Predictors of failure of transoesophageal cardioversion of common atrial flutter.

BACKGROUND: Common atrial flutter is due to a re-entry circuit in the right atrium. It is possible to entrain and interrupt this arrhythmia with transoesophageal pacing (TEAP) in a substantial percentage of patients. The aim of this study is to evaluate factors associated with failure of transoesophageal cardioversion of common atrial flutter. METHODS: One hundred consecutive patients underwent an attempted transoesophageal cardioversion of their common atrial flutter. In order to detect factors associated with failure of this procedure, the following were considered: (a) age and gender; (b) underlying heart disease; (c) time of onset of the arrhythmia; (d) antiarrhythmic treatment at the time of cardioversion; (e) flutter cycle length, (f) A/V deflection ratio at the site of transoesophageal pacing; and (g) longitudinal and transverse diameters of right and left atrium on the echocardiogram. RESULTS: In 84 of 100 patients, TEAP modified the atrial flutter circuit: in 23 of these, sinus rhythm was restored; in 31 patients, flutter was converted into atrial fibrillation which spontaneously reverted to sinus rhythm; and in remaining 30 patients, persistent atrial fibrillation was obtained. In 16 cases, no modification in atrial flutter circuit was obtained by TEAP (Group 2). Using univariate analysis, this group of patients showed no significant difference in flutter cycle length, a smaller A/V ratio at the site of TEAP, a longer transverse diameter of left atrium and a shorter transverse diameter of right atrium. Analysis of the therapy at cardioversion shows that no Group 2 patients was on intravenous amiodarone, while a greater percentage of patients of the former group was on chronic amiodarone treatment. A logistic regression model applied to the data showed that flutter cycle length, transverse diameter of left atrium and A/V deflection ratio at the site of TEAP were independent variables with influence on the failure rate. CONCLUSION: Transoesophageal pacing is able to modify the circuit of common atrial flutter in a large percentage of patients, and can convert this arrhythmia to sinus rhythm in more than 50% of cases. Failure of this procedure is associated with electrophysiological parameters (flutter cycle length, A/V ratio at the site of TEAP), anatomical factors (left and right atrial diameters) and treatment in use at the time of TEAP.

Predictors of tilting test negativization during beta-blocker treatment in patients with neurocardiogenic syncope.

BACKGROUND: The cardioinhibitory and/or vasodepressor reflex, always preceded by adrenergic activation, has recently been accepted as the main mechanism of neuromediated syncope. The aim of this study was to verify if efficacy of beta-blockers, in the treatment of neuromediated syncope, may be predicted on the basis of clinical variables and data derived from tilting test. METHODS: We retrospectively analyzed 23 patients with recurrent or traumatic unexplained syncopal episodes, with a positive tilting test, who repeated the test during beta-blocker therapy. According to the second tilting test results, patients were divided into Group 1 (19 patients) with a positive second test, and Group 2 (4 patients) with a negative second test. RESULTS: No difference was found between the two groups in age, gender, number of syncopal episodes before observation, and period (days) between the two tests. Moreover, there was no difference between the two groups in the kind of positive response to tilting test, in heart rate at tilting (minimum, maximum, delta and slope of increase), and in the minimum, maximum and slope of heart rate increase before syncope. Delta heart rate before syncope was 15 b/min in Group 1, and 28 b/min in Group 2 (p = 0.011). Taking a discriminant value of 20 b/min, 100% sensitivity and 68% specificity were found. CONCLUSIONS: Heart rate increase before syncope identifies patients with negativization of tilting test on beta-blocker therapy. However, the clinical value of the second test for driving therapy is controversial.

Evidence of functional and structural cardiac abnormalities in cirrhotic patients with and without ascites.

Cirrhosis is associated with cardiovascular abnormalities. Scanty information is available as to whether these include left ventricle diastolic dysfunction and wall thickness increase. To this aim in 27 cirrhotic patients with tense ascites, 17 cirrhotic patients with previous episodes of ascites (not actual), and 11 controls we investigated by echocardiography and echocolor Doppler left ventricle diastolic function (E wave, A wave, E/A ratio, deceleration time of E wave), systolic function (ejection fraction), and wall thickness (left ventricle posterior wall thickness + interventricular septum thickness) along with neurohumoral variables. All measurements (supine position) were repeated after total paracentesis (10.7 +/- 0.6 L of ascites) in ascitic patients. Both in patients with and without ascites E/A ratio was reduced as compared with controls (0.93 +/- 0.07 and 0.97 +/- 0.06 vs. 1.18 +/- 0.08, P < .05) while left ventricle wall thickness was increased (18.6 +/- 0.6 and 20.1 +/- 0.8 vs. 17.2 +/- 0.7, P < .05 and P < .01, respectively), irrespective of the postviral or alcoholic cause of liver disease. In all cirrhotics both right and left atrial and right ventricle diameters were significantly greater. Ejection fraction was slightly but significantly (P < .01) reduced in ascitic patients. Paracentesis induced a reduction of the highly increased basal plasma renin activity, aldosterone, norepinephrine (P < .01), and epinephrine (P < .05) and improved diastolic function (E/A, P < .05). Systolic function was unaffected. Thus, irrespective of ascites and cause, advanced cirrhosis is associated with left ventricle diastolic dysfunction and wall thickness increase. We can speculate that neurohumoral overactivity, known to stimulate cardiac tissue growth, may challenge the heart, promoting fibrosis and exerting a further hindrance to ventricular relaxation in patients with cirrhosis experiencing episodes of ascites.

Time course of circulatory and humoral effects of rapid total paracentesis in cirrhotic patients with tense, refractory ascites.

BACKGROUND/AIMS: Tense ascites of cirrhosis can be treated with total paracentesis; however, the short-term effects of this procedure are poorly defined. METHODS: The circulatory and humoral changes induced by total paracentesis (250 mL/min) were studied in 12 cirrhotics with tense, refractory ascites. Data were collected before, during, and after paracentesis and 24 hours later (after albumin infusion). Hormonal parameters were recorded again 48 hours and 6 days thereafter. RESULTS: Paracentesis (10.7 +/- 4.4 L; 64 +/- 20 minutes) caused marked reduction of intra-abdominal, intrathoracic, right atrial, and pulmonary pressures. Heart rate did not change. Cardiac output and heart volumes increased. Systemic vascular resistances and mean arterial pressure slightly decreased. Baseline plasma renin and aldosterone levels were markedly increased; a reduction was already evident during paracentesis with the lowest values at the end of the procedure. All changes were maintained 24 hours later. Hormones regained baseline levels 6 days later. CONCLUSIONS: Rapid total paracentesis is accompanied by marked cardiovascular and humoral changes. Some of these changes can be explained by mechanical factors that are directly or indirectly related to the relief of abdominal pressure. However, other changes (systemic vasodilatation, humoral deactivation) have a non-mechanical nature and may depend on reflexes originating from cardiac volume receptor stimulation. Most changes may beneficially (albeit transiently) influence the cardiovascular system of cirrhotic patients with tense ascites.

Two-dimensional echocardiographic evaluation of right ventricular ejection fraction: comparison between three different methods.

Twelve patients with chronic cor pulmonale due to chronic obstructive pulmonary disease have been examined with 2D echocardiography, performing four-chamber view by apical and subcostal approaches, and the right ventricular outflow tract view by the subcostal approach. These views have permitted evaluation of right ventricular volumes, and hence right ventricular ejection fraction, by the use of three different geometrical formulae: the biplane area-length method, Simpson's rule and the pyramidal method. The ejection fraction values obtained from each method have been compared to those obtained by equilibrium radionuclide angiocardiography. Four-chamber apical and subcostal views were satisfactorily recorded in 10 of the 12 patients (83.3%), and right ventricular outflow tract view in 8 patients (66.6%). No significant statistical differences have been found between measurements obtained from the three different echocardiographic examinations performed on each subject by the same operator, so demonstrating a satisfactory reproducibility of the technique. The highest correlation coefficient for ejection fraction was shown by Simpson's rule (r = 0.96, p less than 0.001), with a very narrow confidence intervals, while the r values for the biplane area-length method was 0.63 (p less than 0.05) and for the pyramidal method 0.50 (not statistically significant), with increasingly wider confidence intervals. The statistically significant difference between the three correlation coefficients demonstrates the higher accuracy of Simpson's rule for the determination of right ventricular ejection fraction.

[Cardiotoxicity of 5-fluorouracil. Personal cases and review of the literature]. / Cardiotossicità da 5-fluorouracile. Casistica personale e revisione della letteratura.

Two cases of 5-Fluorouracil (5FU) cardiotoxicity, chest pain with changes in ECG the former, and myocardial infarction the latter, are described. Review of literature shows the existence of 49 cases of cardiotoxicity due to 5FU (38 angina = 77.5% 8 myocardial infarction = 16.3%). This complication seems due to a "coronary toxicity" whose onset is very precocious and not dose-dependent. Since 5FU therapy could result very dangerous when cardiotoxicity occurs, it is strictly advisable to withdraw further administration of the drug. As a matter of fact 18 patients out of 21 who again were treated with 5FU, had more serious complications which resulted in 3 myocardial infarctions (2 deaths).