Various causes could explain syncope in 70% of patients with coronary disease and DCM, but differences were noted: VT was frequent in coronary disease with a bad prognosis, and ischemia could explain syncope; in DCM, different causes such as atrial tachycardia could be responsible for syncope, but the prognosis only depended on LVEF.
Summary. Background: Elevated plasma homocysteine is a risk factor for coronary artery disease (CAD) and thromboembolic disorders that seems also to be associated with chronic heart failure. Objective: To evaluate the association between homocysteine and left ventricular dysfunction and to assess whether it is independent of CAD. Patients and methods: A prospective study evaluated this relationship in 709 patients referred for diagnostic coronary angiography, including 515 CAD and 194 patients without evidence of coronary artery lesions. Results: The homocysteine level was significantly higher in the 187 patients with a left ventricular ejection fraction (LVEF) dysfunction < 40% (P < 0.0001) than in those without ventricular dysfunction. LVEF, NYHA functional class II or III and CAD, stable angina and hypertension were clinical characteristics that influenced total homocysteine level in univariate analysis. Homocysteine was significantly associated with LVEF and N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) in univariate regression (r = -0.267, 95% CI -0.33 to -0.19, P < 0.0001, and r = 0.381, 95% CI 0.28-0.47, P < 0.0001, respectively) and in multiple regression (P = 0.0022 and P = 0.0001, respectively). Other determinants were creatinine and vitamin B 12 , but not folate. LVEF was a predictor of homocysteine > 15 lmol L )1 in the whole population (P for trend £ 0.0001) and in patients without documented CAD (P for trend = 0.0058). Conclusion: Our results showed an association of homocysteine with left ventricular systolic dysfunction and NT-pro-BNP that existed independently of documented CAD. Whether this association reflects a causative factor or a consequence of CHF and influences the prognosis of the disease remains an open question.
The occurrence of paradoxical bradycardia was a rare finding during isoprenaline infusion (7%); sinus or junctional bradycardia was a sign of hypervagotonia, but was without clinical significance in 35% of these patients. The development of second-degree AV block was always pathological and associated with AV conduction disturbances, which occurred spontaneously during exercise. Isoprenaline infusion appeared to be a simple means to detect organic AV conduction disturbance in patients complaining of exercise or stress-related dizziness/syncope and unable to perform exercise test.
The prevalence of AF is known to increase in the elderly. Some electrophysiological changes were reported in these patients, but the effects of age on AF inducibility and other electrophysiological signs associated with atrial vulnerability are unknown. The purpose of the study was to evaluate the effects of age on atrial vulnerability and AF induction. The study consisted of 734 patients (age 16-85 years, mean 61 +/- 15 years) without spontaneous AF who were admitted for electrophysiological study. Study was indicated for dizziness or ventricular tachyarrhythmia. Programmed atrial stimulation was systematically performed. One and two extrastimuli were delivered in sinus rhythm and atrial driven rhythms (600, 400 ms). Univariate and multivariate analysis of several clinical and electrophysiological data were performed. AF inducibility, defined as the induction of an AF lasting > 1 minute, was paradoxically and significantly decreased in elderly (> 70 years) patients compared to younger patients (< 70 years) (P < 0.01). AF inducibility was present in 40% of 62 patients < 40 years, 39% of 99 patients age 40-50 years, 37% of 130 patients age 50-60 years, 38% of 222 patients age 60-70 years, and only 28% of 221 patients > 70 years. There was no significant correlation with the sex, the presence of dizziness, the presence or not of an underlying heart disease, the left ventricular ejection fraction, and the presence of salvos of atrial premature beats on 24-hour Holter monitoring. There was a significant correlation with a longer atrial effective refractory period in the elderly (226 +/- 41 ms) than in younger patients (208 +/- 31 ms) (P < 0.001). Other electrophysiological parameters of atrial vulnerability did not change significantly. Increased atrial refractory period and age >70 years were independent factors of decreased AF inducibility. Programmed atrial stimulation should be interpreted cautiously before the age of 70 years. AF induction is facilitated by the presence of a short atrial refractory period in these patients. Surprisingly, AF inducibility decreases in patients > 70 years because their atrial refractory period increases. Therefore, increased AF prevalence in these patients should be explained by nonelectrophysiological causes.
AF is frequent after cardiac surgery. However, ventricular arrhythmias are less known. The purpose of the study was to evaluate the causes and the prognostic significance of severe ventricular arrhythmias occurring after cardiac surgery. For 10 years, among 2,100 cardiac surgeries, 16 (0.8%) patients (13 men, 3 women; age 49-71 years, mean 62 +/- 9 years) without previous ventricular arrhythmias, with preserved left ventricular ejection fraction, and without acute cause of ventricular arrhythmias, developed VF (n = 4) or a sustained VT between 3 days and 3 weeks after cardiac surgery (coronary artery bypass grafting [n = 6], valve replacement [n = 10]). Rapid AF (n = 5) or slow AF (n = 1) were present at the time of VT/VF. Programmed ventricular stimulation occurred after up to three extrastimuli in the basal state and after infusion of 20-30 micrograms of isoproterenol. An echocardiogram, coronary angiography, Holter monitoring with heart rate variability (HRV) study were performed. Ventricular stimulation was negative in six patients (with AF); sustained and clinical VT was induced in 10 patients with a left ventricular ejection fraction > 0.40, except in one patient. Valvular prothesis and coronary bypass graftings were normal. In all patients, HRV was normal before surgery and decreased after cardiac surgery; before versus after surgery, respectively, HR 69 +/- 9 and 89 +/- 30 beats/min (P < 0.01), SDNN 117 +/- 31 and 50 +/- 11 ms (P < 0.001), low frequency (LF) 474 +/- 658 and 51 +/- 40 ms2 (P < 0.05), high frequency (HF) 115 +/- 23 and 33 +/- 32 ms2 (P < 0.05), LF:HF 4 +/- 3 and 1 +/- 0.6 (P < 0.01). Follow-up lasted from 6 months to 10 years (mean 3 +/- 2 years). In patients without induced VT, 1 patient died from asystole, 1 had an ICD but no subsequent events, and the other 4 untreated patients are free of events. Patients with induced VT were treated with amiodarone and beta-blockers except in one patient who died from extracardiac complications. Six of nine patients had no inducible VT with this treatment and are alive; 3 patients had inducible VT, 1 died suddenly before implantation of ICD, and 2 patients are alive with an ICD; recurrent VTs were noted in one patient and received an ICD. In conclusion, recent heart surgery may increase the risk of ventricular arrhythmias. The reduction of indexes reflecting sympathetic and parasympathetic tone could facilitate the occurrence of atrial arrhythmias (and then VT) in patients without ventricular arrhythmogenic substrate or the development of VT/VF in patients with a latent previous ventricular arrhythmogenic substrate. In patients without inducible VT, the prognosis is excellent and an ICD is not recommended in these patients. In those with inducible VT, there is a high incidence of responders to antiarrhythmic drugs with a favorable prognosis.
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