Congestive Heart Failure (CHF)
CARDIAC FAILURE
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Last Updated : 5/11/2016
Valerie Schroeder
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Systemic Effects on the Cardiovascular System and End-Stage Heart disease
Systemic Effects on the Cardiovascular System and End Stage Heart disease
There many communications between the heart, circulation, and neuro-hormonal signaling pathways. These pathways, triggered by changes in hemodynamic status, modulate cardiac function (compensated heart failure). Such responses benefit when heart failure is transient but paradoxically become detrimental over time and contribute to end-state heart disease (3-6). Consequently, these effects must be considered in the overall treatment plan.
1) Sympathetic nervous system
Increases in sympathetic tone leads to higher heart rates, greater myocardial contractility and vasoconstriction to sustain tissue perfusion pressure. Sympathetic stimulation increases afterload (blood pressure), myocardial oxygen consumption and promotes fibrosis. Calcium flux within the cardiomyocyte may also be altered which subsequently results in reduced contractility (decompensation). Helpful drugs include beta-blockers.
2) The renin-angiotensin-aldosterone system
These pathways cause vasoconstriction and renal retention of salt and water. This process may augment contractility early in heart failure initially. Over time, systemic and pulmonary venous congestion develops due to volume overload. Helpful drugs include ACE inhibitors and diuretics.
3) Ventricular hypertrophy
Cardiac hypertrophy is thought to relieve cardiac wall stress. However, unrestrained hypertrophy may result in myocardial cell death and fibrosis.
4) Inflammation
Increased wall stress of myocardial fibers may lead to the production of cytokines and free radicals. These substances may cause cell apoptosis, tissues necrosis, fibrosis, cardiac dilation and cardiac dysfunction. Beta-blockers, aldosterone antagonists, and ACE inhibitors may help mitigate these responses.


End-Stage Heart Failure
When heart failure progresses to advanced states, medication may have a limited capacity to provide stabilization. Families can choose between palliative care or mechanical based therapies while awaiting cardiac transplant.

Cardiac resynchronization therapy
Cardiac resynchronization therapy (CRT) involves the use of biventricular pacing to improve ventricular function by optimizing the timing of right and left ventricular contraction. CRT may slow or reverse cardiac remodeling and improve quality of life in adults. However, outcome data are somewhat limited in children (16).

Enlarged, poorly functioning ventricles are prone to rhythm disturbances. Arrhythmias that are not amenable to medication control should be treated by radiofrequency ablation, pacemakers or defibrillators (5).

Mechanical support
Mechanical support is used in the treatment of acute heart failure or in chronic heart failure as a bridge to recovery or to a heart transplant. The choice of support therapy depends on the expected duration of use.

Extracorporeal membrane oxygenation (ECMO) therapy is for unstable patients. The duration of use is limited to days or weeks because of the risks infection or bleeding. It is intended to provide acute temporary support as a bridge to recovery or transplantation (17, 18).

Ventricular assist devices (VAD) may be used to provide long-term ventricular support compared to ECMO. Certain devices are made for children and have graduated sizes to fit children from newborns to adolescents. In children, VADs are used most often as a bridge to transplant as opposed to destination (long-term) therapy (17, 18).

Future Therapies
The finding that adult stem cells have the capacity to differentiate various lineages (endothelial, mesenchymal, etc.) has lead investigators into the early stages using them as therapy for myocardial dysfunction. In one series, 9 pediatric patients were compassionately treated with intracoronary bone marrow derived stem cells. There was an improvement in symptoms in five of the children and the therapy was overall well tolerated (19, 20).

References

Contributor Information and Disclosures

Valerie Schroeder
Pediatric Cardiology Associate Professor
University of Kansas Medical Center Department of Pediatrics
3901 Rainbow Blvd, Kansas City, KS 66160


First Created : 1/12/2001
Last Updated : 5/11/2016

References

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