ABSTRACT
Statins are one of the most commonly prescribed drugs in clinical practice. They are usually well tolerated and effectively prevent cardiovascular events. Most adverse effects associated with statin therapy are muscle-related. The recent statement of the European Atherosclerosis Society (EAS) has focused on statin associated muscle symptoms (SAMS), and avoided the use of the term 'statin intolerance'. Although muscle syndromes are the most common adverse effects observed after statin therapy, excluding other side effects might underestimate the number of patients with statin intolerance, which might be observed in 10-15% of patients. In clinical practice, statin intolerance limits effective treatment of patients at risk of, or with, cardiovascular disease. Knowledge of the most common adverse effects of statin therapy that might cause statin intolerance and the clear definition of this phenomenon is crucial to effectively treat patients with lipid disorders. Therefore, the aim of this position paper was to suggest a unified definition of statin intolerance, and to complement the recent EAS statement on SAMS, where the pathophysiology, diagnosis and the management were comprehensively presented.
ABSTRACT
Statins are one of the most commonly prescribed drugs in clinical practice. They are usually well tolerated and effectively prevent cardiovascular events. Most adverse effects associated with statin therapy are muscle-related. The recent statement of the European Atherosclerosis Society (EAS) has focused on statin-associated muscle symptoms (SAMS), and avoided the use of the term 'statin intolerance'. Although muscle syndromes are the most common adverse effects observed after statin therapy, excluding other side effects might underestimate the number of patients with statin intolerance, which might be observed in 10 - 15% of patients. In clinical practice, statin intolerance limits effective treatment of patients at risk of, or with, cardiovascular disease. Knowledge of the most common adverse effects of statin therapy that might cause statin intolerance and the clear definition of this phenomenon is crucial to effectively treat patients with lipid disorders. Therefore, the aim of this position paper was to suggest a unified definition of statin intolerance, and to complement the recent EAS statement on SAMS, where the pathophysiology, diagnosis and the management were comprehensively presented.
Subject(s)
Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Muscular Diseases/chemically induced , Cardiovascular Diseases/prevention & control , Dyslipidemias/drug therapy , Humans , Muscular Diseases/epidemiologyABSTRACT
Left ventricular hypertrophy (LVH) with intraventricular septum thickness (IVST) between 1.2 and 1.5 cm in athletes represents a "gray zone" between physiologic adaptation and mild hypertrophic cardiomyopathy (HCM). Various echo and laboratory parameters have been reported till now in the literature to discriminate the "gray zone" entities. Aim of this study was to assess the efficacy of these "classic" parameters in differentiating physiologic LVH in athletes from mild HCM in a highly selected population. Nine highly trained athletes with IVST (1.28 ± 0.07 cm), 9 patients with mild HCM (1.38 ± 0.11 cm), and 26 athletes without LVH (1.06 ± 0.09 cm; P < 0.0005) underwent echocardiographic study, cardiopulmonary treadmill exercise stress test, and brain natriuretic peptide (BNP) measurement before and after exercise. Among all parameters tested, 7 were found to significantly differ between "gray zone" groups. After bootstrapping analysis, it was found that athletes with left ventricular end-diastolic diameter <4.74 cm, mitral deceleration time >200 ms, isovolumic relaxation time >94 ms, tricuspid E/A < 1.63, septum Em < 9.5 cm/sec, relative wall thickness >0.445, and a BNP value at rest >9.84 pg/mL had a greater possibility for having underlying cardiomyopathy. A 10-point score based on these parameters showed accuracy (area under the curve = 0.958 [95%CI: 0.738-1.0; P = 0.00005, standard error = 0.0342]) for revealing HCM in a gray zone athletic population. Differentiation of adaptive LVH versus HCM in a gray zone population could be facilitated by recognition of certain features referring to LV dimensions, diastolic function, and BNP.
Subject(s)
Athletes , Cardiomegaly, Exercise-Induced/physiology , Cardiomyopathy, Hypertrophic/diagnostic imaging , Echocardiography/methods , Heart Ventricles/diagnostic imaging , Hypertrophy, Left Ventricular/diagnostic imaging , Natriuretic Peptide, Brain/blood , Adolescent , Adult , Cardiomyopathy, Hypertrophic/blood , Cardiomyopathy, Hypertrophic/physiopathology , Diagnosis, Differential , Exercise Test , Follow-Up Studies , Heart Ventricles/physiopathology , Humans , Hypertrophy, Left Ventricular/blood , Hypertrophy, Left Ventricular/physiopathology , Male , Pilot Projects , Retrospective Studies , Young AdultABSTRACT
There is evidence that small dense low density lipoprotein (sdLDL) subfractions are more atherogenic than buoyant LDL. Therefore, it is relevant to assess the effect of lipid lowering drugs on LDL subfractions. In this editorial we discuss the effect of ezetimibe (EZE; a cholesterol transport inhibitor) alone or in combination with a statin, on sdLDL levels. We conclude that, based on currently available evidence, more studies are needed before a definitive answer can be provided regarding the effect of EZE on sdLDL levels.
Subject(s)
Azetidines/therapeutic use , Cholesterol, LDL/chemistry , Cholesterol, LDL/drug effects , Hypercholesterolemia/drug therapy , Anticholesteremic Agents/pharmacology , Anticholesteremic Agents/therapeutic use , Azetidines/administration & dosage , Azetidines/pharmacology , Chemical Fractionation , Cholesterol/blood , Cholesterol/chemistry , Cholesterol, LDL/blood , Dissent and Disputes , Ezetimibe , Humans , Hypercholesterolemia/blood , Hypercholesterolemia/diagnosis , Lipoproteins, LDL/blood , Lipoproteins, LDL/chemistry , Particle Size , Prognosis , Simvastatin/administration & dosage , Simvastatin/pharmacologyABSTRACT
Carbon dioxide (CO(2)) balneotherapy is a kind of remedy with a wide spectrum of applications which have been used since the Middle Ages. However, its potential use as an adjuvant therapeutic option in patients with cardiovascular disease is not yet fully clarified. We performed a thorough review of MEDLINE Database, EMBASE, ISI WEB of Knowledge, COCHRANE database and sites funded by balneotherapy centers across Europe in order to recognize relevant studies and aggregate evidence supporting the use of CO(2) baths in various cardiovascular diseases. The three main effects of CO(2) hydrotherapy during whole body or partial immersion, including decline in core temperature, an increase in cutaneous blood flow, and an elevation of the score on thermal sensation, are analyzed on a pathophysiology basis. Additionally, the indications and contra-indications of the method are presented in an evidence-based way, while the need for new methodologically sufficient studies examining the use of CO(2) baths in other cardiovascular substrates is discussed.