Diminishment of respiratory sinus arrhythmia foreshadows doxorubicin-induced cardiomyopathy.

Hrushesky, William J. M.; Fader, Darrell J.; Berestka, John S.; Sommer, Marc A.; Hayes, Jennifer; Cope, Frederick O.

doi:10.1161/01.cir.84.2.697

Cited by 33 publications

(18 citation statements)

References 19 publications

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“…Heart rate variability was significantly impaired in patients who received 2400 mg/m2 doxorubicin and was the only parameter showing a correlation with cumulative dose. Similar results were reported by Hrushesky et al [24], who found that diminished respiratory sinus arrhythmia predicted congestive heart failure during treatment with doxorubicin. This suggests that HRV could be a sensitive index for cardiotoxicity.…”

Section: -Hour Ambulatory Eccsupporting

confidence: 90%

Late cardiotoxicity after treatment for a malignant bone tumor

Postma

Bink‐Boelkens

Beaufort‐Krol

et al. 1996

Med. Pediatr. Oncol.

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Section: -Hour Ambulatory Eccsupporting

confidence: 90%

Late cardiotoxicity after treatment for a malignant bone tumor

Postma

Bink‐Boelkens

Beaufort‐Krol

et al. 1996

Med. Pediatr. Oncol.

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“…Effects of anthracycline therapy on HRV in humans have been reported previously [29][30][31][32][33]. Three of these studies were retrospective [29,31,32], and one study evaluated cardiac parasympathetic control [30].…”

Section: Discussionmentioning

confidence: 97%

Neuroendocrine changes during the evolution of doxorubicin-induced left ventricular dysfunction in adult lymphoma patients

et al. 2001

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Doxorubicin-induced cardiotoxicity was used as a model to prospectively investigate neuroendocrine changes during the development of left ventricular dysfunction. Radionuclide ventriculography, frequency domain analysis of heart rate variability (HRV), and plasma noradrenaline and natriuretic peptide measurements were performed in 27 adult lymphoma patients at baseline and after cumulative doxorubicin doses of 200, 400 and 500 mg/m(2). The left ventricular ejection fraction (LVEF) decreased from 58.1+/-1.4% to 50.3+/-1.1% (P<0.001) and 49.3+/-1.7% (P<0.001) after cumulative doxorubicin doses of 400 and 500 mg/m(2) respectively. With a doxorubicin dose of up to 400 mg/m(2) there was an increase in sympathetic tone, characterized by a decrease in the normalized high-frequency (HF(nu)) power (P=0.011), and increases in the normalized low-frequency (LF(nu)) power (P=0.011), the LF/HF ratio (P=0.021) and the plasma noradrenaline concentration (P=0.034). The decrease in LVEF was correlated with the changes in LF(nu) and HF(nu) power (r=0.540, P=0.012) and LF/HF ratio (r=-0.452, P=0.04). However, after the cumulative doxorubicin dose of 500 mg/m(2) the changes in HRV components and plasma noradrenaline levels returned towards baseline. This was accompanied by increased concentrations of plasma atrial natriuretic peptide (P=0.004) and brain natriuretic peptide (P=0.021). Our findings suggest that doxorubicin-induced left ventricular dysfunction is associated with an early change in sympathovagal balance towards sympathetic predominance. Along with further progression of left ventricular dysfunction, there is an attenuation of sympathetic tone, which may be attributable to sympatho-adrenal inhibition by increased secretion of natriuretic peptides.

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“…According to the study of Hrushesky et al [65], it is unlikely that alterations in HRV were provoked by DOX-induced autonomic neuropathy. They proposed that the direct effect of DOX on the heart muscle itself caused HRV changes [65].…”

Section: Discussionmentioning

confidence: 99%

Cardiac autonomic modulation induced by doxorubicin in a rodent model of colorectal cancer and the influence of fullerenol pretreatment

et al. 2017

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The very effective anticancer drug doxorubicin (DOX) is known to have cardiotoxic side effects, which could be accompanied by autonomic modulation. Autonomic disbalance might even be an initiating mechanism underlying DOX-induced cardiotoxicity and can be studied noninvasively by the analysis of heart rate variability (HRV). A number of strategies have been assessed to predict chemotherapy-induced cardiac dysfunction while HRV, a potential detecting tool, has not yet been tested. Thus, we aimed to determine the effect of DOX treatment on HRV in a rat model of colorectal cancer. While pretreatment with fullerenol (Frl) acts protectively on DOX-induced cardiotoxicity, we aimed to test the effect of Frl pretreatment on DOX-induced HRV alterations. After the induction of colorectal cancer, adult male Wistar rats were treated with saline (n = 7), DOX (1.5 mg/kg per week, n = 7) or DOX after pretreatment with Frl (25 mg/kg per week, n = 7) for three weeks (cumulative DOX dose 4.5 mg/kg). One week after treatment rats were anaesthetized, standard ECG was measured and HRV was analyzed in time and frequency domain. During autopsy the intestines and hearts were gathered for biochemical analysis and histopathological examination. DOX treatment significantly decreased parasympathetically mediated high-frequency component (p<0.05) and increased the low-frequency component of HRV (p<0.05), resulting in an increased LF/HF ratio (p<0.05) in cancerous rats. When pretreated with Frl, DOX-induced HRV alterations were prevented: the high-frequency component of HRV increased (p<0.01), the low-frequency decreased (p<0.01), LF/HF ratio decreased consequently (p<0.01) compared to DOX only treatment. In all DOX-treated animals, disbalance of oxidative status in heart tissue and early myocardial lesions were found and were significantly reduced in rats receiving Frl pretreatment. Autonomic modulation accompanied the development of DOX-induced cardiotoxicity in rat model of colorectal cancer and was prevented by Frl pretreatment. Our results demonstrated the positive prognostic power of HRV for the early detection of DOX-induced cardiotoxicity.

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Diminishment of respiratory sinus arrhythmia foreshadows doxorubicin-induced cardiomyopathy.

Cited by 33 publications

References 19 publications

Late cardiotoxicity after treatment for a malignant bone tumor

Late cardiotoxicity after treatment for a malignant bone tumor

Neuroendocrine changes during the evolution of doxorubicin-induced left ventricular dysfunction in adult lymphoma patients

Cardiac autonomic modulation induced by doxorubicin in a rodent model of colorectal cancer and the influence of fullerenol pretreatment

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