Introducción: La angina variante por vasoespasmo coronario y el síndrome X han sido mencionados como responsables de angina en ausencia de lesión coronaria significativa. Sin embargo no todos los pacientes en esta situación clínica cumplen criterios para ser agrupados en estas entidades patológicas.Pacientes y Métodos: Se estudiaron 328 pacientes consecutivos divididos en 4 grupos: A: Angina vasoespástica (n:165). B: Síndrome X (SDX) [sin vasoespasmo (VSP) con prueba de esfuerzo (PE) positiva] (n:47). C: Angina de reposo o mixta, sin VSP y PE negativa (n:93) D: Angina de esfuerzo, sin VSP y PE negativa (n:23). Fueron excluidos del estudio aquellos pacientes con patología extracoronaria que justificase la angina. Se evaluaron antecedentes patológicos, factores de riesgo y características clínicas. Se realizó a todos una prueba de esfuerzo, con gammagrafía en 214 casos, y se analizó en el seguimiento a largo plazo (72±52meses) valorando la mortalidad y la aparición de eventos coronarios.Resultados: La prevalencia global de dislipemia fue elevada (67%) y no mostró diferencias significativa entre los grupos. La prevalencia del tabaquismo fue superior en los pacientes que presentaban VSP (62 vs 22%, p<0,001) y la de HTA fue superior en el SDX que en el resto de los grupos (51 vs 34%, P<0,05). Entre los pacientes vasoespásticos existía una mayor proporción con respuesta a NTG que en los no vasoespásticos (85 vs 54%,p<0,01). Un 43,2% de los pacientes de grupos C y D presentan defectos de perfusión reversibles. No existieron diferencias significativas entre los pacientes con y sin VSP en la aparición de cambios ECG (24,6 vs 29%, p:ns) ni defectos gammagráficos (53 vs 50%,p:ns) durante la PE. En el seguimiento se observó una reducida mortalidad (3%) y una baja incidencia de infarto de miocardio (5%) sin evidenciarse diferencias entre los grupos ni entre pacientes con (4,7%) o sin (7%) defectos gammagráficos de esfuerzo (p:ns).Conclusiones: Nuestros resultados indican que existe una proporción importante de pacientes anginosos sin lesiones coronarias significativas que no presentan vasoespasmo ni cambios en el ECG de esfuerzo. No obstante, casi la mitad de ellos presentan defectos de perfusión durante el esfuerzo, en su mayoría leves. Existe una baja incidencia de infarto de miocardio y de mortalidad cardiaca en el seguimiento a largo plazo. La aparición de defectos gammagráficos de esfuerzo no confiere empeoramiento en el pronóstico. / Introduction: Variant angina due to coronary spasm and syndrome X are known to be responsible for angina in the absence of significant coronary stenosis. However, not all patients in these clinical conditions meet the criteria to be labelled as these pathological entities.Patient and methods: We studied 328 consecutive patients in 4 different groups: A: vasospastic angina (n:165). B: Syndrome X (SDX) [without vasospasm (VSP) with a positive stress test (ST)] (n:47). C: Rest angina or mixed angina, without VSP and with a negative ST (n:93). D: stress angina without VSP and with negative ST (n:23). Those patients with non coronary cause of angina were excluded of this study. We evaluated pathological antecedents, risk factors and clinical characteristics. Stress tests were performed in all patients, 214 of them with scintigraphic perfusion analysis. We study incidence of mortality and coronary events in the long term follow up (72±52month).Result: The global prevalence of dislipidemia was high (67%) without significant differences between groups. The prevalence of smoking was higher in the vasospastic patients (62 vs 22%, p<0,001) and the hypertension's prevalence was higher in Group B than in the remaining groups (51 vs 34%, P<0,05). Among vasospastic patients we observed a greater proportion with response to nitroglicerine than no vasospastic patients (85 vs 54%, p<0,01). Forty tree patients from groups C and D presented reversible perfusion defects. There were not significant differences between patients with and without VSP in the ECG changes (24,6 vs. 29%, p:ns) nor in the scintigraphic defects (53 vs 50%,p:ns) during ST. In the follow-up we observed a low mortality rate (3%) and a low incidence of infarct (5%) without differences among the groups nor between patients with (4,7%) or without (7%) stress scintigraphic defects (p:ns) during ST.Conclusions: Our results indicate than there is an important proportions of patients with angina without significant coronary artery stenosis who do not nither present vasospasm nor ECG changes during ST. However, nearly a half of them present perfusion defects during ST, mild in most of them. There is a low incidence of myocardial infarct and cardiac mortality in the long-term follow-up. The presence of stress scintigraphic defects do not implicate worse prognosis.

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (leaves 73-84).

Spontaneous subarachnoid hemorrhage (SAH) is a form of hemorrhagic stroke that accounts for approximately 7% of all strokes worldwide. Recently, researchers have gained insight into some possible genetic influences involved in the response to SAH. The goal of this study was to investigate the potential contribution of different mouse genetic backgrounds to brain injury after SAH. SAH was induced in 7 inbred strains of mice, and the degree of large artery vasospasm and brain injury was assessed. After 48 hours, SAH mice showed a significant reduction in middle cerebral artery diameter and increased neuronal injury in the cerebral cortex compared to sham controls. The degree of vasospasm and brain injury varied across strains. This data suggests that vasospasm and neuronal injury may not correlate, and that different genetic factors may influence each one. Future investigations may provide invaluable insight into the causes of these inter-strain differences and potential genetic contributors.

Spontaneous subarachnoid hemorrhage (SAH) is a form of hemorrhagic stroke that accounts for approximately 7% of all strokes worldwide. Recently, researchers have gained insight into some possible genetic influences involved in the response to SAH. The goal of this study was to investigate the potential contribution of different mouse genetic backgrounds to brain injury after SAH. SAH was induced in 7 inbred strains of mice, and the degree of large artery vasospasm and brain injury was assessed. After 48 hours, SAH mice showed a significant reduction in middle cerebral artery diameter and increased neuronal injury in the cerebral cortex compared to sham controls. The degree of vasospasm and brain injury varied across strains. This data suggests that vasospasm and neuronal injury may not correlate, and that different genetic factors may influence each one. Future investigations may provide invaluable insight into the causes of these inter-strain differences and potential genetic contributors.

Cerebral vasospasm following subarachnoid hemorrhage has high morbidity and mortality. Mathematical modeling of the progression of the condition provides insight to improve clinical treatment of patients post subarachnoid hemorrhage. An existing model of the clotting cascade is expanded to include the theoretical conditions of cerebral vasospasm. We consider clotting factor XIIIa, which has been implicated as a primary cause of the entrenchment of the smaller diameter. Solutions for clotting are used as boundary conditions to solve the concentration of diffusible clotting factors in the vessel wall and cerebrospinal fluid (CSF). Each domain (clot, vessel wall, CSF) is described by a separate initial-boundary value problem, requiring unique conditions, reaction-diffusion equations, and diffusion coefficients. Additionally, the results from the first domain (the clot) provide a subset of the boundary conditions for the second and third domains (arterial wall and CSF, respectively). Although this approach captures many detailed components of the clotting process, a simpler method for investigating the formation and dissolution of a clot post subarachnoid hemorrhage is to neglect the bulk of the clot cascade to focus on the most salient features, namely, the formation of cross-linked fibrin and the degradation of fibrin by plasmin. By assuming first order kinetics in the initial hours following hemorrhage, we find a simplified expression with kinetic rates that may be adjusted depending on experimental conditions.

No description available.

No / Two different theories of migraine aura exist: In the vascular theory of Wolff, intracerebral vasoconstriction causes migraine aura via energy deficiency, whereas in the neuronal theory of Leão and Morison, spreading depression (SD) initiates the aura. Recently, it has been shown that the cerebrovascular constrictor endothelin-1 (ET-1) elicits SD when applied to the cortical surface, a finding that could provide a bridge between the vascular and the neuronal theories of migraine aura. Several arguments support the notion that ET-1¿induced SD results from local vasoconstriction, but definite proof is missing. If ET-1 induces SD via vasoconstriction/ischemia, then neuronal damage is likely to occur, contrasting with the fact that SD in the otherwise normal cortex is not associated with any lesion. To test this hypothesis, we have performed a comprehensive histologic study of the effects of ET-1 when applied topically to the cerebral cortex of halothane-anesthetized rats. Our assessment included histologic stainings and immunohistochemistry for glial fibrillary acidic protein, heat shock protein 70, and transferase dUTP nick-end labeling assay. During ET-1 application, we recorded (i) subarachnoid direct current (DC) electroencephalogram, (ii) local cerebral blood flow by laser-Doppler flowmetry, and (iii) changes of oxyhemoglobin and deoxyhemoglobin by spectroscopy. At an ET-1 concentration of 1 µM, at which only 6 of 12 animals generated SD, a microarea with selective neuronal death was found only in those animals demonstrating SD. In another five selected animals, which had not shown SD in response to ET-1, SD was triggered at a second cranial window by KCl and propagated from there to the window exposed to ET-1. This treatment also resulted in a microarea of neuronal damage. In contrast, SD invading from outside did not induce neuronal damage in the absence of ET-1 (n = 4) or in the presence of ET-1 if ET-1 was coapplied with BQ-123, an ETA receptor antagonist (n = 4). In conclusion, SD in presence of ET-1 induced a microarea of selective neuronal necrosis no matter where the SD originated. This effect of ET-1 appears to be mediated by the ETA receptor.

Thesis (doctoral)--Lund University, 1999. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (doctoral)--Lund University, 1999. / Added t.p. with thesis statement inserted. Includes bibliographical references.

There is conflicting data on the effects of statins on cerebral vasospasm and clinical outcomes in aneurysmal subarachnoid hemorrhage (aSAH) patients. In this retrospective cohort study, patients were divided into those who received pravastatin (PRAV group) 40mg/d and those who did not (NP group). Data were analyzed using multivariate logistic regression. Eighty-one patients met inclusion criteria. There was a statistically significant decreased in the incidence of vasospasm in the PRAV group; however, this association did not retain significance after adjusting for WFNS, race, elevated WBC, and clipping (59% PRAV vs. 88% NP, p=0.08). There was no statistically significant difference in proportion of severe radiological vasospasm or mortality between groups. However, there was a trend towards a decreased mean length of stay (P=0.06) and a significantly higher proportion of survivors discharged to home in the PRAV group (P<0.0001). In conclusion, there was a trend towards a decrease in the incidence of vasospasm in the aSAH receiving pravastatin, but this trend did not achieve statistical significance after adjusting for potential confounders. Pravastatin was associated with other favorable clinical outcomes.