Elsevier

JACC: Heart Failure

Volume 1, Issue 1, February 2013, Pages 1-20
JACC: Heart Failure

State-of-the-Art Paper
Heart Failure

https://doi.org/10.1016/j.jchf.2012.10.002Get rights and content
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Despite major improvements in the treatment of virtually all cardiac disorders, heart failure (HF) is an exception, in that its prevalence is rising, and only small prolongations in survival are occurring. An increasing fraction, especially older women with diabetes, obesity, and atrial fibrillation exhibit HF with preserved systolic function. Several pathogenetic mechanisms appear to be operative in HF. These include increased hemodynamic overload, ischemia-related dysfunction, ventricular remodeling, excessive neurohumoral stimulation, abnormal myocyte calcium cycling, excessive or inadequate proliferation of the extracellular matrix, accelerated apoptosis, and genetic mutations. Biomarkers released as a consequence of myocardial stretch, imbalance between formation and breakdown of extracellular matrix, inflammation, and renal failure are useful in the identification of the pathogenetic mechanism and, when used in combination, may become helpful in estimating prognosis and selecting appropriate therapy. Promising new therapies that are now undergoing intensive investigation include an angiotensin receptor neprilysin inhibitor, a naturally-occurring vasodilator peptide, a myofilament sensitizer and several drugs that enhance Ca++ uptake by the sarcoplasmic reticulum. Cell therapy, using autologous bone marrow and cardiac progenitor cells, appears to be promising, as does gene therapy. Chronic left ventricular assistance with continuous flow pumps is being applied more frequently and successfully as destination therapy, as a bridge to transplantation, and even as a bridge to recovery and explantation. While many of these therapies will improve the care of patients with HF, significant reductions in prevalence will require vigorous, multifaceted, preventive approaches.

Key Words

biomarkers
calcium cycling
cardiovascular disease
heart failure
left ventricular assist device
review

Abbreviations and Acronyms

ACE
angiotensin-converting enzyme
ACS
acute coronary syndromes
ADHF
acute decompensation heart failure
ANP
atrial natriuretic peptide
ARB
angiotensin II receptor blocker
BNP
brain natriuretic peptide
CAD
coronary artery disease
CPC
cardiac stem/progenitor cell
CRP
C-reactive protein
cTn
cardiac-specific troponin
CVD
cardiovascular disease
ECM
extracellular matrix
EF
ejection fraction
HF
heart failure
HFPEF
heart failure and a preserved ejection fraction
HFREF
heart failure and a reduced ejection fraction
hs
high-sensitivity
LV
left-ventricular
LVAD
left-ventricular assist device
miR
micro RNA
MMP
matrix metalloproteinases
NP
natriuretic peptide
NT-proBNP
N-terminal pro-B-type natriuretic peptide
PINP
pro collagen type I aminoterminal propeptide
PIIINP
collagen III N-terminal propeptide
RyR2
ryanodine receptor
SR
sarcoplasmic reticulum
SERCA2a
sarcoplasmic reticulum Ca2+ adenosine triphosphatase

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Dr. Braunwald has received research support from Johnson & Johnson.