ISSN: 0001-6002
actamedica@medicos.sa.cr
Colegio de Mdicos y Cirujanos de Costa Rica
Costa Rica
Revisin
Actualizacin en los mecanismos
fisiopatolgicos de la insuficiencia
cardiaca
(Update in physiopathological mechanisms in heart failure)
Guido Ulate-Montero, Adriana Ulate-Campos
_____________________________________________________________________________________
Resumen
_____________________________________________________________________________________
* Departamento de Fisiologa,
Escuela de Medicina,Universidad
de Costa Rica
Abreviaturas:
ANGII,
angiotensina II; ET-1: endotelina
1; GC, gasto cardiaco; HAD,
hormona
antidiurtica
(vasopresina); IC, insuficiencia
cardiaca;
LEC,
lquido
extracelular; NE, norepinefrina;
PA, potencial de accin; PAN,
pptido atrial natriurtico; PCN,
pptido cerebral natriurtico;
PKA,
proteinquinasa
A;
PKC,
proteinquinasa
C;
RS, retculo sarcoplsmico;
RyR2, receptor de rianodina,
SERCA2a, ATPasa de calcio de
retculo sarcoplsmico; SRAA,
sistema
renina-angiotensinaaldosterona; VI, ventrculo
izquierdo.
Correspondencia: Apartado
1300 2050, San Pedro.
Abstract
_____________________________________________________________________________________
Heart failure is one of the most frequent clinical syndromes in medical practice; it appears when
the heart is unable to pump enough volume of blood to supply the tissues requirements. This
article reviews the most recent information regarding the mechanisms involved in the
pathophysiology of heart failure, the main goal is to offer the knowledge necessary to understand
and manage properly this condition. In heart failure, as a response to the low cardiac output, a
series of neuroendocrine systemic mechanisms are activated, but they contribute to deteriorate
the clinical status; this happens with the sympathetic and the renin-angiotensin-aldosterone
systems, which end up producing endothelial damage, increase of oxidative radicals, apoptosis,
ISSN 0001-6002/2008/50/1/5-12
Acta Mdica Costarricense, 2008
Colegio de Mdicos y Cirujanos
cardiac fibrosis and generation of arrhythmias. Also there is an increase in the secretion of
natriuretic peptides, which tend to regulate some of the exacerbated neuroendocrine responses,
but with time their effect tend to diminish. At the cellular and molecular level a series of alterations
occur in the regulation of intracellular Ca2+, as well as in some of the ionic currents that play a
role in the generation of action potentials in cardiac myocytes. Cardiac remodeling precedes the
clinical manifestations of heart failure and contributes to its deterioration. Chemical messengers
like endothelin-1, norepinephrine and angiotensin II, activate the MAP kinases cascade and
provoke cardiac hypertrophy favoring the development of ischemia and the appearance of
arrhythmias. Pharmacological management of heart failure must aim the mechanisms affected, it
must block the deleterious actions of the neuroendocrine systems, avoiding the loss of myocytes,
the generation of fibrosis and the production of cardiac arrhythmias, in order to achieve this goal
an appropriate management of intracellular levels of Ca2+ is required.
Key words: Heart failure, cardiac remodeling, neurohumoral activation, excitation-contraction
coupling, arrhythmias, apoptosis
Recibido: 31 de julio de 2007
Liberacin no
antidiurtica
osmtica
de
la
hormona
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