RESUMEN
The pathophysiological mechanisms underlying Myocardial Infarction with Non-Obstructive Coronary Artery Disease (MINOCA) are still under debate. Lipoprotein (a) [Lp(a)] has proinflammatory and prothrombotic actions and has been involved in the pathogenesis of atherosclerosis. However, no previous studies have linked Lp(a) levels with the probability of developing MINOCA. Moreover, the relationship between MINOCA and the plasma levels of other proatherogenic and proinflammatory molecules such as Interleukin-18 (IL18) and proprotein convertase subtilisin/kexin type 9 (PCSK9) has not been studied. We conducted a prospective, multicenter study involving 1042 patients with acute myocardial infarction (AMI). Seventy-six patients had no significant coronary lesions. All patients underwent plasma analysis on admission. MINOCA patients were younger (57 (47-68) vs. 61 (52-72) years; p = 0.010), more frequently female (44.7% vs. 21.0%; p < 0.001), and had lower rates of diabetes and of Lp(a) > 60 mg/dL (9.2% vs. 19.8%; p = 0.037) than those with coronary lesions; moreover, High Density Lipoprotein cholesterol (HDL-c) levels were higher in MINOCA patients. The absence of Lp(a) > 60 mg/dL and of diabetes were independent predictors of MINOCA, as well as female sex, high HDL-c levels, and younger age. IL-18 and PCSK9 levels were not predictors of MINOCA. During a follow-up of 5.23 (2.89, 7.37) years, the independent predictors of the primary outcome (acute ischemic events or death) in the whole sample were Lp(a) > 60 mg/dL, older age, low estimated Glomerular Filtration rate (eGFR), hypertension, previous heart failure (HF), coronary artery bypass graft, use of insulin, and no therapy with acetylsalicylic acid. In conclusion, in AMI patients, the absence of high Lp(a) levels, as well high HDL-c levels, were independent predictors of the inexistence of coronary artery disease. High Lp (a) levels were also an independent predictor of ischemic events or death.
RESUMEN
RESUMEN El síndrome cistocerebral fue descrito por primera vez en 1990 por Blackburn y Dunn. Los casos estudiados fueron varones ancianos con síndrome confusional agudo y retención urinaria aguda que, tras un drenaje vesical, presentaron resolución completa del cuadro clínico. Se reporta el caso de un anciano con disminución rápida del nivel de consciencia, mioclonías, hipotensión arterial, bradicardia y retención aguda de orina que experimentó total remisión del cuadro clínico luego del drenaje vesical correspondiente. Se describen, asimismo, los posibles mecanismos implicados en el origen de este síndrome y las alteraciones hemodinámicas y autonómicas subyacentes. Se sugiere considerar al síndrome cistocerebral en el diagnóstico diferencial de pacientes varones ancianos con síndrome confusional o deterioro cognitivo e hipertrofia prostática y que presenten, además, un episodio de retención urinaria aguda.
SUMMARY Cystocerebral syndrome was first described in 1990 by Blackburn and Dunn, in elderly males with acute confusion syndrome and urinary retention, who after bladder drainage experienced full resolution of the clinical picture. We report the case of an elderly male patient with Cystocerebral syndrome and symptoms such as a rapid decrease in consciousness level, myoclonies, hypotension, bradycardia and acute urinary retention who, after bladder drainage presented a complete remission of the clinical picture. The potential mechanisms involved in the origin of this syndrome are described, as well as its underlying hemodynamic and autonomic alterations. Cystocerebral syndrome should be considered in the differential diagnosis of patients with a confusional syndrome and cognitive impairment, diagnosed with prostatic hypertrophy and presenting, in addition, an episode of acute urinary retention.
RESUMEN
Con el redescubrimiento de las causas vasculares en el deterioro cognitivo, el concepto de trastorno cognitivo vascular (TCV) busca cambiar los paradigmas establecidos en el antiguo concepto de demencia vascular. El TCV sería el resultado de una cascada de eventos: los factores de riesgo vascular conducen a enfermedad vascular cerebral, la cual origina injuria vascular cerebral en las vías nerviosas importantes para la cognición. Tanto el TCV como la enfermedad de Alzheimer (EA) se incrementan exponencialmente con la edad y sus interacciones son comunes y controversiales. No obstante la capacidad de los criterios de consenso actuales para distinguir TCV de EA es limitada, la identificación en estadios tempranos nos va a dar la oportunidad de influir sobre la tasa de progresión de la enfermedad. Actualmente, la prevención primaria y secundaria es esencialmente la misma establecida para ictus, mientras que el tratamiento sintomático de TCV es similar a EA.
With the rediscovering of the importance of vascular causes related to cognitive impairment, the new concept of vascular cognitive impairment (VCI) seeks to change the paradigms established in the old concept of vascular dementia. The VCI is the outcome of a cascade of events: vascular risk factors lead to vascular disease which causes vascular brain injury (VBI) in the nervous network important for cognition. Both VCI and Alzheimers disease (AD) increase exponentially with age, and their interactions are common and controversial. However, the capacity of current consensus criteria to distinguish VCI from AD is limited; the identification of cases at the earliest possible stage will give us the excellent opportunity to provide medical treatment that may retard the disease rate of progression. Currently, the primary and secondary prevention of VCI is essentially the same for stroke, whereas the symptomatic treatment of VCI is similar to AD.
