Biomedical subjects

P D Higham

Publications and source records attributed to P D Higham.

6 recordsLinked to original sources

PubMed2000

Time dependent variability of QT dispersion after acute myocardial infarction and its relation to ventricular fibrillation: a prospective study.

OBJECTIVE: To show whether increased QT dispersion on admission predicts ventricular fibrillation after acute myocardial infarction, and to determine the nature of time related changes in QT dispersion. DESIGN: Prospective cohort study. SETTING: Coronary care units of three teaching hospitals in Newcastle-upon-Tyne over an eight month period. PATIENTS: All had acute myocardial infarction according to World Health Organization criteria. INTERVENTIONS: For all patients, QT dispersion (QTd) and Bazett rate corrected QTc dispersion (QTcd) were measured from a high quality 12 lead ECG recorded on admission at a paper speed of 50 mm/s. In a subset, serial ECGs were recorded regularly to show time related changes in QTcd following acute myocardial infarction. MAIN OUTCOME MEASURES: Occurrence of ventricular fibrillation within the first 24 hours after myocardial infarction. RESULTS: Data collected from 201 patients, 12 of whom (6%) developed ventricular fibrillation within 24 hours. Neither QTd nor QTcd differed between those developing ventricular fibrillation and those who did not: QTd mean (SD), 74 (24) ms (95% confidence interval (CI) 59 to 89) v 66 (24) ms (95% CI 62 to 70), respectively; QTcd, 86 (26) ms(0.5) (95% CI 70 to 102) v 77 (29) ms(0.5) (95% CI 72 to 82), respectively. Significant QTcd changes occurred early after myocardial infarction. CONCLUSIONS: Admission QTd and QTcd do not predict ventricular fibrillation after acute myocardial infarction. There are significant changes in QTcd with time, which may account for this measured lack of correlation.

Aged↗

PubMed1995

QT dispersion and components of the QT interval in ischaemia and infarction.

OBJECTIVE: To evaluate changes in QT dispersion and components of the QT interval in patients admitted with unstable angina and acute myocardial infarction and to study the dynamics of these changes in patients with infarction. METHODS: Prospective study recording electrocardiograms at 50 mm/s in patients admitted with typical cardiac chest pain. Subsequent confirmation of acute myocardial infarction according to standard criteria. Single blind analysis for QT dispersion and QT components using a digitiser and simple computer program. Results are expressed as native QT dispersion, QTc dispersion, and the QT dispersion ratio defined as QT dispersion divided by cycle length and expressed as a percentage. RESULTS: QT dispersion, QTc dispersion, and QT dispersion ratio were all higher in patients with acute myocardial infarction than in those with unstable angina (mean (SD) 66 (18) ms, 75 (26) ms1/2, and 8.1 (2.4)% compared with 38 (13) ms, 39 (13) ms1/2, and 4.5 (1.7) % respectively). Dynamic changes in QTc dispersion were seen after acute infarction with significant differences in the QT components occurring between the different patient groups. Levels of QT dispersion (87 (15) ms), QTc dispersion (105 (17) ms1/2), and QT dispersion ratio (11.7 (0.8)%) in the four patients with ventricular fibrillation were significantly higher. Use of QT dispersion ratio gave a narrower confidence interval. CONCLUSION: QT dispersion is increased after myocardial infarction and levels are higher in patients with ventricular fibrillation. The changes in QT dispersion are dynamic and may reflect the changing pattern of underlying ventricular recovery of ventricular excitability, which is profoundly disturbed in the earliest phase of acute infarction. Expressing QT dispersion as a percentage of cycle length (QT dispersion ratio) rather than using standard rate correction may be superior in identifying patients who develop ventricular fibrillation.

Angina, Unstable↗

PubMed1995

Concentration dependent cardiotoxicity of terodiline in patients treated for urinary incontinence.

OBJECTIVE: Terodiline, an antimuscarinic and calcium antagonist drug, was used to treat detrusor instability but was withdrawn in 1991 after provoking serious ventricular arrhythmias associated with increases in the corrected QT interval (QTc). This research was performed to relate drug induced electrocardiographic changes in asymptomatic recipients to plasma concentrations of the R(+) and S(-) terodiline enantiomers. SETTING: Urological and geriatric clinics and wards. SUBJECTS: Asymptomatic patients taking terodiline in stable dose. METHODS: Electrocardiograms (50 mm/s) were collected from patients while they were taking terodiline and compared with ECGs obtained before or after terodiline. QT interval, heart rate corrected QT interval (QTc), and QT dispersion (QTd) were measured. Drug induced electrocardiographic changes were related to plasma concentrations of R(+) and S(-) terodiline. RESULTS: During terodiline treatment mean QTc and QTd were prolonged (491(43) and 84 (35) ms 1/2) compared with measurements made off therapy (443 (33) and 42 (17) ms 1/2, paired t tests, P < 0.002 and P < 0.01 respectively) in the 12 patients in sinus rhythm. The mean (95% confidence interval) drug induced increases were 48 (23 to 74) ms 1/2 for QTc and 42 (13 to 70) ms 1/2 for QTd. These increases correlated with total plasma terodiline (QTc: r = 0.77, P < 0.006, QTd: r = 0.68, P < 0.025) and with plasma concentrations of both terodiline enantiomers. CONCLUSIONS: Terodiline increases QTc and QTd in a concentration dependent manner. It is not clear whether this is a stereoselective effect and, if so, which enantiomer is responsible. The results suggest that drug induced torsade de pointes is a type A (concentration dependent) adverse drug reaction.

Aged↗

PubMed1994

QT dispersion.

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Arrhythmias, Cardiac↗

PubMed1993

Self-terminating ventricular tachyarrhythmias--a diagnostic dilemma?

Ventricular fibrillation is generally regarded as being lethal unless promptly halted. There have been reports of self-terminating ventricular fibrillation, but similar events are described by some cardiologists as polymorphic ventricular tachycardia or even torsade de pointes. To examine how experienced cardiologists would diagnose such tachyarrhythmias, electrocardiograms of self-terminating ventricular tachyarrhythmias compatible with accepted definitions of ventricular fibrillation (rate > 300/min) were sent to 22 cardiologists. During the study period of 19 months, 2462 patients treated in a 10-bed coronary-care unit were monitored by use of a single bipolar chest lead. 45 (2%) had episodes of ventricular fibrillation that were terminated by direct current (DC) shock. 12 self-terminating tachyarrhythmias (duration 5.2-49.5 s) were recorded from 8 patients, 3 of whom also had sustained ventricular fibrillation terminated by DC shock. The cardiologists offered 264 diagnoses for the self-terminating events; 42 (15.9%) ventricular fibrillation, 99 (37.5%) polymorphic ventricular tachycardia, 98 (37.1%) torsade de pointes, and 25 (9.5%) "other". The cardiologists differed (p < 0.01) in their response patterns. The findings show that rapid self-terminating ventricular tachyarrhythmias are not uncommon in coronary-care unit patients, and that the diagnostic categorisation of these important events is highly subjective and inconsistent.

Cardiology↗

PubMed1993

Plasma potassium, serum magnesium and ventricular fibrillation: a prospective study.

Low plasma potassium and magnesium concentrations have been advanced as risk factors for ventricular fibrillation (VF). For potassium, this assertion is based almost exclusively on retrospective data; for magnesium the evidence shows an association with ventricular arrhythmias but no direct association with VF. We studied the relationship between these electrolytes and VF prospectively. Plasma potassium and serum magnesium concentrations were measured on admission to our coronary care unit. Drug therapy, time from onset of symptoms, ECG, enzyme changes and clinical status were all recorded. VF was confirmed by analysis of 24 h monitoring tapes. Mean plasma potassium in the 21 patients with VF who had measurements prior to their arrhythmia was 3.49 +/- 0.54 mmol/l, lower than that of the 1165 patients without VF (mean K 3.88 +/- 0.57 mmol/l, p < 0.05). Plasma potassium concentrations in the 17 patients with myocardial infarction and VF were lower (mean 3.58 +/- 0.41 mmol/l) than in those without VF (n = 417, mean 3.89 +/- 0.61 mmol/l) (p < 0.05). Mean serum magnesium in the 12 patients with VF, measured prior to their arrhythmia (all with myocardial infarction) was 0.80 +/- 0.07 mmol/l, which was not different from the mean for patients without VF (n = 781, 0.82 +/- 0.09 mmol/l) or from the mean of 0.81 +/- 0.08 mmol/l for those with infarction but not VF (n = 331). Low plasma potassium concentrations are associated with increased risk of ventricular fibrillation, but low serum magnesium concentrations are not.

Female↗