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Sympathetic activation and loss of reflex sympathetic control in mild congestive heart failure
G Grassi1, G Seravalle, B M Cattaneo
1Cattedra di Medicina Interna, Ospedale S. Gerardo, Monza, Milano, Italy.
Insights
Baroreceptor control is impaired in mild congestive heart failure (CHF), leading to early sympathetic overactivation. This study shows significant baroreflex impairment even in early stages of CHF.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Regulation
- Heart Failure Pathophysiology
Background:
- Baroreflex control of sympathetic activity is known to be impaired in severe congestive heart failure (CHF).
- This impairment is thought to contribute to the sympathetic overactivation characteristic of advanced CHF.
- However, whether baroreflex dysfunction and sympathetic activation are present in mild CHF remains unclear.
Purpose of the Study:
- To investigate the status of baroreflex control of sympathetic activity in patients with mild CHF.
- To compare baroreflex sensitivity and sympathetic nerve activity in healthy individuals, mild CHF patients, and severe CHF patients.
Main Methods:
- Studied 17 healthy controls, 17 mild CHF patients (NYHA class I-II), and 19 severe CHF patients (NYHA class III-IV).
- Measured beat-to-beat blood pressure, heart rate, and muscle sympathetic nerve activity (MSNA) at rest and during baroreceptor stimulation/deactivation.
- Utilized phenylephrine and nitroprusside infusions to assess baroreflex responses.
Main Results:
- Muscle sympathetic nerve activity (MSNA) was progressively higher in mild and severe CHF patients compared to controls.
- Baroreflex sensitivity, assessed by heart rate and MSNA responses to blood pressure changes, was significantly impaired in both mild and severe CHF groups.
- Mild CHF patients exhibited a substantial reduction in baroreflex sensitivity (approx. 60%) for both heart rate and MSNA.
Conclusions:
- Baroreceptor-mediated inhibition of heart rate and MSNA is markedly impaired even in mild CHF.
- This early baroreflex impairment likely contributes to the sympathetic overactivation observed in the early stages of congestive heart failure.
Background:
Baroreflex control of sympathetic activity is impaired in severe congestive heart failure (CHF), probably causing the marked sympathetic activation typical of this condition. Little information exists, however, as to whether baroreflex impairment and related sympathetic activation also occur in mild CHF.
Methods And Results:
We studied 19 patients (age, 57.5 +/- 2.2 years, mean +/- SEM) with CHF in New York Heart Association (NYHA) class III or IV and with a marked reduction in left ventricular ejection fraction (LVEF, 30.1 +/- 1.5% from echocardiography) and 17 age-matched patients with CHF in NYHA class I or II and with an only slightly reduced LVEF (44.9 +/- 3.3%) that never was < 40%. Seventeen age-matched healthy subjects served as control subjects. Primary measurements included beat-to-beat arterial blood pressure (with the Finapres technique), heart rate (from ECG), and postganglionic muscle sympathetic nerve activity (MSNA, from microneurography at the peroneal nerve). Measurements were performed at baseline and during baroreceptor stimulation (intravenous phenylephrine infusion), baroreceptor deactivation (intravenous nitroprusside infusion), and cold-pressor test. Baseline blood pressure was similar in the three groups, whereas heart rate was progressively greater from control subjects to patients with mild and severe CHF, MSNA (bursts per 100 heart beats) increased significantly and markedly from control subjects to patients with mild and severe CHF (47.1 +/- 2.9 versus 64.4 +/- 6.2 and 82.1 +/- 3.4, P < .05 and P < .01, respectively). Heart rate and MSNA were progressively reduced by phenylephrine infusion and progressively increased by nitroprusside infusion. Compared with control subjects, the responses were strikingly impaired in severe CHF patients, but a marked impairment also was seen in mild CHF patients. On average, baroreflex sensitivity in mild CHF patients was reduced by 59.1 +/- 5.5% (MSNA) and 64.8 +/- 4.8% (heart rate). In contrast, reflex responses to the cold-pressor test were similar in the three groups.
Conclusions:
These results demonstrate that in mild CHF patients the baroreceptor inhibitor influence on heart rate and MSNA is already markedly impaired. This impairment may be responsible for the early sympathetic activation that occurs in the course of CHF.