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      Neuropsychiatric consequences of cardiovascular medications Translated title: Consecuencias neuropsiquiátricas de los medicamentos cardiovasculaires Translated title: Conséquences neuropsychiatriques des traitements cardiovasculaires

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          Abstract

          The use of cardiovascular medications can have a variety of neuropsychiatric consequences. Many cardiovascular agents cause higher rates of fatigue and sedation than placebo, and case reports of medication-induced mood syndromes, psychosis, and cognitive disturbances exist for many cardiovascular drugs. Depression has been associated with β-blockers, methyldopa, and reserpine, but more recent syntheses of the data have suggested that these associations are much weaker than originally believed. Though low cholesterol levels have been associated with depression and suicide, lipid-lowering agents have not been associated with these adverse effects. Finally, cardiovascular medications may have beneficial neuropsychiatric consequences; for example, the use of clonidine in patients with attention deficit-hyperactivity disorder, the use of prazosin for patients with post-traumatic stress disorder, and the use of propranolol for performance anxiety and akathisia.

          Translated abstract

          El empleo de medicamentos cardiovasculares puede tener una variedad de consecuencias neuropsiquiátricas. Muchos fármacos cardiovasculares provocan con mayor frecuencia fatiga y sedación respecto del placebo y también existen muchos reportes de casos de síntomas afectivos, psicosis y trastornos cognitivos inducidos por varios de estos medicamentos. Se ha asociado la depresión con beta-bloqueadores, metildopa y reserpina, pero análisis recientes de estos datos han sugerido que estas asociaciones son mucho más débiles que lo que originalmente se pensaba. Aunque los niveles reducidos de colesterol se han asociado con depresión y suicidio, los fármacos reductores de lípidos no se han asociado con estos efectos adversos. Por último, los fármacos cardiovasculares pueden tener efectos neuropsiquiátricos útiles; por ejemplo, el empleo de clonidina en pacientes con trastorno por déficit atencionaI con hiperactividad, el uso de prazosin en pacientes con trastorno por estrés postraumático y la indicación de propranolol en la ansiedad de rendimiento y en la acatisia.

          Translated abstract

          Les traitements cardiovasculaires peuvent avoir des conséquences neuropsychiatriques variées. De nombreux produits cardiovasculaires induisent une fatigue et une sédation plus importantes que le placebo. Des troubles cognitifs, de l'humeur et psychotiques ont été considérés comme provoqués par un grand nombre de ces traitements cardiotropes. La dépression a parfois été associée aux β-bloquants, à la méthyldopa et à la réserpine, mais des données plus récentes laissent penser que ces associations sont beaucoup moins importantes qu'initialement pressenties. Bien que des cholestérolémies basses aient été associées à la dépression et au suicide, les hypolipémiants n'ont pas été incriminés dans de tels effets indésirables. Les traitements cardiovasculaires peuvent finalement avoir des conséquences neuropsychiatriques bénéfiques : par exemple, l'utilisation de la clonidine chez les patients atteints d'un déficit de l'attention/hyperactivité, l'utilisation de la prazosine pour ceux souffrant d'un syndrome de stress post-traumatique, et l'utilisation du propranolol pour l'anxiété de performance (trac) et l'akathisie.

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          Most cited references 303

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          Prognostic association of depression following myocardial infarction with mortality and cardiovascular events: a meta-analysis.

          To assess the association of depression following myocardial infarction (MI) and cardiovascular prognosis. The authors performed a meta-analysis of references derived from MEDLINE, EMBASE, and PSYCINFO (1975-2003) combined with crossreferencing without language restrictions. The authors selected prospective studies that determined the association of depression with the cardiovascular outcome of MI patients, defined as mortality and cardiovascular events within 2 years from index MI. Depression had to be assessed within 3 months after MI using established psychiatric instruments. A quality assessment was performed. Twenty-two papers met the selection criteria. These studies described follow up (on average, 13.7 months) of 6367 MI patients (16 cohorts). Post-MI depression was significantly associated with all-cause mortality (odds ratio [OR], fixed 2.38; 95% confidence interval [CI], 1.76-3.22; p <.00001) and cardiac mortality (OR fixed, 2.59; 95% CI, 1.77-3.77; p <.00001). Depressive MI patients were also at risk for new cardiovascular events (OR random, 1.95; 95% CI, 1.33-2.85; p = .0006). Secondary analyses showed no significant effects of follow-up duration (0-6 months or longer) or assessment of depression (self-report questionnaire vs. interview). However, the year of data collection (before or after 1992) tended to influence the effect of depression on mortality (p = .08), with stronger associations found in the earlier studies (OR, 3.22; 95% CI, 2.14-4.86) compared with the later studies (OR, 2.01; 95% CI, 1.45-2.78). Post-MI depression is associated with a 2- to 2.5-fold increased risk of impaired cardiovascular outcome. The association of depression with cardiac mortality or all-cause mortality was more pronounced in the older studies (OR, 3.22 before 1992) than in the more recent studies (OR, 2.01 after 1992).
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            Statins and the risk of dementia.

            Dementia affects an estimated 10% of the population older than 65 years. Because vascular and lipid-related mechanisms are thought to have a role in the pathogenesis of Alzheimer's disease and vascular dementia, we did an epidemiological study of the potential effect of HMGCoA (3 hydroxy-3methylglutaryl-coenzyme A) reductase inhibitors (statins) and other lipid-lowering agents on dementia. We used a nested case-control design with information derived from 368 practices which contribute to the UK-based General Practice Research Database. The base study population included three groups of patients age 50 years and older: all individuals who had received lipid-lowering agents (LLAs); all individuals with a clinical diagnosis of untreated hyperlipidaemia; and a randomly selected group of other individuals. From this base population, all cases with a computer-recorded clinical diagnosis of dementia were identified. Each case was matched with up to four controls derived from the base population on age, sex, practice, and index date of case. The study encompassed 284 cases with dementia and 1080 controls. Among controls 13% had untreated hyperlipidaemia, 11% were prescribed statins, 7% other LLAs, and 69% had no hyperlipidaemia or LLA exposure. The relative risk estimates of dementia adjusted for age, sex, history of coronary-artery disease, hypertension, coronary-bypass surgery and cerebral ischaemia, smoking and body mass index for individuals with untreated hyperlipidaemia (odds ratio 0.72 [95% CI 0.45-1.14]), or treated with nonstatin LLAs (0.96 [0.47-1.97], was close to 1.0 and not significant compared with people who had no diagnosis of hyperlipidaemia or exposure to other lipid-lowering drugs. The adjusted relative risk for those prescribed statins was 0.29 (0.13-0.63; p=0.002). Individuals of 50 years and older who were prescribed statins had a substantially lowered risk of developing dementia, independent of the presence or absence of untreated hyperlipidaemia, or exposure to nonstatin LLAs. The available data do not distinguish between Alzheimer's disease and other forms of dementia.
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              Pilot study of secondary prevention of posttraumatic stress disorder with propranolol.

              Preclinical considerations suggest that treatment with a beta-adrenergic blocker following an acute psychologically traumatic event may reduce subsequent posttraumatic stress disorder (PTSD) symptoms. This pilot study addressed this hypothesis. Patients were randomized to begin, within 6 hours of the event, a 10-day course of double-blind propranolol (n = 18) versus placebo (n = 23) 40 mg four times daily. The mean (SD) 1-month Clinician-Administered PTSD Scale (CAPS) score of 11 propranolol completers was 27.6 (15.7), with one outlier 5.2 SDs above the others' mean, and of 20 placebo completers, 35.5 (21.5), t = 1.1, df = 29, p =.15. Two propranolol patients' scores fell above, and nine below, the placebo group's median, p =.03 (sign test). Zero of eight propranolol, but six of 14 placebo, patients were physiologic responders during script-driven imagery of the traumatic event when tested 3 months afterward, p =.04 (all p values one-tailed). These pilot results suggest that acute, posttrauma propranolol may have a preventive effect on subsequent PTSD.
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                Author and article information

                Contributors
                Department of Psychiatry, Massachusetts General Hospital, Boston, Mass, USA; Harvard Medical School, Boston, Mass, USA
                Department of Psychiatry, Massachusetts General Hospital, Boston, Mass, USA; Harvard Medical School, Boston, Mass, USA
                Journal
                Dialogues Clin Neurosci
                Dialogues Clin Neurosci
                Dialogues in Clinical Neuroscience
                Les Laboratoires Servier (France )
                1294-8322
                1958-5969
                March 2007
                March 2007
                : 9
                : 1
                : 29-45
                Affiliations
                Department of Psychiatry, Massachusetts General Hospital, Boston, Mass, USA; Harvard Medical School, Boston, Mass, USA
                Department of Psychiatry, Massachusetts General Hospital, Boston, Mass, USA; Harvard Medical School, Boston, Mass, USA
                Author notes
                Article
                3181843
                17506224
                Copyright: © 2007 LLS

                This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Pharmacological Aspects

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