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Objectives: To describe children with pertussis who require intensive care., Design, Setting and Patients: An audit in Auckland, New Zealand, of pertussis admissions to the national paediatric intensive care unit (PICU) from 1991 to 2003., Results: 72 children, 97% of whom were <12 months old. The annual number of cases increased with time (p = 0.04). Forty patients (56%) were coughing for less than 8 days before admission. Apnoea or paroxysmal cough was present in 33 (83%) of these children. Thirty five (49%) received assisted ventilation. Four died. 19% were readmitted to PICU. Those readmitted presented with more atypical disease and had a shorter first admission but longer total PICU admission (9 vs 5 days, p = 0.009). Of the 58 children from Auckland, nine either died (three) or had subsequent respiratory or neurodevelopmental problems (six). There was an increased risk (relative risk, 95% CI) of death or disability associated with having a co-morbidity (RR = 5.56, 1.50 to 8.15), an elevated lymphocyte count (RR = 5.75, 1.54 to 13.65), presenting with seizures/encephalopathy (4.87, 1.18 to 8.34) or shock (6.50, 1.89 to 8.94), having a PIM score of 1% or more (RR = 6.20, 1.22 to 21.72), any abnormal neurological signs (RR = 9.65, 3.32 to 15.23) or being readmitted to PICU (RR = 4.63, 1.44 to 8.82)., Conclusions: Apnoea and paroxysmal cough are key symptoms of pertussis in those with shorter cough duration. Death or disability are frequent. Clinical factors define children at increased risk of these poor outcomes. Early discharge from PICU is associated with an increased risk of readmission and poor outcome.

Objective: To determine the prognosis in patients with diphtherial myocarditis and bradyarrhythmias and to assess the results of ventricular pacing in those with third degree atrioventricular block., Design: Case series., Setting: Referral department of cardiology in a teaching hospital., Patients: Twenty four out of 46 patients admitted with diphtherial myocarditis over 10 years had bradyarrhythmias. Six had sinus bradycardia, 15 atrioventricular or intraventricular conduction disturbances, and three atrioventricular dissociation., Main Outcome Measure: Death rate., Results: Eleven patients died (46%): all seven patients with third degree atrioventricular block, the patient with bifascicular block, and three of the six patients with bundle branch block. Seven died of cardiogenic shock and four of ventricular fibrillation. All nine patients with sinus bradycardia or atrioventricular dissociation survived., Conclusion: Conduction system disturbances in patients with diphtherial myocarditis are markers of severe myocardial damage and a poor prognosis. In addition, ventricular pacing does not improve survival.

Objective: To search for possible serum factors (immunochemical abnormalities) that reflect HLA-B27 associated inflammatory process with the proliferative endarteritis, which is an important cause of severe bradycardia and aortic valve regurgitation., Patients and Methods: Seventy four men with pacemakers were studied: 24 were HLA-B27 positive and had associated rheumatic and cardiac disorders, 13 were B27 positive but had no clinical or radiographic signs of a related rheumatic condition, and 37 were B27 negative controls. Randomly obtained serum samples were examined for a series of serum factors., Results: Thirteen (57%) of the 23 patients with HLA-B27 and associated rheumatic and cardiac conditions had platelet aggregating activity in their serum. No such activity was found in sera from patients in the other groups. None the less, immunochemical abnormalities were common among patients of all groups; 30 (41%) had antinuclear antibodies or rheumatoid factor or both., Conclusion: The platelet aggregating activity found in patients with HLA-B27 and associated rheumatic and cardiac conditions may reflect serum factors that increase the stickiness of platelets and increase their adhesion to the vessel wall. This suggests a link via release of platelet derived growth factor(s) with the characteristic histopathological feature of proliferative endarteritis. Immunochemical abnormalities were common in serum from all men with pacemakers.

Pseudo second degree atrioventricular block resulting from blocked His premature beats was successfully treated with quinidine. The diagnosis was proved by His bundle electrogam which showed both blocked and conducted His premature beats. The blocked His prematures produced second degree atrioventricular block by making the atrioventricular junction refractory. Quinidine abolished both conducted and blocked His extrasystoles. There has been no recurrence of arrhythmia during a one-year follow-up.

A Welsh multicentre trial of early (fifth day) compared with late (tenth day) mobilisation in 742 patients after uncomplicated myocardial infarction, reported previously, found that there were no significant differences in survival during the first year, but a partial follow up beyond the first year survival showed a significantly reduced survival during the second and third years among patients mobilised early. A full 10 year follow up of all patients admitted to the trial was therefore carried out. A small difference in survival was confirmed, which reached about 5% at four years; but the difference was not statistically significant. Further analysis suggested the possibility of real differences in survival in certain subgroups, but the present evidence was not sufficient to provide contraindication to mobilisation five days after uncomplicated myocardial infarction.

Premature opening of the aortic valve in late diastole has been demonstrated by echocardiography in a patient with severe aortic regurgitation. Valve opening coincided with the end of the diastolic murmur and equalization of aortic and left ventricular diastolic pressures. Echocardiography of the aortic valve in severe aortic reflux may, therefore, provide valuable information about the underlying haemodynamic disturbance.

A patient with a peculiar interatrial block is reported. The electrocardiogram showed a short PR interval and negative P waves in II, III, and aVF, which were preceded, 0-07 s earlier, by another positive P wave present in the right praecordial leads which were absent in the limb leads. From the study with His bundle electrograms, high right atrial electrograms, and bipolar oesophageal electrocardiograms, it could be proved that atrioventricular, His-Purkinje, and right intra-atrial conduction were normal, and that P waves recorded in limb leads represented left atrial depolarization; whereas the ones in the right praecordial leads corresponded to right atrial activation. The vectorial analysis from both P waves and atrial potentials showed that the left atrium was activated in a retrograde fashion, because of an interatrial block. This block was bradycardia dependent and it disappeared in the cycles shorter than 800 ms.

Symptomatic bradycardia-independent atrioventricular block occurred in a patient with right bundle-branch block, left anterior hemiblock, and prolonged HV interval. The arrhythmia, triggered by a spontaneous or induced premature beats, appeared when the post-extrasystolic PP and HH intervals increased to a critical value. Reinitiation of atrioventricular conduction required the presence of ventricular escapes. Bradycardia-dependent atrioventricular block was related to either an enhanced or slightly rising slope of diastolic depolarization, or to a decrease in membrane responsiveness. The patient also, most probably, had tachycardia-dependent atrioventricular block. Both types of conduction disturbance occurred in the same part of the intraventricular conducting system, either in the low His bundle or left bundle-branch or its posteroinferior division. It is suggested that the electrophysiological study of cases with prolonged HV intervals should include procedures which can expose bradycardia-dependent atrioventricular block.

A 41-year-old man presented with dizziness associated with sinus bradycardia and sinus arrest. An attempt to implant a transvenous pacing lead was frustrated by absence of the right superior vena cava. The left superior vena cava persisted and drained via the coronary sinus into the right atrium. Absence of the right superior vena cava may present with symptomatic sinus node dysfunction and may require an epicardial demand pacing system.

Fifty-six patients with symptomatic chronic sinus bradycardia because of sick sinus syndrome (SSS) were followed for periods from one month to 11 years (average 3-2 years). Eleven developed stable atrial fibrillation persisting for 8 to 61 months; 52 had permanent demand pacemakers implanted before atrial fibrillation commenced. In the 11 patients with atrial fibrillation, 10 had adequate ventricular rate, 8 with rates greater than 100 beats/min requiring digoxin for rate control. The 8 patients with atrial fibrillation with pacemakers remained asymptomatic for 13 to 18 months without requiring reimplantation; battery failure occurred in 2 whose rapid ventricular rates were controlled by digoxin. In the other 6 patients with pacemakers who developed atrial fibrillation, adequate ventricular rates persisted resulting in overdrive suppression. No patient had systemic embolisation. The previous duration of symptomatic sinus bradycardia was longer in patients developing atrial fibrillation (average 5-5 years) compared (P less than 0-01) with patients without atrial fibrillation (1-9 years). Further, premature atrial contractions occurred in all 11 patients before atrial fibrillation in contrast to only 21 of the 45 patients without atrial fibrillation. It is concluded that occurrence of atrial fibrillation in SSS with symptomatic sinus bradycardia provides a natural cure of symptoms caused by bradycardia. These data indicate that permanent ventricular pacing may not be necessary if persistent atrial fibrillation develops in SSS.