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| Home | ||||||||||||||||||||||||
| ACS and Inflammation | ||||||||||||||||||||||||
| 1. Plaque rupture and Inflammation 2002: A review of the basic science behind the theory of inflammation as the unifying cause of acute coronary syndromes | ||||||||||||||||||||||||
| 2. HOPE 2000: Patients aged 55 or older with CAD, stroke, or PVascDz, OR DM and one additional RF (defined as HTN, increased total cholesterol, tobacco, low HDL, or microalbuminuria). Ramipirl decreased CVS death by 25%, MI by 20%, stroke by 32%, and revascularization by 15%. | ||||||||||||||||||||||||
| 3. HPS 2002: A 1 mmol/L (39 mg/dL) reduction in LDL from 4 (155 mg/dL) to 3 (166 mg/dL) reduces risk of major vascular events (defined as major coronary event, stroke, or revascularization) by about a quarter, and reducing from 3 (166) to 2 (77) also reduces risk by about a quarter. Results are similiar for major coronary events (defined as non-fatal MI, or coronary death). Largest RCT of CHD prevention to date. Overall, LDL level was irrelevant. Patients with known vascular disease, or at high risk for vascular disease benefit from a statin. | ||||||||||||||||||||||||
| 4. VA-HIT 1999: 24% reduction in combined end point of CHD death, non-fatal MI, or stroke with the use of gemfibrozil in patients with isolated low HDL. | ||||||||||||||||||||||||
| 5. VA-HIT and insulin resistance 2003: Benefit of gemfibrozil more apparent and more important in patients with insulin resistance than effects of HDL, as these patients explained the benefit of the study, but had little effect on HDL. | ||||||||||||||||||||||||
| 6. AHA/CDC Inflammation and CRP: Test inermediate rsk pts, i.e. those c 10-20% 10 yr Frammingham risk of CHD for hsCRP as a motivator for behavior change, and consider treating c asa, acei, statin (those studies ongoing) | ||||||||||||||||||||||||
| 7. CRP and LDL: CRP was more predictive than LDL of CVS events. High CRP and low LDL still poor outcome, which could be a new subset of pts who are at high risk. | ||||||||||||||||||||||||
| 8. Unstable angina and inflammation: Coronary arteries are all inflammed in USAngina. | ||||||||||||||||||||||||
| 9. MPO and ACS: New prognostic marker, better detecting CP pts at high risk at presentation, even in those pts c nl initial troponin, and those without any troponin elevation during admission. Predicted 30 day and 6 month outcomes better than other markers. ROC curves better for those with negative troponin. | ||||||||||||||||||||||||
| 10. and 11. Consensus articles that summarizes above literature into new concept of identifying vulnerable patients who have vulnerable plaque, vulnerable blood, and/or vulnerable myocardium. | ||||||||||||||||||||||||
| 12. EBM and ACS: Asa, beta-blocker, stain, acei: Using all 4 meds compared to none decreased 6 month mortality by 90%; using 2 or 3 compared to none decreased it by ~80%. | ||||||||||||||||||||||||
| 13. PROVE-IT: Pts c ACS did better on intensive lipid lowering c statin, atorvastatin 80 mg v pravastatin 40 mg. Both meds significantly decreased CRP by ~65%. | ||||||||||||||||||||||||
| 14. REVERSAL: In stable CAD pts, higher dose atorvastatin, 80 mg, stopped progression of atheroosclerosis compared to 40 mg of pravastatin via IVUS. Atorvastatin also decreased CRP (36%), and pravastatin did not. | ||||||||||||||||||||||||
| 15. AFCAPS/TexCAPS: Young (men and women in 50s-60s) people c average tchol (221) and LDL (150) and low HDL (36) had 37% reduction to first major coronary event. A f/u study showed that this decreased costs by 11% | ||||||||||||||||||||||||
| 17. Integrative Plaque Rupture: An integrative approach to the pathophysiology of plaque rupture involving local and systemic factors. Reviews experimental models of plaque rupture. | ||||||||||||||||||||||||
| 18. Interacitve lipid tool: Gives you the Frammingham risk score for the PDA | ||||||||||||||||||||||||