natriuretic-peptide--brain and Muscular-Atrophy

COPD affects up to one third of patients with chronic heart failure. The coexistence of COPD and chronic heart failure presents clinicians with diagnostic and therapeutic challenges. Measurement of B-type natriuretic peptide plasma levels facilitates the diagnosis of acute dyspnea in patients known to have both COPD and chronic heart failure. Patients with COPD or chronic heart failure have skeletal muscle abnormalities that limit functional capacity independently from primary organ failure. Exercise training reverses skeletal muscle abnormalities in patients with COPD or chronic heart failure and may be particularly indicated in patients with coexistent COPD and chronic heart failure.

Topics: Biomarkers; Exercise; Heart Failure; Humans; Muscle Weakness; Muscular Atrophy; Natriuretic Peptide, Brain; Pulmonary Disease, Chronic Obstructive; Treatment Outcome

The angiotensin receptor/neprilysin inhibitor Sacubitril/Valsartan (Sac/Val) has been shown to be beneficial in patients suffering from heart failure with reduced ejection fraction (HFrEF). However, the impact of Sac/Val in patients presenting with heart failure with preserved ejection fraction (HFpEF) is not yet clearly resolved. The present study aimed to reveal the influence of the drug on the functionality of the myocardium, the skeletal muscle, and the vasculature in a rat model of HFpEF. Female obese ZSF-1 rats received Sac/Val as a daily oral gavage for 12 weeks. Left ventricle (LV) function was assessed every four weeks using echocardiography. Prior to organ removal, invasive hemodynamic measurements were performed in both ventricles. Vascular function of the carotid artery and skeletal muscle function were monitored. Sac/Val treatment reduced E/é ratios, left ventricular end diastolic pressure (LVEDP) and myocardial stiffness as well as myocardial fibrosis and heart weight compared to the obese control group. Sac/Val slightly improved endothelial function in the carotid artery but had no impact on skeletal muscle function. Our results demonstrate striking effects of Sac/Val on the myocardial structure and function in a rat model of HFpEF. While vasodilation was slightly improved, functionality of the skeletal muscle remained unaffected.

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Animals; Biphenyl Compounds; Connectin; Cyclic GMP; Diastole; Disease Models, Animal; Drug Combinations; Electrocardiography; Female; Fibrosis; Glycated Hemoglobin; Heart Failure; Muscle, Skeletal; Muscular Atrophy; Natriuretic Peptide, Brain; Peptide Fragments; Phosphorylation; Rats, Mutant Strains; Valsartan; Ventricular Function, Left

Cardiac cachexia is a wasting syndrome characterized by chronic inflammation and high mortality. Fibroblast growth factor 21 (FGF-21) and monocyte chemoattractant protein 1 (MCP-1) are associated with cardiovascular disease and systemic inflammation. We investigated FGF-21 and MCP-1 in relations to cardiac function, inflammation, and wasting in patients with heart failure with reduced ejection fraction (HFrEF) and cardiac cachexia.. Plasma FGF-21 and MCP-1 were measured in a cross-sectional study among the three study groups: 19 patients with HFrEF with cardiac cachexia, 19 patients with HFrEF without cachexia, and 19 patients with ischaemic heart disease and preserved ejection fraction. Patients with HFrEF and cardiac cachexia displayed higher FGF-21 levels median (inter quantile range) 381 (232-577) pg/mL than patients with HFrEF without cachexia 224 (179-309) pg/mL and ischaemic heart disease patients 221 (156-308) pg/mL (P = 0.0496). No difference in MCP-1 levels were found among the groups (P = 0.345). In a multivariable regression analysis, FGF-21 (logarithm 2) was independently associated with interleukin 6 (logarithm 2) (P = 0.015) and lower muscle mass (P = 0.043), while no relation with N-terminal pro-hormone brain natriuretic peptide was observed.. Fibroblast growth factor 21 (FGF-21) levels were elevated in patients with HFrEF and cardiac cachexia, which could be mediated by increased inflammation and muscle wasting rather than impaired cardiac function.

Topics: Aged; Aged, 80 and over; Biomarkers; Cachexia; Cardiovascular Diseases; Case-Control Studies; Chemokine CCL2; Chronic Disease; Cross-Sectional Studies; Denmark; Female; Fibroblast Growth Factors; Heart Failure; Humans; Inflammation; Interleukin-6; Male; Muscular Atrophy; Myocardial Ischemia; Natriuretic Peptide, Brain; Stroke Volume; Wasting Syndrome

Recent papers discussed include two large, multicentre, high-positive end-expiratory pressure trials in acute lung injury and reflects upon the usefulness of such trial designs. Further papers considered include the emerging story of beta2-agonists for pulmonary oedema, highlights the newly described, iatrogenic demon, of ventilator-induced diaphragm injury, promotes the addition of B-type natriuretic peptide testing to the prediction of extubation success, and muses again over the oxygen debate.

Topics: Adrenergic beta-Agonists; Animals; Critical Illness; Diaphragm; Humans; Hyperoxia; Muscular Atrophy; Natriuretic Peptide, Brain; Oxygen Inhalation Therapy; Positive-Pressure Respiration; Pulmonary Edema; Randomized Controlled Trials as Topic; Respiration, Artificial; Respiratory Distress Syndrome; Sepsis; Ventilator Weaning

To determine whether the plasma brain natriuretic peptide level increases differentially in muscular dystrophy and idiopathic dilated cardiomyopathy, we investigated the plasma brain natriuretic peptide level and echocardiographic parameters in patients with similarly low left ventricular ejection fraction. The plasma brain natriuretic peptide level was lower, and the left ventricular end-diastolic diameter was shorter in the patients with muscular dystrophy than in those with idiopathic dilated cardiomyopathy. The correlation between the plasma brain natriuretic peptide and left ventricular ejection fraction was shifted downward in the patients with muscular dystrophy compared with those with idiopathic dilated cardiomyopathy. Those between the brain natriuretic peptide and left ventricular end-diastolic diameter were superimposable, although the data from the muscular dystrophy patients were located at the shorter left ventricular end-diastolic diameter side. The plasma brain natriuretic peptide level may differentially increase in the two diseases with similar left ventricular systolic dysfunction. Differences in the left ventricular distension and in the physical activity might explain at least partially the different plasma brain natriuretic peptide levels.

Topics: Adult; Cardiomyopathy, Dilated; Echocardiography; Female; Heart Ventricles; Humans; Immunoradiometric Assay; Male; Muscular Atrophy; Natriuretic Peptide, Brain; Statistics, Nonparametric; Ventricular Dysfunction, Left