Congestive Heart Failure Abnormalities Research Articles

A Comparative Review of Vagal Nerve Stimulation Versus Baroreceptor Activation Therapy in Cardiac Diseases.

Sympathetic imbalance coupled with impairment of baroreceptor control is a key factor responsible for hemodynamic abnormalities in congestive heart failure. Vagal nerve stimulation (VNS) and baroreceptor activation therapy (BAT) are two novel interventions for the same. In this paper, we review the role of sympathovagal alterations in cardiac diseases like heart failure, arrhythmia, hypertension (HTN), etc. Studies like neural cardiac therapy for heart failure (NECTAR-HF), autonomic regulation therapy to enhance myocardial function and reduce progression of heart failure (ANTHEM-HF), and baroreflex activation therapy for heart failure (BEAT-HF), which comprise the history, efficacy, limitations, and current protocols, were extensively analyzed in contrast to one another. Vagal nerve stimulation reverses the reflex inhibition of cardiac vagal efferent activity, which is caused as a result of sympathetic overdrive during the course for heart failure. It has shown encouraging results in certain pre-clinical studies; however, there is also a possibility of serious cardiovascular adverse events if given in higher than the recommended dosage. Attenuated baroreflex sensitivity is attributed to cardiac arrhythmogenesis during heart failure. Baroreceptor activation therapy reverses this phenomenon. However, the surgical procedure for baroreceptor stimulation can have unwarranted complications, including worsening heart failure and hypertension. Considering the effectiveness of the given modalities and taking into account the inconclusive evidence of their adverse events, more clinical trials are needed for establishing the future prospects of these interventional approaches.

Complexity analysis from EEG data in congestive heart failure: A study via approximate entropy.

Congestive heart failure (CHF) is a very complex clinical syndrome that may lead to ischemic cerebral hypoxia condition. The aim of the present study is to analyze the effects of CHF on brain activity through electroencephalographic (EEG) complexity measures, like approximate entropy (ApEn). Twenty patients with CHF and 18 healthy elderly people were recruited. ApEn values were evaluated in the total spectrum (0.2-47 Hz) and main EEG frequency bands: delta (2-4 Hz), theta (4-8 Hz), alpha 1 (8-11 Hz), alpha 2 (11-13 Hz), beta 1 (13-20 Hz), beta 2 (20-30 Hz), and gamma (30-45 Hz) to identify differences between CHF group and control. Moreover, a correlation analysis was performed between ApEn parameters and clinical data (i.e., B-type natriuretic peptides (BNP), New York Heart Association (NYHA), and systolic blood pressure (SBP)) within the CHF group. Statistical topographic maps showed statistically significant differences between the two groups in the total spectrum and theta frequency band. Within the CHF group, significant negative correlations were found between total ApEn and BNP in O2 channel and between theta ApEn and NYHA scores in Fp1, Fp2, and Fz channels; instead, a significant positive correlation was found between theta ApEn and SBP in C3 channel and a nearly significant positive correlation was obtained between theta ApEn and SBP in F4 channel. EEG abnormalities in CHF are very similar to those observed in cognitive-impaired patients, suggesting analogies between the effects of neurodegeneration and brain chronic hypovolaemia due to heart disorder and underlying high brain sensitivity to CHF.

Developed CorrNN within IoMT to enhance CKD and CVD accuracy

Chronic Kidney Disease (CKD) &Cardiovascular Disease (CVD) would both be life-threatening parts of the process by renal impairment or reduced kidney functioning. Kidney cancer has been one of the worst cancers in the current study field, and while it was critical for the survival of clients' diagnostic and categorization. Early detection and treatment could prevent or delay the progression of this chronic illness to the point whereby hemodialysis or a kidney transplant have been the only options for preserving the person's life. Congestive Heart Failure (CHF) seems to be a chronic cardiac ailment that causes debilitating headaches & leads to higher mortality, disability, insurance premiums, and even a lower standard of living. The Electrocardiogram (ECG) seems to be a noninvasive & straightforward diagnostic tool that could reveal abnormalities in CHF. Manually ECG signal identification, on the other hand, was subject to mistakes due to the limited amplitude & length of ECG signals, which is neither accurate nor selective for CHF prognosis when used alone. The diagnosis accuracy & reproducibility of ECG signals in CHF may well be improved by using a technological and mechanical method.

Soluble, platelet-bound, and total P-selectin as indices of platelet activation in congestive heart failure

Background. Many complications associated with congestive heart failure (CHF) have a thrombosis-related aetiology. Platelets play an important role in thrombogenesis, but it is not clear whether circulating platelets actively participate in thrombosis-related complications associated with CHF.Objective. To determine whether soluble P-selectin, platelet surface P-selectin, and total platelet P-selectin as indices of platelet activation in CHF patients—compared to ‘disease controls’ and ‘healthy controls’—and to assess their prognostic value in CHF.Methods. We measured soluble P-selectin (sP-sel, by enzyme-linked immunosorbent assay, ELISA), total platelet P-selectin (pP-sel, by a novel ‘platelet lysate’ assay), platelet surface P-selectin (CD62P%G) and platelet surface CD63 (CD63%G) expression by flow cytometry—in 108 patients with stable congestive heart failure (all with left ventricular ejection fraction (LVEF) <50%). Levels were compared with 50 healthy controls and 70 ‘disease controls’ (patients with coronary artery disease with normal left ventricular systolic function).Results. CHF patients and disease controls had higher sP-sel, CD62P%G and CD63%G than healthy controls. There were no significant correlations between sP-sel, pP-sel, CD62P%G and CD63%G with ejection fraction (all P>0.05). There were no differences in these markers when ischaemic and non-ischaemic aetiologies of CHF were compared. After a median follow-up of 490 days (range 340–535), there were 7 deaths, 15 hospitalizations for worsening heart failure, 1 for cardiac resynchronization therapy, 4 for revascularizations, 4 for myocardial infarctions, and 1 stroke. None of the platelet markers were predictive of the composite end-point at follow-up.Conclusions. Patients with stable CHF exhibit evidence of abnormal platelet activation, despite usage of antiplatelet agents. These abnormalities did not determine prognosis and were broadly similar to those seen in ‘disease controls’ indicating that platelet abnormalities in CHF may simply be related to associated comorbidities.

Cerebral metabolic abnormalities in congestive heart failure detected by proton magnetic resonance spectroscopy

OBJECTIVESUsing proton magnetic resonance spectroscopy, we investigated cerebral metabolism and its determinants in congestive heart failure (CHF), and the effects of cardiac transplantation on these measurements.BACKGROUNDFew data are available about cerebral metabolism in CHF.METHODSFifty patients with CHF (ejection fraction ≤35%) and 20 healthy volunteers were included for this study. Of the patients, 10 patients underwent heart transplantation. All subjects performed symptom-limited bicycle exercise test. Proton magnetic resonance spectroscopy (1H MRS) was obtained from localized regions (8 to 10 ml) of occipital gray matter (OGM) and parietal white matter (PWM). Absolute levels of the metabolites (N-acetylaspartate, creatine, choline, myo-inositol) were calculated.RESULTSIn PWM only creatine level was significantly lower in CHF than in control subjects, but in OGM all four metabolite levels were decreased in CHF. The creatine level was independently correlated with half-recovery time and duration of heart failure symptoms in PWM (r = −0.56, p < 0.05), and with peak oxygen consumption and serum sodium concentration in OGM (r = 0.58, p < 0.05). Cerebral metabolic abnormalities were improved after successful cardiac transplantation.CONCLUSIONSThis study shows that cerebral metabolism is abnormally deranged in advanced CHF and it may serve as a potential marker of the disease severity.

Myocardial imaging with 123I-BMIPP in patients with congestive heart failure.

First, we studied the diagnostic utility of myocardial imaging with 123I-BMIPP (BMIPP), a 3-methyl-branched fatty acid analog, in patients with various types of cardiomyopathy and left ventricular dysfunction (ejection fraction below 40%) by comparing with myocardial flow tracer imaging. The incidence of a dissociation between myocardial BMIPP and 201Tl distributions (BMIPP < 201Tl) as a marker of metabolic abnormality in viable tissue varied considerably among various heart diseases. Patients with ischemic cardiomyopathy and the dilated form of hypertrophic cardiomyopathy had a higher incidence while those with idiopathic dilated, alcoholic and hypertensive cardiomyopathy had a lower incidence. These results suggest that the marked difference between ischemic and idiopathic dilated cardiomyopathies may contribute to the differential diagnosis between these two diseases which are main basic abnormalities in congestive heart failure. Second, we investigated the relationship between myocardial BMIPP uptake and ventricular stress in patients with right ventricular pressure overload due to pulmonary hypertension. Myocardial BMIPP uptake in the right ventricle estimated by referring to uptake in the left ventricle showed a significant correlation with mean pulmonary artery pressure (mPAP) and no significant difference with myocardial 99mTc-sestamibi uptake in the 15-81 mmHg mPAP range. These results suggest that myocardial utilization of free fatty acid may be preserved in the presence of higher ventricular wall stress.

Mesangiolytic glomerulopathy in severe congestive heart failure

To study the glomerular morphological abnormalities in congestive heart failure (CHF), we analyzed 27 autopsy cases without other causes of renal disease. Their mean age was 59 years, and they showed mild prerenal azotemia. They had generally been treated with digitalis and diuretics, and a few of them with captopril or nifedipine. The abnormal glomerular findings of enlargement, hyperemia, and mesangial thickening were observed at high frequencies (61%, 64%, and 57%, respectively). They characteristically showed mesangiolysis (ML) by the findings of microaneurysms (81%) and mesangial degeneration (70%) such as loose reticular matrix and poor matrix area. In addition, glomerular infiltration of mononuclear leukocytes including macrophages was noted in 70% of the cases. Glomerular enlargement was not correlated with the grade of hyperemia, but it was correlated with the grade of ML index of % glomeruli with microaneurysms (F = 7.22, p < 0.004). There was an inverse relationship between the grades of mesangial thickening and of the ML index (P < 0.005). The number of glomerular leukocytes was positively correlated with mean glomerular size (P < 0.002) and with the ML index (P < 0.03). Notably, the glomerular macrophage-positive cases showed a prominently higher mean ML index than the negative cases (P < 0.005). There was an inverse correlation between the mean glomerular size and the partial oxygen pressure in arterial blood (PaO2; P < 0.01), and a positive correlation between the mean glomerular size and hematocrit (Hct) levels (P < 0.02). The cases positive for mesangiolytic mesangial degeneration showed significantly lower PaO2 values than the cases negative for this lesion (P < 0.04). In the analysis of the various causes of CHF, the patients with congenital cardiac anomalies showed mean levels of the lowest PaO2 (P < 0.02) and the highest Hct (P < 0.03) and histologically the largest mean glomerular size (P < 0.04). There was no difference in the ML index and the glomerular leukocyte number among the subgroups classified by the causes. These results indicate that ML associated with glomerular enlargement is the major glomerular abnormality characteristic in patients with severe CHF and suggest that glomerular infiltration of leukocytes, especially of macrophages, should play an important role in the progression of both ML and glomerulomegaly. The contributions of persistent hypoxia and up-regulated angiotensin II as the causative factors of these glomerular abnormalities in congestive heart failure are discussed.

Skeletal muscle phosphate metabolism abnormalities in volume-overload experimental heart failure.

We studied skeletal muscle phosphate metabolism abnormalities to examine their contribution at an early stage of congestive heart failure (CHF) in rats with aortocaval fistula (ACF) 4 wk after the procedure. In a group of 26 rats (13 with ACF and 13 sham operated), we assessed the degree of CHF. The ACF produced a significant rise in heart weight and plasma atrial natriuretic peptide. In a second group of 26 rats (13 ACF and 13 sham operated), we performed 31P-magnetic resonance spectroscopy in the gastrocnemius muscle during motor activity produced by electrical stimulation. The rate of phosphocreatine depletion, expressed by its initial slope, was higher in the ACF rats compared with controls (0.078 +/- 0.01 vs. 0.041 +/- 0.007; P < 0.03). pH and ATP decreased and phosphodiesters increased in all rats during electrical stimulation, with no difference between ACF rats and controls. The kinetics of phosphocreatine recovery were not different between ACF rats and controls. Together with previous studies, our present results suggest that muscle metabolism abnormalities in CHF may vary according to the experimental model and may be observed early in the course of the disease.

Clinical relevance and management of the major electrolyte abnormalities in congestive heart failure: Hyponatremia, hypokalemia, and hypomagnesemia

Electrolyte disturbances are a common complication of CHF. CHF provides a perfect milieu for the development of these disturbances; renal dysfunction, elevation of neurohormonal substances, activation of the renin-angiotensin-aldosterone axis, and diuretic therapy represent the major contributory factors. Hyponatremia is closely aligned with an unfavorable clinical course. Hypokalemia is associated with increased ventricular dysrhythmias. Hypomagnesemia noted in advanced CHF can be accompanied by arrhythmias and refractory hypokalemia. CHF also offers the ideal milieu (diseased, ischemic, and arrhythmogenic myocardium; elevated catecholamines; and arrhythmogenic drugs) for the threatening clinical consequences (clinical deterioration, dysrhythmias, or death) of these disturbances. These consequences underscore the importance of the recognition, appreciation, and management of these electrolyte abnormalities.

Cardiac noradrenergic nerve terminal abnormalities in dogs with experimental congestive heart failure.

We have shown previously that norepinephrine (NE) uptake activity is reduced in the failing right ventricle of animals with right heart failure (RHF) produced by tricuspid avulsion and progressive pulmonary constriction. However, it is unknown whether this defect in neuronal NE uptake is related to reduction of noradrenergic nerve terminals or whether these changes also occur in animals with left heart failure (LHF). It is also unknown whether increased NE release in heart failure contributes to the noradrenergic nerve abnormalities. We measured myocardial NE content. NE uptake function, and noradrenergic nerve profiles in dogs with either RHF or LHF induced by rapid ventricular pacing. NE uptake activity was measured using [3H]NE, and noradrenergic nerve profiles were visualized by glyoxylic acid (SPG)-induced histofluorescence and tyrosine hydroxylase immunocytochemical staining. To study the effects of excess NE, we exposed normal dogs to 8 weeks of chronic NE infusion using subcutaneous osmotic minipumps. RHF and LHF animals exhibited reduced myocardial contractile function and congestive heart failure, as evidence by reduced cardiac output and elevated right atrial pressure. However, unlike that in LHF, left atrial pressure was not increased in RHF. The animals also showed an increase in plasma NE and a decrease in cardiac NE. In addition, SPG-induced histofluorescence correlated significantly with NE uptake activity (r = .712, P < .001) and tyrosine hydroxylase immunoreactive profiles (r = .569, P < .001) in the right ventricles of RHF dogs and in both ventricles of LHF dogs. The numbers of catecholaminergic profiles and tyrosine hydroxylase profiles significantly correlated with cardiac filling pressures. Chronic infusion of NE decreased heart rate in normal dogs but had no effect on either mean aortic pressure or left atrial pressure; like heart failure, it resulted in significant decreases in myocardial NE uptake activity and numbers of SPG-induced catecholaminergic histofluorescence and immunoreactive tyrosine hydroxylase profiles. Myocardial NE uptake activity was reduced only in the failing ventricles with elevated filling pressure in RHF and LHF. These changes probably were caused by loss of noradrenergic nerve terminals in the failing ventricles, as evidenced by the reductions of catecholaminergic histofluorescence and tyrosine hydroxylase immunostained profiles. Furthermore, since similar reductions of myocardial NE uptake and noradrenergic nerve profiles could be produced by chronic NE infusion in normal dogs, elevated NE levels may play a role in the development of cardiac noradrenergic nerve abnormalities in congestive heart failure.

Baroreflex Abnormalities in Congestive Heart Failure

Abnormalities in reflex control of the circulation in heart failure are mediated by afferent and target organ alterations. Depression of afferent function is especially prominent in arterial baroreceptors. This depression is mediated by an augmentation of responses that are dependent on the action of Na+-K+-ATPase.

Skeletal muscle metabolic abnormalities in congestive heart failure are not due to muscle atrophy

Skeletal muscle metabolic abnormalities in congestive heart failure are not due to muscle atrophy

Skeletal muscle response to exercise training in congestive heart failure.

To examine the ability of the skeletal muscle of congestive heart failure (CHF) patients to adapt to chronic exercise, five patients performed localized nondominant wrist flexor training for 28 d. Inorganic phosphate (Pi) and phosphocreatine (PCr) were monitored by magnetic resonance spectroscopy in both forearms at rest and during submaximal wrist flexion exercise at 6, 12, 24, and 36 J.min-1 before and after exercise training. Simultaneous measurements of limb blood flow were made by plethysmography at 12, 24, and 36 J.min-1. Forearm muscle mass and endurance were measured by magnetic resonance imaging and wrist flexion exercise before and after training. The Pi/PCr ratio and pH were calculated from the measured Pi and PCr. Exercise cardiac output, heart rate, plasma norepinephrine, and lactate measured during training were not elevated above resting values, confirming that training was localized to the forearm flexor muscles. After training, muscle bioenergetics, as assessed by the slope of the regression line relating Pi/PCr to submaximal workloads, were improved in the trained forearm of each patient, although muscle mass, limb blood flow, and pH were unchanged. Forearm endurance increased by greater than 260% after training. In the dominant untrained forearm, none of the measured indices were affected. We conclude that localized forearm exercise training in CHF patients improves muscle energetics at submaximal workloads in the trained muscle, an effect which is independent of muscle mass, limb blood flow, or a central cardiovascular response during training. These findings indicate that peripheral muscle metabolic and functional abnormalities in CHF can be improved without altering cardiac performance.

Renal and hormonal effects of phosphodiesterase III inhibition in congestive heart failure

Evaluation of the impact of therapeutic interventions in congestive heart failure (CHF) with compounds such as the phosphodiesterase (PDE) III inhibitors must include the determination of regional blood flow and functional changes. Thus, whereas PDE III inhibitors produce a significant increase in cardiac output and reduction of systemic vascular resistance, it is necessary to understand their effects on the kidney and neurohormonal parameters. The evaluation of these effects must take into consideration both the baseline renal and neurohormonal abnormalities in CHF, and the cellular actions of PDE III inhibition, which include an increase in cyclic adenosine monophosphate and cytosolic calcium. In a group of 13 patients with CHF, milrinone therapy for 1 month did not increase renal blood flow or glomerular filtration rate, or favorably affect neurohormonal parameters. However, forearm blood flow increased proportionately with cardiac output. Therefore PDE III inhibition produces a preferential increase in skeletal muscle blood flow, which may be a relative shunting of blood from the kidney. Alternatively, PDE III inhibition may activate renal cellular mechanisms that offset the anticipated favorable response to the increase of cardiac output produced by milrinone.

Sodium and water excretion abnormalities in congestive heart failure. Determinant factors and clinical implications.

The renal hemodynamic and neurohumoral determinants of sodium and water excretion abnormalities were studied in 66 patients with severe chronic congestive heart failure. Abnormalities were not closely related to any one variable but were the result of the convergence of a number of determinants. The most important determinants for sodium excretion were activation of the renin-angiotensin system and ventricular function; and the most important for water excretion were plasma vasopressin, plasma norepinephrine, and renal and ventricular functions. In a subgroup of patients, neurohumoral overactivation led to severe sodium and water excretion abnormalities and to increased furosemide requirements. A 17-month follow-up of all 66 patients showed a less favorable clinical course for this subgroup even when compared with hemodynamically matched patients.

Activity of the sympathetic nervous system and renin-angiotensin system assessed by plasma hormone levels and their relation to hemodynamic abnormalities in congestive heart failure

Resting hemodynamic measurements and plasma levels of catecholamines and renin activity were studied in 55 hospitalized treated patients with congestive heart failure in clinically stable condition. Plasma norepinephrine (mean ± standard error of the mean 594 ± 51 pg/ml, range 153 to 1,868) and plasma renin activity (mean 12.9 ± 2.4 ng/ml per hr, range 0.6 to 85.2) values were significantly (probability [p] < 0.01) higher than in normal subjects. In 26 of these patients plasma norepinephrine and plasma renin activity measured on 3 successive days including the day of hemodynamic study did not change significantly. In contrast, plasma epinephrine (mean 138 ± 26 pg ml, range 24 to 1,099) increased significantly at the time of invasive studies, probably because of stress-induced adrenal discharge. When baseline plasma norepinephrine was compared with resting hemodynamic values, significant correlations were found with right atrial pressure (correlation coefficient [r] = +0.44), pulmonary arterial pressure (r = +0.45), pulmonary capillary wedge pressure (r = +0.42), pulmonary vascular resistance (r = +0.55), pulmonary arteriolar resistance (r = +0.41), cardiac index (r = −0.42), systemic vascular resistance (r = +0.30) and heart rate (r = +0.52). Plasma renin activity was only weakly correlated with plasma norepinephrine (r = +0.38) and did not correlate significantly with any hemodynamic measurement. It is concluded that patients with congestive heart failure can be categorized on the basis of neurohumoral activity. The statistically significant correlations between plasma norepinephrine and hemodynamic evidence of cardiac dysfunction suggest that the sympathetic response is either a marker of or a contributor to the hemodynamic derangement. Because hemodynamic abnormalities did not correlate with plasma renin activity despite a statistically significant correlation between plasma norepinephrine and plasma renin activity, it appears that the two systems are independently activated in congestive heart failure but that sympathetic stimulation may be one factor contributing to renin release. Further studies are needed to assess the usefulness of plasma hormone levels in evaluating and treating patients with congestive heart failure.

Local effects of hypokalemia on coronary resistance and myocardial contractile force.

ARTICLESLocal effects of hypokalemia on coronary resistance and myocardial contractile forceRA Brace, DK Anderson, WT Chen, JB Scott, and FJ HaddyRA Brace, DK Anderson, WT Chen, JB Scott, and FJ HaddyPublished Online:01 Sep 1974https://doi.org/10.1152/ajplegacy.1974.227.3.590MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAdmission serum potassium levels and prognosis of vasospastic angina11 March 2021 | Scientific Reports, Vol. 11, No. 1Individualizing the Dialysate to Address Electrolyte Disturbances in the Dialysis PatientStructure and Function of the HeartRegional CirculationNormokalemic adenosine–lidocaine cardioplegia: Importance of maintaining a polarized myocardium for optimal arrest and reanimationThe Journal of Thoracic and Cardiovascular Surgery, Vol. 139, No. 6Electrolyte Disturbances in DialysisStructure and Function of the HeartRegional CirculationModifying the dialysis prescription to reduce intradialytic hypotensionAmerican Journal of Kidney Diseases, Vol. 38, No. 4Individualizing the Dialysate in the Hemodialysis Patient7 July 2008 | Seminars in Dialysis, Vol. 14, No. 1Regulation of Na + ,K + -ATPase α-Subunit Expression by Mechanical Strain in Aortic Smooth Muscle CellsHypertension, Vol. 27, No. 3Role of dietary salt in hypertension.Journal of the American College of Nutrition, Vol. 14, No. 5Regulation of Na+,K+-ATPase α-subunit isoforms in rat tissues during hypertensionEuropean Journal of Pharmacology: Environmental Toxicology and Pharmacology, Vol. 292, No. 2Clinical relevance and management of the major electrolyte abnormalities in congestive heart failure: Hyponatremia, hypokalemia, and hypomagnesemiaAmerican Heart Journal, Vol. 128, No. 3Chronic blood pressure effects of bufalin, a sodium-potassium ATPase inhibitor, in rats.Hypertension, Vol. 23, No. 1_supplementSalt loads attenuate potassium-induced vasodilation of forearm vasculature in humans.Hypertension, Vol. 21, No. 6_pt_1The Effect of Dialysate Composition on Systemic Hemodynamics1 October 2007 | Seminars in Dialysis, Vol. 5, No. 1Chronic hypokalemia and the left ventricular responses to epinephrine and preloadJournal of the American College of Cardiology, Vol. 18, No. 4Effects of three sodium-potassium adenosine triphosphatase inhibitors.Hypertension, Vol. 18, No. 3Dialysis hypotension: A hemodynamic analysisKidney International, Vol. 39, No. 2Attenuated vasodilator responses to Mg2+ in young patients with borderline hypertension.Circulation, Vol. 82, No. 2Contraction Induced by Ouabain and Potassium-free Solution in Human Umbilical ArteriesThe Pathophysiologic Basis for Hemodialysis-Related Hypotension1 October 2007 | Seminars in Dialysis, Vol. 1, No. 3Importance of magnesium and potassium concentration on basal tone and 5-HT-induced contractions in canine isolated coronary artery19 July 2012 | British Journal of Pharmacology, Vol. 94, No. 2Humoral sodium transport inhibitor in acute volume expansion and low renin hypertension.Hypertension, Vol. 10, No. 5_pt_2Dietary sodium and potassium in the genesis, therapy, and prevention of hypertension.Journal of the American College of Nutrition, Vol. 6, No. 3Demonstration of a ouabainlike plasma compound in hypertension prone and hypertension resistant rats.Hypertension, Vol. 7, No. 5Phasic vascular sodium pump changes in deoxycorticosterone-hypertensive rats.Circulation Research, Vol. 55, No. 3Local Regulation of Blood FlowSodium-potassium pump activity in reduced renal-mass hypertension.Hypertension, Vol. 5, No. 2_pt_2Reduced Sodium-Potassium Dependent Atpase and its Possible Role in the Development of Hypertension in Spontaneously Hypertensive Rats3 July 2009 | Clinical and Experimental Hypertension. Part A: Theory and Practice, Vol. 5, No. 1Natriuretic hormone—the missing link in low renin hypertension?Biochemical Pharmacology, Vol. 31, No. 20Increased circulating levels of an endogenous digoxin-like factor in hypertensive monkeys.Hypertension, Vol. 4, No. 3Demonstration of a humoral inhibitor of the Na+-K+ pump in some models of experimental hypertension.Hypertension, Vol. 3, No. 6_pt_2Position Paper: Sodium Metabolism: The Sodium-Potassium Membrane Pump and Volume Overload HypertensionEffect of Local Metabolic Factors on Vascular Smooth Muscle1 January 2011Commentary on a Commentary3 July 2009 | Clinical and Experimental Hypertension, Vol. 2, No. 2Humoral factors and the sodium-potassium pump in volume expanded hypertensionLife Sciences, Vol. 24, No. 23Effect of changes in Na, K, and Ca ion concentrations in the medium on frequency-strength of contraction relations in the pathologically changed myocardiumBulletin of Experimental Biology and Medicine, Vol. 86, No. 1Possible role of Na?Ca exchange mechanism in the contractions induced in guinea-pig aorta by potassium free solution and ouabainNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 304, No. 3The mechanism of K+-induced vasodilation of the coronary vascular bed of the dog.Circulation Research, Vol. 42, No. 1The Sodium-Potassium Pump in Volume Expanded Hypertension3 July 2009 | Clinical and Experimental Hypertension, Vol. 1, No. 3The role of humoral agents in volume expanded hypertensionLife Sciences, Vol. 19, No. 7Studies on potassium induced coronary dilation in the isolated guinea pig heartPfl�gers Archiv European Journal of Physiology, Vol. 363, No. 1Effects of potassium ion on the microcirculation of the hamster.Circulation Research, Vol. 37, No. 3Potassium and blood vesselsLife Sciences, Vol. 16, No. 10 More from this issue > Volume 227Issue 3September 1974Pages 590-597 Copyright & PermissionsCopyright © 1974 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1974.227.3.590PubMed4414503History Published online 1 September 1974 Published in print 1 September 1974 Metrics

The Pathogenesis of Cardiac Cachexia.

This little volume, originating in studies by the authors on intestinal absorption in congestive heart failure, presents a well-ordered, reasonably comprehensive review of the factors involved in overall energy metabolism in such patients. In the process, the multisystem physiologic aberrations of heart failure are noted and sometimes illuminated. A strong effort is made to organize available data and thinking in a meaningful way, usually with success. The chief attractiveness of the book, in this reviewer's opinion, lies in its insistent physiological orientation and exploration of this common clinical syndrome, and we, as clinicians, are in the authors' debt for this and for the comprehensiveness of their review as well as for its extensive documentation. They have considered dietary factors, metabolic abnormalities in congestive heart failure, abnormal losses of nutrients (including the nephrotic syndrome, malabsorption, and protein-losing gastroenteropathy), and iatrogenic factors as the primary areas in which the abnormalities leading to

Hepatic abnormalities in congestive heart failure; needle biopsy studies.

Needle biopsies of the liver were performed on 30 patients with heart failure and correlated with clinical features and biochemical liver function studies. Hepatic biopsy served as a useful adjunct to other methods in deciding the status of the liver in this group. Type of heart disease, degree of heart failure and length of heart failure could not be correlated with the observed histology. Neither history, physical examination, nor biochemical functional studies provided sufficient information to predict anatomy with certainty. A histologic diagnosis improved both therapeutic and prognostic perspective.