21 research outputs found

    Achieving secondary prevention low-density lipoprotein particle concentration goals using lipoprotein cholesterol-based data

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    BACKGROUND: Epidemiologic studies suggest that LDL particle concentration (LDL-P) may remain elevated at guideline recommended LDL cholesterol goals, representing a source of residual risk. We examined the following seven separate lipid parameters in achieving the LDL-P goal of \u3c1000 nmol/L goal for very high risk secondary prevention: total cholesterol to HDL cholesterol ratio, TC/HDL, \u3c3; a composite of ATP-III very high risk targets, LDL-C\u3c70 mg/dL, non-HDL-C\u3c100 mg/dL and TG\u3c150 mg/dL; a composite of standard secondary risk targets, LDL-C\u3c100, non-HDL-C\u3c130, TG\u3c150; LDL phenotype; HDL-C ≥ 40; TG\u3c150; and TG/HDL-C\u3c3. METHODS: We measured ApoB, ApoAI, ultracentrifugation lipoprotein cholesterol and NMR lipoprotein particle concentration in 148 unselected primary and secondary prevention patients. RESULTS: TC/HDL-C\u3c3 effectively discriminated subjects by LDL-P goal (F = 84.1, p\u3c10(-6)). The ATP-III very high risk composite target (LDL-C\u3c70, nonHDL-C\u3c100, TG\u3c150) was also effective (F = 42.8, p\u3c10(-5)). However, the standard secondary prevention composite (LDL-C\u3c100, non-HDL-C\u3c130, TG\u3c150) was also effective but yielded higher LDL-P than the very high risk composite (F = 42.0, p\u3c10(-5)) with upper 95% confidence interval of LDL-P less than 1000 nmol/L. TG\u3c150 and TG/HDL-C\u3c3 cutpoints both significantly discriminated subjects but the LDL-P upper 95% confidence intervals fell above goal of 1000 nmol/L (F = 15.8, p = 0.0001 and F = 9.7, p = 0.002 respectively). LDL density phenotype neared significance (F = 2.85, p = 0.094) and the HDL-C cutpoint of 40 mg/dL did not discriminate (F = 0.53, p = 0.47) alone or add discriminatory power to ATP-III targets. CONCLUSIONS: A simple composite of ATP-III very high risk lipoprotein cholesterol based treatment targets or TC/HDL-C ratio \u3c3 most effectively identified subjects meeting the secondary prevention target level of LDL-P\u3c1000 nmol/L, providing a potential alternative to advanced lipid testing in many clinical circumstances

    How to Handle Conflict With Poise?: A Fellow\u27s Perspective

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    A rare cause of coagulopathy Acquired factor V inihibitor

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    Vasodilators and management of hypertensive emergencies

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    Hypertensive emergency is an important clinical entity, which may result in end-organ damage involving neurological, cardiovascular, and renal systems. If not recognized and acted upon promptly, it can result in life-threatening adverse outcomes. Vasodilators form the mainstay of treatment in hypertensive emergencies. There are different classes of vasodilators based on the site and mechanism of action. The most commonly used vasodilators include directly acting drugs that act via the vascular nitric oxide pathway, calcium channel blockers, beta blockers, alpha blockers, and peripheral dopamine agonists. The various classes of vasodilators act via different neurohormonal signaling pathways and reduce the blood pressure by decreasing the peripheral resistance. Despite the availability of several medications, there is still paucity of literature regarding the best antihypertensive medication to be employed as well as the ideal rate of decreasing the elevated blood pressure in a given clinical scenario. This chapter reviews the basic pharmacology and the mechanism of action of commonly used vasodilators. It also reviews the approach to choosing the most appropriate drug based on the target organ involvement in diverse clinical scenarios of hypertensive emergency
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