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

Monitoring and management of intravascular volume status is of crucial importance in critically ill patients. Hypovolemia, induced by hemorrhage or pathologic fluid shifts in the presence of systemic inflammation, is frequently the cause for hemodynamic instability and hypotension. This deficit of central blood volume leads to a reduction in biventricular cardiac preload. With respect to the Frank-Starling mechanism, this causes an alteration in left ventricular stroke volume. If this reduction in stroke volume cannot be compensated by an increase in heart rate, this finally results in a decline of cardiac output. In this clinical situation fluid loading is the treatment of choice. However, insufficient peripheral vascular resistance and thus reduced cardiac afterload as well as impaired myocardial contractility also have to be taken in account to be causative for hypotension. Potential hazards of fluid loading specifically in the latter situation include pulmonary edema, worsening of pulmonary gas exchange and myocardial failure. Thus, prediction of fluid responsiveness, i.e. the prediction of the hemodynamic response to fluid loading is of utmost importance in critically ill patients. Several conventional parameters of systemic hemodynamic monitoring such as the cardiac filling pressures CVP and PAOP, the estimation of the left ventricular end-diastolic area (LVEDA) by echocardiography and measurement of central blood volumes as the right-ventricular end-diastolic volume (RVEDV) or the global end-diastolic volume (GEDV) by thermodilution are frequently used for preload monitoring. Further, functional preload parameters such as the left ventricular stroke volume variation (SW), describing the specific interactions of the heart and the lungs under mechanical ventilation, have been recently proposed to be useful for predicting fluid responsiveness. Thus, it is the aim of the present article to analyze these different concepts of hemodynamic monitoring regarding their usefulness and clinical applicability to predict fluid responsiveness at the bedside.
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PMID:[Assessment of volume responsiveness in mechanically ventilated patients]. 1499 86

The New Energy and Industrial Technology Development Organization (NEDO) project was started in 1995. The goal is the development of a multipurpose, totally implantable biventricular assist device (BVAD) that can be used for any patient who suffers from severe heart failure. Our C1E3 (two-week pump) centrifugal pump, called the Gyro pump, has three design characteristics: a magnetic coupling and double pivot bearing system, an eccentric inlet port, and secondary vanes on the bottom of the impeller. The pump was miniaturized. The C1E3 evolved into the NEDO PI-601, a totally implantable centrifugal pump for BVAD. The current NEDO PI-710 pump (five-year pump) system includes a centrifugal pump with pivot bearings, a hydraulically-levitated impeller, an rpm-controlled miniaturized actuator (all-in-one actuator plus controller), an emergency clamp on the left outflow, and a Frank-Starling-type flow control. The final mass production model is now finalized, and the final animal study and two-year endurance studies are ongoing.
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PMID:Current status of the gyro centrifugal blood pump--development of the permanently implantable centrifugal blood pump as a biventricular assist device (NEDO project). 1538 4

The "stretch-sensitization" response is essential to the regulation of heart contractility. An increase in diastolic volume improves systolic contraction. The cellular mechanisms of this modulation, the Frank-Starling law, are still uncertain. Moreover, their alterations in heart failure remains controversial. Here, using left ventricular skinned rat myocytes, we show a nonuniform stretch-sensitization of myofilament activation across the ventricular wall. Stretch-dependent Ca2+ sensitization of myofilaments increases from sub-epicardium to sub-endocardium and is correlated with an increase in passive tension. This passive tension-dependent component of myofibrillar activation is not associated with expression of titin isoforms, changes in troponin I level, and phosphorylation status. Instead, we observe that stretch induces phosphorylation of ventricular myosin light chain 2 isoform (VLC2b) in sub-endocardium specifically. Thus, VLC2b phosphorylation could act as a stretch-dependent modulator of activation tuned within normal heart. Moreover, in postmyocardial infarcted rat, the gradient of stretch-dependent Ca2+ sensitization disappears associated with a lack of VLC2b phosphorylation in sub-endocardium. In conclusion, nonuniformity is a major characteristic of the normal adult left ventricle (LV). The heterogeneous myocardial deformation pattern might be caused not only by the morphological heterogeneity of the tissue in the LV wall, but also by the nonuniform contractile properties of the myocytes across the wall. The loss of a contractile transmural gradient after myocardial infarction should contribute to the impaired LV function.
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PMID:Transmural stretch-dependent regulation of contractile properties in rat heart and its alteration after myocardial infarction. 1549 94

We investigated the effects of the agent SCH00013 on Ca(2+)-induced force generation in rabbit skinned cardiac muscle fibers and in vivo cardiac function in high-pacing-induced heart failure dogs. The Ca(2+)-induced force generation in skinned cardiac muscle fibers was determined at pH 6.2 - 7.4, and SCH00013 was found to have a significant Ca(2+) sensitizing effect at pH 7.2 to 7.4. There was no significant difference in the Ca(2+) sensitizing action between the enantiomers of SCH00013. The Ca(2+) sensitizing effect of SCH00013 was dependent on the sarcomere length, being significant only at a long sarcomere length. SCH00013 elicited a positive inotropic effect at more than 0.3 and 1 mg/kg, i.v. in normal and heart failure dogs, respectively, with no chronotropic action. These results strongly suggested that SCH00013 is a novel Ca(2+) sensitizer that elicits a positive inotropic and no chronotropic effect in heart failure, probably through enhancing the Frank-Starling mechanism.
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PMID:SCH00013, a novel Ca(2+) sensitizer with positive inotropic and no chronotropic action in heart failure. 1564 93

Progressive chamber remodeling plays a major role in the pathophysiology of chronic cardiac failure. Recent studies have begun exploring the potential for a passive external containment to impede such progressive dilation. In dogs with ischemic dilated cardiomyopathy, surgical placement of a thin external polyester mesh led to reversal of chronic chamber dilation after 3 to 6 months. Systolic function was preserved compared with the earlier time point. Both end-systolic and end-diastolic chamber volumes were reduced by about 20%, whereas end-diastolic pressure and chamber diastolic stiffness were not altered. These findings differ from the natural progression of this model, which involves progressive dilation and systolic dysfunction. In conjunction with reverse remodeling, cardiac inotropic reserve to beta-receptor agonists was markedly enhanced. Furthermore, these changes were induced without adversely affecting Frank-Starling reserve, supporting the lack of constriction.
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PMID:Reverse remodeling and enhanced inotropic reserve from the cardiac support device in experimental cardiac failure. 1580 53

Myofilament dysfunction is a common point of convergence for many forms of heart failure. Recently, we showed that cardiac overexpression of PKC epsilon initially depresses myofilament activity and then leads to a progression of changes characteristic of human heart failure. Here, we examined the effects of PKC epsilon on contractile reserve, Starling mechanism, and myofilament activation in this model of end-stage dilated cardiomyopathy. Pressure-volume loop analysis and echocardiography showed that the PKC epsilon mice have markedly compromised systolic function and increased end-diastolic volumes. Dobutamine challenge resulted in a small increase in contractility in PKC epsilon mice but failed to enhance cardiac output. The PKC epsilon mice showed a normal length-dependent tension development in skinned cardiac muscle preparations, although Frank-Starling mechanism appeared to be compromised in the intact animal. Simultaneous measurement of tension and ATPase demonstrated that the maximum tension and ATPase were markedly lower in the PKC epsilon mice at any length or Ca2+ concentration. However, the tension cost was also lower indicating less energy expenditure. We conclude 1) that prolonged overexpression of PKC epsilon ultimately leads to a dilated cardiomyopathy marked by exhausted contractile reserve, 2) that PKC epsilon does not compromise the Frank-Starling mechanism at the myofilament level, and 3) that the Starling curve excursion is limited by the inotropic state of the heart. These results reflect the significance of the primary myofilament contractilopathy induced by phosphorylation and imply a role for PKC epsilon-mediated phosphorylation in myofilament physiology and the pathophysiology of decompensated cardiac failure.
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PMID:Protein kinase C epsilon induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism. 1595 44

A 60-year-old woman was admitted to a hospital complaining of dizziness and general fatigue in October, 2004. Because of heart failure and severe anemia, she was referred to our hospital. Based on a positive direct Coombs test and an elevated level of platelet-associated IgG (PAIgG), the patient was diagnosed as having autoimmune hemolytic anemia (AIHA) associated with idiopathic thrombocytopenic purpura (ITP), i.e., Evans syndrome. Basedow disease was also diagnosed due to hyperthyroidism with an elevation of anti-thyroid stimulating hormone (TSH) receptor antibodies. Both the Evans syndrome and Basedow disease were considerably ameliorated with plasma exchange, corticosteroid and thiamazole therapy. Although Basedow disease is known to be associated with hematological disorders such as AIHA or ITP, the combination of Basedow disease and Evans syndrome is rare. We report here a case of Basedow disease associated with Evans syndrome.
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PMID:[Basedow disease associated with Evans syndrome]. 1644 Jul 74

The role of the Frank-Starling mechanism in the regulation of cardiac systolic function in the ischemic failing heart was examined in conscious dogs. Left ventricular (LV) dimension, pressure and systolic function were assessed using surgically implanted instrumentations and non-invasive echocardiogram. Heart failure was induced by daily intra-coronary injections of microspheres for 3-4 weeks via implanted coronary catheters. Chronic coronary embolization resulted in a progressive dilation of the left ventricle (12+/-3%), increase in LV end-diastolic pressure (118+/-19%), depression of LV dP/dt(max) (-19+/-4%), fractional shortening (-36+/-7%), and cardiac work (-60+/-9%), and development of heart failure, while the LV contractile response to dobutamine was depressed. A brief inferior vena caval occlusion in dogs with heart failure decreased LV preload to match the levels attained in their control state and caused a further reduction of LV dP/dt(max), fractional shortening, stroke work and cardiac work. Moreover, in response to acute volume loading, the change in the LV end-diastolic dimension-pressure (DeltaLVEDD-DeltaLVEDP) curve in the failing heart became steeper and shifted significantly to the left, while the increases in LV stroke work and cardiac work were blunted. Thus, our results suggest that the Frank-Starling mechanism is exhausted in heart failure and unable to further respond to increasing volume while it plays an important compensatory role in adaptation to LV dysfunction in heart failure.
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PMID:Exhaustion of the Frank-Starling mechanism in conscious dogs with heart failure induced by chronic coronary microembolization. 1662 28

Technology and techniques of cardiac catheterization to assess the ventricular function have been developed in the recent decades. The approach for assessing function is based on the measurement of cardiac output which depends on preload, afterload and ventricular contractility. Clinical application of Frank-Starling principle is useful for characterizing human heart failure. Conventionally, the isovolumic phase index(peak positive dP/dt) and ejection phase index (ejection fraction) have been applied to evaluate ventricular systolic function. Recently, ventricular diastolic function as well as systolic function can be estimated using ventricular pressure-volume loops obtained by simultaneous measurement of pressure and volume. The slope of end-systolic pressure-volume relation represents a load-independent index of ventricular contractility and assessing ventricular end-diastolic pressure-volume relation can express ventricular passive diastolic compliance for the evaluation of human heart failure.
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PMID:[Invasive diagnostic technique and technology for heart failure]. 1668 69

Although the physiological states of hypertrophic remodeling and congestive heart failure have been intensively studied, less is known about the transition from one to the other. The use of genetically engineered murine models of heart failure has proven valuable in characterizing the progression of remodeling and its ultimate decompensation to failure. Mice deficient in the cytoskeletal muscle LIM-only protein (MLP) are known to present with a clinical picture of dilated cardiomyopathy and transition to failure as adults. Longitudinal high-field magnetic resonance (MR) cardiac imaging provided a time course of remodeling where an improvement in ejection fraction and stroke volume (15- vs. 31-wk MLP(-/-) mice; P < 0.0001) was temporally concurrent with an abrupt phase of end-diastolic chamber dilatation. Hemodynamic analysis conducted throughout that dilatation phase showed improved ratio of maximum first derivative of pressure to end-diastolic pressure (dP/dt(max)/EDP; 15- vs. 31-wk MLP(-/-) mice; P < 0.0005), ratio of minimum first derivative of pressure to EDP (dP/dt(min)/EDP; 15- vs. 31-wk MLP(-/-) mice; P < 0.003), and developed pressure (15- vs. 31-wk MLP(-/-) mice; P < 0.0001) levels in the MLP(-/-) mice. Computational modeling techniques were used to estimate the EDP volume relationship, revealing that although MLP hearts possess a stiffer stress-strain relation, chamber compliance increased as a function of dilatation. This detailed physiological characterization during a phase of rapid anatomical remodeling suggests that systolic function in the MLP(-/-) mice may temporarily improve as a result of alterations in chamber compliance, which are mediated by dilatation. In turn, a balance may exist between exploiting the Frank-Starling mechanism and altering chamber compliance that maintains function in the absence of hypertrophic growth. Though initially compensatory, this process may exhaust itself and consequently transition to a maladaptive course.
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PMID:Role of diastolic properties in the transition to failure in a mouse model of the cardiac dilatation. 1686 93


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