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Tel Aviv, Israel

Webster M.W.I.,Green City
Current Opinion in Cardiology | Year: 2011

PURPOSE OF REVIEW: Diabetes is an increasingly prevalent risk factor for coronary and other vascular disease. Recent trials in patients with diabetes have examined the effects of intensive glycemic control on cardiovascular outcomes, and treatment of common concomitant risk factors, in particular hypertension and dyslipidemia. Optimal revascularization strategies have also been examined. RECENT FINDINGS: Intensive glycemic control has a beneficial effect on microvascular but not macrovascular endpoints, with one major trial reporting increased mortality out to 5 years with intensive treatment. Similarly, aggressive lowering of SBP to below 120 mmHg produced no advantage over treatment to 130-140 mmHg. Statins are the best treatment for diabetic dyslipidemia, with little benefit from adding a fibrate. Medical treatment may be appropriate for many with diabetes and stable coronary disease. When revascularization is needed, coronary bypass graft surgery has an advantage over percutaneous coronary intervention in those at the severe end of the coronary disease spectrum. SUMMARY: Patients with type 2 diabetes often have multiple cardiovascular risk factors and require multiple cardiac and diabetes medications. Caution over aggressive glucose and blood pressure lowering is needed, at least with currently available drugs. © 2011 Lippincott Williams & Wilkins, Inc.

White H.,Green City
New Zealand Medical Journal | Year: 2013

The New Zealand branch of the Cardiac Society of Australia and New Zealand have produced guidelines on the management of acute coronary symptoms since 2005. These have been developed by clinicians throughout New Zealand with the aim to improve quality of care. They focus on the most effective strategies based on evidence from clinical trials. The evidence is graded and the recommendations are patient focused. Patients should be informed of the risks and benefits of treatment and share in decision making. © NZMA.

Despite the proven efficacy of dual antiplatelet therapy with aspirin and one of the first-generation P2Y 12 antagonists (clopidogrel, prasugrel) in patients with atherothrombotic disease, residual ischemic risk remains substantial, and bleeding rates are increased. Incomplete protection against ischemic events can be attributed to the fact that these therapies each target a single platelet activation pathway, allowing continued platelet activation via other pathways, including the protease-activated receptor-1 (PAR-1) pathway stimulated by thrombin. Increased bleeding with dual antiplatelet therapy can be attributed to blockade of the thromboxane A 2 (by aspirin) and adenosine diphosphate (by P2Y 12 antagonist) platelet activation pathways that are essential to hemostasis. The second-generation P2Y 12 inhibitor ticagrelor plus aspirin demonstrated superior ischemic outcomes, including reduction in total mortality, versus clopidogrel plus aspirin, but event rates remain high, and major bleeding not related to coronary artery bypass grafting is increased. The novel P2Y 12 antagonist elinogrel, available in intravenous and oral formulations, may have a more favorable benefit-to-risk profile than existing agents in this class because of reversible and competitive binding to the P2Y 12 receptor. Inhibition of PAR-1 is an attractive, novel approach in antiplatelet therapy because it may provide incremental ischemic protection without increasing bleeding. The PAR-1 antagonist vorapaxar (SCH 530348) has been associated with favorable efficacy and safety in phase 2 trials. Two phase 3 trials are evaluating the efficacy and safety of vorapaxar in patients presenting with non-ST-segment elevation acute coronary syndromes and in patients with documented atherothrombotic disease. © 2011 Mosby, Inc. All rights reserved.

Lipoprotein-associated phospholipase A2 (Lp-PLA2) levels are associated with coronary heart disease (CHD) in healthy individuals and in patients who have had ischemic events. The Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) study randomized 9014 patients with cholesterol levels of 4.0 to 7.0 mmol/L to placebo or pravastatin 3 to 36 months after myocardial infarction or unstable angina and showed a reduction in CHD and total mortality. We assessed the value of baseline and change in Lp-PLA2 activity to predict outcomes over a 6-year follow-up, the effect of pravastatin on Lp-PLA2 levels, and whether pravastatin treatment effect was related to Lp-PLA2 activity change. Lp-PLA2 was measured at randomization and 1 year, and levels were grouped as quartiles. The prespecified end point was CHD death or nonfatal myocardial infarction. Baseline Lp-PLA2 activity was positively associated with CHD events (P < 0.001) but not after adjustment for 23 baseline factors (P = 0.66). In 6518 patients who were event free at 1 year, change in Lp-PLA2 was a significant independent predictor of subsequent CHD events after adjustment for these risk factors, including LDL cholesterol and LDL cholesterol changes (P < 0.001). Pravastatin reduced Lp-PLA2 by 16% compared with placebo (P < 0.001). After adjustment for Lp-PLA2 change, the pravastatin treatment effect was reduced from 23% to 10% (P = 0.26), with 59% of the treatment effect accounted for by changes in Lp-PLA2. Similar reductions in treatment effect were seen after adjustment for LDL cholesterol change. Reduction in Lp-PLA2 activity during the first year was a highly significant predictor of CHD events, independent of change in LDL cholesterol, and may account for over half of the benefits of pravastatin in the LIPID study.

Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an uncommon inherited myocardial disorder characterised by fibro-fatty inflammation affecting the right and left ventricles. It most commonly presents with palpitations or syncope but sudden death may occur, especially in young males. Methods: Diagnosis is not possible with a single test and may be difficult. Task Force criteria agreed in 1994 comprise major and minor criteria spanning structural abnormalities, ECG appearances, arrhythmias, family history of premature death and myocardial histology. Modified criteria were introduced in 2010 to improve sensitivity. Results: Arrhythmogenic right ventricular cardiomyopathy is a desmosomal disease. Mutations have been detected in five desmosomal genes, most frequently in plakophilin-2 (PKP2) and multiple mutations are also reported. Antiarrhythmic drugs such as sotalol and amiodarone may improve symptoms but are unproven to increase survival. An implantable defibrillator is appropriate in individuals surviving cardiac arrest or sustained ventricular tachycardia, but there is not yet consensus about prophylactic treatment of Task Force positive but asymptomatic individuals. Conclusions: Arrhythmogenic right ventricular cardiomyopathy is more common than previously believed. Preliminary evidence supports improved sensitivity without loss of specificity using the revised Task Force criteria. The genetics of the disease are complex but should ultimately advance diagnosis and management. © 2011 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand.

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