Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heart failure, cause notwithstanding, is characterized by adaptive (but harmful) increases in sympathetic activity and hormone levels, as well as by abnormal cardiovascular reflexes. Such reflex derangements may contribute to neurohumoral excitation. Consequently, normalization of the reflexes may be an important determinant of the effectiveness of therapy.
Hosp Pract (Off Ed) 1991 Jun 15
PMID:Reflex control in heart failure: a primer for physicians. 167 44

A central feature of the excitation-contraction cycle-myocardial Ca2+ handling--is altered in humans with cardiomyopathy. Many adaptive changes in excitation-contraction mechanisms observed in aged or hypertensive animals also supervene in the failing human heart. Heart failure may thus emerge when such changes lead to systolic or diastolic insufficiency.
Hosp Pract (Off Ed) 1991 Jul 15
PMID:Excitation-contraction coupling in heart failure. 167 9

After nearly three decades of intense investigation, the precise cellular mechanisms underlying impaired contractility in heart failure remain to be defined. Nevertheless, growing use of the tools of molecular biology promises new insights into how alterations of contractile proteins mediate the functional derangements of failure.
Hosp Pract (Off Ed) 1991 Dec 15
PMID:Contractile protein alterations in heart failure. 174 87

This first article of a new series on "cellular" gastroenterology focuses on the embryogenesis and neonatal development of the gut. In this context, the effects of malnutrition, morbidity, and trauma on intestinal histodynamics are discussed, as are compensatory adaptations analogous to those in the circulatory responses to heart failure.
Hosp Pract (Off Ed) 1990 Jan 15
PMID:Intestinal development and regeneration. 210 60

Although the role of the autonomic nervous system in the pathophysiology of heart failure has been studied for decades, only within the past few years have adrenergic receptors and their alterations occupied center stage. There is now considerable evidence linking such receptors to many of the phenomena of heart failure; recent work appears to have significant therapeutic implications.
Hosp Pract (Off Ed) 1983 Nov
PMID:The beta-adrenergic receptor in heart failure. 613 6

Research findings to date indicate that there may not be a discrete change in contractile proteins in the common forms of heart failure. While the search for a defective myosin molecule in this context no longer seems promising, it remains plausible to propose "up-regulation" to a myosin variant with high ATPase activity as a means of increasing contractility in the failing heart.
Hosp Pract (Off Ed) 1983 Jun
PMID:Contractile proteins of the heart. 622 89

Whether left ventricular hypertrophy is a useful compensatory process rather than the first step in heart failure is under debate. Early experimental data indicate that events during hypertrophy indeed hasten the progression of failure. Since it is often possible to reverse hypertrophy with some forms of antihypertensive treatment, it makes sense to try to do so.
Hosp Pract (Off Ed) 1983 Aug
PMID:The progression from hypertrophy to heart failure. 622 73

The introduction of new pharmacotherapies for long-term treatment of chronic cardiac failure has underscored the need for serial measurement of ventricular function in the ambulatory patient. Management strategies can best be guided by physiologic assessment of the heart's function as a muscular pump that must serve to propel gases to the metabolizing tissues on a moment-to-moment basis.
Hosp Pract (Off Ed) 1983 May
PMID:The mechanics of ventricular function. 640 87

Cardiac failure can begin with metabolic disturbances within the myocardial cell--in the mitochondria, contractile proteins, or other cellular organelles. It also can result from faulty adrenergic regulation of contraction. New technology is making it possible to synthesize the contributing factors into a clinical model that will greatly enhance our understanding of these mechanisms.
Hosp Pract (Off Ed) 1983 Sep
PMID:The biochemical basis of myocardial failure. 641 2

Altered loading conditions can sometimes produce serious heart failure, even though myocardial contractility is not depressed. The role of afterload in some forms of heart failure is emphasized, as are the conditions termed afterload mismatch, in which afterload is excessive "absolutely" or relative to diminished contractility. A related aspect is the role of the peripheral circulation.
Hosp Pract (Off Ed) 1983 Oct
PMID:The failing heart and the circulation. 641 66


1 2 3 Next >>