Symposium on Congestive Heart Failure

Katz, Louis N.; Feinberg, Harold; Shaffer, Aaron B.

doi:10.1161/01.cir.21.1.95

Cited by 38 publications

(7 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The concept that congestive circulatory failure and cardiac muscle failure are not synonymous under clinical circumstances in man is well described (30,31). However, the cardiac lesions leading to fluid retention in the presence of normal myocardial function usually have been confined to mechanical abnormalities such as valvular or constrictive lesions, and adequate techniques for the assessment of myocardial function in the intact animal have not been available.…”

Section: Discussionmentioning

confidence: 99%

Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention

Taylor¹,

Covell²,

Ross³

1968

J. Clin. Invest.

108

View full text Add to dashboard Cite

A B S T R A C T The mechanical properties of left ventricular contraction were described in terms of tension, velocity, length, and time in closed-chest, sedated dogs in which a large aorto-caval fistula had resulted in circulatory congestion, and the results were compared with those in normal dogs. Instantaneous contractile element velocity was calculated from left ventricular pressure and its first derivative during isovolumic left ventricular contractions produced by sudden balloon occlusion of the ascending aorta during diastole. A range of ventricular end-diastolic volumes was induced and heart rate was controlled at 150 beats/min. Wall tension (stress) was derived from ventricular pressure and volume, the latter being obtained from the pressure-volume relation of the passive ventricle. Extrapolated velocity at zero tension, Vmax, averaged 3.0 circ/sec in the normal dogs and 2.9 circ/sec in the seven dogs with an aortocaval fistula and fluid retention; in only one of these seven animals was Vmax below the lower limit of normal of 2.7 circ/sec. Isovolumic tension (PO) in dogs with aorto-caval fistulas tended to be slightly greater than normal at low ventricular filling pressures, and there was no difference in P. between the two groups of animals at high ventricular filling pressures. Time to peak pressure averaged 151 ± 6 (SE) msec (normal 139 ± 3). Left ventricular weight averaged 6.32 ±0.23 Dr. Taylor is a

show abstract

Section: Discussionmentioning

confidence: 99%

Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention

Taylor¹,

Covell²,

Ross³

1968

J. Clin. Invest.

108

View full text Add to dashboard Cite

show abstract

“…Other diseases spare the myocardium only to involve the heart's valvular structures, its pericardium, or the pulmonary or systemic circulations. These disorders are considered causes of circulatory failure [3]. In both car diac and circulatory failure, the primary de ficit resides in the ability of the heart to maintain cardiac output and thereby sustain oxygen delivery to the tissues at a rate com mensurate with their V02.…”

Section: Assessing the Severity Of Heart Diseasementioning

confidence: 99%

Cardiopulmonary Exercise Testing in Clinical Practice

Weber¹,

Janicki²,

McElroy³

et al. 1987

Cardiology

View full text Add to dashboard Cite

Cardiopulmonary exercise testing refers to the noninvasive measurement of respiratory gas exchange and air flow, together with heart rate, blood pressure, and the electrocardiogram. These data, obtained during an incremental exercise test, can be used to derive the aerobic capacity or Vo_2max, which is an objective measure of the severity of chronic cardiac and circulatory failure, as well as to predict the maximum cardiac output response to exercise. The additional monitoring of minute ventilation and arterial oxygen saturation can be used to distinguish ventilatory from cardiac or circulatory causes of exertional dyspnea. Finally, this information serves as an objective measure of functional capacity which can be monitored over time to assess the natural history of disease as well as its response to medical therapy.

show abstract

“…However, small, long-term, or localized alterations in uptake of exogenous substrates might not have been detected by acute measurements of arteriovenous * Submitted for publication December 19, 1963; accepted October 15, 1964. Supported by grant H-3312 from the National Institutes of Health, U. S. Public Health Service. differences across intact hearts in situ (12). Concentrations of high energy phosphates have been reported to be normal in isolated, acutely failing dog hearts, guinea pig atria, and cat papillary muscles (13)(14)(15) and in chronically failing hearts from dogs with tricuspid insufficiency and pulmonary stenosis or with aortic insufficiency ( 11,16).…”

mentioning

confidence: 99%

High Energy Phosphate Compounds in the Myocardium during Experimental Congestive Heart Failure. Purine and Pyrimidine Nucleotides, Creatine, and Creatine Phosphate in Normal and in Failing Hearts*

Fox¹,

Wikler²,

Reed³

1965

J. Clin. Invest.

View full text Add to dashboard Cite

High energy phosphate compounds are generally considered essential for muscular contraction although it is not clear how their chemical energy is ultimately made available for transformation into mechanical work (1-3). According to classical concepts, hydrolysis of adenosine triphosphate (ATP) by myofibrillar .ATPase (adenosine triphosphatase) occurs at some time during repetitive cycles of muscular contraction and relaxation, and as a result adenosine diphosphate (ADP) is produced. Delivery of this ADP to mitochondria for regeneration into ATP can serve as an important regulator of the activity of mitochondrial oxidative phosphorylation (4, 5). In failing hearts, changes in oxidative phosphorylation or its products might accordingly reflect primary changes at the mitochondria or altered delivery of ADP from the failing myofibrils (6).Many studies of normal and failing hearts have examined the processes involved in the formation and utilization of high energy phosphate compounds (7). During spontaneous heart failure in man (8-10) and induced heart failure in dogs (11), there were no significant changes in uptake by the myocardium of oxygen or of the diverse substrates from which chemical energy is liberated and then conserved as nucleoside triphosphates or as creatine phosphate (CrP). However, small, long-term, or localized alterations in uptake of exogenous substrates might not have been detected by acute measurements of arteriovenous * Submitted for publication December 19, 1963; accepted October 15, 1964. Supported by grant H-3312 from the National Institutes of Health, U. S. Public Health Service. differences across intact hearts in situ (12). Concentrations of high energy phosphates have been reported to be normal in isolated, acutely failing dog hearts, guinea pig atria, and cat papillary muscles (13)(14)(15) and in chronically failing hearts from dogs with tricuspid insufficiency and pulmonary stenosis or with aortic insufficiency ( 11,16). Muscle preparations from failing canine and human hearts have shown decreased contractility (17, 18) and decreased ATPase activity (19), but myofibrillar proteins from failing canine hearts have been reported to be both normal (20) and altered (21).Recently, changes have been observed in the morphology of mitochondria from failing hearts of dogs with aortic stenosis (22) and in the metabolic responses of mitochondria from failing hearts of guinea pigs with aortic stenosis (23,24). Improved methods for isolation, separation, and specific assay of high energy phosphate compounds have made possible more precise measurements of tissue levels of these labile compounds (25)(26)(27). With the use of such improved techniques, a recent study found significant decreases in levels of ATP, CrP, and creatine (Cr) in failing hearts from guinea pigs with aortic stenosis (28). Since the status of labile phosphate compounds in the chronically failing heart did not yet seem settled, it was considered pertinent to re-examine the content of purine and pyrimidine nucleotides and CrP in h...

show abstract

Symposium on Congestive Heart Failure

Abstract: The 3 articles in this issue on congestive heart failure comprise the first of 10 contributions on this subject. The remaining 7 articles will be published in the February and March issues.—EDITOR.

Cited by 38 publications

References 63 publications

Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention

Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention

Cardiopulmonary Exercise Testing in Clinical Practice

High Energy Phosphate Compounds in the Myocardium during Experimental Congestive Heart Failure. Purine and Pyrimidine Nucleotides, Creatine, and Creatine Phosphate in Normal and in Failing Hearts*

Contact Info

Product

Resources

About