The Effect Of Two Intensive Statin Regimens On Progression Of Coronary Disease

A higher level of fats in the body puts the patient at higher risk for Cardiovascular diseases(CAD). The patient's' family has a history of CAD. Her mom and one of her sister have CAD (Lewis et al., 2014, pp. 733-734). The patient states that she has been taking her meds for cholesterol atorvastatin regularly. Her lipase level was 8272 on 11/11/16 and 2829 on 11/12/16 U/L 1069 on 11/13/16 (Ref range 73-393 U/L). Her HDL cholesterol level was 21 ( ref range>49 mg/dl), LDL Cholesterol level 148 ( ref range: <130 mg/dL). Patient statin drug was on hold because it is contradicted on the patient with an elevated level of ALT 80, 61(Ref range 0-50 U/L) and AST 61 on 11/12/16 and 64 on 11/13/16 (ref range 0-45 U/L). The uncontrolled level of could be the cause of concern for stroke or acute myocardial

MR. David likewise takes atorvastatin (Lipitor); 10 mg every day, for hypercholesterolemia (hoisted LDL cholesterol, low HDL cholesterol, and raised triglycerides). He has endured this medicine and holds fast to the day by day plan. Amid the previous 6 months, he has likewise taken chromium picolinate,

Current guidelines state that ezetimibe,is considered the best alternative for LDL reduction and tolerability in statin-intolerant patients and considered an adjuvant in this trial. The primary end point was percentage change from baseline to week 12 in LDL cholesterol. Other end points included measures of safety and tolerability of different doses of AMG145 and AMG145 plus ezetimibe. Other objectives included assessment of the safety and tolerability of 3 different doses of AMG145 and AMG145 plus ezetimibe compared with placebo plus ezetimibe. One hundred sixty patients were randomized into 5 groups, to take AMG 145 as monotherapy once a month at 280mg, 320mg and 420mg, to take AMG 145 420mg once a month with ezetimibe 10mg daily or placebo once a month with ezetimibe 10mg daily. At week 12 the AMG 145 groups had a percent change of blood levels of LDL from baseline from -40.8 % to -50.7 % dose ascending monotherapy and -63.0% with combination with ezetimibe versus -14.8% with combination of placebo and ezetimibe. Reduction in total cholesterol percentwise was from -29.8 % to -37.7 % dose ascending monotherapy and -43.3% with combination with ezetimibe versus -10.7% with combination of placebo and ezetimibe. The overall incidence of all adverse effects was similar among patients receiving

The examples of drugs in this class are atorvastatin (Lipitor), rosuvastatin (Crestor), and simvastatin (Zocor). Statins is the first line to use for lowing blood cholesterol levels. Statins works by blocking the enzyme called HMG-CoA reductase in the liver which is necessary for making cholesterol. The statins blocks the active site of the HMG-CoA reductase enzyme so that it cannot converse to mevalonate. Therefore, there is more LDL receptor available in the liver. These receptors bind to passing LDL and VLDL (very low-density lipoprotein). The LDL and VLDL then enter the liver and are digested. So that there is less LDL level in blood stream. Even though, many drugs are in the same class, but the effectiveness of each drug is different. For example, 5-40 mg of Crestor seems to work best by lowering LDL by 47-65%; whereas 10-40 mg of pravachol can lower LDL by 22-34%. Most people who take statins do not experience serious side effects. The most common minor side effects include headache, pins and needle sensations, abdominal pain, bloating, diarrhea, feeling sick, and a rash. The provider normally starts statins in a low. The dosage may be increased if this target is not reached. Statins are contradicated in patient with active liver disease and consume a large amount of alcohol. The common side effects are GI upset and

She has been off simvastatin because of the myalgias. Her lipids were most recently checked back in June and were elevated. Total cholesterol 270, triglycerides 199, HDL 59, LDL 171. She really wanted to work on healthier lifestyle choices, which she is trying to do, but is still struggling with. She has not been using her exercise bike of late, as her basement was being renovated, though she plans to start doing that soon. She would like to continue to work on those things, but does admit that she has difficulty. She would be willing to consider an alternative statin than simvastatin because of her prior issues, but would perhaps like to recheck them

ASSESMENT OF THE EFFECT OF STATINS IN LOWRING THE RISK OF STROKE AND PREVENTING CEREBRAL ISCHEMIA IN PATIENTS WITH HYPERCHOLESTEROLEMIA

Robert is a 70-year-old male who suffers from pure hypercholesterolemia (E78.0), along with multiple cardiac risk factors including diabetes, hypertension, myocardial infarction, peripheral artery disease, sleep apnea, hypothyroidism, bullous pemphigus, hemochromatosis, and hypogonadism. Robert has tried and failed various treatments including Lipitor, cholestyramine, and Zetia, in which his LDL still does not meet criteria of being less than 80 in the presence of known vascular disease. Robert is not candidate for additional statin therapy due to his cholesterol levels were sub-optimally controlled. Repatha is his best treatment option at this time, in addition to him monitoring his diet. Repatha is Robert’s best treatment option at this

Coronary Artery Disease (CAD) is the end result of the accumulation of atheromatous plaques within the walls of the coronary arteries that supply the myocardium with oxygen and nutrients. While the symptoms and signs of (CAD) are noted in the advanced state of disease, most individuals with (CAD) show no evidence of disease for decades as the disease progress before the first onset of symptoms, often a “Sudden” heart attack, After decades of progression, some of these atheromatous plaques may rupture (along with the activation of the blood clotting system) limiting blood flow to the heart muscle.

McGarry PA, McMohan CA, Montenegro MR et al. General findings ‎of the International Atherosclerosis Project. Lab Invest 1968; 18:498-‎‎502.‎

A detailed medical history was taken about other systemic and/ or CVD. Macrovascular disease was defined as a history of MI, presence of angina, revascularization procedures or stenosis >50% of the coronary artery, a history of cerebrovascular diseases or PAD based on a previous L.L Doppler U/S examination [13]. DM was defined according to American Diabetes Association (ADA) criteria [14]. Hypertension was defined as blood pressure above 140/90 mmHg or taking antihypertensive

The key terms searched include, secondary prevention, heart attack, atorvastatin, simvastatin, and pravastatin. The terms were combined with an “and” operator, and the following limits were applied: English language, human, and randomized controlled trial. The search returned 39 articles of which only 1 included a study which compared 2 different statins. The other articles were excluded because they were guidelines, review articles or were not specific to preventing a recurrence of myocardial infarction.

Cardiac Disease /Circulatory-Medium risk: Cholesterol, triglycerides and HDL levels will improve through the use of medication and diet within the next 12 months (current levels 204, 244, 33 respectively)

The patient was put on a low fat and low cholesterol diet to see if the symptoms would improve and the cholesterol levels would decrease along with some statin medication of Atorvastatin, to help lower the cholesterol within the blood and help to prevent the patient from gaining any associated symptoms that are related with cardiovascular disease. The medication was given as it inhibits HMG-CoA reductase of the enzyme found within the liver that has a huge role in the production of cholesterol. This should show a dramatic reduction in the levels of LDL-C.

Treatment with fibrate drugs acting to decrease free fatty acid production on the peroxisome proliferator-activated receptors (PPARs), specifically PPARα is for both the conditions. The synthetic statin drugs, namely, rosuvastatin and atorvastatin can increase hepatic reuptake of LDL due to increased LDL-receptor expression, resulting in the decrease of LDL

Primary prevention of dyslipidemia is aimed at management of persons at increased risk, and does not - in present or past have any clinically apparent atherosclerotic cardiovascular disease (ASCVD) like myocardial infarction with or without coronary intervention, angina, stroke, and peripheral vascular disease, and who have not undergone revascularization. The 3 P’s of “Risk stratification and management of dyslipidemia from a primary prevention perspective can be labelled as predict, prioritize and prevent. In other words primary prevention of dyslipidemia aims to prevent new onset of ASCVD.