Q-T interval prolongation in cirrhosis: Prevalence, relationship with severity, and etiology of the disease and possible pathogenetic factors

Abstract

Prolonged Q-T interval predicts severe arrhythmias and sudden death, and has been shown to occur in alcoholic liver disease and cirrhotic patients who are candidates for liver transplantation. This study first evaluated the prevalence of prolonged Q-T interval in a large population of unselected patients with cirrhosis, and assessed the relationship between abnormal Q-T, etiology, and severity of liver disease and mortality of patients. Possible causes of Q-T abnormality were also explored. Ninety-four patients with cirrhosis without overt heart disease and 37 control subjects with mild chronic active hepatitis were enrolled. Rate-corrected Q-T interval (Q-T c ) was assessed along with routine liver tests, Child-Pugh score, serum bile salts, electrolytes and creatinine, plasma renin activity, aldosterone, norepinephrine, atrial natriuretic factor and, gonadal hormones. Q-T c was longer in patients with cirrhosis than in controls (440.3 ؎ 3.2 vs. 393.6 ؎ 3.7 ms; P F .001) and prolonged (G440 ms) in 44 patients (46.8%) and 2 controls (5.4%; P F .001). Q-T c length was not influenced by the etiology of cirrhosis and correlated with Child-Pugh score (r ‫؍‬ .53; P F .001), liver tests such as prothrombin activity, and serum concentrations of albumin and bilirubin, plasma bile salts, and plasma norepinephrine. Multivariate analysis showed that only Child-Pugh score and plasma norepinephrine were independently correlated with Q-T c duration. Over a median follow-up period of 19 months (range, 2-33 months), patients with Q-T c longer than 440 ms had a significantly lower survival rate than those with normal Q-T c . Q-T interval is frequently prolonged in patients with cirrhosis, regardless the etiology of the disease, worsens in parallel with the severity of the disease, and may have an important prognostic meaning. In addition to other undefined factors related to the severity of cirrhosis, sympathoadrenergic hyperactivity may play a pathogenetic role. (HEPA-TOLOGY 1998;27:28-34.)

Cirrhotic cardiomyopathy

“…Few years later, human studies in nonalcoholic cirrhosis showed similar results. Bernardi et al [12] measured systolic time intervals that has been validated as a reliable method of assessing ventricular contractile performance [20] and found the ratio of pre-ejection period to left ventricular ejection time to be prolonged in 22 alcoholic and nonalcoholic cirrhotic patients both at rest and after exercise, an indication of contractile dysfunction. Grose et al [21] reported a submaximal increase in cardiac output following exercise in both alcoholic and nonalcoholic cirrhotic patients compared with controls.…”

“…Its prevalence is about 45%, which is strikingly higher than the 5% prevalence in the general population, and is broadly proportional to the severity of cirrhosis, rising from 25% in class A to 51% in class B and up to 60% or more in class C of Child-Pugh classification [12]. The presence of prolonged QT interval provides the substrate for ventricular arrhythmias and therefore may be responsible for the sudden deaths observed following stressful procedures such as TIPS insertion or liver transplantation.…”

“…QT prolongation, a common electrophysiological abnormality in cirrhosis [12], also worsens after the TIPS insertion, especially in the first 3 months post-TIPS [91]. This is thought to be due to the translocation of cardiotoxic substances from the splanchnic to the systemic circulation through the TIPS shunt, affecting ventricular repolarization, hence prolonging the QT interval.…”

“…Over the last 2 decades, there is accumulating evidence to suggest that the presence of cirrhosis per se is associated with significant cardiovascular abnormalities, irrespective of the cause of cirrhosis. These include resting increased cardiac output; decreased systemic vascular resistance [1]; reduced myocardial contractility or systolic incompetence, especially under conditions of stress, whether physiological [5], physical [6,7], or pharmacological [8]; increased thickness of the left ventricle [9][10][11], associated with diastolic dysfunction; and electrophysiological abnormalities [12][13][14]. This constellation of abnormalities has been termed cirrhotic cardiomyopathy [15].…”

Heart Function and Myocardial Tissue Characterization in Patients with HCV Related Cirrhosis: Diastolic Dysfunction and Cardiac Hypertrophy

“…Hyperdinamic circulation [3], QTc prolongation [4,5], beta-receptors desensitization [6,7], reduced systolic competence under strains [8][9][10][11] and diastolic dysfunction [12][13][14][15][16][17] are the key features of cirrhotic cardiomyopathy. Diastolic dysfunction, characterized by an altered pattern of transmitral flow due to impaired diastolic relaxation of left ventricle, can be easily assessed by echocardiography and accordingly can be considered as a marker of this condition.…”