Searches / Australian And New Zealand Journal Of Medicine[JOURNAL]

Australian And New Zealand Journal Of Medicine[JOURNAL]

Sun 200 papers
RSS

Mechanical circulatory support devices in the treatment of heart failure.

Knight JL

Aust N Z J Med · 1999 Jun · PMID 10868513 · Publisher ↗

With an increasingly aging population, heart failure is a major health issue, affecting more than 10% of the population over 65 years of age, and costing hundreds of millions of dollars per year for ongoing care. Even wi... With an increasingly aging population, heart failure is a major health issue, affecting more than 10% of the population over 65 years of age, and costing hundreds of millions of dollars per year for ongoing care. Even with maximal medical therapy, annual mortality rates of in excess of 25% are commonly reported. Over the last three decades, various surgical approaches have been examined in the hope of improving the outcome of congestive cardiac failure. These procedures range from simple coronary revascularisation to left ventricular reduction surgery and cardiac transplantation. Although of value in selected situations, no surgical approach, beyond transplantation, has had significant impact on the outcome of heart failure. In the last decade, development in the area of mechanical support for the failing heart has continued to expand at a rapid rate. Strong evidence now exists to show that in many patients with advanced heart failure, prolonged mechanical support results in significant myocardial recovery. There are currently several mechanical support devices available for clinical use, although most are considered experimental in this country. These devices are expensive and are not without significant complications, but early results of their use as either a bridge to transplantation or as a stand alone treatment, have been very encouraging. Currently available mechanical assist devices are described, with discussion of indications for implantation, complications and results of their use.

Animal models of heart failure.

Arnolda LF, Llewellyn-Smith IJ, Minson JB

Aust N Z J Med · 1999 Jun · PMID 10868512 · Publisher ↗

Animal models of heart failure present homogenous groups of animals all with heart failure produced by a well defined lesion at a particular stage of evolution, in contrast to humans, who present with heart failure of un... Animal models of heart failure present homogenous groups of animals all with heart failure produced by a well defined lesion at a particular stage of evolution, in contrast to humans, who present with heart failure of uncertain duration from a wide variety of causes and with marked variation in age and pre-morbid health and fitness. Animal models of heart failure provide diseased groups of animals in which experimental procedures, not possible in humans, can be evaluated and in which new treatments can be tested before their safety is established in humans. An ideal model should have a common human counterpart and should closely mimic heart failure in humans. Thus the haemodynamic changes should include increased cardiac filling pressures and low cardiac output. There should be evidence of activation of the sympathetic nervous system and increased secretion of hormones such as renin, angiotensin, aldosterone, vasopressin, atrial natriuretic factor and endothelin. The clinical features of the human syndrome such as cardiomegaly, lung and peripheral oedema and decreased exercise tolerance should be present. Lastly, the model should be inexpensive and technically simple to produce and study. This paper reviews some commonly used models of heart failure in relation to the criteria listed above. There is no perfect animal model of heart failure and in practice one should match the model to the purpose of the study.

Large animal models of heart failure.

Power JM, Tonkin AM

Aust N Z J Med · 1999 Jun · PMID 10868511 · Publisher ↗

Congestive heart failure (HF) is a major focus of medical research. Its incidence has greatly increased in recent decades because of an aging population base and the increasingly successful treatment of other forms of ch... Congestive heart failure (HF) is a major focus of medical research. Its incidence has greatly increased in recent decades because of an aging population base and the increasingly successful treatment of other forms of chronic cardiac disease. Relevant large animal models of HF should reflect the complex interactions of cardiac dysfunction, neurohumoral dynamics and peripheral vascular abnormalities found in human HF. A number of large animal models have been developed, especially in dogs, sheep and swine, using naturally occurring HF, or single or combinations of interventions, as instruments to trigger the development of HF. Naturally occurring HF models are not commonly used because of ethical or perceived ethical grounds, however, King Charles Cavalier Spaniel and Yucatan Mini Pig models have been described. Tachycardia induced HF is the most commonly used HF model. Ventricular pacing at 220-240 bpm results in profound low output, biventricular, oedematous failure in two to three weeks. Lower pacing rates result in a more stable, sustainable, lesser degree of failure. Positive features of this model include 'acceptance', aetiological relevance to patient tachycardia induced HF, neurohumoral and functional profile similar to most human HF, relatively low cost simple preparation, ability to manipulate the degree of failure with pacing rate, reversibility, reliability and a large amount of published multi species data. Limitations to the use of the model are the rapid onset, the fact that reversibility is only relevant to the tachycardia induced patient HF, the absence of hypertrophy in failure, the diminished plasma atrial natriuretic peptide (ANP) levels, absence of ANP of ventricular origin, and the interference between rapid pacing and therapeutic interventions. Myocardial damage models of HF include those models induced by ischaemia, eg due to coronary occlusion (ligation or aneroid) or intracoronary microembolism, transmyocardial DC shock, toxic cardiomyopathy from adriamycin, doxorubicin or catecholamines. Overload models of HF may be induced by high pressure from aortic constriction, aortic regurgitation, renal artery constriction, pulmonary stenosis or aortocaval shunts, or by induction of mitral regurgitation from chordae or leaflet damage. No single, all-encompassing, large animal model of HF exists to date. Selection of the type of model to be used should be based primarily on the hypotheses to be tested and secondarily on the available resources and facilities.

Arsenic trioxide treatment of relapsed acute promyelocytic leukaemia: initial Australian experience.

Spencer A, Firkin F

Aust N Z J Med · 1999 Jun · PMID 10868510 · Publisher ↗

Abstract loading — click title to view on PubMed.

Haemolytic uraemic syndrome and prostatic cancer.

Perkovic V, Came NA, Grigg AP … +1 more , Becker GJ

Aust N Z J Med · 1999 Jun · PMID 10868509 · Publisher ↗

Abstract loading — click title to view on PubMed.

Herpes simplex encephalitis in multiple myeloma.

Chim CS, Ho PL, Yuen KY … +1 more , Pieres JS

Aust N Z J Med · 1999 Jun · PMID 10868508 · Publisher ↗

Abstract loading — click title to view on PubMed.

Hyperemesis gravidarum, transient hyperthyroxinaemia and primary hyperparathyroidism in a Chinese woman.

Li JK, Yeung VT, Chow CC … +3 more , Ko GT, Lau TK, Cockram CS

Aust N Z J Med · 1999 Jun · PMID 10868507 · Publisher ↗

Abstract loading — click title to view on PubMed.

Delayed diagnosis of recurrent visceral angio-oedema secondary to ACE inhibitor therapy.

Jardine DL, Anderson JC, McClintock AD

Aust N Z J Med · 1999 Jun · PMID 10868506 · Publisher ↗

Abstract loading — click title to view on PubMed.

Focal necrotising vasculitis with secondary myositis following fluoxetine administration.

Fisher A, McLean AJ, Purcell P … +3 more , Herdson PB, Dahlstrom JE, Le Couteur DG

Aust N Z J Med · 1999 Jun · PMID 10868505 · Publisher ↗

Abstract loading — click title to view on PubMed.

Vegebilia'--a late complication of endoscopic sphincterotomy.

Hashimi H, Stewart AL

Aust N Z J Med · 1999 Jun · PMID 10868504 · Publisher ↗

Abstract loading — click title to view on PubMed.

Cardiac toxicity associated with ciguatera poisoning.

Miller RM, Pavia S, Keary P

Aust N Z J Med · 1999 Jun · PMID 10868503 · Publisher ↗

Abstract loading — click title to view on PubMed.

Olanzapine: extrapyramidal side effects in the elderly.

Granger AS, Hanger HC

Aust N Z J Med · 1999 Jun · PMID 10868502 · Publisher ↗

Abstract loading — click title to view on PubMed.

Sudden cardiac death in familial hypertrophic cardiomyopathy: an Australian experience.

Semsarian C, Richmond DR

Aust N Z J Med · 1999 Jun · PMID 10868501 · Publisher ↗

Abstract loading — click title to view on PubMed.

A review of isoniazid-related hepatotoxicity during chemoprophylaxis.

Stuart RL, Grayson ML

Aust N Z J Med · 1999 Jun · PMID 10868500 · Publisher ↗

Abstract loading — click title to view on PubMed.

The insulin-like growth factor system: basic and clinical aspects.

Bach LA

Aust N Z J Med · 1999 Jun · PMID 10868499 · Publisher ↗

Abstract loading — click title to view on PubMed.

Problem-based learning: process and practice.

Johnson SM, Finucane PM, Prideaux DJ

Aust N Z J Med · 1999 Jun · PMID 10868498 · Publisher ↗

Abstract loading — click title to view on PubMed.

Growth hormone deficiency in adults: to treat or not to treat.

Hoffman DM, Ho KK

Aust N Z J Med · 1999 Jun · PMID 10868497 · Publisher ↗

Abstract loading — click title to view on PubMed.

Comparison of the long-term efficacy of implantable defibrillators and sotalol for documented spontaneous sustained ventricular tachyarrhythmias secondary to coronary artery disease.

Kovoor P, Yung A, Byth K … +4 more , Eipper VE, Uther JB, Cooper MJ, Ross DL

Aust N Z J Med · 1999 Jun · PMID 10868496 · Publisher ↗

BACKGROUND: The relative efficacy of antitachycardia pacing implantable cardioverter defibrillators (ATPICD) and sotalol in the treatment of ventricular tachyarrhythmias is controversial. AIM: To compare the mortality in... BACKGROUND: The relative efficacy of antitachycardia pacing implantable cardioverter defibrillators (ATPICD) and sotalol in the treatment of ventricular tachyarrhythmias is controversial. AIM: To compare the mortality in patients treated with ATPICD and sotalol for documented spontaneous sustained ventricular tachyarrhythmias occurring late after previous myocardial infarction. METHODS: In this non-randomised retrospective study of 139 consecutive patients all patients had inducible ventricular tachycardia at baseline electrophysiological studies. Before the availability of ATPICD, 22 patients were treated with sotalol as part of a randomised study comparing the efficacy of sotalol to amiodarone. After ATPICD became available sotalol was used in 49 patients in whom intravenous testing predicted sotalol to be effective and ATPICD were implanted in 68 patients in whom sotalol was predicted to be ineffective at electrophysiological testing. Thus, 68 patients were treated with an ATPICD and 71 with sotalol. RESULTS: The two groups were well-matched for age, type of presenting arrhythmia, severity of coronary artery disease and ventricular function. At 36 months Kaplan-Meier estimates of mortality from ventricular tachyarrhythmia were 0% with ATPICD and 15% with sotalol (p=0.03). Kaplan-Meier estimates of total mortality at 36 months were 12% with ATPICD and 25% with sotalol (p=0.09). Multivariate analysis showed hazard ratio of 7.9 (p=0.06) for death from ventricular tachyarrhythmia in patients treated with sotalol compared to ATPICD. CONCLUSIONS: While no difference in total mortality was demonstrated, treatment with ATPICD is probably superior to sotalol for preventing deaths due to ventricular tachyarrhythmia.

Opinion of New Zealand physicians on management of acute ischaemic stroke: results of a national survey.

Ardern-Holmes SL, Raman R, Anderson NE … +2 more , Charleston AJ, Bennett P

Aust N Z J Med · 1999 Jun · PMID 10868495 · Publisher ↗

BACKGROUND: Randomised trials have evaluated various treatments for acute ischaemic stroke, but it is unclear how the results of these studies are used in everyday practice. AIMS: To obtain the opinions of physicians on... BACKGROUND: Randomised trials have evaluated various treatments for acute ischaemic stroke, but it is unclear how the results of these studies are used in everyday practice. AIMS: To obtain the opinions of physicians on the management of acute ischaemic stroke. METHODS: A questionnaire was sent to 368 New Zealand Fellows of the Royal Australasian College of Physicians. The survey included questions about the availability of hospital services for stroke patients, management of acute ischaemic stroke and opinion on the efficacy of treatments used in acute ischaemic stroke. RESULTS: Of the 293 physicians who responded to the questionnaire, 171 managed patients in the first week after stroke. Forty-seven per cent of these physicians were general physicians. Ninety-five per cent usually managed these patients in a general medical ward. Only five physicians admitted patients to an acute stroke unit and only 57% considered acute stroke units were beneficial. Aspirin was usually or sometimes used for patients with acute ischaemic stroke by 92% of physicians, intravenous heparin by 43%, low-dose subcutaneous heparin by 41%, low-molecular-weight heparin by 25% and tissue-plasminogen activator (t-PA) by 3%. Two thirds considered that aspirin was definitely beneficial, but most were uncertain about the efficacy of intravenous heparin, low-dose subcutaneous heparin, low-molecular-weight heparin and t-PA. Sixty-two per cent were prepared to begin aspirin and 21% subcutaneous heparin before computerised tomography (CT). Twenty-three per cent used anti-hypertensive treatment in the first few hours after an ischaemic stroke. CONCLUSIONS: Several common deficiencies in the management of acute ischaemic stroke were identified. The widespread lack of stroke units, use of aspirin and heparin before CT, and lowering of blood pressure after an acute ischaemic stroke differed from accepted guidelines. Many physicians used heparin despite lack of evidence from randomised trials that it is beneficial. The development of stroke units and the appointment of physicians with a special interest in the management of stroke may improve the management of patients with acute stroke.

Cerebrovascular disease as a general medicine discharge diagnosis: assessment of diagnostic agreement on case note review.

Lunt H, Beard ME, Wilson MA … +2 more , Kendall D, Frampton CM

Aust N Z J Med · 1999 Jun · PMID 10868494 · Publisher ↗

BACKGROUND: Accurate clerical coding of discharge diagnoses is important partly because results may be used to derive a recommended costing for hospital length of stays (LOS). Some authors think that discharge coding und... BACKGROUND: Accurate clerical coding of discharge diagnoses is important partly because results may be used to derive a recommended costing for hospital length of stays (LOS). Some authors think that discharge coding undertaken by clinicians will result in less diagnostic misclassification than clerical coding. This presupposes a high degree of between-observer diagnostic agreement between clinicians. AIMS: To compare discharge coding undertaken by two general physicians, for patients receiving a clerical discharge code of cerebrovascular disease. The recommended LOS was then calculated from each observer's discharge codes using the Physicians Diagnosis Related Group Working Guidebook. RESULTS: Eighty-two cases were coded as stroke by the clerical coder. Both medical coders agreed with this diagnosis in 68 (83%) of these cases. The corresponding figure for cases coded by the clerical coder as transient cerebral ischaemia was 47% (32/68) agreement between all three observers. Correcting for chance agreement between medical observers using the kappa statistic, a value of 0.64 was obtained for the combined stroke and transient cerebral ischaemia discharges, suggesting moderate diagnostic agreement. Using the clerical coder's results, the mean recommended LOS for all cases of cerebrovascular disease over the study period was calculated at 6.68 days. The corresponding values for the two medical coders were 6.68 days and 6.75 days. CONCLUSIONS: Diagnostic agreement between clinicians was moderate. Consideration of alternative diagnostic possibilities and the difficulty in determining the duration of neurological deficit were the main reasons for diagnostic disagreement. The mean recommended LOS was similar, however, when comparing results from all three observers.
← Prev Page 7 of 10 Next →

About

Frequency
Sun
Papers found
200
RSS feed
Subscribe