Background/aims: QT interval prolongation is frequent in cirrhosis, predicts a poor prognosis and may trigger severe ventricular arrhythmias. Our aim was to evaluate the effect of chronic beta-blockade on QT prolongation.
Methods: Clinical and laboratory evaluation, ECG and hepatic vein pressure gradient (HVPG) measurement were performed in 30 cirrhotic patients before and 1-3 months after prophylactic nadolol. QT was corrected for heart rate by the cirrhosis-specific formula and other formulas.
Results: QT(cirrhosis) was prolonged in 10 patients (33%); HVPG was increased in all cases. QT(cirrhosis) was correlated with the Child-Pugh score (r=0.40; p=0.027). Nadolol shortened QT interval only with the Bazett formula (p=0.01), remaining unchanged with the other formulas. The QT interval shortened only if prolonged at baseline (from 473.3+/-5.5 to 458.4+/-6.5 ms; p=0.007), while it lengthened when normal (from 429.8+/-3.1 to 439.3+/-2.9 ms; p=0.01). QTc changes were directly related to the baseline value (p<0.001). HVPG decreased from 19.4+/-0.8 to 15.6+/-1.3 mmHg (p=0.004). The HVPG changes did not correlate with QTc changes.
Conclusions: Chronic beta-blockade shortens the QT interval only in patients with prolonged baseline values, and this is likely due to a direct cardiac effect.
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http://dx.doi.org/10.1016/j.jhep.2007.11.012 | DOI Listing |
J Trauma Acute Care Surg
November 2024
From the Department of Surgery and Sepsis and Critical Illness Research Center (J.A.M., L.S.K., E.E.P., C.G.A., K.B.K., L.E.B., P.A.E., A.M.M.), University of Florida College of Medicine, Gainesville; and The Gut Biome Lab, Department of Health, Nutrition, and Food Sciences (G.P., R.N.), Florida State University College of Education, Health, and Human Sciences, Tallahassee, Florida.
Background: Traumatic injury leads to gut dysbiosis with changes in microbiome diversity and conversion toward a "pathobiome" signature characterized by a selective overabundance of pathogenic bacteria. The use of non-selective beta antagonism in trauma patients has been established as a useful adjunct to reduce systemic inflammation. We sought to investigate whether beta-adrenergic blockade following trauma would prevent the conversion of microbiome to a "pathobiome" phenotype.
View Article and Find Full Text PDFAnn Thorac Surg
February 2025
Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee.
Background: Atrial fibrillation (AF) occurs commonly after cardiac surgery and is associated with multiple adverse outcomes. Older randomized trials suggested that perioperative β- blockade reduced postoperative AF, and The Society of Thoracic Surgeons (STS) coronary artery bypass grafting (CABG) composite measure includes β-blocker administration preoperatively within 24 hours of surgery and at discharge. However, some more recent studies suggest preoperative β-blockade has limited value and question its continuation as an STS quality measure.
View Article and Find Full Text PDFJ Physiol
July 2024
Knight Cardiovascular Institute, Oregon Health and Science University, Portland, OR, USA.
Curr Med Res Opin
April 2024
Hypertension Unit, Renal Division, University of São Paulo Medical School, Sao Paulo, Brazil.
Cardiovascular disease (CVD) remains the most prevalent cause of premature death worldwide. It had been suspected for decades that increased activity of the sympathetic nervous system (SNS) might play a pathogenetic role in the development and progression of hypertension, heart failure (HF) and CVD. The use of microneurographic techniques to directly assess the SNS has allowed this field to advance considerably in recent years.
View Article and Find Full Text PDFCurr Med Res Opin
April 2024
Department of Cardiology, National Heart Centre Singapore, Singapore.
β-blockers are a heterogeneous class, with individual agents distinguished by selectivity for β- vs. β- and α-adrenoceptors, presence or absence of partial agonist activity at one of more β-receptor subtype, presence or absence of additional vasodilatory properties, and lipophilicity, which determines the ease of entry the drug into the central nervous system. Cardioselectivity (β-adrenoceptor selectivity) helps to reduce the potential for adverse effects mediated by blockade of β-adrenoceptors outside the myocardium, such as cold extremities, erectile dysfunction, or exacerbation of asthma or chronic obstructive pulmonary disease.
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