Intensive statin treatment improves baroreflex sensitivity: another cardioprotective mechanism for statins?

Patterson, D.

doi:10.1136/heart.88.4.415

Cited by 19 publications

(13 citation statements)

References 7 publications

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“…17) In humans, Patterson, et al demonstrated an improvement in baroreflex sensitivity in patients receiving intensive simvastatin treatment. 47) Augmentation of HRR in HF patients, who receive fluvastatin treatment as shown in our trial, may be an indicator of improvement in sympathetic overactivity or enhancement of parasympathetic tonus which is introduced by statin therapy.…”

Section: Discussionmentioning

confidence: 61%

Decreased Heart Rate Recovery in Patients With Heart Failure Effect of Fluvastatin Therapy

et al. 2005

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SUMMARYHeart rate recovery is the difference in heart rate at peak exercise and at a specific time interval following the onset of recovery. Attenuated heart rate recovery is an independent predictor of mortality in patients with a history of coronary artery disease. The aim of the present study was to evaluate the effect of a statin on heart rate recovery, particularly in patients with ischemic heart failure and hyperlipidemia. Twenty-nine consecutive hyperlipidemic, stable coronary artery disease patients with heart failure and 19 healthy subjects were enrolled. Heart rate recovery values at the 1st and 3rd minutes and lipid profiles of the patients were evaluated at baseline and following 3 months of treatment with fluvastatin. Compared with healthy subjects, the heart rate recovery values were significantly lower in the heart failure patients in both the 1st and 3rd minutes, respectively (31 ± 6 versus 19 ± 7, P < 0.0001; 66 ± 7 versus 47 ± 8, P < 0.0001). Heart rate recovery in the 1st and 3rd minutes increased from 19 ± 7 to 24 ± 9 and 47 ± 8 to 57 ± 11, respectively, following treatment (P < 0.001, P < 0.001). There were no significant correlations among the changes in lipid parameters or HRR in the first and third minutes in the recovery period. The results revealed an improvement in heart rate recovery in heart failure patients by fluvastatin treatment. If this association can be confirmed by other studies, it would be interesting to perform further studies into the mechanism underlying this finding. (Int Heart J 2005; 46: 845-854)

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Section: Discussionmentioning

confidence: 61%

Decreased Heart Rate Recovery in Patients With Heart Failure Effect of Fluvastatin Therapy

et al. 2005

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“…[25][26][27] Sympathetic overactivity might be partly explained by peripheral mechanisms, including elevated peripheral chemoreceptor activity, reduced baroreceptor sensitivity and reduced nitric oxide synthesis. [28][29][30][31][32] Statins can affect baroreceptor sensitivity, 33 endothelial function 17 and nitric oxide synthesis; 18 thus, the speculation arose that statins might modulate sympathetic outflow in cardiovascular disorders. 17,18,33 Accordingly, our study provided insight into the modulatory role of statins on sympathetic activation in patients with hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…However, several mechanisms have been suggested; for example, statin inhibition of atherosclerosis within the aortic arch and carotid arteries might improve the sensitivity of the high pressure baroreceptors. 33 As a decreased baroreflex contributes to impaired sympathovagal balance, it is possible that an improvement in BRS will lead to an inhibition of sympathetic activity. Indeed, in this study, simvastatin improved the baroreflex control of HR, and this was inversely related to the decrease in MSNA.…”

Section: Discussionmentioning

confidence: 99%

Simvastatin reduces sympathetic activity in men with hypertension and hypercholesterolemia

et al. 2010

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Beyond their hypolipidemic effect, statins reduce cardiovascular risk in hypertensive subjects via various mechanisms; one suggested mechanism is that they reduce sympathetic activity. We investigated the hypothesis that simvastatin decreased muscle sympathetic nerve activity (MSNA) in 31 hypertensive subjects with hypercholesterolemia (aged 38.7±10 years). In this randomized, placebocontrolled, double-blinded study, patients were treated with simvastatin (40 mg day À1 ; n¼15) or placebo (n¼16) for 8 weeks. Before and after treatment, we measured MSNA, blood pressure and heart rate. Baroreceptor control of the heart rate, or baroreceptor sensitivity (BRS), was computed by the sequence method, a cross-analysis of systolic blood pressure and the electrocardiogram R-R interval. Blood samples were tested for plasma levels of catecholamines, neuropeptide Y, aldosterone, endothelin and renin activity. Simvastatin significantly reduced MSNA (from 36.5 ± 5 to 27.8 ± 6 bursts per min, P¼0.001), heart rate (from 77 ± 6.7 to 71 ± 6.1 beats per min, P¼0.01) and both total and low-density lipoprotein cholesterol (from 249±30.6 to 184±28.3 mg dl À1 , P¼0.001 and from 169±30.6 to 117±31.2 mg dl À1 , P¼0.01, respectively). Simvastatin also improved BRS (from 10.3 ± 4.1 to 17.1 ± 4.3 ms per mm Hg, P¼0.04). No changes were observed in systolic or diastolic blood pressures, or in plasma levels of catecholamines, neuropeptide Y, endothelin, aldosterone and renin activity. After simvastatin therapy, MSNA and BRS were inversely related (r¼À0.94, Po0.05). In conclusion, we found that, in patients with hypertension and hypercholesterolemia, simvastatin reduced MSNA, and this was related to increased baroreceptor sensitivity.

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“…Variables associated with BRS in univariate analysis with a P value of Յ0.1 were then tested in a logistic regression model. In addition, taking into account reports on BRS increase in patients under antihypertensive medications 16 or statins, 17 the variable "antihypertensive or statin therapy" was forced into the model. We used the median BRS as a cut-off point.…”

Section: Discussionmentioning

confidence: 99%

Baroreflex Sensitivity Is Impaired in Bilateral Carotid Atherosclerosis

Nasr

Traon

Larrue

2005

Stroke

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Background and Purpose-The arterial baroreflex is an important determinant of the short-term regulation of blood pressure and cardiovascular variability. The purpose of our study was to determine whether baroreflex sensitivity (BRS) and heart rate (HR) variability are altered in patients with carotid atherosclerosis (CA) and to assess the impact of characteristics of CA on BRS. Methods-BRS and HR variability were prospectively evaluated in 75 consecutive patients undergoing carotid duplex examination in our neurosonology unit. Resting BRS was measured with the sequence method. HR variability was evaluated using spectral analysis. Results-BRS was significantly reduced in patients with bilateral CA compared with patients without CA (Pϭ0.015) and patients with unilateral CA (Pϭ0.045). BRS was unaltered in patients with unilateral CA compared with patients with no CA. BRS was already reduced in mild (stenosis Ͻ50%), bilateral CA and was not further impaired in more severe CA. The association of BRS impairment with bilateral CA remained significant after adjustment for age, hypertension, and a history of stroke or transient ischemic attack. The study of HR variability demonstrated a reduction in the power of high-frequency band in patients with bilateral CA compared with patients with unilateral CA or without CA (Pϭ0.015). Conclusion-Bilateral

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Intensive statin treatment improves baroreflex sensitivity: another cardioprotective mechanism for statins?

Cited by 19 publications

References 7 publications

Decreased Heart Rate Recovery in Patients With Heart Failure Effect of Fluvastatin Therapy

Decreased Heart Rate Recovery in Patients With Heart Failure Effect of Fluvastatin Therapy

Simvastatin reduces sympathetic activity in men with hypertension and hypercholesterolemia

Baroreflex Sensitivity Is Impaired in Bilateral Carotid Atherosclerosis

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