Higher hepatic venous pressure gradient (P=0.003), alcoholic etiology (P<0.001), and lower plasma calcium (P<0.001) were significantly associated with QTc prolongation in cirrhotic patients.
Observational (n=48)
What are the clinical and biochemical determinants of QT interval prolongation and decreased heart rate variability in male patients with cirrhosis?
In male cirrhotic patients, QT prolongation and reduced heart rate variability correlate with disease severity, portal hypertension, alcoholic etiology, and lower plasma calcium levels, potentially predisposing to arrhythmias.
p-value: p=0.001
A prolongation of QT interval has been shown in patients with cirrhosis and it is considered as part of the definition of the so-called 'cirrhotic cardiomyopathy'. The aim of the present study was to assess the determinants of QT interval prolongation in cirrhotic patients. Forty-eight male patients with different stages of liver disease were divided into three subgroups according to the Child-Pugh classification. All patients underwent a 24-h ECG Holter recording. The 24-h mean of QT intervals corrected for heart rate (termed QTc) and the slope of the regression line QT/RR were calculated. HRV (heart rate variability), plasma calcium and potassium concentration and HVPG (hepatic venous pressure gradient) were measured. QTc was progressively prolonged from Child A to Child C patients (P=0.001). A significant correlation between QTc and HVPG was found (P=0.003). Patients with alcohol-related cirrhosis presented QTc prolongation more frequently than patients with post-viral cirrhosis (P<0.001). The QT/RR slope was steeper in subjects with alcoholic aetiology as compared with viral aetiology (P=0.02), suggesting that these patients have a further QTc prolongation when heart rate decreases. The plasma calcium concentration was inversely correlated with QTc (P<0.001). The presence of severe portal hypertension was associated with decreased HRV (P<0.001). Cirrhotic patients with a more severe disease, especially of alcoholic aetiology, who have greater HVPG and lower calcium plasma levels, have an altered ventricular repolarization and a reduced vagal activity to the heart, which may predispose to life-threatening arrhythmias.
Genovesi et al. (Thu,) conducted a observational in Cirrhosis (n=48). Higher hepatic venous pressure gradient (P=0.003), alcoholic etiology (P<0.001), and lower plasma calcium (P<0.001) were significantly associated with QTc prolongation in cirrhotic patients.