[Pathophysiology and treatment of congestive heart failure--recently advanced strategy for heart failure].
The principle functions of the heart are to accept blood from the systemic and the pulmonary circulatory system, pump and deliver it to the whole body tissues and lungs. The term "heart failure" is used to describe the pathophysiological state in which an abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues, or to do so only from an elevated filling pressure. Thus, for a long period, heart failure has been thought of as a mechanical disorder of the heart and vessels, and its treatment has been based on improving impaired cardiac function and hemodynamic disorder. Recently multi-center, randomized placebo-controlled survival trials revealed that pure inotropic agents such as phosphodiesterase inhibitors succeeded in mechanical improvement, yet not only failed to prolong the patient's life, but also increased mortality. A number of neurohumoral mechanisms, which are activated in heart failure, were thought to be compensatory ones. However, survival trials demonstrated that two types of drug interfering with the renin-angiotensin system and the sympathetic nervous system reduced mortality. Those drugs are angiotensin-converting enzyme (ACE) inhibitors and beta blockers. ACE inhibitors reduce the direct effects of angiotensin II on myocardial cells, which may lead to cell necrosis, imbalanced remodeling through fibrosis, and attenuate the progressive ventricular dilatation. Local tissue renin-angiotensin system may be potentially important in regulating the angiotensin II production in both heart and vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
Kitabatake
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Department of Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002986:Clinical Trials as Topic; D006333:Heart Failure / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D012084:Renin-Angiotensin System
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D011943:Receptors, Adrenergic, beta; D002118:Calcium