Improving survival in the 6 months after diagnosis of heart failure in the past decade: population-based data from the UK.

OBJECTIVE: To investigate the secular trend in survival after a new diagnosis of heart failure in the UK population. DESIGN AND SETTING: Comparison of all-cause mortality in the 6 months after diagnosis of heart failure in population-based studies in the south east of England in 2004-5 (Hillingdon-Hastings Study) and 1995-7 (Hillingdon-Bromley Studies). PARTICIPANTS: 396 patients in the 2004-5 cohort and 552 patients in the 1995-7 cohort with incident (new) heart failure. MAIN OUTCOME MEASURES: All-cause mortality. RESULTS: All-cause mortality rates were 6% (95% CI 3% to 8%) at 1 month, 11% (8% to 14%) at 3 months and 14% (11% to 18%) at 6 months in the 2004-5 cohort compared with 16% (13% to 20%), 22% (19% to 25%) and 26% (22% to 29%), respectively, in the 1995-7 cohort (difference between the two cohorts, p<0.001). The difference in survival was not explained by any difference in the demographics or severity of heart failure at presentation. There was a difference at baseline and thereafter in the use of neurohormonal antagonists (beta-blockers and angiotensin-converting enzyme inhibitors). CONCLUSIONS: Although early mortality remains high among patients with newly diagnosed heart failure in the UK general population, there is strong evidence of a marked improvement in survival from 1995-7 to 2004-5, perhaps partly explained by an increased usage of neurohormonal antagonists.

Physiological changes in ventricular filling alter cardiac electrophysiology in patients with abnormal ventricular function.

OBJECTIVE: To explore the hypothesis that patients with abnormal ventricular function have an altered electrophysiological response to physiological changes in ventricular filling which is not evident in people with normal ventricles. DESIGN: The influence of an acute alteration in ventricular filling on dispersion of repolarisation, measured as QT dispersion, was examined in subjects with normal (n = 9) and abnormal ventricles (n = 9). A physiological reduction in ventricular filling was achieved using dual chamber atrioventricular (AV) pacing in two different modes-AV pacing: atrial activation 120 ms before ventricular activation such that atrial contraction occurred normally in late diastole; and VA (ventriculoatrial) pacing: atrial activation 50 ms after ventricular activation, such that atrial contraction occurred after closure of the AV valves. The absence of effective atrial contraction was confirmed by echocardiography. Ventricular cycle length and sequence of excitation through the ventricle was constant throughout both VA and AV sequences within each patient. RESULTS: During AV pacing (normal ventricular filling) there was no significant difference in QT dispersion between the two groups. In contrast during VA pacing, when the atrial component to ventricular filling was abolished, there was an immediate and consistent increase in QT dispersion compared with baseline in subjects with abnormal ventricular function (p < 0.001) but not in those with normal ventricles. CONCLUSIONS: An abrupt change in ventricular filling, within the physiological range, increased QT dispersion in subjects with abnormal ventricular function but not in subjects with normal ventricles. The findings suggest an altered electrophysiological response to ventricular load in patients with abnormal ventricular function.

Cerebral microembolism detected by transcranial Doppler during cardiac procedures.

BACKGROUND AND PURPOSE: Cerebral embolism with clinical sequelae may rarely complicate cardioversion and cardiac catheterization. Transcranial Doppler sonography has recently been introduced to monitor microemboli entering the middle cerebral artery in cardiac and carotid surgery. We therefore used this technique to evaluate the risk of asymptomatic embolism during common cardiac procedures. METHODS: Patients were monitored by transcranial Doppler while undergoing direct current cardioversion (n=15) and cardiac catheterization (n=17). RESULTS: Microemboli were detected in all patients having cardiac catheterization but in only 1 patient after cardioversion. CONCLUSIONS: Microembolism occurred frequently during cardiac catheterization and rarely during cardioversion. It is not yet known whether this has clinical relevance.

Acute psychological stress and the propensity to ventricular arrhythmias; evidence for a linking mechanism.

AIMS: This study was designed to test the hypothesis that acute psychological stress is capable of inducing an increase in the dispersion of repolarization in patients with underlying coronary artery disease. METHODS AND RESULTS: Twenty four patients undergoing elective coronary angiography were studied, 17 with significant coronary artery disease and seven with normal coronary arteries. Following coronary angiography they were subjected to a series of timed cognitive tests, well known to induce acute psychological stress. An individual's perception of stress was assessed by visual analogue scales. Serial ECGs were recorded during the cognitive tests and QT, QRS and JT intervals measured from which QT, QRS and JT dispersion were calculated. Psychological stress was reported by the seven patients with normal coronaries and 14 of the 17 with coronary artery disease. In patients who experienced stress a marked increase in QT dispersion, reflecting JT dispersion, was observed in those with coronary artery disease (F=22.4, P=0.0001) but not in those without. At baseline there was no difference in QT dispersion between those with and without coronary artery disease (27-57 ms, 17-53 ms, P > or = 0.5). CONCLUSION: Acute psychological stress induces an increase in QT dispersion in patients with underlying coronary artery disease due to changes in JT dispersion (rather than QRS dispersion). This suggests that psychological stress modifies the dispersion of repolarization through ischaemia related changes in action potential duration.

Osteomyelitis and possible endocarditis secondary to Lactococcus garvieae: a first case report.

Although osteomyelitis is commonly caused by staphylococcal infection, the first case of a lumbar osteomyelitis secondary to Lactococcus garvieae is reported. The case was complicated by possible endocarditis of an aortic valve prosthesis.

Is there a place for the late cardioversion of atrial fibrillation? A long-term follow-up study of patients with post-thyrotoxic atrial fibrillation.

AIMS: As atrial fibrillation is associated with significant mortality and morbidity, restoration of sinus rhythm is desirable. However, previous data suggest that cardioversion should be restricted to patients in whom the fibrillation is of limited duration (<1-2 years) because of high relapse rates. It may be the frequent association with cardiac disease, rather than the duration of fibrillation itself, which determined the high relapse of earlier studies. The aim of this study was to investigate rates of cardioversion, maintenance of sinus rhythm and predictors of subsequent relapse in a homogeneous group of patients without evidence of any co-existent cardiac disease. METHODS AND RESULTS: We report on a retrospective series of 106 patients with thyrotoxicosis-induced fibrillation but no other heart disease: 87% had been in atrial fibrillation for >12 months (median duration 28.5, interquartile range 15-47 months). Cardioversion was attempted using disopyramide and then electric shock. Ninety-eight patients were successfully cardioverted: at late follow-up, 80.6+/-37 months (mean+/-SD), 67% were in sinus rhythm. CONCLUSION: Although a relationship between the duration of fibrillation and maintenance of sinus rhythm was found, the high proportion remaining in sinus rhythm, compared with other series, suggests this influence may be less important than the presence or absence of structural heart disease.

Evidence for an influence of mechanical restitution on beat-to-beat variations in haemodynamics during chronic atrial fibrillation in patients.

OBJECTIVE: We tested the hypothesis that beat-to-beat changes in haemodynamics during atrial fibrillation include an effect of each preceding R-R interval through the interval-strength relationship (mechanical restitution). BACKGROUND: The variation in stroke volume and pulse pressure characteristic of atrial fibrillation is usually ascribed to time dependent ventricular filling. METHODS: We measured the maximum rate of rise of left ventricular pressure (LVdP/dtmax), and aortic blood velocity and its integral in patients with atrial fibrillation undergoing cardiac catheterisation. The contractile response of isometric human myocardial trabeculae to sequences of atrial fibrillation was also studied, using the recorded ECGs as stimuli. The trabeculae were obtained from the resected right ventricular outflow tracts of patients with Fallot's tetralogy undergoing operative correction. RESULTS: Beat-to-beat variations in contractile function during atrial fibrillation in the patients were recorded as LVdP/dtmax and left ventricular ejection (ascending aortic) velocity integral (proportional to stroke volume). Both these indices correlated well with the response to the same ECG (R wave) sequences in the isometric model measured as the maximum rate of rise of force, dF/dtmax, r = 0.72 to 0.81, p, 0.0001. When short pre-preceding intervals were excluded (minimizing the effect of post-extrasystolic potentiation), these variables showed a positive curvilinear relationship to preceding interval typical of mechanical restitution. CONCLUSIONS: Mechanical restitution, which causes beat-to-beat changes in inotropic state, accounts in part for the changes in stroke volume in atrial fibrillation.

Acute ischaemia: a dynamic influence on QT dispersion.

BACKGROUND: The aim of this study was to test the hypothesis that acute myocardial ischaemia increases QT dispersion measured from the 12-lead electrocardiogram. METHODS: Incremental atrial pacing was used to induce myocardial ischaemia in 18 patients with coronary artery disease and QT dispersion was measured. Six patients with normal coronary arteries served as the control group. FINDINGS: All the patients with coronary artery disease developed angina and/or ST depression accompanied by marked increases in QT dispersion (mean increase 38 ms, 95% CI 30 to 45 ms, p < 0.001). In contrast, in the six patients with normal coronary arteries who remained without symptoms and without ST changes, there was no significant change in QT dispersion in response to pacing. Baseline QT dispersion did not distinguish those patients with coronary artery disease from those with normal coronary arteries (44 ms [95% Cl 39-49 ms] vs 40 ms [25-55 ms]), respectively. INTERPRETATION: These results demonstrate that myocardial ischaemia induced by incremental atrial pacing in patients with coronary artery disease causes an acute increase in QT dispersion. Such "inducible" QT dispersion may prove more useful than resting QT dispersion in assessing the individual risk of arrhythmic events in patients with coronary artery disease.

Mechanical restitution and recirculation fraction in cardiac myocytes and left ventricular muscle of adult rats.

Unloaded cell shortening was measured in electrically stimulated myocytes from adult rat hearts to compare the contractile response to stimulation with that in isometrically contracting left ventricular papillary muscles under similar experimental conditions, but preloaded to produce maximum twitch tension. Mechanical restitution in cells followed a biexponential function with time constants of 0.19 +/- 0.03 s and 36.4 +/- 10.2 s (7 cells from 5 hearts, n = 7/5). The time constants for papillary muscles were 0.58 +/- 0.05 s and 14.6 +/- 1.0 s (n = 6/6). In myocytes, maximum post-rest potentiation occurred after 30 to 60 s of rest. The potentiation after 60 s of rest was 2.48 +/- 0.31 times the steadystate in cells and 2.63 +/- 0.16 in papillary muscles. Recirculation fraction of C2+ as calculated from the decay of post-rest potentiation was 0.84 +/- 0.04 in single cells and 0.59 +/- 0.02 in papillary muscles (p < 0.005). Caffeine (3mM) abolished post-rest potentiation in both types of preparations. The numerical values for the time constants of mechanical restitution, potentiation factor and recirculation fraction in papillary muscles did not depend on preload. It is concluded that interval-dependent changes of contractility are preserved in single cardiac cells but the kinetics of decay of potentiation appear to have changed quantitatively.

Analysis of left ventricular contractile behaviour during atrial fibrillation.

OBJECTIVES: The purpose of this study was to explore the physiology underlying the beat-to-beat variations of ventricular function during atrial fibrillation (AF). METHODS: Left ventricular pressure, and its first derivative (LVdP/dtmax, an index of contractility, and aortic blood velocity (and its integral AVI, an ejection index), were recorded using cathetermounted transducers in 15 patients with AF during cardiac catheterisation. Transfer function modelling was used to examine the influence of preceding intervals on LVdP/dtmax, and of LVdP/dtmax on AVI. The technique also allowed simulation of the behaviour of LVdP/dtmax in response to specific manipulations of interval. RESULTS: The variations in LVdP/dtmax recorded from the AF patients were shown to be dependent on up to six preceding intervals; a maximum of 91% of the variation was explicable in this way. The influences of mechanical restitution (MR, the relationship between preceding interval and contractility), postextrasystolic potentiation (PESP, the inverse relationship between pre-preceding interval and contractility) and the decay of that potentiation were all demonstrated. These influences collectively appeared to be powerful determinants of AVI. Simulations of LVdP/dtmax, following single interval perturbations, were entirely consistent with these interval force effects. CONCLUSIONS: The cardiac interval force relationship in man is an important determinant of the beat-to-beat variations of contractile and ejection function during AF: the beat-to-beat variations in contractile (or inotropic) function are independent of changes in ventricular filling or fibre-length.