Neuroendocrine response in acute heart failure and the influence of treatment

Broqvist, Mats; Dahlström, Ulf; Karlberg, B. E.; Karlsson, E.; Marklund, Tage

doi:10.1093/oxfordjournals.eurheartj.a059429

Cited by 50 publications

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“…One site of interaction is the peripheral sympathetic neuroeffector junction, where NE release is thought to be facilitated by prejunctional Ang II receptors (21)(22)(23)(24)(25)(26). It has been widely proposed that one of the mechanisms for the efficacy of angiotensin-converting enzyme (ACE) inhibitors in CHF is the inhibition of the effect of Ang II to facilitate NE release, especially in the heart (5,14,15,17). Prejunctional Ang II receptors have been demonstrated in tissue preparations (21)(22)(23) and in animal models (24)(25)(26)(27), but have been very difficult to demonstrate in humans.…”

Section: Introductionmentioning

confidence: 99%

Prejunctional angiotensin II receptors. Facilitation of norepinephrine release in the human forearm.

et al. 1994

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To determine if peripheral angiotensin II (Ang II) prejunctional receptors facilitating NE release exist in humans, we used 13H INE kinetic methodology to measure forearm NE spillover during intrabrachial arterial Ang II infusions in eight normal male subjects. We used the following protocol to optimize conditions for demonstrating these receptors: (a) lower body negative pressure (-15 mmHg) to increase sympathetic nerve activity to skeletal muscle; and (b) intraarterial nitroprusside to maintain a high constant forearm blood flow (-10 ml/ min* 100 ml) to maximize the proportion of neuronally released NE that spills over into the circulation. During lower body negative pressure, the following were infused intraarterially for three consecutive 20-min periods: saline, Ang II (4 ng/min), and Ang 11( 16 ng/min). During the Ang II infusions, forearm venous NE increased significantly from 173 to 189 and 224 pg/ml (P < 0.01), and forearm NE spillover increased from 384 to 439 and 560 ng/min. 100 ml (P < 0.05 for high Ang II). Forearm NE clearance was unchanged. During low and high dose Ang II, the plasma venous Ang II concentrations were 25 and 97 pM, respectively. Since normal subjects increase plasma Ang II from 4 to 20-22 pM with exercise, standing, or diuretic administration, and patients with severe congestive heart failure can have a plasma Ang II of -25 pM at rest, we suggest that Ang II might facilitate NE release in severe congestive heart failure, especially under conditions of stress. (J. Clin. Invest. 1994. 93:684-691.) Key words: congestive heart failure* angiotensin-converting enzyme inhibitors . 13H1-norepinephrine kinetics . norepinephrine spillover

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Section: Introductionmentioning

confidence: 99%

Prejunctional angiotensin II receptors. Facilitation of norepinephrine release in the human forearm.

et al. 1994

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“…A nor mal or low ANP level might indicate either sufficient or too much treatment, as most medical treatments which improve the pa tients. also lower the ANP level [16], In this situation, the medical therapy should be re considered. The follow-up administration can be accompanied with a few echocardiograph examinations until the optimal treatment has been reached.…”

Section: Discussionmentioning

confidence: 99%

Atrial Natriuretic Peptide in Congestive Heart Failure after Acute Myocardial Infarction

Svanegaard¹,

Angelo-Nielsen

Pindborg

1993

Cardiology

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The concentration of atrial natriuretic peptide, a newly discovered hormone produced in the atrial wall, was measured in 55 patients during the first 72 h after acute myocardial infarction. 37 patients became clinically congested, while 18 patients avoided this complication. 13 patients (9 congested and 4 uncongested) experienced tachycardia, known to raise the concentration of atrial natriuretic peptide both with and without congestive heart failure. In the remaining 42 patients, the congested group had a significantly higher plasma atrial natriuretic peptide concentration than the uncongested group (p < 0.05) on all 3 days. In the congested group the concentration of atrial natriuretic peptide did not normalize after initiation of treatment. We conclude that the concentration of atrial natriuretic peptide is increased in all patients with acute myocardial infarction and that the level of atrial natriuretic peptide declines during the first 24 h in all patients and normalizes in the uncongested patients while the level of atrial natriuretic peptide is still elevated (at least for 72 h) in the congested patients.

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“…27 (Suppl. V), V-19-V-20 (2004) sin II, 6 aldosterone, 5 and arginine vasopressin 3 ), reflex vasoconstriction, 7 and permanent hearing loss 8 in some cases. In addition, high diuretic doses have been related to significant increases in total and cause-specific mortality.…”

Section: Discussionmentioning

confidence: 99%

“…1 It can be caused by a host of factors, including excessive sodium intake, decreased renal function, 2 and reduced/delayed peak concentrations of diuretics in the tubular fluid. 2 High diuretic doses have been associated with neurohormonal activation (plasma elevations of norepinephrine, 3, 4 renin, 3,5,6 angioten- …”

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confidence: 99%

Assessment and treatment of acute heart failure-Case study: Wet and warm profile-Diuretic refractory

Michota

2004

Clin Cardiol

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A 62-year-old man presented to the emergency department (ED) with severe shortness of breath. His symptoms had begun 4 days previously when he ran out of his "water pills." He also complained of dyspnea on exertion, difficulty breathing when lying supine, and swelling of his feet. His past medical history was significant for hypertension and congestive heart failure (CHF). His normal medications included furosemide 40 mg b.i.d. and a clonidine 0.4 mg patch. He reported having no money to refill any of his prescriptions, and he had not taken any of his medications for almost a week. ExaminationIn general, he appeared anxious and in mild respiratory distress. His vital signs were: temperature 36.8°C, heart rate 119 beats/min, respiratory rate 32 breaths/min, blood pressure 178/86 mmHg, and SO 2 by pulse oximetry 89% on room air. His neck veins were grossly distended with elevated jugular venous pressure (JVP). Lungs demonstrated diffuse wheezes and crackles in all lung fields. Cardiac examination showed tachycardia. Abdominal and neurological examinations were normal. Lower extremities showed 3+ peripheral edema bilaterally. Laboratory Findings• Hemoglobin 11.4 mg/dl • Serum creatinine 1.6 mg/dl • Blood urea nitrogen 35 mg/dl • Sodium 139 mEq/l • B-type natriuretic peptide (BNP) 1740 pg/ml • Troponin T < 0.02 ng/ml Hospital CourseChest radiography was consistent with pulmonary edema, and an electrocardiogram showed sinus tachycardia with left ventricular strain. The patient was started on supplemental oxygen and given furosemide 60 mg intravenously (IV). He was admitted to a telemetry unit, and the furosemide was continued every 12 h. Enalapril was initiated at 10 mg orally b.i.d., and a clonidine patch delivering 0.4 mg/h was replaced. By the next morning, the patient was still short of breath with signs of volume overload. Diuresis was ineffective, with only a 500 cc net negative fluid balance. Cardiac enzymes remained normal. His furosemide was increased to 80 mg IV q 12 h, and a nesiritide bolus of 2 mcg/kg was given followed by a continuous infusion at 0.01 mcg/kg/min. Over the next 12 h the patient had 1.5 l of urine output, and by the next hospital day he was on room air with good oxygen saturations. Total fluid balance was now 3 l net negative, and his systolic blood pressure was now controlled at 135 mmHg. A social work consult was obtained, and the patient was provided with a temporary Medicaid number so his prescriptions would be filled. The nesiritide infusion was stopped at a total of 20 h of therapy. A repeat BNP was 356 pg/ml at the time of discharge. He was discharged home on clonidine, enalapril, and furosemide. DiscussionPatients can become diuretic refractory (clinically defined as the failure to remove edema despite a high diuretic dose) over time with increased diuretic dosage requirements; this typically occurs in one out of every three patients with CHF. 1 It can be caused by a host of factors, including excessive sodium intake, decreased renal function, 2 and reduced/delayed peak concentrat...

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Neuroendocrine response in acute heart failure and the influence of treatment

Cited by 50 publications

References 0 publications

Prejunctional angiotensin II receptors. Facilitation of norepinephrine release in the human forearm.

Prejunctional angiotensin II receptors. Facilitation of norepinephrine release in the human forearm.

Atrial Natriuretic Peptide in Congestive Heart Failure after Acute Myocardial Infarction

Assessment and treatment of acute heart failure-Case study: Wet and warm profile-Diuretic refractory

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