Wiley

Background: Conventional methods of quantifying heart rate variability using summary statistics have shown that decreased variability is associated with increased mortality in heart failure. However, many patients with heart failure have arrhythmias which make the ‘raw’ heart rate variability data less suitable for the use of summary statistical measures.

Aims: To examine the clinical potential of a new measure of heart rate variability data, presented by the Poincare plot pattern, as an adjunct to the summary statistical measures of R‐R interval

Methods: We used the Poincaré plot pattern to display beat‐to‐beat heart rate variability data from a group of 23 patients with heart failure and compared them with data collected from 20 healthy age‐matched control subjects. The data, which consisted of 2000 consecutive R‐R intervals, were gathered over 20–40 minutes while the subjects rested supine in a quiet darkened room.

Results: The morphological classification scheme proposed reflected the functional status of patients in heart failure. There was a significant difference (chi‐square = 27.5, df = 6, ρ < 0.0001) in the different pattern types between patients with NYHA Class I and II compared to patients with NYHA Class III and IV. All healthy subjects displayed a ‘cluster’ type of pattern characterised by normally distributed data. Sixteen of the 23 patients in heart failure also produced data which were normally distributed but the remaining seven produced data which required careful filtering to make them suitable for analysis using summary statistics, but which could be analysed by the Poincare plot.

Conclusions: The Poincaréot pattern is a semi‐quantitative tool which can be applied to the analysis of R‐R interval data. It has potential advantages in that it allows assessment of data which are grossly non‐Gaussian in distribution, and is a simple and easily implemented method which can be used in a clinical setting to augment the standard electrocardiogram to provide ‘real time’ visualisation of data.

Background: Sub‐optimal use of prescribed medication is often associated with unplanned hospitalisation among the chronically ill.

Aims: To examine the extent of sub‐optimal use of prescribed medication in a ‘high risk’ patient cohort recently discharged from acute hospital care.

Methods: Chronically ill patients discharged from acute hospital care (n=342) were studied. At one week post discharge a home visit was performed by a nurse and a pharmacist during which medication management (including compliance and medication—related knowledge) was assessed.

Results: During the majority of home visits at least one medication‐related problem was detected: approximately half of the cohort subject to a ‘reliable’ pill‐count were found to be mal‐compliant and almost all demonstrated inadequate medication‐related knowledge. Mal‐compliance was correlated with ≥ five prescribed medications (Odds ratio [OR] 2.6: p <0.002). Comparatively, lower medication‐related knowledge was correlated with age >75 years (OR 2.2: p <0.001), exacerbation of a pre‐existing chronic illness (OR 2.7: p=0.044) and six years formal education (OR 1.9: p≥0.004). Neither were modulated by extent of in‐hospital counselling. Other previously unknown problems detected during the home visit included hoarding of previously prescribed medication (35%) and reducing medication intake to minimise costs (21%).

Conclusions: Management of prescribed medications among chronically ill patients recently discharged from acute hospital care is often sub‐optimal. Assessment of medication management in the home provides an invaluable opportunity to detect and address problems likely to result in poorer health outcomes.

The Sydney AIDS Project is a prospective immunoepidemiological study of 996 homosexual/bisexual men enrolled between February 1984 and January 1985. By January 1987, 32 of 386 homosexual men who were seropositive at enrolment in the study had developed AIDS, yielding a crude progression rate of between 2.8% and 4.2% per annum. Of these subjects, 23 (72%) developed AIDS within 12 months of enrolment.

In univariate analysis, the only lifestyle differences between seropositive subjects who progressed to AIDS and those that did not progress were less frequent oral sex activity and more use of marijuana in the three months prior to enrolment. In multivariate analysis, seropositive subjects who progressed to AIDS were more likely to have a lower percentage of CD4+ cells, a higher percentage of CD8+ cells and to have used marijuana in the three months prior to enrolment than the seropositive subjects who did not progress. No HIV seropositive subject who was asymptomatic and had normal T‐cell subsets at enrolment had developed AIDS by January 1987. Persistent generalised lymphadenopathy was not associated with progression to AIDS.

Although there are a number of lifestyle factors that may be associated with HIV infection, this study did not implicate most of these in the progression of HIV seropositive subjects to end‐stage AIDS. We conclude that antecedent changes in T‐cell subsets are associated with progression to AIDS and we emphasise the prognostic value of enumeration of T‐cell subsets in HIV seropositive persons. (Aust NZ J Med 1988; 18: 8–15).

We studied 925 consecutive patients hospitalised with acute stroke to determine how stroke type, age, gender and risk factors influence acute, in‐hospital outcome. Stroke types included carotid territory cortical or large subcortical infarction (52%), vertebrobasilar infarction (12%), lacunar infarction (11%), intracerebral haemorrhage (16%), and subarachnoid haemorrhage (9%). Mean age (mean ± 1 SD) was 66 ± 15 years, but patients with cerebral infarction were older than those with cerebral haemorrhage. The prevalence of hypertension, diabetes mellitus and cardiac disease increased with age across all stroke types, while the prevalence of smoking decreased with age. Mortality was 19% overall, but varied significantly between stroke types, highest in intracerebral haemorrhage (34%), and lowest in lacunar infarction (1%). Age had a marked adverse effect on mortality, independent of stroke type, the probability of death increasing by 3 ± 0.5% per year from 20–92 years, whereas gender had no effect. Cardiac disease and diabetes were independent adverse prognostic factors (Odds Ratios 1.6 and 1.5 respectively). Cerebral haemorrhage, age, cardiac disease and diabetes all independently worsen acute stroke outcome. (Aust NZ J Med 1992; 22: 30–35.)

Lipoprotein(a) is an independent risk factor for cardiovascular disease. Lipoprotein(a) levels were measured in 196 patients (103 Male [M]: 93 Female [F]) with chronic renal diseases and in 116 controls. Median levels of Lipoprotein(a) [Lp(a)] were found to be significantly elevated in patients with untreated chronic renal disease (285, 285 mg/L; M, F; range 30–1675 mg/L) and in those treated with continuous ambulatory peritoneal dialysis (320, 603; M, F; range 50–1450) compared with controls (70, 51; M, F; range 1–750; p<0.01 Males, p<0.001 Females). Lp(a) levels in patients treated by haemodialysis (133, 35; M, F; range 5–685) and renal transplantation (100, 95; MJF; range 10–1700) were not significantly different from controls. Lipoprotein(a) levels correlated inversely with serum albumin in the combined dialysis group (r= ‐034, p < 0.001), and with urinary protein loss in the combined transplant and chronic renal diseases groups (r = 0.29, p <0.01). This correlation of Lp(a) with protein metabolism suggests a similarity with changes in other apolipoprotein‐B containing lipoproteins in nephrosis. These findings may be relevant to the increased risk of atherosclerosis in patients with chronic renal disease and to their optimum mode of renal replacement therapy. (Aust NZ J Med 1992; 22:243–248.)

Abstract Sixty‐four patients with chronic bronchitis with a history of recurrent respiratory tract infections were admitted to a double‐blind randomised controlled study in which the efficacy of an oral vaccine containing killed Haemophilus influenzae in preventing acute exacerbations of chronic bronchitis was compared with placebo. Patients given vaccine developed fewer acute infective episodes. Although the numbers of patients who required antibiotic therapy in the two groups were not significantly different, the number of antibiotic prescriptions given to the vaccinated group of patients was significantly less than that required by the control group. A reduction in colonisation with Haemophilus influenzae occurred in the active group, which was maximal 14 weeks after the onset of the study. (Aust NZ J Med 1991; 21: 427–432.)

Abstract: The influence of the xanthine derivative pentoxifylline (‘Trental’ or BL191; Hoechst–Roussel) on exercise tolerance was measured in 38 subjects with stable, severe to moderately severe, intermittent claudication who completed a randomised, double–blind, placebo controlled, cross–over clinical trial. Patients received placebo tablets or 400 mg slow–release pentoxifylline tablets (‘Trental 400’) twice a day for one week, followed by three times daily for seven weeks, and then crossed over to receive the alternate preparation for another eight weeks.

Claudication distance and walking distance were measured on a treadmill before starting treatment and again at four–week intervals during the trial. At the same times, red blood cell filterability, plasma fibrinogen concentration and blood viscosity, resting and post–ischemic calf muscle blood flow, and the resting and post–exercise ankle/brachial systolic pressure ratio were also measured.

In this study, the observed effects of pentoxifylline treatment were no greater than those of placebo, even though serum levels of pentoxifylline and its hydroxy–metabolite were within the anticipated range. This was shown by a ‘therapeutic effect ratio’ of 0.98 for treadmill claudication distance and 0.96 for treadmill walking distance after within–patient analysis at the end of the cross–over (where a ratio of 1.0 means the test drug and placebo effects are identical). These ratios have 95% confidence limits of 0.72–1.34 and 0.74–1.25, respectively.

Abstract Allergic bronchopulmonary fungal disease (ABPFD) usually manifests in asthmatics as allergic bronchopulmonary aspergillosis. In a few instances other fungi have been implicated. Serological testing in Western Australia between 1979 and 1986 revealed precipitins to Bipolaris and Curvularia species in 40 of 503 patients tested. Eight of these were patients with ABPFD due to Bipolaris and/or Curvularia and are reported here.

Geographical location appeared to be significant as seven of eight of those with ABPFD (and at least 18 of 40 with positive serology) were living in the more remote and sub‐tropical northern part of the state.

ABPFD due to fungi other than Aspergillus species may be more common than previously recognised and further epidemiological assessment is warranted. (Aust NZ J Med 1991; 21: 871–874.)

Summary: The aetiology of the sudden infant death syndrome: Current ideas on breathing and sleep and possible links to deranged thiamine Neurochemistry.

The sudden infant death syndrome (SIDS) is now the commonest cause of death between one week and one year of age in most western countries. An asphyxia/ death, with unrecognised hypoxic episodes during sleep in the preceding weeks, has been postulated from autopsy evidence for both acute and chronic hypoxia; the evidence includes Po₂ values, intra‐thoracic distribution of petechiae, pulmonary arteriolar and right ventricular hypertrophy. Long‐term monitoring of infants resuscitated from a “near miss” SIDS demonstrates sleep apnoea, sometimes associated with episodic collapse and obstruction of the upper airway.

Physiological studies in healthy babies and animals highlight factors leading to vulnerability to asphyxia in different phases of sleep. In REM‐sleep (rapid‐eye‐movement), inhibition of intercostal muscle activity leads to: inspiratory collapse of the rib‐cage, impaired reflex compensation for airway obstruction, overall lung‐deflation with reduction of O₂‐stores and rapid hypoxaemia during apnoea. In REM‐sleep, breathing efforts are not augmented by hypercapnia and the defense against asphyxia depends on reflex responses to hypoxia.

Sleep apnoea sometimes occurs in infants with a rare congenital defect of brain thiamine triphosphate. This draws attention to many similarities of modern SIDS and other infantile syndromes reported historically which involve deranged thiamine neurochemistry. Sudden unexpected deaths occur in apparently thriving infants of asymptomatic thiamine deficient mothers. Other similarities include: a peak incidence at 2–4 months of age; precipitation often by minor febrile episodes; seasonal and familial risk factors, with increased risk in twins; many common findings at autopsy.

Although asymptomatic maternal thiamine deficiency is common in western communities ingesting high carbohydrate diets containing various thiamine antagonists, the effect on infant thiamine stores has received little attention.

Future research is needed to evaluate SIDS incidence after identification and elimination of low thiamine states. Defective neural control of breathing during sleep should be evaluated in relation to thiamine‐neurochemistry, particularly to the leaky blood‐brain barrier, to glutamate and GAB A, to sympathetic denervation and to defective vagal reflexes of the lungs and larynx.

Neurological manifestations of unknown cause occurring in patients who become or are HIV antibody positive with presumed normal immune function have been described recently. This report adds a further six cases, all of whom had normal CD4 + cell counts either throughout the period of observation or after the episode of seroconyersion. Three had an acute presentation, two in the context of documented seroconversion consisting of one of the following: an encephalitis, an ataxia, and confusion with neuralgic amyotrophy. Three had a subacute disorder occurring at a later phase of HIV infection but before opportunistic infections or neoplasms, and marked by a static mild cognitive deficit. This report extends the range of abnormalities that may be seen at seroconversion and documents the presence of a non‐progressive cognitive deficit occurring in the latent phase of HIV infection.