Frmacos con acciones

sobre la circulacn
Los AVC son la causa #3 de
muerte en EEUU
Cada ao, ms de 600 mil personas en
los Estados Unidos mueren de un ataque
al cerebro

Definiciones
Accidente vascular cerebral

Corresponde a un sndrome clnico de
rpida o brusca aparicin de un dficit
neurolgico focal no convulsivo, de
ms de 24 horas de evolucin.
Stroke; Accidente Vascular Enceflico (AVE); Ictus;
Clasificacin
Desde un punto de vista fisiopatolgico:

ACV
ISQUMICO
(68,8%)*
HEMORRGICO
(31,1%)
Lacunar (12,5%)
Aterotrombtico (4,4%)
Cardioemblico (33,5%)
Intraparenquimatosa
(28%)
Subaracnodea (3,3%)
* 14% no se especifica etiologa
Estudio prospectivo multidisciplinario Nacional del AVE, 1992. Jorge Tapia et al.
Tratamiento
1) Tratamiento antitrombtico:
Arterias: evitar propagacin del trombo y
la re-embolizacin.
Venas: evitar trombosis venosa profunda
y TEP.
Uso de antiagregantes plaquetarios,
heparina, uso de medias elsticas.
Qu es tPA?
tPA es activador tisular de
plasmingeno, un medicamento
administrado para disolver cogulos
tPA puede reducir el nivel de incapacidad
provocada por un ataque al cerebro si se
administra antes de que pasen tres horas
desde el comienzo del evento
Subarachnoid hemorrhage (SAH)
Is a common and often devastating occurrence;
each year approximately 30,000 Americans
have nontraumatic SAH.
Despite considerable advances in diagnostic
techniques, surgical, and anesthetic techniques
and perioperative management, the outcome for
patients with SAH remains poor, with overall
mortality rates of 25% and significant morbidity
among approximately 50% of survivors.
(http://www.americanheart.org/presenter.jhtml?identifier=1192
consultado el 25 de febrero del 2007)
Calcium-Channel Antagonists
(http://www.americanheart.org/presenter.jhtml?identifier=1192
consultado el 25 de febrero del 2007)

A number of prospective, randomized
trials for the oral agent nimodipine were
initiated in the past decade.
Allen G, N Engl J Med. 1983;308:619-624.
Pickard JD, Br Med J . 1989;298:636-642.
Several prospective nonrandomized
trials,have reported a lower incidence of
permanent deficit or death from
vasospasm after intravenous
administration of calcium-channel
antagonists, with rates ranging from 1% to
10%.
Auer L. Neurosurgery. 1984;15:57-66.
Gilsbach J, Neurosurgery. 1990;26:458-464.
Dihydropyridine calcium antagonists increase
fibrinolytic activity: a systematic review.
Calcium antagonists have been shown to
be superior over other antihypertensive
drugs to prevent stroke.
Vergouwen MD, Dihydropyridine calcium antagonists increase
fibrinolytic activity: a systematic review. J Cereb Blood Flow
Metab. 2006 Dec 27;
Because this cannot be fully attributed to
blood pressure lowering effects, other
mechanisms seem to play a role.

Vergouwen MD, Dihydropyridine calcium antagonists increase
fibrinolytic activity: a systematic review. J Cereb Blood Flow
Metab. 2006 Dec 27;
We systematically studied the entire
PUBMED and EMBASE
Twenty-six prospective studies were
identified and 22 manuscripts were
included (802 investigated individuals).
Vergouwen MD, Dihydropyridine calcium antagonists increase
fibrinolytic activity: a systematic review. J Cereb Blood Flow
Metab. 2006 Dec 27;
The results show that calcium antagonists

1.-significantly increase fibrinolysis
2.- and an increase of tPA activity
Vergouwen MD, Dihydropyridine calcium antagonists increase
fibrinolytic activity: a systematic review. J Cereb Blood Flow
Metab. 2006 Dec 27;
In conclusions
Calcium antagonists increase fibrinolytic
activity. This may add to the beneficial
pharmacological effect of calcium
antagonists to prevent ischemic events in
patients with hypertension and
subarachnoid hemorrhage
Vergouwen MD, Dihydropyridine calcium antagonists increase
fibrinolytic activity: a systematic review. J Cereb Blood Flow
Metab. 2006 Dec 27;
Nimodipino
(Vlazquez 17)
En pacientes con hemorragia
subaracnoidea, aumenta el flujo cerebral.
Suprime cuadros de vasoespasmo.
Mejora el deterioro neurolgico.
No mejora la supervivencia
No es efectivo en Ictus isquemico
Manejo profilctico de migraa.

Migraine is the most
common type of
headache disorder,
characterized by
recurring headaches,
which vary in intensity
Usually affects only one
side of the head, is often
accompanied by
decreased appetite,
nausea, vomiting and
intolerance to light and
sound
World prevalence of migraine:
A disorder of First World
1-year prevalence rates
Population-based studies
IHS criteria (or modified)
USA 12%
Chile 7%
Japan 8%
Italy 16%
Denmark 10%
France 8%

Switzerland 13%
Rasmussen and Olesen (1994); Rasmussen (1995);
Lipton et al (1994); Lavados and Tenhamm (1997);
Sakai and Igarashi (1997)

Prevalence measured over a few years

Prevalence of migraine by
sex and age
Females
Males
30
25
20
15
10
5
0
20 30 40 50 60 70 80 100
Migraine prevalence (%)
Age (years)
Lipton and Stewart (1993)
The American Migraine Study (n=2479 migraine sufferers)
Migraine Triggers
Alcoholic
beverages
Hormonal
changes
Weather
Stress
Glare or
flickering light
Changes in
sleep habit
Fisiopatologa
Desencadenante


Dilatacin de los vasos


Activacin del trignimo


Mayor sensibilidad de las fibras nerviosas
Mechanisms for treatment
CGRP
NK
SP
5-HT
1F
5-HT
1D
5-HT
1B
Blood vessel
Trigeminal
nerve
Adapted from Goadsby (1997)
CGRP calcitonin gene
related peptide
NK neurokinin A
SP substance P
triptan
CONSTRICTION
INHIBITION
Are all migraine medications
the same?
Acute:
Triptans
Analgesics
Preventives
Antiepileptics
Beta-blockers
Antidepressants (TCAs)
Dihidroergotamina.
Agonista parciales de los receptores alfa
Agonista de los receptores
serotoninrgicos.
Biodisponibilidad por va oral de 1 a 5 %
Efecto del primer paso muy importante
Su eliminacin es bifsica con una inicial
muy rpida y otra muy rpida.
Se metaboliza en el hgado y se elimina
por las heces
Efectos adversos
Nauseas
Vomitos
Parestesias
Crisis anginosas
Insuficiencia vascular
Isquemia del miocardio
Gangrena de las extremidades
Cefalea de rebote
Sumatriptan
Agonista de receptores 5-HT
1B
y 5-HT
1D

Diseado especficamente para el
tratamiento agudo de la migraa.
Eficaz en el 70 a 80 % de la cefalea
migraosa y sntoma asociados.
Su efecto inicia 30 a 60 minutos de su
adm.

Concentracin mxima a los 90 min.
Vida media de 2 hrs.
Es mas eficaz cuando se adm, por va
intranasal.
Inicio de accin 12 min.

Riego de efectos
vasoconstrictores en:
arterias coronarias,
enfermedades cerebrovasculares y en
la hipertensin arterial no controlada.
Pentoxifilina
Derivado xntico que aumenta la
flexibilidad de las membrana de los
hemates.
As como tiene efecto antiagregante
plaquetario.
Usos antiagregantes plaquetarios
Prevencin de los accidentes trombticos
en el sector arterial.
Riesgo de sangrado en personas sanas.
Solo a personas con 3 o ms factores de
riesgo

Prevencin secundaria
Manejo de antiagregantes a pacientes que
han sufrido uno o varios accidentes
trombticos.
Angina
Infarto agudo del miocardio
Implantacin de prtesis
Procesos vasculares cerebrales
Procesos vasculares perifricos