AUStralian Indigenous Chronic Disease Optimisation Study (AUSI-CDS) prospective observational cohort study to determine if an established chronic disease health care model can be used to deliver better heart failure care among remote Indigenous Australians: Proof of concept-study rationale and protocol.

BACKGROUND: The congestive heart failure syndrome has increased to epidemic proportions and is cause for significant morbidity and mortality. Indigenous patients suffer a greater prevalence with greater severity. Upon diagnosis patients require regular follow-up with medical and allied health services. Patients are prescribed life saving, disease modifying and symptom relieving therapies. This can be an overwhelming experience for patients. To compound this, remoteness, differentials in conventional health care and services pose special problems for Indigenous clients in accessing care. Additional barriers of language, culture, socio-economic disadvantage, negative attitudes towards establishment, social stereotyping, stigma and discrimination act as barriers to improved care. Recent focus supported by clinical evidence support the role of chronic disease self-management programs. A patient focused, problem identification, goal setting and psychosocial modification based program should in principal highlight these issues and help tailor a patient focused comprehensive care plan to complement guideline based care. At present there are no Indigenous focused chronic disease self-management programs. There is a need for research on ways to provide chronic disease management to this group. We therefore designed a study to assess a model of patient focussed comprehensive care for Indigenous Australians with heart failure. STUDY DESIGN: AUSI-CDS is a prospective, cohort, observational study to evaluate the efficacy of the standard "Flinders Program of Chronic Condition Management" for Indigenous patients with chronic heart failure. Eligible patients will be Indigenous, suffering from chronic heart failure, in the Northern Territory. The primary end-point is the satisfaction score based on the PACIC. The study will recruit 20 patients and is expected to last 12 months. SUMMARY: The rationale and design of the AUSI-CDS using the Flinders Model is described.

Prediction of right ventricular and posterior wall ST elevation by coronary care nurses: the 12-lead electrocardiograph versus the 18-lead electrocardiograph.

OBJECTIVES: To determine the value of routine versus selective use of the 18-lead electrocardiogram in determining the size of an acute inferior myocardial infarction (MI). DESIGN: Prospective, quasi-experimental, random assignment. SETTING: The coronary care unit (CCU) of a major teaching hospital in South Australia. PATIENTS: Fifty-two patients admitted to the CCU with acute evolving inferior MI. OUTCOME MEASURES: Correlation and comparison of the predictions of the right ventricular (RV) and posterior wall (PW) lead ST elevation with prospectively chosen markers on the 12-lead electrocardiogram--ST elevation in lead III > II and precordial ST depression, and the predictions by coronary care nurses. PROCEDURE: The results of 18-lead electrocardiograms of 52 consecutive patients admitted to the CCU with acute evolving inferior MI were classified according to prospectively chosen criteria. Coronary care nurses were randomly assigned four 12-lead electrocardiograms and asked to "blindly" predict ST elevation in the concurrent RV and PW leads. RESULTS: ST elevation in lead III > II demonstrated a sensitivity and positive predictive accuracy of 86% to 1 mm of ST elevation in the RV leads. ST depression in V1, V2, and V3 similarly demonstrated a 75% sensitivity and 89% positive predictive accuracy to 1 mm of ST elevation in the PW leads. In comparison, coronary care nurses proved to be as accurate in their predictions of additional PW ST elevation (p = 0.73), but were significantly less able to predict RV ST elevation (p = 0.049). These predictions were independent of the level of experience and qualifications. CONCLUSIONS: Discriminating between smaller and larger types of inferior MIs has the potential to alter patient management: Thirty-two percent of patients in the study demonstrated additional ST elevation in both the RV and PW leads. Both of the 12-lead electrocardiogram markers used in this study proved reasonably accurate in predicting additional ST elevation in the leads that normally comprise the 18-lead electrocardiogram. Recognition of these markers has the potential to expedite the need for the additional 18-lead electrocardiogram when rapid assessment of infarction size is required. However, the routine use of the 18-lead electrocardiogram is supported by this study.

Streptokinase-induced transient aggravation of myocardial injury.

We examined the relationship between streptokinase infusion, intensity of myocardial injury and systemic hypotension in patients receiving streptokinase for treatment of evolving acute myocardial infarction. Twenty consecutive patients treated with streptokinase for evolving acute myocardial infarction received continuous blood pressure and S-T segment monitoring of the 12 lead electrocardiogram (ECG) for at least 5 h, commencing prior to commencement of the streptokinase infusion. Aggravation of injury, manifested both by episodic increases in S-T segment elevation on the electrocardiogram (ECG) (P < 0.001), and in mean S-T segment elevation (P < 0.05) occurred within the first 20 min after initiation of streptokinase infusion. Hypotension also occurred transiently in most patients, with a mean minimum systolic blood pressure of 92 +/- 22 (S.D.) mmHg occurring 16 +/- 5 min after commencement of streptokinase. There was no correlation between the extent of aggravation of injury and that of hypotension. All patients showed ECG evidence of reperfusion, with a reduction of S-T elevation in the reference lead to 50% of maximal value, after a median of 62 min (range 9-174 min). It is concluded that streptokinase aggravates injury prior to reperfusion, although probably not via the induction of hypotension: It is possible that this effect contributes to the 'early hazard' of thrombolytic therapy.