vs 37 +/- 4 mmHg, respectively). The magnitude of the early pressor response of androgenized female tats (50 +/- 2 mmHg) was similar to that of male rats (45 +/- 2 mmHg) but the late sustained response was 19% smaller (26 +/- 2 mmHg). Common carotid occlusion caused increases in heart rate which were greater in female (51 +/- 9 and 34 +/- 9 beats/min in the early pressor response and late sustained response, respectively) than in male rats (31 +/- 5 and 8 +/- 4 beats/min, respectively). In androgenized female rats, heart rate decreased during common carotid occlusion (34 +/- 7 and 35 +/- 8 beats/min after 20 s and 1 min, respectively). These data provide evidence that there are substantial sex-related differences in the cardiovascular responses to common carotid occlusion in conscious rats and indicate that administration of androgens to newborn female rats affects the baroreceptor reflex control of their arterial pressure.

Validação da técnica de angiotomografia helicoidal cerebral em cães hígidos

Pós-graduação em Medicina Veterinária - FMVZ

Development of Clinical Decision Support Systems based on Mathematical Models of Physiological Systems

In the last years of research, I focused my studies on different physiological problems. Together with my supervisors, I developed/improved different mathematical models in order to create valid tools useful for a better understanding of important clinical issues. The aim of all this work is to develop tools for learning and understanding cardiac and cerebrovascular physiology as well as pathology, generating research questions and developing clinical decision support systems useful for intensive care unit patients. I. ICP-model Designed for Medical Education We developed a comprehensive cerebral blood flow and intracranial pressure model to simulate and study the complex interactions in cerebrovascular dynamics caused by multiple simultaneous alterations, including normal and abnormal functional states of auto-regulation of the brain. Individual published equations (derived from prior animal and human studies) were implemented into a comprehensive simulation program. Included in the normal physiological modelling was: intracranial pressure, cerebral blood flow, blood pressure, and carbon dioxide (CO2) partial pressure. We also added external and pathological perturbations, such as head up position and intracranial haemorrhage. The model performed clinically realistically given inputs of published traumatized patients, and cases encountered by clinicians. The pulsatile nature of the output graphics was easy for clinicians to interpret. The manoeuvres simulated include changes of basic physiological inputs (e.g. blood pressure, central venous pressure, CO2 tension, head up position, and respiratory effects on vascular pressures) as well as pathological inputs (e.g. acute intracranial bleeding, and obstruction of cerebrospinal outflow). Based on the results, we believe the model would be useful to teach complex relationships of brain haemodynamics and study clinical research questions such as the optimal head-up position, the effects of intracranial haemorrhage on cerebral haemodynamics, as well as the best CO2 concentration to reach the optimal compromise between intracranial pressure and perfusion. We believe this model would be useful for both beginners and advanced learners. It could be used by practicing clinicians to model individual patients (entering the effects of needed clinical manipulations, and then running the model to test for optimal combinations of therapeutic manoeuvres). II. A Heterogeneous Cerebrovascular Mathematical Model Cerebrovascular pathologies are extremely complex, due to the multitude of factors acting simultaneously on cerebral haemodynamics. In this work, the mathematical model of cerebral haemodynamics and intracranial pressure dynamics, described in the point I, is extended to account for heterogeneity in cerebral blood flow. The model includes the Circle of Willis, six regional districts independently regulated by autoregulation and CO2 reactivity, distal cortical anastomoses, venous circulation, the cerebrospinal fluid circulation, and the intracranial pressure-volume relationship. Results agree with data in the literature and highlight the existence of a monotonic relationship between transient hyperemic response and the autoregulation gain. During unilateral internal carotid artery stenosis, local blood flow regulation is progressively lost in the ipsilateral territory with the presence of a steal phenomenon, while the anterior communicating artery plays the major role to redistribute the available blood flow. Conversely, distal collateral circulation plays a major role during unilateral occlusion of the middle cerebral artery. In conclusion, the model is able to reproduce several different pathological conditions characterized by heterogeneity in cerebrovascular haemodynamics and can not only explain generalized results in terms of physiological mechanisms involved, but also, by individualizing parameters, may represent a valuable tool to help with difficult clinical decisions. III. Effect of Cushing Response on Systemic Arterial Pressure. During cerebral hypoxic conditions, the sympathetic system causes an increase in arterial pressure (Cushing response), creating a link between the cerebral and the systemic circulation. This work investigates the complex relationships among cerebrovascular dynamics, intracranial pressure, Cushing response, and short-term systemic regulation, during plateau waves, by means of an original mathematical model. The model incorporates the pulsating heart, the pulmonary circulation and the systemic circulation, with an accurate description of the cerebral circulation and the intracranial pressure dynamics (same model as in the first paragraph). Various regulatory mechanisms are included: cerebral autoregulation, local blood flow control by oxygen (O2) and/or CO2 changes, sympathetic and vagal regulation of cardiovascular parameters by several reflex mechanisms (chemoreceptors, lung-stretch receptors, baroreceptors). The Cushing response has been described assuming a dramatic increase in sympathetic activity to vessels during a fall in brain O2 delivery. With this assumption, the model is able to simulate the cardiovascular effects experimentally observed when intracranial pressure is artificially elevated and maintained at constant level (arterial pressure increase and bradicardia). According to the model, these effects arise from the interaction between the Cushing response and the baroreflex response (secondary to arterial pressure increase). Then, patients with severe head injury have been simulated by reducing intracranial compliance and cerebrospinal fluid reabsorption. With these changes, oscillations with plateau waves developed. In these conditions, model results indicate that the Cushing response may have both positive effects, reducing the duration of the plateau phase via an increase in cerebral perfusion pressure, and negative effects, increasing the intracranial pressure plateau level, with a risk of greater compression of the cerebral vessels. This model may be of value to assist clinicians in finding the balance between clinical benefits of the Cushing response and its shortcomings. IV. Comprehensive Cardiopulmonary Simulation Model for the Analysis of Hypercapnic Respiratory Failure We developed a new comprehensive cardiopulmonary model that takes into account the mutual interactions between the cardiovascular and the respiratory systems along with their short-term regulatory mechanisms. The model includes the heart, systemic and pulmonary circulations, lung mechanics, gas exchange and transport equations, and cardio-ventilatory control. Results show good agreement with published patient data in case of normoxic and hyperoxic hypercapnia simulations. In particular, simulations predict a moderate increase in mean systemic arterial pressure and heart rate, with almost no change in cardiac output, paralleled by a relevant increase in minute ventilation, tidal volume and respiratory rate. The model can represent a valid tool for clinical practice and medical research, providing an alternative way to experience-based clinical decisions. In conclusion, models are not only capable of summarizing current knowledge, but also identifying missing knowledge. In the former case they can serve as training aids for teaching the operation of complex systems, especially if the model can be used to demonstrate the outcome of experiments. In the latter case they generate experiments to be performed to gather the missing data.

Einfluss moderater intraischämischer Hypothermie auf die Proliferation und Differenzierung neuronaler Stammzellen 28 Tage nach inkompletter Vorderhirnischämie und Reperfusion der adulten Ratte

Hypothermie schützt Neurone vor hypoxischen, ischämischen und traumatischen Schädigungen. Bisher ist jedoch unklar, ob Hypothermie auch endogene Reparaturmechanismen beeinflusst. Die vorliegende Arbeit untersucht daher den Einfluss intraischämischer Hypothermie auf das neuroregenerative Potential des Gehirns nach zerebraler Ischämie.rn50 männliche Sprague-Dawley Ratten wurden hierzu anästhesiert, intubiert und in folgende Versuchsgruppen randomisiert: Normotherme Ischämie (Normo/BACO), intraischämische Hypothermie (Hypo/BACO) sowie korrespondierende scheinoperierte Kontrollgruppen (Normo/Sham und Hypo/Sham). In den Gruppen Normo/Sham und Normo/BACO wurde die perikranielle Temperatur konstant bei 37 °C gehalten während sie in den Gruppen Hypo/Sham und Hypo/BACO für 85 min auf 33 °C gesenkt wurde. Durch bilaterale Okklusion der Aa. carotides communes in Kombination mit hämorrhagischer Hypotension wurde in BACO-Tieren eine 14-minütige inkomplette globale zerebrale Ischämie induziert. Tiere der Kontroll-Gruppen (Sham) blieben ohne Induktion einer Ischämie in Narkose. 15 weitere Tiere durchliefen nicht den operativen Versuchsteil und bildeten die Nativ-Gruppe, die als Referenz für die natürliche Neurogenese diente. Zur in-vivo-Markierung der Stammzellen wurde vom ersten bis siebten postoperativen Tag Bromodeoxyurindine (BrdU) injiziert. Nach 28 Tagen wurden die Gehirne entnommen. Die Analyse des histopathologischen Schadens erfolgte anhand HE-gefärbter Hirnschnitte, die Quantifikation der absoluten Anzahl neu gebildeter Zellen im Gyrus dentatus erfolgte mittels BrdU-Färbung. Anhand einer BrdU/NeuN-Immunfluoreszenz-Doppelfärbung konnte der Anteil neu generierter Neurone bestimmt werden.rnNach zerebraler Ischämie zeigten Tiere mit Normothermie eine Schädigung der CA 1-Region von über 50 % während hypotherme Ischämietiere einen Schaden von weniger als 10 % aufwiesen. Tiere ohne Ischämie (Hypo/Sham, Normo/Sham, Nativ) zeigten keinen histopathologischen Schaden. Die Anzahl neu gebildeter Neurone im Gyrus dentatus lag für normotherme Ischämietiere (Normo/BACO) bei 18819 und für Tiere mit intraischämischer Hypothermie (Hypo/BACO) bei 15175 neuen Neuronen. In den Kontroll-Gruppen wiesen Tiere der Gruppe Normo/Sham 5501, Tiere der Gruppe Hypo/Sham 4600 und Tiere der Nativ-Gruppe 5974 neu generierte Neurone auf.rnDiese Daten bestätigen frühere Studien, die eine Reduktion des neuronalen Schadens durch intraischämische Hypothermie zeigten. Infolge des ischämischen Stimulus kam es im Vergleich zu beiden Kontroll- und der Nativ-Gruppe zu einem signifikanten Anstieg der Anzahl neuer Neurone in beiden Ischämiegruppen unabhängig von der Temperatur. Somit scheint das Ausmaß der histopathologischen Schädigung keinen Einfluss auf die Anzahl neu gebildeter Neurone zu haben. Darüber hinaus beeinflusste die therapeutische Hypothermie auch nicht die natürliche Neurogeneserate. Die erhobenen Daten lassen vermuten, dass Hypothermie keinen Effekt auf die Anzahl und Differenzierung neuronaler Stammzellen aufweist, unabhängig davon, ob eine zerebrale Schädigung vorliegt.

Screening renal artery angiography in hypertensive patients undergoing coronary angiography and 6-month follow-up after ad hoc percutaneous revascularization

OBJECTIVE: To determine the prevalence and independent predictors of significant atherosclerotic renal artery stenosis (RAS) in unselected hypertensive patients undergoing coronary angiography and to assess the 6-month outcome of those patients with a significant RAS. METHODS: One thousand, four hundred and three consecutive hypertensive patients undergoing drive-by renal arteriography were analyzed retrospectively. Univariate and multivariate logistic regression analyses were performed to identify independent predictors of RAS. In patients with significant RAS (>or=50% luminal narrowing), 6-month follow-up was assessed and outcome was compared between patients with or without renal revascularization. RESULTS: The prevalence of significant RAS was 8%. After multivariate analysis, coronary [odds ratio 5.3; 95% confidence interval (CI) 2.7-10.3; P < 0.0001], peripheral (odds ratio 3.3; 95% CI 2.0-5.5; P < 0.0001), and cerebral artery (odds ratio 2.8; 95% CI 1.5-5.3; P = 0.001) diseases, and impaired renal function (odds ratio 2.9; 95% CI 1.8-4.5; P < 0.0001) were found as independent predictors. At least one of these predictors was present in 96% of patients with RAS. In 74 patients (66%) with significant RAS, an ad hoc revascularization was performed. At follow-up, creatinine clearance was significantly higher in revascularized than in nonrevascularized patients (69.2 vs. 55.5 ml/min per 1.73 m, P = 0.029). By contrast, blood pressure was comparable between both groups, but nonrevascularized patients were taking significantly more antihypertensive drugs as compared with baseline (2.7 vs. 2.1, follow-up vs. baseline; P = 0.0066). CONCLUSION: The prevalence of atherosclerotic RAS in unselected hypertensive patients undergoing coronary angiography was low. Coronary, peripheral, and cerebral artery diseases, and impaired renal function were independent predictors of RAS. Ad hoc renal revascularization was associated with better renal function and fewer intake of antihypertensive drugs at follow-up.

Active regulation of cerebral venous tone: simultaneous arterial and venous transcranial Doppler sonography during a Valsalva manoeuvre

The aim of this study was to analyse the cerebral venous outflow in relation to the arterial inflow during a Valsalva manoeuvre (VM). In 19 healthy volunteers (mean age 24.1 +/- 2.6 years), the middle cerebral artery (MCA) and the straight sinus (SRS) were insonated by transcranial Doppler sonography. Simultaneously the arterial blood pressure was recorded using a photoplethysmographic method. Two VM of 10 s length were performed per participant. Tracings of the variables were then transformed to equidistantly re-sampled data. Phases of the VM were analysed regarding the increase of the flow velocities and the latency to the peak. The typical four phases of the VM were also found in the SRS signal. The relative flow velocity (FV) increase was significantly higher in the SRS than in the MCA for all phases, particularly that of phase IV (p < 0.01). Comparison of the time latency of the VM phases of the MCA and SRS only showed a significant difference for phase I (p < 0.01). In particular, there was no significant difference for phase IV (15.8 +/- 0.29 vs. 16.0 +/- 0.28 s). Alterations in venous outflow in phase I are best explained by a cross-sectional change of the lumen of the SRS, while phases II and III are compatible with a Starling resistor. However, the significantly lager venous than the arterial overshoot in phase IV may be explained by the active regulation of the venous tone.