Changes in Cardiovagal Baroreflex Sensitivity Are Related to Increased Ventricular Mass in Patients With Liver Cirrhosis

Song, Jae-Kwan; Kim, Young‐Kug; Shin, Won-Jung; Hwang, Gyu‐Sam

doi:10.1253/circj.cj-12-0380

Cited by 11 publications

(5 citation statements)

References 32 publications

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“…The ratio of the LF/HF power was calculated as an index of autonomic balance. 27, 28 After basal recordings, baroreflex responses were generated with intravenous doses of phenylephrine administered in a random order (PE; Sigma, UK: 10, 20, 40 and 80 µg i.a. ), then by sodium nitroprusside (SNP; Sigma, UK; 0.6, 1.25, 2.5, 5, 10 and 20 µg/kg i.a.)…”

Section: Experimental Protocolmentioning

confidence: 99%

Vitamin C Prevents Intrauterine Programming of in vivo Cardiovascular Dysfunction in the Rat

Kane

Herrera

Camm

et al. 2013

Circ J

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Background: Fetal hypoxia is common and in vitro evidence supports its role in the programming of adult cardiovascular dysfunction through the generation of oxidative stress. Whether fetal chronic hypoxia programmes alterations in cardiovascular control in vivo, and if these alterations can be prevented by antioxidant treatment, is unknown. This study investigated the effects of prenatal fetal hypoxia, with and without maternal supplementation with vitamin C, on basal and stimulated cardiovascular function in vivo in the adult offspring at 4 months of age in the rat. Methods and Results:From days 6 to 20 of pregnancy, Wistar rats were subjected to Normoxia, Hypoxia (13% O2), Hypoxia+Vitamin C (5 mg/ml in drinking water) or Normoxia+Vitamin C. At 4 months, male offspring were instrumented under urethane anaesthesia. Basal mean arterial blood pressure, heart rate and heart rate variability (HRV) were assessed, and stimulated baroreflex curves were generated with phenylephrine and sodium nitroprusside. Chronic fetal hypoxia increased the LF/HF HRV ratio and baroreflex gain, effects prevented by vitamin C administration during pregnancy. Conclusions:Chronic intrauterine hypoxia programmes cardiovascular dysfunction in vivo in adult rat offspring; effects ameliorated by maternal treatment with vitamin C. The data support a role for fetal chronic hypoxia programming cardiovascular dysfunction in the adult rat offspring in vivo through the generation of oxidative stress in utero. (Circ J 2013; 77: 2604 -2611

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Section: Experimental Protocolmentioning

confidence: 99%

Vitamin C Prevents Intrauterine Programming of in vivo Cardiovascular Dysfunction in the Rat

Kane

Herrera

Camm

et al. 2013

Circ J

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“…In fact, it has been shown that baroreceptor sensitivity is reduced in cirrhosis and that was significantly related to serum sodium, heart rate and central circulation time [44]. Moreover, reduced baroreceptor reflex sensitivity has been shown to inversely correlate with left ventricular mass [45]. These results suggest a link between reduced baroreceptor sensitivity and end organ damage in cirrhosis.…”

Section: Cardiac Autonomic Dysfunctionmentioning

confidence: 97%

Cirrhosis-Associated Cardiomyopathy

Zaky

Lang

2012

J Anesthe Clinic Res

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“…19,28 Chronotropic incompetence is associated with more perioperative complications in cirrhotic patients undergoing liver transplantation. 31 In their study, Song et al 72 found that impaired autonomic function in cirrhotics correlates with cardiac remodeling revealed by increased left ventricular (LV) mass, suggesting the connection between cardiovagal baroreflex sensitivity and cardiac morphology.…”

Section: Electrophysiological Abnormalitiesmentioning

confidence: 99%

Cirrhotic Cardiomyopathy—A Veiled Threat

Scărlătescu

Марченко

Tomescu

2020

Cardiology in Review

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Cirrhotic cardiomyopathy (CCM) is defined as cardiac dysfunction in patients with liver cirrhosis without preexisting cardiac disease. According to the definition established by the World Congress of Gasteroenterology in 2005, the diagnosis of CCM includes criteria reflecting systolic dysfunction, impaired diastolic relaxation, and electrophysiological disturbances. Because of minimal or even absent clinical symptoms and echocardiographic signs at rest according to the 2005 criteria, CCM diagnosis is often missed or delayed in most clinically stable cirrhotic patients. However, cardiac dysfunction progresses in time and contributes to the pathogenesis of hepatorenal syndrome and increased morbidity and mortality after liver transplantation, surgery, or other invasive procedures in cirrhotic patients. Therefore, a comprehensive cardiovascular assessment using newer techniques for echocardiographic evaluation of systolic and diastolic function, allowing the diagnosis of CCM in the early stage of subclinical cardiovascular dysfunction, should be included in the screening process of liver transplant candidates and patients with cirrhosis in general. The present review aims to summarize the most important pathophysiological aspects of CCM, the usefulness of contemporary cardiovascular imaging techniques and parameters in the diagnosis of CCM, the current therapeutic options, and the importance of early diagnosis of cardiovascular impairment in cirrhotic patients.

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Changes in Cardiovagal Baroreflex Sensitivity Are Related to Increased Ventricular Mass in Patients With Liver Cirrhosis

Cited by 11 publications

References 32 publications

Vitamin C Prevents Intrauterine Programming of in vivo Cardiovascular Dysfunction in the Rat

Vitamin C Prevents Intrauterine Programming of in vivo Cardiovascular Dysfunction in the Rat

Cirrhosis-Associated Cardiomyopathy

Cirrhotic Cardiomyopathy—A Veiled Threat

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