Objectives This study addressed to compare plasma B-type natriuretic peptide （BNP） and endothelin-1 （ET-1） levels with hemodynamics in heart failure（HF） patients. Methods Plasma BNP and ET-1 levels were obtaine...Objectives This study addressed to compare plasma B-type natriuretic peptide （BNP） and endothelin-1 （ET-1） levels with hemodynamics in heart failure（HF） patients. Methods Plasma BNP and ET-1 levels were obtained from 75 patients with HF by rapid immunofluorescence assay and radio-immunity method, respectively, and left ventricular end-diastolic diameter （LVEDD） were observed by echocardiogram. Hemodynamic data of 53 HF patients were determined by Swan-Ganz catheterization. Results Hemodynamics （PCWP, MPAP and RAP） and plasma BNP, ET-1 levels were proportional to New York Heart Association （NYHA） class（P〈 0.001-0.05）. Both BNP and ET-1 had positive linear relations with PCWP, MPAP, RAP （P〈 0.05- 001 ）. Moreover, plasma ET-1 was an independent and significant predictor of BNP （P〈0.001）. Plasma levels of BNP （968.23±478.63 pg/ml）and ET-1 （129.45± 88.56 pg/ml）in group with LVEDD （n=31） ≥60 mm were much higher than those in LVEDD （n = 44） 〈 60 mm group （BNP：286.26 ±156.89 pg/mL, ET-1 ： 87.45±43.65 pg/mL, P〈 0.001）. Conclusions BNP level is as a direct result of ventricular volume expansion and pressure overload. BNP is a sensitive biochemical maker of left ventricular injury and ET-1 may stimulate the secretion of cardiac BNP independent of hemodynamics in patients with HF.展开更多
It is traditionally considered that angiotensin-converting enzyme inhibitor(ACEI) and spironolactone could not be used simultaneously because of the assumed risk of hyperkalemia.
Since only oral preparations of captopril are clinically available, intravenous captopril was studied in 10 patients with mild heart failure and in 20 severe. The results showed that intravenous captopril may rapidly ...Since only oral preparations of captopril are clinically available, intravenous captopril was studied in 10 patients with mild heart failure and in 20 severe. The results showed that intravenous captopril may rapidly reduce cardiac preload and afterload, increase cardiac output, inhibit renin-angiotensin-aldosterone system, and depress plasma levels of catecholamine. After captopril infusion, a rapid symptomatic improvement occurred and the infusion could be well tolerated in patients with acute or severe heart failure. In addition, reversing hyponatremia and hypokalemia or improving azotemia may benefit the patients with acute or severe heart failure.展开更多
Congestive heart failure is a disease in which initially compensatory changes in cardiac , vascular, and renal functions become detrimental over time. The changes are mediated by a large number of neurohormones and cy...Congestive heart failure is a disease in which initially compensatory changes in cardiac , vascular, and renal functions become detrimental over time. The changes are mediated by a large number of neurohormones and cytokines. Counter-regulatory hormones also play a role, but are generally insufficient to offset the adverse effects of the neurohormones or progression of the disease. Symptoms of heart failure occurs in the 'presence of systolic dysfunction, usually documented by a decrease in ejection fraction, or can present with impaired diastolic function occasionally labeled as heart failure with preserved systolic function of the left ventricle. Heart failure and its treatment represent a medical problem of significant importance because of the high mortality associated with it despite the current therapy , which has substantial evidence of reduction in mortality and morbidity. Prevention or slowing of the progressive deterioration in function of the heart and other organs involved through utilizing new agents that affect more or different neurohormonal pathways may be beneficial and forms the focus of heart failure research and drug development. However , the multiplicity of hormonal effects mandate the use of complex therapy in the management of congestive heart failure(CHF). The new agents in addition to the conventional therapy used in the management of heart failure are; Human B-type nalriuretic peptide (in the treatment of decompensated CHF) , endothelin receptor antagonists, calcium sensitizers, neutral endopeptidase (NEP) and vasopeptidase inhibitors, vasopressin antagonists and cytokine inhibitors.展开更多
文摘Objectives This study addressed to compare plasma B-type natriuretic peptide （BNP） and endothelin-1 （ET-1） levels with hemodynamics in heart failure（HF） patients. Methods Plasma BNP and ET-1 levels were obtained from 75 patients with HF by rapid immunofluorescence assay and radio-immunity method, respectively, and left ventricular end-diastolic diameter （LVEDD） were observed by echocardiogram. Hemodynamic data of 53 HF patients were determined by Swan-Ganz catheterization. Results Hemodynamics （PCWP, MPAP and RAP） and plasma BNP, ET-1 levels were proportional to New York Heart Association （NYHA） class（P〈 0.001-0.05）. Both BNP and ET-1 had positive linear relations with PCWP, MPAP, RAP （P〈 0.05- 001 ）. Moreover, plasma ET-1 was an independent and significant predictor of BNP （P〈0.001）. Plasma levels of BNP （968.23±478.63 pg/ml）and ET-1 （129.45± 88.56 pg/ml）in group with LVEDD （n=31） ≥60 mm were much higher than those in LVEDD （n = 44） 〈 60 mm group （BNP：286.26 ±156.89 pg/mL, ET-1 ： 87.45±43.65 pg/mL, P〈 0.001）. Conclusions BNP level is as a direct result of ventricular volume expansion and pressure overload. BNP is a sensitive biochemical maker of left ventricular injury and ET-1 may stimulate the secretion of cardiac BNP independent of hemodynamics in patients with HF.
文摘It is traditionally considered that angiotensin-converting enzyme inhibitor(ACEI) and spironolactone could not be used simultaneously because of the assumed risk of hyperkalemia.
文摘Since only oral preparations of captopril are clinically available, intravenous captopril was studied in 10 patients with mild heart failure and in 20 severe. The results showed that intravenous captopril may rapidly reduce cardiac preload and afterload, increase cardiac output, inhibit renin-angiotensin-aldosterone system, and depress plasma levels of catecholamine. After captopril infusion, a rapid symptomatic improvement occurred and the infusion could be well tolerated in patients with acute or severe heart failure. In addition, reversing hyponatremia and hypokalemia or improving azotemia may benefit the patients with acute or severe heart failure.
文摘Congestive heart failure is a disease in which initially compensatory changes in cardiac , vascular, and renal functions become detrimental over time. The changes are mediated by a large number of neurohormones and cytokines. Counter-regulatory hormones also play a role, but are generally insufficient to offset the adverse effects of the neurohormones or progression of the disease. Symptoms of heart failure occurs in the 'presence of systolic dysfunction, usually documented by a decrease in ejection fraction, or can present with impaired diastolic function occasionally labeled as heart failure with preserved systolic function of the left ventricle. Heart failure and its treatment represent a medical problem of significant importance because of the high mortality associated with it despite the current therapy , which has substantial evidence of reduction in mortality and morbidity. Prevention or slowing of the progressive deterioration in function of the heart and other organs involved through utilizing new agents that affect more or different neurohormonal pathways may be beneficial and forms the focus of heart failure research and drug development. However , the multiplicity of hormonal effects mandate the use of complex therapy in the management of congestive heart failure(CHF). The new agents in addition to the conventional therapy used in the management of heart failure are; Human B-type nalriuretic peptide (in the treatment of decompensated CHF) , endothelin receptor antagonists, calcium sensitizers, neutral endopeptidase (NEP) and vasopeptidase inhibitors, vasopressin antagonists and cytokine inhibitors.
