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Cardiovascular highlights from non-cardiolody journals

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ISCHAEMIC HEART DISEASE

Older people seem at major risk of cognitive dysfunction after CABG: There is a risk of stroke after coronary bypass grafting (CABG), but also a risk of cognitive dysfunction. Newman and colleagues undertook detailed evaluation up to five years and found that over 50% of patients have a decline in cognitive function at discharge, and 24% have a decline at six months. Worryingly, the number rises again to 42% at five years compared to preoperatively. The effect was most dramatic in the over 70s. Part of the observed effect is an age related decline, and part was associated with any operation, but the concern remains that cardiopulmonary bypass and aortic manipulation have long term effects on the brain.

 1 Newman M, Kirchner J, Phillips-Bute B, Gaver V, Grocott H, Jones RH, Mark DB, Reves JG, Blumenthal JA. Longitudinal assessment of neurocognitive function after coronary-artery bypass surgery.

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Women who have had an MI at an early age remain at higher risk for at least two years:Women who have suffered a myocardial infarction (MI) before the age of 60 years do worse than age matched men, despite correction for MI characteristics, complications, risk factors, and co-morbidity. The exact cause is not clear.

 2 Vaccarino V, Krumholz HM, Yarzebski J, Gore JM, Goldberg RJ. Sex differences in 2-year mortality after hospital discharge for myocardial infarction

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Treat cardiogenic shock post-MI with early revascularisation: The SHOCK (should we emergently revascularise occluded coronaries for cardiogenic shock) trial has shown that at one year, early revascularisation leads to a survival benefit over standard care (survival 47%v 34%). Standard treatment included intra-aortic balloon pump (IABP) in 86% and thrombolysis in 63%. Revascularisation was with coronary angioplasty (PTCA) in 55% and CABG in 33%. The benefit was only evident in those less than 75 years old. The American Heart Association/American College of Cardiology guidelines now suggest early revascularisation if cardiogenic shock develops within 36 hours of an MI.

 3 Hochman JS, Sleeper LA, White HD, Dzavik V, Wong SC, Menon V, Webb JG, Steingart R, Picard MH, Menegus MA, Boland J, Sanborn T, Buller CE, Modur S, Forman R, Desvigne-Nickens P, Jacobs AK, Slater JN, LeJemtel TH, for the SHOCK Investigators. One-year survival following early revascularization for cardiogenic shock.

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Exercise (or at least walk faster) if you are diabetic: The nurses health study followed 5125 female nurses with diabetes and asked about their exercise habits. Those performing > 4 hours per week moderate or vigorous exercise had an approximately 40% lower risk for cardiovascular disease. However, only 20% of nurses with diabetes managed even > 1 hour/week exercise. The trends withstood correction for standard risk factors and the fact that regular exercise takers also took hormone replacement therapy more often as well as folate.

 4 Hu FB, Stampfer MJ, Solomon C, Liu S, Colditz GA, Speizer FE, Willett WC, Manson JE. Physical activity and risk for cardiovascular events in diabetic women.

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Use DNA analysis and cholesterol measurement to pick up all the familial hypercholesterolaemics coming to the lipid clinic: Population screening for a familial disorder is especially worthwhile if a treatment, such as statin therapy in familial hypercholesterolaemia (FH), is available. This study used an elevated cholesterol (greater than the age and sex specific 90th centile for the population) as a cut off to diagnose FH in relatives of patients with the disorder. This gave 18% false positives (not FH) and 18% false negatives (FH missed). Use of lipid lowering treatment increased from a third before screening to > 90% in these relatives.

 5 Umans-Eckenhausen MAW, Defesche JC, Sijbrands EJG, Scheerder RLJM, Kastelein JJP. Review of first 5 years of screening for familial hypercholesterolaemia in the Netherlands.

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HYPERTENSION

Vitamin C lowers blood pressure, but the endothelium is not made normal in hypertensive patients: Vitamin C, perhaps acting as an antioxidant on resistance vessels, seems to lower blood pressure. This study of 500 mg/day vitamin C for one month confirmed blood pressure reduction (about 10 mm Hg mean pressure), but showed no improvement in arterial endothelial function measured non-invasively.

 1 Duffy SJ, Gokce N, Holbrook M, Hunter LM, Biegelsen ES, Huang A, Keaney JF, Vita JA. Effect of ascorbic acid treatment on conduit vessel endothelial dysfunction in patients with hypertension.

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GENERAL CARDIOLOGY

What is the best blood thinning for non-rheumatic AF? Warfarin produces a 68% reduction and aspirin a 28% reduction in non-fatal stroke in patients with atrial fibrillation (AF) not caused by rheumatic heart disease when compared to placebo. This systematic review assessed five trials directly comparing the two treatments. It casts doubt on how much better warfarin really is in reducing non-fatal and fatal events. The authors point out, however, that the absence of a significant benefit does not rule out a real difference between treatments. The result must be regarded with caution and a very large trial is needed.

 1 Taylor FC, Cohen H, Ebrahim S. Systematic review of long term anticoagulation or antiplatelet treatment in patients with non-rheumatic atrial fibrillation.

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Large plaques in the descending aorta may predispose to stroke and peripheral embolism: Tenenbaum and associates found large, mobile plaques in the thoracic aorta on transoesophageal echocardiography in patients with cerebral and peripheral emboli. They suggest that these may actually be the source of the emboli rather than just a marker of severe atherosclerosis.

 2 Tenenbaum A, Motro M, Feinberg MS, Schwammenthal E, Stroh CI, Vered Z, Fisman EZ. Retrograde flow in the thoracic aorta in patients with systemic emboli: a transesophageal echocardiographic evaluation of mobile plaque motion

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Even a 3 cm left ventricular wall thickness does not necessarily indicate a bad prognosis in HOCM: Last year, Spirito and colleagues suggested that having severe left ventricular hypertrophy (LVH) alone was enough to predict poor outcome in hypertrophic obstructive cardiomyopathy (HOCM), and raised the possibility of a dramatic increase in the use of implantable defibrillators. Now Eliot and associates have shown that although LVH is a marker of risk, it has a poor predictive value when used alone. It is, however, possible to say that if a patient has HOCM but no family history of sudden death, a normal exercise test, no serious rhythm problems on a Holter, and the LVH is not severe, they have a good prognosis.

 3 Spirito P, Bellone P, Harris KM, Bernabo P, Bruzzi P, Maron BJ. Magnitude of left ventricular hypertrophy and risk of sudden death in hypertrophic cardiomyopathy.

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  4 Elliott PM, Gimeno Blanes GR, Mahon NG, Poloniecki JD, McKenna WJ. Relation between severity of left-ventricular hypertrophy and prognosis in patients with hypertrophic cardiomyopathy.

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“Breathe that insulin in”: Although cardiologists do not often initiate novel diabetic treatments, Skyler and colleagues may have helped the quality of life of many a person with insulin-dependent diabetes by reducing the number of injections they have to take. A once daily injection of long acting insulin and three preprandial insulin inhalations gave as good control as two or three injections of insulin. This is only a very preliminary assessment, however.

 5 Skyler JS, Cefalu WT, Kourides IA, Landschulz WH, Balagtas CC, Cheng S-L, Gelfand RA, for The Inhaled Insulin Phase II Study Group. Efficacy of inhaled human insulin in type 1 diabetes mellitus: a randomised proof-of-concept study.

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BASIC RESEARCH

Mouse models of platelet dysfunction suggest another possible antiplatelet treatment:Angelillio and colleagues have studied mice deficient in a little known vitamin K dependent protein Gas6produced by platelets. Mice deficient inGas6 did not bleed more, but were less likely to get thrombosis. In addition, treatment with antibodies toGas6 protected against fatal thromboembolism without causing bleeding. This finding may lead on to another generation of antiplatelet agents.

 1 Angelillo-Scherrer A, de Frutos PG, Aparicio C, Melis E, Savi P, Lupu F, Arnout J, Dewerchin M, Hoylaerts MF, Herbert J-M, Collen D, Dahlbäck B, Carmeliet P. Deficiency or inhibition of Gas6 causes platelet dysfunction and protects mice against thrombosis.

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Footnotes

  • Journals scanned—American Journal of Medicine; American Journal of Physiology: Heart and Circulatory Physiology; Annals of Emergency Medicine; Annals of Thoracic Surgery; Annals of Internal Medicine; Archives of Internal Medicine; BMJ; Canadian Medical Association Journal; Chest; European Journal of Cardiothoracic Surgery; Lancet; JAMA; Journal of Clinical Investigation; Journal of Diabetes and its Complications; Journal of Immunology; Journal of Thoracic and Cardiovascular Surgery; Nature Medicine; New England Journal of Medicine; Pharmacoeconomics; Thorax.

    Reviewers—C Baker, E Barnes, V Bhatia, R Desilva, M Earley, K Fox, D Gorog, G Jenkins, R Kaprilian, A Kapur, M Khan, P Lambiese, V Markides, M Poullis, P Ramrakha, J Strange, B Wasan, H Walker.

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