Can Smoking Cause High Cholesterol – High cholesterol is a known risk factor for developing ischemic stroke. Concern regarding the relationship between very low cholesterol levels and an increased risk of intracerebral hemorrhage (ICH), however, has led some experts to hesitate to prescribe statins to individuals at risk of stroke. The mechanism by which high cholesterol increases the risk of ICH is not fully understood; However, ischemic strokes resulting from atherosclerosis are consistently associated with elevated levels of total cholesterol (TC) and LDL cholesterol (LDL-C). As a result, LDL-C is a lipid subset that is a therapeutic target for preventing vascular events.
Several studies have investigated the effect of lipid lowering on the risk of incident stroke (Table). A 2010 meta-analysis of 26 trials included people with and without prior stroke and for every 39 mg/dL (1 mmol/L) reduction in LDL-C there was a significant 21% reduction in ischemic stroke risk. found (relative risk [RR], 0.79; 95% CI 0.74 to 0.85). Conversely, there was a significant 12% increase in ICH risk for every 39 mg/dL (1 mmol/L) reduction in LDL-C (RR, 1.12; 95% CI 0.93 to 1.35).
Can Smoking Cause High Cholesterol
Among people with prior stroke, 2 large trials focused specifically on lipid-lowering therapy. In one trial in 4, 731 participants with a recent transient ischemic attack (TIA) thought to be atherosclerotic in origin, stroke, or ICH and without a history of coronary artery disease, received high-dose atorvastatin (80 mg/day) significantly reduced the incidence. Fatal and nonfatal stroke compared with placebo, with 11.2 vs 13.1% events per year (1.9% 5-year absolute risk reduction [ARR]; HR, 0.84; 95% CI 0.71 to 0.99; P=.03) .
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A second trial focused on LDL treatment goals in 2,860 participants with recent ischemic stroke or TIA and atherosclerosis, with low (<70 mg/dL) versus high (90–110 mg/dL) target LDL-C at baseline. Compare using label lipids. Medication reduction (eg, any statin, ezetimibe, or both). A lower LDL-C target was associated with significantly fewer major vascular events, mostly ischemic stroke, when compared with a higher target, with 8.5% vs 10.9% of events, respectively ( adjusted HR, 0.78; 95% CI 0.61– 0.98; P=.04).
Both trials also assessed the risk of ICH as a result of LDL-C reduction. Although there was a significant increase in ICH in those treated with atorvastatin vs placebo (HR, 1.68; 95% CI 1.08 to 2.55), post-hoc analysis found that ICH was associated with secondary hypertension, prior ICH. , and was strongly associated with age. There was also no association between low LDL-C levels and risk of ICH, either at baseline or after treatment with statins.
Along these lines, there was no significant difference in ICH between patients with low target LDL-C and patients with high target LDL-C. Recently, a Danish population-based study of more than 55,000 people found that statins did not increase the risk of ICH in people with a history of ischemic stroke or ICH.
Given the high risk of recurrent stroke in individuals with heart failure due to atherosclerosis, the benefit of lipid-lowering therapy outweighs any known risk of ICH.
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Several lipid-altering therapies are available, including high- and low-potency statins, ezetimibe, protein convertase subtilisin-kixin type 9 (PCSK9) inhibitors, eicosapentaenoic acid ethyl ester, gemfibrozil, and niacin. Here we focus on lipid management with statins, ezetimibe, and PCSK9 inhibitors.
Statins lower serum cholesterol by inhibiting hydroxymethyl-glutaryl-coenzyme A (HMG-CoA) reductase, which in turn lowers serum cholesterol; However, statins reduce the risk of stroke through several mechanisms beyond lowering cholesterol. In addition to their lipid-dependent effect, statins have also been shown to improve endothelial function, reduce inflammatory and oxidative stress, and modulate thrombogenesis. The effect of statins on endothelial function is associated with an increase in endothelial nitric oxide synthesis, which may mediate vasodilation and reduce vascular smooth muscle cell proliferation. By reducing the production of thromboxin A2 in the platelet and erythrocyte membrane, statins act to reduce thrombogenesis. The damage caused by inflammation and oxidative stress is reduced by the recruitment, adhesion and migration of inflammatory cells as well as reduction of reactive oxygen species by angiotensin III.
These added benefits, or pleiotropic effects, likely provide additional protection against stroke by making statins the first-line choice for LDL-lowering in people who have had a stroke. Commonly used statins are available in generic form and are inexpensive, compared to other lipid-lowering drugs.
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And has been shown to reduce LDL-C by about 10% to 18% alone, with an additional 25% reduction in LDL-C when used in combination with statins.
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A subanalysis of ezetimibe clinical trials showed a reduced risk of ischemic stroke with the addition of ezetimibe to a statin compared with a statin alone in people with a pre-existing acute coronary syndrome (Table).
PCSK9 is a protein that regulates LDL receptor degradation in response to cellular cholesterol concentrations. PCSK9 inhibition increases the number of LDL receptors on liver cell surfaces, increasing the clearance of LDL-C from the circulation. Inherited variants in the PCSK9 gene cause loss of function resulting in very low plasma concentrations of LDL-C and cardiovascular events,
Which led to the development of PCSK9 inhibitors as a therapeutic approach to lower LDL. PCSK9 inhibitors have been shown to reduce LDL-C levels by 50% to 60% and, when added to statins in people with atherosclerotic disease and elevated LDL-C, reduce the risk of cardiovascular events.
Another study showed that adding a PCSK9 inhibitor to statin therapy in people with previous acute coronary syndrome (ACS) and high cholesterol reduced the risk of recurrent ischemic heart events, including ischemic stroke, when compared with statin monotherapy. (. table).
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Despite being highly effective, the use of PCSK9 inhibitors is limited by their high cost (average retail cost over $450/month).
Adhering to lifestyle changes can also help lower LDL-C. Studies have shown that reducing caloric intake by 20% to 25% for at least 3 months leads to reductions in LDL-C and triglycerides, in addition to having positive effects on both blood pressure and glucose levels.
The American Heart Association (AHA) recommends moderate to vigorous physical activity, defined as activity that raises the heart rate for at least 150 minutes per week.
Given the strong evidence supporting lowering LDL for stroke prevention, the most recent AHA stroke prevention guidelines recommend an LDL goal of less than 70 mg/dL in people with ischemic stroke or TIA and atherosclerotic disease. -C is recommended to reduce the risk of major cardiovascular events. Events (pictured).
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Atherosclerotic disease to be considered for this purpose is present in intra or extraocular arteries, aortic arch or coronary arteries. This can be achieved with a statin and ezetimibe, if needed. Ezetimibe should be added to the maximum tolerated statin dose if additional lipid lowering is required. For patients who cannot achieve this goal with these 2 drugs, the use of PCSK9 inhibitors is a suitable adjunct to treatment to prevent further cardiovascular events.
Shape Management of hyperlipidemia after ischemic stroke or at very high risk of subsequent events. The AHA definition of very high risk includes those with a history of multiple major ASCVD events or 1 major ASCVD event and multiple high-risk conditions defined below. Major ASCVD events included acute coronary syndrome, history of myocardial infarction, ischemic stroke, or symptomatic peripheral artery disease (ABI<0.85, or previous revascularization or amputation) within the previous 12 months. High-risk conditions include age 65 years or older, heterozygous familial hypercholesterolemia, history of prior coronary artery surgery or coronary intervention outside of an ASCVD event, diabetes mellitus, hypertension, chronic kidney disease (presumed by glomerular filtration) 59 ml/min/1.73m
), current smoking, persistently elevated LDL-C (≥100 mg/dL despite maximally tolerated statin therapy and ezetimibe), and history of heart failure. Abbreviations: ABI, acquired brain injury; AHA, American Heart Association; ASCVD, atherosclerotic cardiovascular disease; LDL, low-density lipid; LDL-C, LDL-cholesterol; PCSK9, proprotein convertase subtilisin-kexin type 9.
For effective attainment of an LDL goal of less than 70 mg/dL, a lipid panel should be repeated approximately 1 month after initiation or adjustment of lipid-lowering therapy and medications titrated as needed. Once on target, a repeat lipid panel is only needed once a year to assess adherence. However, if an individual has a significant change in medication use (for example, reduces the dose or stops the medication), a lipid panel should be checked. A lipid panel can be performed with or without fasting, but if non-fasting triglycerides are above 400 mg/dL, a lipid panel should be performed with fasting.
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Similar to the atherogenic effects of LDL, triglyceride-rich lipoproteins (very low-density lipoprotein [VLDL] and chylomicrons) promote the development of atherosclerosis and contribute to the risk of heart disease and stroke. Although treatment with niacin and fibrates in combination with statin therapy may lower triglycerides, it has not shown a significant reduction in cardiovascular events. However, a purified omega-3 fatty acid, icosapentaenoic acid (IPE), has shown benefit in preventing vascular events. In a clinical trial in 8, 179 participants with atherosclerotic heart disease, 70% of whom had a history of ischemic stroke or TIA, were treated with IPE 4 g/day in 2 divided doses and statin and statin alone therapy. Fatal or non-fatal stroke is reduced.
