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Enalapril restores depressed circulating insulin-like growth factor 1 in patients with chronic heart failure
R Corbalan1, M Acevedo, I Godoy
1Catholic University of Chile, Santiago.
Insights
Angiotensin-converting enzyme (ACE) inhibition therapy improved insulin-like growth factor 1 (IGF-1) levels in patients with congestive heart failure (CHF). This treatment also enhanced cardiac function and exercise capacity in these patients.
Area of Science:
- Cardiology
- Endocrinology
- Pharmacology
Background:
- Congestive heart failure (CHF) is linked to elevated renin-angiotensin system activity.
- Experimental data show angiotensin II reduces insulin-like growth factor 1 (IGF-1) and body weight.
- Previous research indicated diminished growth hormone (GH)-IGF1 axis activity in stable CHF patients.
Purpose of the Study:
- To investigate the effect of angiotensin-converting enzyme (ACE) inhibition on the GH-IGF1 axis in CHF patients.
- To determine if ACE inhibition can restore suppressed IGF-1 levels in CHF.
Main Methods:
- Nine stable CHF patients (NYHA class III) received 8 weeks of Enalapril (10 mg twice daily).
- Measurements included plasma IGF-1 levels, radionuclide left ventricular ejection fraction (EF), and peak oxygen consumption (PVO2).
Main Results:
- Seven out of nine patients initially presented with low IGF-1 levels (0.2-0.5 mU/ml).
- Enalapril therapy normalized IGF-1 levels (0.36 +/- 0.03 to 0.8 +/- 0.14 mU/ml, P = .004).
- Significant improvements were observed in EF (27.4% to 31.4%) and PVO2 (14.8 to 18.6 ml/kg/min, P < .05).
Conclusions:
- Chronic ACE inhibition effectively restored reduced IGF-1 plasma levels in CHF patients.
- The therapeutic benefits are likely mediated by the reduction of angiotensin II activity.
- ACE inhibition improved cardiac function and exercise capacity alongside hormonal normalization.
Background:
Congestive heart failure (CHF) is characterized by increased activity of the renin-angiotensin system. Recent experimental studies have shown that infusion of angiotensin II results in depressed plasma levels of insulin-like growth factor 1 (IGF-1) and weight loss. We have previously reported that stable patients with CHF have decreased activity of the growth hormone (GH)-IGF1 axis. We have hypothesized, therefore, that angiotensin-converting enzyme (ACE) inhibition therapy should restore GH-IGF1 activity in CHF patients.
Methods And Results:
Nine patients with stable CHF who were taking digitalis and diuretics, New York Heart Association functional class III were studied before and after 8 weeks of therapy with Enalapril (10 mg twice daily). We measured IGF1 levels, radionuclide left ventricular ejection fraction (EF) and peak oxygen consumption (PVO2). We found that 7 of 9 patients had abnormally low levels of IGF1 (0.2-0.5 mU/ml). IGF1 levels reverted to normal after Enalapril therapy (0.36 +/- 0.03 to 0.8 +/- 0.14 mU/ml, P = .004). This was associated with a significant increase in EF (27.4 +/- 1.1 to 31.4 +/- 0.9%) and PVO2 (14.8 +/- 1.2 to 18.6 +/- 1.5 ml/kg/min) values (P < .05).
Conclusion:
Chronic ACE inhibition therapy restored previously reduced IGF1 plasma levels in patients with CHF, most likely by reducing angiotensin II activity.