A: número de altas hospitalarias por insuficiencia cardíaca.

B: porcentaje de altas hospitalarias por insuficiencia cardíaca

sobre el total de altas hospitalarias en España (1989-1999).

Rodriguez-Artalejo F. Y cols.: Rev Esp Cardiol 2004; 57: 163 - 170

 TTº INSUFICIENCIA CARDIACA
Inotrópicos
DIGOXINA
agonistas β−adrenérgicos
α2 Inhibidores de FDEs

Transmisión Simpática
BLOQUEANTES β–ADRENÉRGICOS

Vasodilatadores
DIURETICOS
HIDRALAZINA
α1 DINITRATO ISOSORBIDE
angiotensinogeno
β1 β1 renina

angiotensina 1
tripsina
ECA catepsina
- quimasa
IECAs angiotensina 2 ARA-2
-
+ +
+
vc Aldosterona
NA

Bloqueantes R. de Aldosterona
Spironolactona
Eplerenona
In 1775 William Withering demonstrated that the leaves of
the foxglove plant alleviated certain forms of dropsy
(edema), and in 1799 John Ferriar ascribed their beneficial
effects to a primary action on the heart. All physicians have
learned about digitalis, but few recognize its plant source.
Digoxin, the preparation most commonly used in the United
States, is derived from related plants, Digitalis lanata and D.
orientalis
 MECANISMO DE ACCIÓN DE DIGOXINA

1. Acción Directa:

K+ Na+

ATPasa
Na+-K+ Ca+2/Na+

-
Na+ Ca+2
DIGOXINA
RS

2. ↑ Sensibilidad a Ach.
EFECTOS PROARRITMICOS DE DIGOXINA
 TOXICIDAD DIGITÁLICA

1.- Sintomatología precoz:

- Nauseas
- Vómitos
- Anorexia
- Diarrea
- Alteración visión de colores
2.- Arritmias Cardiacas

3.- Síntomas Neurológicos:

- Cefaleas
- Somnolencia
- Confusión
- Neuralgia

4.- Otros: - Visión Borrosa

- Ginecomastia
Farmacocinética

Farmacodinámica
Cumulative Percentages (Time to First Event) for the Combined End Point of Total Mortality or
All-Cause Hospitalization

Hjalmarson, A. et al. JAMA 2000;283:1295-1302.

Copyright restrictions may apply.
Kaplan-Meier Analysis of the Probability of Freedom from the Combined End Point (Death from
Any Cause, Cardiac Arrest with Resuscitation, Hospitalization for Worsening Heart Failure, or
Therapy with Intravenous Inotropes or Vasodilators)

Cohn J et al. N Engl J Med 2001;345:1667-1675

Kaplan-Meier Analysis of the Probability of Survival among Patients in the Placebo Group and
Patients in the Spironolactone Group

Pitt B et al. N Engl J Med 1999;341:709-717

Cohn J. y cols. (1991) N EnglJ Med 325: 303-10
Terapia Vasodilatadora en pacientes Afro-americanos con ICC

Taylor AL y cols, (2005) N Engl J Med 351:2049-2057

Incidence of Death or Hospitalization Due to Worsening Heart Failure in the Digoxin and Placebo Groups

The Digitalis Investigation Group (1997) N Engl J Med 336:525-533

Kaplan-Meier Estimates of Survival among Men and Women, According to Whether They Were
Randomly Assigned to Receive Digoxin or Placebo

Rathore S et al. N Engl J Med 2002;347:1403-1411

Wang L. y cols. (2007) J Pharmacol Exptl Ther 320: 525-34
Pérez-Villa F. (2004) Med Clin 123: 149
Common Clinical Problems in Patients with Heart Failure and Recommended Solutions

Jessup M and Brozena S. N Engl J Med 2003;348:2007-2018

Stress signals (such as hemodynamic overload) activate signal-transduction pathways that lead to either the up-regulation or down-
regulation of specific microRNAs (miRNAs). Stress-induced up-regulation of miRNAs can then lead to the down-regulation of several
target messenger RNAs (mRNAs) through gene silencing or translational blockade of the target mRNA. Conversely, stress-induced down-
regulation of miRNAs can result in up-regulation of target mRNAs because of the loss of tonic inhibitory control of the miRNA on its
target mRNA. Ultimately, it is the miRNA-induced pattern of change in gene expression that contributes to the resultant disease phenotype.
Van Rooij and colleagues recently showed that the absence of a specific mRNA prevents cardiac hypertrophy and up-regulation of -myosin
heavy chain after an overload of hemodynamic pressure, indicating that this miRNA is critical to the development of heart failure

Mann D. N Engl J Med 2007;356:2644-2645

ESTATINAS Y MORTALIDAD EN PACIENTES ANCIANOS CON INSUFICIENCIA
CARDIACA

JM Foody. Y cols (2006) Circulation 113: 1086-92

 POSIBILIDADES TERAPEUTICAS EN INSUFICIENCIA CARDIACA

α2 MOXONIDINA OMAPATRILAT

- TOLVAPTAN
-
ADH degradación
NEP
Actividad simpática + NESIRITIDE
-
ANP

Apoptosis

+ VC -Aldosterona
caspasas RESINCRONIZACION
VD T. CELULAR
↑GFR T. CARDIACO
↓RENINA
- +
+ + +
INHIBIDORES

AT-2
BOSENTAL - ET-1 CITOKINAS (TNF,IL-6)
Murray DR y cols.(2000) Circulation 101:2338
-
INFLIXIMAB