Successful surgical treatment of Q fever endocarditis with mitral valve repair.

We report a case of successful surgical treatment of Q fever endocarditis with mitral valve repair in a 66-year old retired British soldier. Valve replacement is invariably undertaken in Q fever endocarditis due to the degree of valvular damage and concerns about eradicating the organism, Coxiella burnetii. Our unique case allowed valve repair since pre-existing myxomatous degeneration and subsequent posterior mitral valve leaflet prolapse resulted in significant excess valve tissue, allowing quadrangular resection of the damaged and perforated P2 portion of this leaflet. Follow-up at four years (including three years of antibiotic treatment) has confirmed excellent valve repair, with no echocardiographic, clinical or microbiological evidence of recurrence. We are only the second group to describe valve repair in a patient with chronic Q fever endocarditis. Valve repair is preferable to valve replacement for Q fever endocarditis, if technically possible.

Can abnormalities of ventricular repolarisation identify insulin dependent diabetic patients at risk of sudden cardiac death?

OBJECTIVE: To study the possible association or QT dispersion and mean QTc intervals, as measured from standard 12 lead electrocardiograms, with baroreceptor-cardiac reflex sensitivity (BRS) in insulin dependent diabetic patients. DESIGN: Comparative study of non-invasive assessment of BRS, QT interval, and QT dispersion. SETTING: Large teaching hospital. SUBJECTS: 31 young asymptomatic, normotensive, insulin dependent diabetic patients, aged 20-55 years with normal clinical autonomic function. METHODS: QT intervals and QT dispersion were measured by a single observer blinded to other data about the patients. BRS was measured after activating the baroreflex with a Valsalva manoeuvre, and the rate in change of R-R interval to increasing systolic pressure during phase 4 was measured; in addition sequence analysis of resting systolic blood pressure and heart rate was performed during standing. The alpha coefficient--an index of the overall gain of the baroreflex mechanisms--was estimated from spectral analysis data of systolic blood pressure and pulse interval variability. RESULTS: Mean (SD) QTc interval was 406 (23) ms, QT dispersion was 44 (13) ms. There was no association between QT dispersion and any measurement of BRS. There was a negative correlation between mean QTc intervals and sequence analysis BRS (r = -0.355, P = 0.049), but no association with Valsalva BRS. The alpha coefficient, showed a significant negative correlation with mean QTc (r = -0.42, P = 0.008). CONCLUSIONS: Abnormal BRS may be reflected in the heart by global prolongation of ventricular repolarisation, but not by dispersion of ventricular repolarisation. This may, in part, explain the increase in sudden cardiac death seen in IDDM patients.

Dynamics of QT dispersion during myocardial infarction and ischaemia.

We studied the dynamics of QT dispersion over the first few days of myocardial infarction and during coronary angioplasty. Ten patients with anterior myocardial infarction and an equal number with inferior infarction had electrocardiograms (ECGs) recorded on admission to hospital (day 1), on the subsequent 2 days (day 2, 3), and prior to discharge (day 6). Ten patients undergoing therapeutic coronary angioplasty were studied; ECGs were recorded prior to, during, and after balloon inflation. Simultaneous 12-lead ECGs were scanned into a personal computer; specially designed software skeletonised and joined each image. The images were then available for user-interactive measurement of QT dispersion. Mean (S.D.) QTc dispersion on day 1 of acute myocardial infarction was 107 (44.8) ms, rose further over the next 48 h, reaching a maximum on day 3 (QTc dispersion, 162.3 (64.8) ms, P < 0.01), and was falling by hospital discharge (QTc dispersion, 117.4 (67.4) ms). There was no difference in QT dispersion measurement during coronary angioplasty. It is unlikely that acute ischaemia plays an important role in the dynamic changes seen in QT dispersion over the first few days of myocardial infarction. These rapid changes in QT dispersion have important implications in the design of any study of QT dispersion after myocardial infarction, and in comparison of studies.

QT dispersion and mortality after myocardial infarction.

QT dispersion may serve as a measure of variability in ventricular recovery time and may be a means of identifying patients at risk of arrhythmias and sudden death after acute myocardial infarction. We investigated this possibility on electrocardiograms (ECGs) recorded 2 or 3 days after infarction (early) and at least 4 weeks later (late). 163 patients who died between 1 day and 5 years after infarct were compared with an equal number of survivors matched for age and sex. 53 of the patients who died and 82 survivors also had late ECGs. There was no difference in early QT dispersion between the patients who died and the survivors (mean QTc dispersion 112.1 [SD 44.4] vs 109.9 [42.7] ms1/2). QTc dispersion fell significantly from early to late ECGs in survivors (110.9 [48.5] to 76.5 [28.8] ms1/2), but not in patients who died during follow-up (108.0 [51.0] to 98.9 [43.1] ms1/2). The difference between the groups in the mean change was significant (34.4 [55.2] vs 9.1 [60.8] ms1/2, p = 0.016). QT dispersion measured on an ECG recorded 2 or 3 days after acute myocardial infarction does not predict mortality during the next 5 years. Increased QT dispersion on ECGs recorded at least 4 weeks after infarct may be associated with subsequent mortality, but this finding must be confirmed in a prospective trial.

Use of lead adjustment formulas for QT dispersion after myocardial infarction.

OBJECTIVE: To determine whether lead adjustment formulas for correcting QT dispersion measurements are appropriate in patients after myocardial infarction. DESIGN: Retrospective analysis of QTc dispersion measurements in 461 electrocardiograms (ECGs). Data are presented as uncorrected QTc dispersion "adjusted" for a number of measurable leads and coefficient of variation of QTc intervals for ECGs in which between six and 12 leads had a QT interval that could be measured accurately. PATIENTS: Patients were drawn from the placebo arm of the second Leicester Intravenous Magnesium Intervention Trial. Some 163 patients who subsequently died and an equal number of known survivors had ECGs recorded on day 2 or 3 of acute myocardial infarction. ECGs were also available in 135 of these patients from at least 1 month postinfarct. RESULTS: The most common lead in which a QT interval measurement was omitted was aVR (n = 176), the least common lead was V3 (n = 13). The longest QTc interval measured was most usually in lead V4 (n = 72) and the shortest in lead V1 (n = 67). As the number of measurable leads decreased there was a small, nonsignificant increase in QTc dispersion from 12 lead to eight lead ECGs (mean (SD) 100 (35.5) v 109.5 (47.9) ms). Lead adjusted QTc dispersion (QTc dispersion/square root of the number of measurable leads) showed a large, significant increase when the number of measurable leads decreased from 12 to eight (28.9 (10.3) v 38.7 (16.1) ms, P < 0.001). A similar trend was seen for coefficient of variation of QTc intervals (standard deviation of QTc intervals/mean QTc interval 64.3 (2.19) v 8.45 (3.94)%, P < 0.001). CONCLUSIONS: Lead adjustment formulas for QT dispersion are not appropriate in patients with myocardial infarction. Large differences in lead adjusted QTc dispersion are produced, dependent on the number of measurable leads, for very small differences in QTc dispersion. It is recommended that QT dispersion is presented as unadjusted QT and QTc dispersion, stating the mean (SD) of the number of leads in which a QT interval was measured.

Three-lead measurement of QTc dispersion.

INTRODUCTION: QTc dispersion has traditionally been calculated from all 12 leads of a standard electrocardiogram (ECG). It is possible that alternative, quicker methods using fewer than 12 leads could be used to provide the same information. METHODS AND RESULTS: We have previously shown a difference in QTc dispersion from ECGs recorded at least 1 month after myocardial infarction between patients who subsequently died and long-term survivors. In the current study, we recalculated QTc dispersion in these ECGs using different methods to determine if the observed difference in QTc dispersion measurements between the two groups, as calculated from 12-lead ECGs, persisted when using smaller sets of leads. QTc dispersion was recalculated by four methods: (1) with the two extreme QTc intervals excluded; (2) from the six precordial leads; (3) from the three leads most likely to contribute to QTc dispersion (aVF, V1, V4); and (4) from the three quasi-orthogonal leads (aVF, I, V2). For each of the 270 12-lead ECGs examined, a mean of 9.9 leads (SD 1.5 leads) had a QT interval analyzed; the QT interval could not be accurately measured in the remaining leads. Using the standard 12-lead measurement of QTc dispersion, there was a difference in the fall in QTc dispersion from early to late ECG between the groups: 9.1 (SD 60.8) msec for deaths versus 34.4 (55.2) msec for survivors (P = 0.016). This difference in QTc dispersion between early and late ECGs was maintained using either three-lead method (quasi-orthogonal leads: -2.6 [56.2] msec for deaths vs 26.9 [54.3] msec for survivors [P = 0.003]; "likeliest" leads: 8.6 [64.9] msec vs 29.5 [50.2] msec [P = 0.05]), but not when using the other two methods (precordial leads: 19.1 [55.5] msec vs 22 [50.8] msec [P = 0.76]; extreme leads removed: 9.2 [50.1] msec vs 21.8 [42] msec [P = 0.13]). CONCLUSION: QTc dispersion calculated from three leads may be as useful a measurement as QTc dispersion calculated from all leads of a standard ECG. Its advantages over the standard measurement are its simplicity and the lack of problems with lead adjustment.

Reproducibility and automatic measurement of QT dispersion.

This study investigated interobserver (two observers) and intrasubject (two measurements) reproducibility of QT dispersion from abnormal electrocardiograms in patients with previous myocardial infarction, and compared a user-interactive with an automatic measurement system. Standard 12-lead electrocardiograms, recorded at 25 mm.s-1, were randomly chosen from 70 patients following myocardial infarction. These were scanned into a personal computer, and specially designed software skeletonized and joined each image. The images were then available for user-interactive (mouse and computer screen), or automatic measurements using a specially designed algorithm. For all methods reproducibility of the RR interval was excellent (mean absolute errors 3-4 ms, relative errors 0.3-0.5%). Reproducibility of the mean QT interval was good; intrasubject error was 6 ms (relative error 1.4%), interobserver error was 7 ms (1.8%), and observers' vs automatic measurement errors were 10 and 11 ms (2.5, 2.8%). However QTc dispersion measurements had large errors for all methods; intrasubject error was 12 ms (17.3%), interobserver error was 15 ms (22.1%), and observers' vs automatic measurement were errors 30 and 28 ms (35.4, 31.9%). QT dispersion measurements rely on the most difficult to measure QT intervals, resulting in a problem of reproducibility. Any automatic system must not only recognize common T wave morphologies, but also these more difficult T waves, if it is to be useful for measuring QT dispersion. The poor reproducibility of QT dispersion limits its role as a useful clinical tool, particularly as a predictor of events.