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1.
Management of patients with statin intolerance.
Fischer, S, Julius, U
Atherosclerosis. Supplements. 2017;:33-37
Abstract
In recent years statins have become an established option in lipid-lowering pharmacotherapy despite the fact that statin intolerance is fairly common. When muscle pains and/or an elevation of the creatine kinase appear, the dose must be lowered in patients with slight symptoms or stopped altogether if the symptoms are more severe. When the symptoms are alleviated and creatine kinase is normalized, re-exposition can be considered. If symptoms recur, treatment with another statin should be attempted - in these cases pravastatin or fluvastatin are recommended, although they are less effective in reducing LDL cholesterol. As a rule, at least 3 statins should be tested. In some patients an intake of atorvastatin or rosuvastatin twice weekly may be tolerated and effective. Alternative drugs for patients who cannot tolerate any of the statins are ezetimibe and/or bile acid sequestrants. If LDL cholesterol targets are not reached, PCSK9 inhibitors may be used. In high-risk patients with multiple cardio-vascular events and sub-optimal LDL cholesterol despite lipid-lowering drug therapy a lipoprotein apheresis should be started. In this context, we present the history of a patient, who also had high lipoprotein(a) levels, for whom lipoprotein apheresis therapy was indicated.
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2.
My Approach to the Patient With Familial Hypercholesterolemia.
Safarova, MS, Kullo, IJ
Mayo Clinic proceedings. 2016;(6):770-86
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Abstract
Familial hypercholesterolemia (FH), a relatively common Mendelian genetic disorder, is associated with a dramatically increased lifetime risk of premature atherosclerotic cardiovascular disease due to elevated plasma low-density lipoprotein cholesterol (LDL-C) levels. The diagnosis of FH is based on clinical presentation or genetic testing. Early identification of patients with FH is of great public health importance because preventive strategies can lower the absolute lifetime cardiovascular risk and screening can detect affected relatives. However, low awareness, detection, and control of FH pose hurdles in the prevention of FH-related cardiovascular events. Of the estimated 0.65 million to 1 million patients with FH in the United States, less than 10% carry a diagnosis of FH. Based on registry data, a substantial proportion of patients with FH are receiving no or inadequate lipid-lowering therapy. Statins remain the mainstay of treatment for patients with FH. Lipoprotein apheresis and newly approved lipid-lowering drugs are valuable adjuncts to statin therapy, particularly when the LDL-C-lowering response is suboptimal. Monoclonal antibodies targeting proprotein convertase subtilisin/kexin type 9 provide an additional approximately 60% lowering of LDL-C levels and are approved for use in patients with FH. For homozygous FH, 2 new drugs that work independent of the LDL receptor pathway are available: an apolipoprotein B antisense oligonucleotide (mipomersen) and a microsomal triglyceride transfer protein inhibitor (lomitapide). This review attempts to critically examine the available data to provide a summary of the current evidence for managing patients with FH, including screening, diagnosis, treatment, and surveillance.
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Nephrology Update: Chronic Kidney Disease.
Saha, S, Rahman, M
FP essentials. 2016;:18-22
Abstract
Chronic kidney disease (CKD) affects more than 1 in 10 individuals in the United States. The care of these patients must be managed by family physicians and nephrology subspecialists. The kidneys often are affected by systemic processes such as diabetes and hypertension, and optimal management of these conditions is critical to slow decline in renal function in CKD patients. These patients are at high risk of cardiovascular disease, and statin therapy is recommended for adults with CKD who are at least age 50 years and not receiving dialysis. Patients with CKD and anemia can be treated with iron therapy and often with an erythropoietin-stimulating agent. Electrolyte abnormalities are managed with dietary changes and drugs. Sodium restriction and modification of dietary protein intake also may be needed. Consultation with a renal dietitian may be helpful. Because many drugs are metabolized by the kidneys, physicians should ensure that drug dosages are appropriate for the level of renal function. Early consultation with or referral to a nephrology subspecialist for patients with reduced renal function, resistant hypertension or electrolyte levels, and other conditions have been associated with improved outcomes in CKD patients.
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An Unusual Case of Statin-Induced Myopathy: Anti-HMGCoA Necrotizing Autoimmune Myopathy.
Nichols, L, Pfeifer, K, Mammen, AL, Shahnoor, N, Konersman, CG
Journal of general internal medicine. 2015;(12):1879-83
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Abstract
Statins are some of the most widely prescribed medications, and though generally well tolerated, can lead to a self-limited myopathy in a minority of patients. Recently, these medications have been associated with a necrotizing autoimmune myopathy (NAM). Statin-associated NAM is characterized by irritable myopathy on electromyography (EMG) and muscle necrosis with minimal inflammation on muscle biopsy. The case presented is a 63-year-old woman who has continued elevation of creatine kinase (CK) after discontinuation of statin therapy. She has irritable myopathy on EMG and NAM is confirmed by muscle biopsy. She subsequently tests positive for an experimental anti-3-hydroxy-3-methylglutaryl-coenzyme A (anti-HMGCoA) antibody that is found to be present in patients with statin-associated NAM. Though statin-associated NAM is a relatively rare entity, it is an important consideration for the general internist in patients who continue to have CK elevation and weakness after discontinuation of statin therapy. Continued research is necessary to better define statin-specific and dose-dependent risk, as well as optimal treatment for this condition.
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Cardiac risk factors: new cholesterol and blood pressure management guidelines.
Anthony, D, George, P, Eaton, CB
FP essentials. 2014;:28-43
Abstract
The 2013 American College of Cardiology/American Heart Association cholesterol guidelines depart from low-density lipoprotein (LDL) treatment targets and recommend treating four specific patient groups with statins. Statins are the only cholesterol-lowering drugs with randomized trial evidence of benefit for preventing atherosclerotic cardiovascular disease (ASCVD). The groups are patients with clinical ASCVD; patients ages 40 to 75 years with diabetes and LDL of 70 to 189 mg/dL but no clinical ASCVD; patients 21 years or older with LDL levels of 190 mg/dL or higher; and patients ages 40 to 75 years with LDL of 70 to 189 mg/dL without clinical ASCVD or diabetes but with 10-year ASCVD risk of 7.5% or higher. Ten-year ASCVD risk may be calculated using the Pooled Cohort Equations. The Eighth Joint National Committee (JNC 8) guidelines for blood pressure management recommend a blood pressure goal of less than 140/90 mm Hg for all adults except those 60 years or older. For the latter group, the JNC 8 recommends a systolic blood pressure goal of less than 150 mm Hg. In another notable change from prior guidelines, the JNC 8 recommends relaxing the systolic blood pressure goal for patients with diabetes and chronic kidney disease to less than 140 mm Hg from less than 130 mm Hg.
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Statin prescription is essential in peripheral vascular disease.
Leyon, JJ, Jaiveer, S, Connolly, DL, Babu, S
Journal of vascular and interventional radiology : JVIR. 2010;(2):175-7, quiz 178
Abstract
Hypercholesterolemia is an important and easily modifiable risk factor for peripheral arterial disease (PAD), but is frequently not adequately addressed by vascular interventionists. Patients with PAD often have extensive atherosclerotic disease elsewhere and have a 1-year mortality rate as high as 20%, mainly from cardiovascular events. This case discussion briefly addresses the evidence for treating hypercholesterolemia in this subgroup of patients. Statins not only lower cholesterol, but also are antiinflammatory, antiproliferative, and antithrombogenic, and improve endothelial function. Current guidelines are reviewed and an approach to initiation of statins and their management is discussed.
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[Atherosclerotic carotid stenosis. How to decide endarterectomy versus stenting versus only medical treatment?].
CantĂș-Brito, C
Revista de investigacion clinica; organo del Hospital de Enfermedades de la Nutricion. 2009;(1):53-65
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Rosuvastatin-induced rhabdomyolysis probably via CYP2C9 saturation.
Gallelli, L, Ferraro, M, Spagnuolo, V, Rende, P, Mauro, GF, De Sarro, G
Drug metabolism and drug interactions. 2009;(1):83-7
Abstract
A 66 year-old woman with no history of renal or liver disease presented with progressive asthenia and diffuse myalgia. She cited 5 months history of mild hyperlipidemia under treatment with rosuvastatin (10 mg/day). Clinical examination documented both an increase in liver size and proximal muscle weakness, with difficulty in raising arms above the head. Blood tests showed the presence of renal, liver and muscle failure, with no evidence of virological, immunological or haematological diseases. Rosuvastatin treatment was stopped and blood values normalised within five days; but because of an increase in cholesterol plasma levels, rosuvastatin (10 mg/day) was restarted. Two days later, the patient returned to our observation due to the development of asthenia and muscle weakness, with an increase in creatine phosphokinase, 12,165 U/l. Rosuvastatin was discontinued and replaced with pravastatin (40 mg/day) with a complete resolution of clinical and laboratory findings in about six days. Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.
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Reduction of intima-media thickness in subjects with asymptomatic carotid disease: two cases from the Asymptomatic Carotid Atherosclerosis DIsease Manfredonia Study (ACADIM Study).
Riccioni, G, D'Orazio, N
La Clinica terapeutica. 2007;(5):431-3
Abstract
The intima-media thickness (IMT) of carotid common arteries (CCA) represents an important step of carotid plaque formation and progression, and is a characteristic marker of atherosclerosis, one of the most principal determinants of coronary artery disease (CAD). Change in IMT is one of the currently used markers to evaluate the progression of atherosclerotic process. In particular rosuvastatin (ROS) has demonstrated in a large scale controlled study with placebo a significant reduction of coronary atherosclerosis. Two subjects with normal lipidic profile underwent a carotid ultrasound investigations (CUI) and received ROS (10 mg/day). The CUI documented a bilateral IMT of CCDX and CCSX for the case A (0.101 cm dx-0.105 cm sx; mean 0.103 cm) and B (0.114 cm dx-0.108 cm sx; mean 0.111 cm), in absence of stenosis or occlusion. After 16 treatment-weeks with ROS it has found a significant reduction of IMT for both case A (0.081 cm dx -0.096 cm sx; mean 0.088 cm) than case B (0.082 cm dx-0.084 cm sx; mean 0.083 cm). The treatment with ROS has been well tolerated and no adverse effects has been reported. ROS represents an efficacious IMT-lowering agent of the statin class. The two presented case reports confirm the benefit of ROS in the IMT reduction in subjects with normal LDL-C values.
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10.
Short-term memory loss associated with rosuvastatin.
Galatti, L, Polimeni, G, Salvo, F, Romani, M, Sessa, A, Spina, E
Pharmacotherapy. 2006;(8):1190-2
Abstract
Memory loss and cognitive impairment have been reported in the literature in association with several 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), but we found no published case reports associated with rosuvastatin. To our knowledge, this is the first reported case of rosuvastatin-related short-term memory loss. A 53-year-old Caucasian man with hypercholesterolemia experienced memory loss after being treated with rosuvastatin 10 mg/day. He had no other concomitant conditions or drug therapies. After discontinuation of rosuvastatin, the neuropsychiatric adverse reaction resolved gradually, suggesting a probable drug association. During the following year, the patient remained free from neuropsychiatric disturbances. Clinicians should be aware of possible adverse cognitive reactions during statin therapy, including rosuvastatin.