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High Cholesterol board


Regression Growth Evaluation Statin Study (REGRESS)5

Restenosis (re-narrowing) after a type of angioplasty called percutaneous transluminal coronary angioplasty (PTCA) is one limitation of the long-term success of this procedure. In previous studies statins have failed to prevent restenosis. However their lack of success in the past may have been due in part to the fact that the studies did not allow a long enough follow-up time. Also, a better understanding of restenosis has led to a better evaluation of it. The REGRESS study investigated the efficacy of pravastatin in reducing restenosis after PTCA. The study considered 221 patients who had undergone PTCA. Patients were randomly selected to receive pravastatin or placebo. The pravastatin group showed a lower percentage of the artery blocked—based on the ratio of blockage to artery diameter (32% vs 45%). In addition, pravastatin provided a 7% reduction in clinical restenosis over placebo. Pravastatin, therefore, is an effective treatment to prevent restenosis after PTCA.

Effect of aggressive lipid lowering on progression of atherosclerosis after coronary artery bypass graft (CABG)6

This follow-up study investigated the difference between moderate LDL lowering therapy and aggressive LDL therapy on the progression of athersclerosis. Four hundred and two patients were randomly assigned into the two treatment groups (aggressive and moderate). The aggressive group received 75-80 mg of lovastatin daily and the moderate group received 2.5-5 mg of lovastatin. Patients in the aggressive group showed average LDL levels of 92-97 mg/dL (a 40% decrease from baseline) while patients in the moderate group had levels of 131-135 (a 12% decrease). More significantly, patients treated with the aggressive treatment had less atherosclerosis than the moderately treated group. Athersclerosis was measured by minimum lumen diameter or by the average change in maximum arterial stenosis. This study, like the Heart Protection Study and the Reversal study demonstrates that at in patients with CABG there are clear benefits to receiving aggressive LDL lowering therapy with a goal of lowering LDL cholesterol to below 100 mg/dl.

Arterial Biology for the Investigation of the Treatment of Effects of Reducing Cholesterol (ARBITER)7

This study further assessed the question of whether lowering LDL cholesterol to well under 100 mg/dl will have benefits above and beyond lowering levels to 100 mg/dl. This study compared pravastatin and atorvastatin, at different doses, on carotid intima-media thickness (CIMT) which is a measure commonly used as a surrogate for vascular atherosclerosis. One hundred and sixty one patients with known cardiovascular disease were randomly divided into a pravastatin (40mg/d) group (n=82) and an atorvastatin (80 mg/d) group (n=79). After one year the average LDL in the pravastatin group was 110 mg/dL and was 76 mg/dL in the atorvastatin group. The CIMT was stable in the pravastatin group while the atorvastatin group showed a regression in CIMT over 12 months. An aggressive reduction in LDL is an efficient way to induce the regression of atherosclerosis which may in turn lead to fewer coronary events.

Pravastatin in the secondary prevention of cardiovascular events in patients with kidney insufficiency8

Since statins have been overwhelmingly shown to reduce cardiovascular disease in the general population, this study investigated the ability of statins to reduce cardiovascular events in patients with renal insufficiency (when the kidneys lose their ability to remove waste from the body). There were 1711 participants in this study who were identified as having chronic kidney insufficiency by having a creatinine clearance of =75 mL/min. Patients were given either pravastatin or placebo. Pravastatin was associated with a lower occurrence of major coronary events but there was not a difference in total mortality between the two groups. The incidence of side effects was similar in patients receiving pravastatin to those receiving placebo. A significant finding is that patients will see the observed benefits whether or not they have kidney insufficiency and regardless of its severity. Pravastatin is therefore a safe and effective method of secondary prevention for patients who have mild chronic kidney insufficiency.

Fluvastatin and prevention of cardiac events after a successful, first percutaneous coronary intervention9 (LIPS study)

Percutaneous coronary intervention (PCI) is effective for short-term improvement in ischemic symptoms but has less long-term efficacy. Sixty percent of patients are free of a major adverse cardiac event (MACE) 5 years after PCI and only 33% after 10 years. The goal of this study was to assess whether fluvastatin reduces major cardiac events. A total of 1677 patients at 77 centers in Europe, Canada, and Brazil were studied. Eight hundred and forty four patients with unstable angina or silent ischemia after their first PCI were randomly assigned to receive 80 mg/d of fluvastatin and 833 a placebo. After a median follow-up time of 3.9 years 21.4% of the patients in the fluvastatin group had a MACE, compared to 26.7% in the placebo group. Also, there was a longer time before a MACE in the fluvistatin group. This study suggests that patients with average cholesterol levels will benefit from fluvistatin treatment after the first successful PCI. The LIPS study has also shown that patients treated with a stent and fluvistatin show a 28% reduction in MACE.

Atorvastatin versus simvastatin on atherosclerosis progression (ASAP) study10,11

The purpose of the ASAP study was to assess the difference of aggressive versus traditional cholesterol treatment on the progression of atherosclerosis in patients with familial high cholesterol. Three hundred and twenty five patients with a family history of high cholesterol were randomly divided into an aggressive group (atorvastatin) and a traditional treatment group (simvastatin). After two years of treatment, the progression of atherosclerosis was compared between the two groups. In one test, the levels of hs-CRP were lower in patients taking atorvastatin compared to simvastatin. hs-CRP is a good marker of inflammation in atherosclerotic vascular disease. In another test—a measurement of the carotid intima media thickness—the atorvastatin group showed a regression of atherosclerosis, whereas the simvastatin group did not. These results show that aggressive lowering of LDL was accompanied by a regression of atherosclerosis in the carotid artery but conventional LDL lowering by simvastatin did not show any benefit.

The Benefit of Aggressive Lipid Lowering12 (AVERT study)

This study examined 341 patients with stable coronary heart disease (CHD). They were randomly assigned to receive atorvastatin (80 md/d) and conventional treatment or angioplasty followed by usual care. The differences in LDL and subsequent ischemic events were compared between the two groups. The atorvastatin/conventional treatment group showed a 48% decrease in LDL compared to an 18% decrease following angioplasty. The atorvastatin group had fewer ischemic events (13% vs 21%, p=.048) and a longer time before the first ischemic event (p=.027) when compared with the angioplasty group. Therefore aggressive lipid lowering is beneficial in patients with existing CHD.

Aggressive LDL lowering provides the greatest reduction in carotid atherosclerosis13

The purpose of this study was to investigate the effects on atherosclerosis of lowering LDL well below the current recommended level of 100 mg/dL. The investigators used the carotid intima media thickness (CIMT) as an indicator of atherosclerosis progression. The study compared the effects of pravastatin (40 mg/d) and atorvastatin (80mg/d) among 161 patients. The final LDL level was directly correlated with the amount of CIMT regression. Sixty-one percent of subjects with final LDL levels of < 70 mg/dL showed a regression whereas only 29% of those with final LDL of = 114 mg/dL. The amount of atherosclerotic regression is directly related to absolute LDL level. The investigators recommend a lower National Cholesterol Education Program guideline.

The relation between atherosclerotic progression and cholesterol levels14

This study assessed the long-term (average of 18.3 months) progression or regression of atherosclerotic plaque in the left main coronary artery (LMCA) by intravascular ultrasound (IVUS). IVUS studies were performed on the LMCA of 60 patients. LDL and plaque progression were positively correlated (i.e. the more LDL, the more plaque). The researchers calculated that LDL levels below 75 mg/dL would not predict any progression of atheroclerosis (i.e. it would be essentially stopped, but not necessarily regress). Also, there was an negative correlation between HDL and plaque (i.e. more HDL less plaque). Therefore lower LDL (at least below 75 mg/dL) and higher HDL slows or halts progression of atherosclerosis. This study is particularly useful because unlike other similar studies it examined the effects of HDL cholesterol on atherosclerotic plaque.
My 2 cents...If you have a significant blockage, then a RADICAL procedure (ie, stent..bypass) is required...without question.

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The relation of elevated LDL cholesterol to the development of CHD must be viewed as a multi-step process beginning relatively early in life.35-37 The first stage of atherogenesis is the fatty streak, which consists largely of cholesterol-filled macrophages; most of the cholesterol in fatty streaks is derived from LDL cholesterol. The second stage consists of fibrous plaques in which a layer of scar tissue overlies a lipid-rich core. Other risk factors contribute to plaque growth at this phase. The third stage is represented by the development of unstable plaques that are prone to rupture and formation of luminal thrombosis. Plaque rupture (or erosion) is responsible for most acute coronary syndromes (myocardial infarction, unstable angina, and coronary death).38-41 Elevated LDL cholesterol plays a role in the development of the mature coronary plaque, which is the substrate for the unstable plaque. Recent evidence also indicates that elevated LDL cholesterol contributes to plaque instability as well; conversely, LDL cholesterol lowering stabilizes plaques and reduces the likelihood of acute coronary syndromes. Clinical intervention with LDL-lowering therapy in patients with advanced coronary atherosclerosis (short-term risk reduction) thus aims to stabilize plaques and to prevent acute coronary sydromes.42,43 In contrast, LDL lowering earlier in life slows atherosclerotic plaque development, the foundation of the unstable plaque. This fact provides a rationale for long-term lowering of LDL cholesterol using both public-health and clinical approaches.