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[Plasma catecholamines and hemodynamics in patients with heart failure (author's transl)]
Insights
Patients with coronary artery disease heart failure exhibit elevated plasma catecholamines and impaired cardiac function. Reduced adrenergic receptor sensitivity may explain decreased heart rate at higher catecholamine levels.
Area of Science:
- Cardiology
- Physiology
Context:
- Investigated hemodynamic and neuroendocrine responses in heart failure patients.
- Utilized Swan-Ganz catheter and bicycle ergometry for comprehensive assessment.
Purpose:
- To evaluate plasma catecholamine levels and hemodynamic changes in coronary artery disease-induced heart failure.
- To correlate these changes with disease severity and functional myocardial impairment.
Summary:
- Patients with heart failure showed increased cardiac volumes, elevated pressures, and reduced cardiac output compared to controls.
- Plasma catecholamine concentrations rose with pressure elevations and inversely with cardiac output.
- Functional impairment correlated with decreased cardiac output and heart rate, suggesting reduced adrenergic sensitivity.
Impact:
- Highlights the neuroendocrine dysregulation in heart failure.
- Provides insights into the mechanisms of reduced cardiac efficiency and heart rate response.
- Suggests potential therapeutic targets related to adrenergic signaling in heart failure.
Abstract:
Plasma catecholamines and hemodynamic were assessed in 32 patients with heart failure of varying degrees due to coronary artery disease as well as in twelve healthy control subjects. The studies employed the use of a (Swan-Ganz) semi-floating, balloon-tipped, thermodilution catheter during supine bicycle ergometry at incremented workloads (except in four patients with overt symptoms at heart failure at rest). As compared with control subjects, the patients showed increases in radiologically-determined cardiac volumes, right atrial, right ventricular, pulmonary artery and pulmonary capillary wedge pressures proportionately expressing increasing degrees of severity and, accordingly, decreasing values of cardiac output and stroke volume as well as a severity-dependent tendency to increasingly rapid heart rates. Similarly, as compared with control subjects, catecholamine concentrations increased in proportion with the pathologic elevation of pressures and inversely proportional to the cardiac output. With respect to a given catecholamine concentration, the patients showed a severity-dependent decrease in cardiac output, as an expression of the degree of functional myocardial impairment, as well as a lower heart rate and higher total peripheral resistance (at the same catecholamine level). The heart rate reduction at the same catecholamine concentration may be due to a reduced adrenergic receptor sensitivity.