Psychometric properties of the Minnesota Living with Heart Failure Questionnaire (MLHF-Q)

Objective: To evaluate the psychometric properties of the Minnesota Living with Heart Failure Questionnaire (MLHF-Q) in patients with atrial fibrillation. Design: A prospective study of the patients who underwent DC electrical cardioversion. Setting: Clinics of cardiology and thoracic surgery of the University Hospital in Groningen, the Netherlands. Main outcome measures: The disease-specific MLHF-Q and generic measures of quality of life were administered. The sensitivity to change over time was tested with effect sizes (ES). Internal consistency of MLHF-Q scales was estimated with Cronbach's alpha. To evaluate the construct validity multitrait-multimethod analysis was applied. The 'known group validity' was evaluated by the comparison of mean scores and effect sizes between two groups of the New York Heart Association (NYHA) classification (NYHA I versus II-III). Stability of MLHF-Q scales was estimated in a subgroup of patients who remained stable. Perfect congruence analysis and factor analysis were applied to confirm the a priori determined structure. Results: Cronbach's alpha was :0.80 of the MLHF-Q scales. Perfect congruence analysis (PCA) showed that the results resemble quite well the a priori assumed factor structure. Multitrait-multi method analysis showed convergent validity coefficients ranging from 0.59 to 0.73 (physical impairment dimension) and 0.39 to 0.69 (emotional dimension). The magnitude of change can be interpreted as medium (ES = 0.50). The results of a 'test-retest' analysis in a stable group can be valued as satisfactory for the MLHF-Q scales (Pearson's r > 0.60). The physical dimension and the overall score of the MLHF-Q discriminated significantly between the NYHA I and II-III groups (p <0.001) with large effect sizes (ES > 1.0). Conclusions: The MLHF-Q has solid psychometric properties and the outcome of the current study indicates that the MLHF-Q is an effective and efficient instrument

Atrioventricular nodal response to retrograde activation in atrial fibrillation

Retrograde (ventriculoatrial) conduction that reaches the atrioventricular node simultaneous with, or just before an atrial impulse can facilitate subsequent anterograde conduction. However, a spontaneous or programmed ventricular extrasystole during atrial fibrillation is generally followed by a compensatory pause indicating subsequent delayed anterograde transmission. This characteristic response was used as a model to study the mechanism of atrioventricular nodal behavior during atrial fibrillation. In eight medically-treated patients with chronic atrial fibrillation and a relatively slow but random ventricular response, single premature right ventricular stimuli were delivered after every eighth spontaneous R wave during at least 1 hour. A fixed coupling interval of the extrastimulus, considerably shorter than the shortest spontaneous RR interval, was used. The histograms of the postextrasystolic intervals were compared with those of the spontaneous noninterrupted RR intervals. The average postextrasystolic interval was 180 to 300 msec longer than the mean control RR interval, and in six of eight patients, the shape of the histogram of the postextrasystolic cycles was insignificantly different from that of the spontaneous RR intervals. This suggests that in those six patients, the retrograde impulse had reset the random timing cycle of atrioventricular nodal discharge during atrial fibrillation. This observation is compatible with the hypothesis that electrotonically-mediated propagation across a weakly coupled junctional area within the atrioventricular node, rather than decremental conduction and extinction of anterograde atrial impulses at different levels within the node, may be the mechanism of atrioventricular transmission in atrial fibrillation

Competitive anterograde and retrograde atrioventricular junctional activation in atrial fibrillation

In eight medically-treated patients with chronic atrial fibrillation and a random ventricular rhythm, we studied the effect of single right ventricular stimuli delivered after each eighth spontaneous R wave during at least 1 hour. The coupling interval of the extrastimulus was fixed and differed marginally from the shortest spontaneous RR interval. The histograms of spontaneous RR intervals and of the "compensatory" pauses following the ventricular extrasystoles were calculated. Analysis of these histograms and simulation of the interaction between anterograde and retrograde impulses in a computer model suggests that in seven of the eight patients the compensatory pause may be caused by two distinctly different mechanisms: (1) reset of the timing cycle of atrioventricular nodal activation by relatively early retrograde impulses; and (2) interception of anterograde impulses by relatively late ventricular extrasystoles. The finding that early retrograde impulses are not blocked by concealed atrioventricular nodal conduction makes the existence of decremental conduction and extinction of atrial impulses at different levels within the node unlikely. The results of this study support the hypothesis that the distal side of a weakly coupled junctional area inside the AV node behaves as a pacemaker for the ventricular rhythm during atrial fibrillation

Effect of right ventricular pacing on ventricular rhythm during atrial fibrillation

In 13 patients with atrial fibrillation, the effect of right ventricular pacing at various rates on spontaneous RR intervals was studied. Five hundred consecutive RR intervals were recorded and measured before and during varying right ventricular pacing rates. As anticipated, all RR intervals longer than the right ventricular pacing intervals were abolished. However, RR intervals shorter than the right ventricular pacing intervals were also eliminated. It is difficult to explain the elimination of RR intervals shorter than the pacing intervals with the accepted concepts concerning the mechanisms governing the rate and rhythm of the ventricular response to atrial fibrillation. An alternative explanation may be that during atrial fibrillation the atrioventricular node behaves as a nonprotected pacemaker that is electrotonically modulated by the chaotic atrial electrical activity. The result is a random ventricular rhythm. With right ventricular pacing, the automatic focus is depolarized by the retrogradely concealed conducted ventricular impulses, the short RR intervals are not generated as a consequence and the rhythm becomes pacemaker dependent