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Pathophysiology of Heart Failure

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ABSTRACT

Heart failure is considered an epidemic disease in the modern world affecting approximately 1% to 2% of adult population. It presents a multifactorial, systemic disease, in which–‐after cardiac injury‐–structural, neurohumoral, cellular, and molecular mechanisms are activated and act as a network to maintain physiological functioning. These coordinated, complex processes lead to excessive volume overload, increased sympathetic activity, circulation redistribution, and result in different, parallel developing clinical signs and symptoms. These signs and symptoms sum up to an unspecific clinical picture; thus invasive and noninvasive diagnostic tools are used to get an accurate diagnosis and to specify the underlying cause. The most important, outcome determining factor in heart failure is its constant progression. Constant optimizing of pharmatherapeutical regimes, novel targets, and fine regulation of these processes try to keep these compensatory mechanisms in a physiological range. Beside pharmacological therapy, interventional and surgical therapy options give new chances in the management of heart failure. For the optimization and establishment of these and novel therapeutical approaches, complete and comprehensive understanding of the underlying mechanisms is essentially needed. Besides diagnosis and treatment, efforts should be made for better prevention in heart failure by treatment of risk factors, or identifying and following risk groups. This summary of the pathophysiology of heart failure tries to give a compact overview of basic mechanisms and of the novel unfolding, progressive theory of heart failure to contribute to a more comprehensive knowledge of the disease. © 2016 American Physiological Society. Compr Physiol 6:187‐214, 2016.

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Figure 1. Figure 1. PV loop showing the correlation of pressure and volume alterations in physiological and pathological conditions.
Figure 2. Figure 2. Beta‐adrenergic signaling pathways and their effects in the heart.
Figure 3. Figure 3. Major effects and further metabolization of angiotensin II.
Figure 4. Figure 4. Macro‐ and microstructural changes in eccentric, concentric, and combined remodeling.
Figure 5. Figure 5. Excitation‐contraction coupling in physiological and pathological state.
Figure 6. Figure 6. Oxidative stress in heart failure.


Figure 1. PV loop showing the correlation of pressure and volume alterations in physiological and pathological conditions.


Figure 2. Beta‐adrenergic signaling pathways and their effects in the heart.


Figure 3. Major effects and further metabolization of angiotensin II.


Figure 4. Macro‐ and microstructural changes in eccentric, concentric, and combined remodeling.


Figure 5. Excitation‐contraction coupling in physiological and pathological state.


Figure 6. Oxidative stress in heart failure.
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Edit Tanai, Stefan Frantz. Pathophysiology of Heart Failure. Compr Physiol 2015, 6: 187-214. doi: 10.1002/cphy.c140055