RESUMEN
Extremitovascular arterial ischemic disease (lower extremity peripheral arterial disease - PAD) is an important manifestation of systemic atherosclerosis and other arterial diseases of vascular system. The lower the ankle-brachial pressure index, the greater the risk of serious acute instable organovascular events (e. g. acute myocardial infarction, stroke). Complex prevention and treatment of extremitovascular arterial disease is discussed in this article. Angiology/vascular medicine is the fastest growing field of internal medicine.
Asunto(s)
Aterosclerosis , Complicaciones de la Diabetes , Diabetes Mellitus , Enfermedad Arterial Periférica , Índice Tobillo Braquial , Humanos , Extremidad Inferior , Enfermedad Arterial Periférica/terapia , Factores de RiesgoRESUMEN
Antiplatelet therapy by acetylsalicylic acid (ASA, aspirin) provided pivotal advances in the prevention and treatment of organovascular (angiovascular, cardiovascular, cerebrovascular, extremitovascular, renovascular, genitovascular, mesenteriointestinokolonovascular, bronchopulmovascular, oculovascular, otovascular and other) arterial ischemic diseases. Currently available antiplatelet drugs have some limitations which might be overcomed by improved dosing regimens, use of combination of agents affecting different platelet functions and, in particular, by the new antiplatelet drugs (new arterial antithrombotics) with distinct pharmacodynamic properties offering new advantages, including faster onset of action, greater potency, and reversibility of effects.Key words: arteriothromboprophylaxis - arterial thrombosis - classic antiplatelet drugs - new antiplatelet agents - organovascular arterial diseases.
Asunto(s)
Aspirina/uso terapéutico , Inhibidores de Agregación Plaquetaria/uso terapéutico , Trombosis/prevención & control , Enfermedades Vasculares/prevención & control , Humanos , Activación Plaquetaria , Pruebas de Función Plaquetaria , Enfermedades Vasculares/tratamiento farmacológicoRESUMEN
BACKGROUND: The goal of the retrospective observatory cross-sectional study was to evaluate the benefit of alanine aminotransferase screening of blood donors in prevention of hepatitis B and C transmission by haemotherapy in context of actual screening methods. METHODS: Donations with elevated ALT more than the defined limit (ALT men 80 IU/l, women 64 IU/l, spectrophotometric UV test, KUADRO(TM), BPC BioSed Srt, Castelnuovo di Porto Roma, Italy) and/or reactivity any of the hepatitis screening parameters HBsAg, anti-HBc, anti-HCV (chemiluminescence method, ARCHITECT i2000(TM), Illinois, USA) were evaluated. Donors were confirmatory retested. They were classified into groups with common biological properties according to their final virological status and statistically evaluated in programs Graph Pad Prism 6.05 and Microsoft Excel 2003. RESULTS: From a total of 61 214 donations elevated ALT was found in 420 (0.69 %), active HBV in 25 (0.04 %), active HCV infection in 5 (0.01 %) blood donors. Coincidental elevation of ALT and active HBV infection occured in 1 donor (0.002 %), as well as HCV (0.002 %). Levels of ALT were higher in the group with elevated ALT without active HBV or HCV infection than in groups with active HCV and HCV infection (p < 0.05). Occurence of blood donor in seronegative anti-HCV window was not observed. Elevated ALT was low specific (69.14 %) and senzitive (6.45 %) for active hepatitis. We did not prove positive correlation of ALT and S/CO (signal-to-cut-off) anti-HBc (Spearman r = -0,565, p < 0.0001), ALT and S/CO anti-HCV (Spearman r = -0.1046, p = 0.0022), in ALT and S/CO HBsAg the result was not statistically significant (Spearman r = -0.00968, p = 0.77). Positive but statistically insignificant correlation ALT and S/CO anti-HCV occured in the group of 5 blood donors with active HCV infection (Spearman r = 0.4, p = 0.51). Screening scheme for HCV infection testing anti-HCV + ALT was per one donation by 0.18 more expensive than the scheme anti-HCV + HCV RNA due to amount of waisted donations with ALT elevation (825 TU, 41 388.89). CONCLUSION: Elevation of ALT in blood donors was not pathognomonic for hepatitis B and C infection. Screening of HCV consisting of anti-HCV + HCV RNA (nucleic acid testing method, COBAS AmpliScreen HCV 2.0(TM), ROCHE Diagnostics, Hague Road, Indianapolis, USA) is more cost-effective than the scheme anti-HCV + ALT.
Asunto(s)
Alanina Transaminasa/sangre , Donantes de Sangre , Anticuerpos contra la Hepatitis B/sangre , Hepatitis B/sangre , Anticuerpos contra la Hepatitis C/sangre , Hepatitis C/sangre , ARN Viral/sangre , Transfusión Sanguínea , Estudios Transversales , Femenino , Hepacivirus/genética , Hepacivirus/inmunología , Hepatitis B/diagnóstico , Hepatitis B/prevención & control , Hepatitis B/transmisión , Antígenos del Núcleo de la Hepatitis B/inmunología , Antígenos de Superficie de la Hepatitis B/inmunología , Virus de la Hepatitis B/inmunología , Hepatitis C/diagnóstico , Hepatitis C/prevención & control , Hepatitis C/transmisión , Humanos , Masculino , Tamizaje Masivo , Estudios Retrospectivos , Conducta de Reducción del Riesgo , Espectrofotometría UltravioletaRESUMEN
Until recently, vitamin K antagonists (VKA; predominantly warfarin) were the only oral anticoagulants for primary and secondary prevention of venous thromboembolism. Prevention and therapy with novel, direct, non-VKA oral anticoagulant agents (NOACs; DOACs: dabigatran, rivaroxaban, apixaban, edoxaban), have recently become available as an alternative to VKA. NOACs have been shown to be non-inferior or superior to VKA in clinical trials. Available results suggest that real world safety of NOACs is mostly consistent with results observed in clinical trials. The most effective method is triple simultaneous prevention of venous thromboembolism (pharmacoâkinezioâmechanoâphlebothromboemboloprophylaxis).Key words: oral anticoagulants - NOAC/DOAC - thromboprophylaxis - venous thromboembolism - VKA.
Asunto(s)
Anticoagulantes/uso terapéutico , Tromboembolia Venosa/tratamiento farmacológico , Tromboembolia Venosa/prevención & control , Administración Oral , Humanos , Tromboembolia Venosa/etiologíaRESUMEN
In addition to organovascular arterial ischemic diseases (cardiovascular, vasculovascular, neurovascular, extre-mitovascular, renovascular, genitovascular, bronchopulmovascular, mesenteriovascular, osteoarthromusculovascular, dermovascular, oculovascular, otovascular, stomatovascular etc.), aortic diseases contribute to the wide spectrum of arterial diseases: aortic aneurysms (AA), acute aortic syndromes (AAS) including aortic dissection (AD), intramural haematoma (IMH), penetrating atherosclerotic ulcer (PAU) and traumatic aortic injury (TAI), pseudoaneurysm, aortic rupture, atherosclerosis, vasculitis as well as genetic diseases (e.g. Turner syndrome, Marfan syndrome, Ehlers-Danlos syndrome) and congenital abnormalities including the coarctation of the aorta (CoA). Similarly to other arterial diseases, aortic diseases may be diagnosed after a long period of subclinical development or they may have an acute presentation. Acute aortic syndrome is often the first sign of the disease, which needs rapid diagnosis and decisionmaking to reduce the extremely poor prognosis. Key clinical-etiology-anatomy-patophysiology (CEAP) diagnostic aspects of aortic diseases are discussed in this document (project Vessels).
Asunto(s)
Aorta Abdominal , Aorta Torácica , Enfermedades de la Aorta/clasificación , Enfermedades de la Aorta/diagnóstico , Enfermedad Aguda , Enfermedades de la Aorta/etiología , Enfermedades de la Aorta/fisiopatología , Enfermedad Crónica , HumanosRESUMEN
The prevalence and the incidence of chronic and acute venous vascular disease has been shown to be globally very high, in both industrialized and developing countries. Chronic venous diseases of lower extremities are being an integral part of the third millennium's deadly angiopandemy, at the present time. The rate of the most severe cases with advanced stage of venous failure is approximately twice as high in the population (2.1 %) as has been assumed so far. Among venoactive drugs (VAD), micronized purified flavonoid fraction (MPFF) of diosmin hesperidin remains the agent with the highest degree of recommendation and it also indicated to pharmacotherapeutical support of leg ulcer healing, along with sulodexide and pentoxifylline. Compressive sclerotherapy, liquid or foam, is a safe and effective invasive method to treat telangiectasias, reticular varicose veins and subcutaneous varicose veins. Direct oral anticoagulants (DOAC) represent one of the therapeutic and preventive options of deep venous thrombosis (DVT) and of venous thromboembolism (VTE) with a limitation in patients with malignant conditions and in pregnancy. The most effective is triple simultaneous pharmaco-kinezio-mechano-phlebothromboemboloprophylaxis. Superficial vein thromboses longer than 5 cm are indicated to anticoagulant therapy too.
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Várices/terapia , Insuficiencia Venosa/terapia , Trombosis de la Vena/terapia , Anticoagulantes/uso terapéutico , Enfermedad Crónica , Humanos , Extremidad Inferior/irrigación sanguínea , Escleroterapia , Cicatrización de HeridasRESUMEN
Pelvic congestion syndrome: chronic symptoms, which may include pelvic pain, perineal heaviness, urgency of micturition, and post-coital pain, caused by ovarian and/or pelvic vein reflux and/or obstruction, and which may be associated with vulvar, perineal, and/or lower extremity varices. The VEIN-TERM consensus document was developed by a transatlantic interdisciplinary faculty of experts under the auspices of the American Venous Forum (AVF), the European Venous Forum (EVF), the International Union of Phlebology (IUP), the American College of Phlebology (ACP), and the International Union of Angiology (IUA). It provides recommendations for fundamental venous terminology. Project Vessels of AS SMC.
Asunto(s)
Hiperemia/diagnóstico , Hiperemia/terapia , Extremidad Inferior/irrigación sanguínea , Consenso , Humanos , Hiperemia/complicaciones , Dolor Pélvico/complicaciones , Dolor Pélvico/diagnóstico , Dolor Pélvico/terapia , Guías de Práctica Clínica como Asunto , Síndrome , Várices/complicaciones , Várices/diagnóstico , Várices/terapiaRESUMEN
Erectile dysfunction is a highly prevalent and progressive condition affecting the quality of life of man and his sexual partner. Evidence is accumulating in favour of erectile dysfunction as a sign of a genitovascular disease (GVD) in the majority of patients. Erectile dysfunction may be considered as the clinical manifestation of a organovascular disease affecting penis (male genitovascular disease - MGVD) as well as angina pectoris is the typical manifestation of a vascular disease affecting coronary arteries of a heart (cardiovascular disease - CVD). Several studies confirm the assumption that erectile dysfunction symptoms were found to come prior to cardiovascular disease symptoms in 60-95 % of CVD patients with mean interval of 2-3 years and likewise of all organovascular diseases (OVD). Four potent selective PDE5Is have been approved by the EMA for the treatment of erectile dysfunction. Physicians should systematically look for erectile dysfunction in any male with vascular risk factors.
Asunto(s)
Arteriopatías Oclusivas/complicaciones , Disfunción Eréctil/complicaciones , Enfermedades Vasculares/diagnóstico , Enfermedades Vasculares/fisiopatología , Arteriopatías Oclusivas/fisiopatología , Enfermedades Cardiovasculares/fisiopatología , Disfunción Eréctil/tratamiento farmacológico , Disfunción Eréctil/epidemiología , Disfunción Eréctil/fisiopatología , Humanos , Masculino , Inhibidores de Fosfodiesterasa 5/uso terapéutico , Calidad de Vida , Factores de Riesgo , Enfermedades Vasculares/epidemiologíaRESUMEN
UNLABELLED: Hyperuricaemia represents nowaday the new risk factor for cardiovascular diseases. Prevalence data and its treatment in our patient´s population are still missing. Literature data shows, that its prevalence differs in various populations significantly from 4 % up to 40 % with race and geographical means. In the hospital population its prevalence is about 7 % and represents the important predictor of hospital mortality, e.i with heart failure. From the Framingham data relative risk was estimated of 25 % for cardiovascular diseases, coronary heart disease and all-course mortality. From the epidemiologic survey Mirror Slovakia hyperuricaemia was evaluated from the sample of 20â¯000 patients from the primare care physicians in order to see the picture on this newer risk factor. KEY WORDS: cardiovascular diseases - epidemiology - hyperuricaemia - therapy.
RESUMEN
Despite significant improvement in the diagnosis and therapy of cardiovascular diseases their global risk and proportion of their clinical forms remains very high. Still the large part of the patients cannot reach the estimated target lipid levels despite statin therapy. Low adherence to preventive programmes with physical training and diet leads to progression of the pathological process of atherothrombosis. One possible therapeutic approach could be the combined hypolipidemic treatment. In this context we followed-up the size of lipoprotein particles among very high risk patients on statin monotherapy, where phytosterole was added. Lipoprotein profile among very high risk patients during combined therapy lead to improvement and therefore may contribute to lowering of their residual risk.
Asunto(s)
Enfermedades Cardiovasculares , Inhibidores de Hidroximetilglutaril-CoA Reductasas/uso terapéutico , Lipoproteínas/sangre , Fitosteroles/uso terapéutico , Enfermedades Cardiovasculares/sangre , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/prevención & control , Quimioterapia Combinada , Salud Global , Humanos , Incidencia , Lipoproteínas/efectos de los fármacos , Factores de RiesgoRESUMEN
Hyperuricaemia represents nowaday the new risk factor for cardiovascular diseases. Prevalence data and its treatment in our patient's population are still missing. Literature data shows, that its prevalence differs in various populations significantly from 4% up to 40% with race and geographical means. In the hospital population its prevalence is about 7% and represents the important predictor of hospital mortality, e.i with heart failure. From the Framingham data relative risk was estimated of 25% for cardiovascular diseases, coronary heart disease and all-course mortality. From the epidemiologic survey Mirror Slovakia hyperuricaemia was evaluated from the sample of 20 000 patients from the primare care physicians in order to see the picture on this newer risk factor.
Asunto(s)
Enfermedad de la Arteria Coronaria/epidemiología , Hiperuricemia/epidemiología , Atención Primaria de Salud , Enfermedades Cardiovasculares/epidemiología , Enfermedad Coronaria/epidemiología , Mortalidad Hospitalaria , Humanos , Pacientes Internos , Prevalencia , Factores de Riesgo , Eslovaquia/epidemiologíaRESUMEN
AIM: The aim of this review is to address documents and a number of studies on hypertension published in the last years in order to assess their contribution to our expanding knowledge of arterial hypertension. DISCUSSION: Arterial hypertension is not defined by symptoms and signs but by numbers of blood pressure values. Arterial hypertension is vascular disease (vascular risk factor) of many vascular diseases (atherosclerosis; arteriolosclerosis/arteriolonecrosis/arteriolocalcinosis; arterial thrombosis; arterial embolism; arterial thromboembolism; arterial dissection; complicated arterial aneurysm) and other. CONCLUSION: Arterial hypertension is cause and consequence of functional (endothelial dysfunction) and of structural organovascular injury (multiorganomultivascular disease). Blood vessels are culprits, implements and victims of arterial hypertension and of organovascular arterial diseases. KEY WORDS: angiology/vascular medicine - arterial hypertension - blood vessels - internal medicine - organovascular arterial diseases - vascular.
RESUMEN
AIM: The aim of this review is to address documents and a number of studies on hypertension published in the last years in order to assess their contribution to our expanding knowledge of arterial hypertension. DISCUSSION: Arterial hypertension is not defined by symptoms and signs but by numbers of blood pressure values. Arterial hypertension is vascular disease (vascular risk factor) of many vascular diseases (atherosclerosis; arteriolosclerosis/arteriolonecrosis/arteriolocalcinosis; arterial thrombosis; arterial embolism; arterial thromboembolism; arterial dissection; complicated arterial aneurysm) and other. CONCLUSION: Arterial hypertension is cause and consequence of functional (endothelial dysfunction) and of structural organovascular injury (multiorganomultivascular disease). Blood vessels are culprits, implements and victims of arterial hypertension and of organovascular arterial diseases.
Asunto(s)
Aneurisma/epidemiología , Aterosclerosis/epidemiología , Embolia/epidemiología , Hipertensión/epidemiología , Tromboembolia/epidemiología , Trombosis/epidemiología , Calcificación Vascular/epidemiología , Presión Sanguínea , Humanos , Factores de RiesgoRESUMEN
OBJECTIVE: To assess the relationship of high density lipoprotein subfractions to newly-diagnosed lower extremity artery disease (LEAD) in individuals without diabetes mellitus and without hypolipidemic therapy. METHODS: This cross-sectional study involves 106 subjects: 51 had newly diagnosed LEAD and no diabetes anamnesis and were not on hypolipidemic therapy; and 55 controls were without clinical presentation of LEAD and were normolipidemic. Analysis of HDL subclasses was performed by an innovative electrophoresis method on polyacrylamide gel (PAG), the Lipoprint HDL System. RESULTS: In LEAD subjects, total HDL-C levels as well as HDL2 (intermediate-to-large particles) subfraction levels were decreased (p<0.0001 and p<0.019 respectively). Interestingly the HDL3 (small particles) subfraction was significantly higher and lost its proportional relationship within the HDL cholesterol fraction (p<0.025, p<0.01 respectively). CONCLUSION: These findings pointed out that: (i) the reduction of HDL-C and especially HDL2 subpopulation opposite to the increase of small HDL3 subclass may be considered as important predictors of cardiovascular diseases. (ii) there are undisputable advantages of using Lipoprint HDL to identify HDL subfractions; the presence of high concentration of small HDL in patients with PAD/LEAD emphasizes that the potentially proatherogenic subclass of HDL family is linked to small HDL.
Asunto(s)
Electroforesis/métodos , Lipoproteínas HDL2/sangre , Lipoproteínas HDL3/sangre , Enfermedad Arterial Periférica/metabolismo , Anciano , Aterosclerosis/metabolismo , Estudios Transversales , Diabetes Mellitus , Femenino , Humanos , Lipoproteínas HDL2/química , Lipoproteínas HDL3/química , Masculino , Persona de Mediana Edad , Valor Predictivo de las Pruebas , EslovaquiaRESUMEN
Angioedema is defined as a vascular reaction of the deep dermis/mucous and/or subcutaneous/submucosal tissues with localized vasodilatation and increased permeability of blood vessels resulting in tissue swelling. Angioedema can be mediated by bradykinin or mast cell mediators including histamine. Bradykinin-mediated angioedema can occur either on a hereditary (HAE) or acquired (AAE) basis, due to a deficiency/defect of C1 inhibitor (C1-INH) or not. Three forms of HAE have been defined: HAE due to C1-INH deficiency (type 1 HAE, HAE-1), characterized by low antigenic and functional C1-INH levels; HAE due to C1-INH dysfunction (type 2 HAE, HAE-2), characterized by normal (or elevated) antigenic but low functional C1-INH levels; and HAE with normal C1-INH antigenic and functional levels (HAE-3). Acquired C1-INH deficiency refers to patients with angioedema due to C1-INH deficiency on an acquired basis. There are a variety of acquired types of angioedema not due to C1-INH deficiency, and these may be bradykinin mediated (e.g. angiotensin-converting enzyme inhibitor-induced angioedema) or mast cell mediator histamine mediated (e.g. anaphylactic angioedema and urticarial angioedema). In recent years there have been several changes on how we look at the anaphylaxis. The spectrum of trigger factors and diagnostic and therapeutic algorithms has changed significantly. The anaphylaxis is regarded as any sudden severe hypersensitive reaction, which potentially can lead to death. Term anaphylactoid reaction is no more recommended to be used. Drug of first choice is adrenaline/epinephrine administered intramuscularly. Each patient at risk of angioedema should have a written individual rescue plan and knowledge how to use the first aid medicines.
Asunto(s)
Angioedema/diagnóstico , Guías de Práctica Clínica como Asunto , Angioedema/terapia , HumanosRESUMEN
Organovascular arterial ischemic diseases (cardiovascular, cerebrovascular, extremitovascular, renovascular, genitovascular, pulmovascular, mesenterovascular, dermovascular, oculovascular, otovascular, stomatovascular etc.) are an important manifestations of systemic atherosclerosis and other arterial diseases of vascular system (arteriolosclerosis/arteriolonecrosis; diabetic macroangiopathy; diabetic microangiopathy; Mönckeberg´s mediosclerosis/mediocalcinosis; arteritis - vasculitis; syndromes of arterial compression; fibromuscular dysplasia; cystic adventitial degeneration; arterial thrombosis; arterial embolism/thromboembolism; traumatic and posttraumatic arteriopathies; physical arteriopathies; chemical and toxic arteriopathies; iatrogenic arterial occlusions; dissection of aorta and of arteries; coiling; kinking; complicated arterial aneurysms; arteriovenous fistula, rare vascular diseases). Key clinical-etiology-anatomy-pathophysiology (CEAP) aspects of the mesenteriovascular arterial ischemic diseases are discussed in this article (project Vessels).
Asunto(s)
Arteriopatías Oclusivas/clasificación , Arteriopatías Oclusivas/prevención & control , Arteriopatías Oclusivas/diagnóstico , Humanos , EslovaquiaRESUMEN
OBJECTIVE: The identification of an atherogenic and a non-atherogenic lipoprotein profile, athero phenotype B vs. non-athero phenotype A, in a group of healthy normolipidemic subjects reveals a new clinical phenomenon in lipoprotein profiles, an atherogenic normolipidemia. Individuals with atherogenic normolipidemia are at increased risk to develop premature atherothrombosis and experience a sudden cardiovascular event. METHODS: A quantitative analysis of non-atherogenic and atherogenic lipoproteins in plasma in a group of healthy normolipidemic volunteers who had no clinical signs of cardiovascular system impairment was performed. An innovative electrophoresis method on polyacrylamide gel (PAG) (Lipoprint LDL System, USA) was used for the analysis of plasma lipoproteins. With regard to lipids, total cholesterol and triglycerides in plasma were analyzed with an enzymatic method, CHOD PAP (Roche Diagnostics, FRG). Prostacyclin and thromboxane A2 were analyzed with an ELISA analysis (DRG USA). A new parameter, the score for anti-atherogenic risk (SAAR), was calculated as the ratio between non-atherogenic to atherogenic plasma lipoproteins in examined subjects. RESULTS: There was a high concentration of LDL3-7 subfraction (p<0.0001) and a slowly increasing triglyceride concentration (p<0.05) in the atherogenic subgroup. The non-atherogenic subgroup of healthy subjects was characterized by high SAAR scores, as well as a low concentration of LDL3-7 subfractions (p<0.0001). Other statistically significant differences between the atherogenic and non-atherogenic subgroup, including total cholesterol, prostanoid parameters (prostacyklin, thromboxane A2), and lipoproteins values, were not confirmed. CONCLUSIONS: The advantages of this new method include: (i) identification of an atherogenic and a nonatherogenic lipoprotein profile in an individual's plasma (ii) identification of an atherogenic normolipidemic lipoprotein profile in plasma (iii) introduction of a new risk measure, the score for anti-atherogenic risk (SAAR), for an estimation of a patient's atherogenic risk of atherothrombosis development. (iv) the presence of small dense LDL in plasma is decisive for declaration of an atherogenic lipoprotein profile. It is valid for hyperlipidemia and for normolipidemia as well.
Asunto(s)
Aterosclerosis/genética , Lípidos/sangre , Lipoproteínas/sangre , Aterosclerosis/sangre , Aterosclerosis/epidemiología , Enfermedades Cardiovasculares/sangre , Enfermedades Cardiovasculares/genética , Colesterol/sangre , Ensayo de Inmunoadsorción Enzimática , Femenino , Humanos , Masculino , Prostaglandinas/sangre , Valores de Referencia , Medición de Riesgo , Factores de Riesgo , Trombosis/sangre , Trombosis/epidemiología , Trombosis/genética , Adulto JovenRESUMEN
OBJECTIVE: In the subjects, who survived a stroke, an atherogenic lipoprotein profile phenotype B, was identified and a predominance of atherogenic lipoproteins of the lipoprotein families, VLDL and LDL, in the lipoprotein spectrum, was confirmed. The higher total cholesterol, triglycerides, and low HDL concentrations were accompanied by high serum levels of small dense LDL - strong atherogenic subfractions of the LDL family. High LDL2 also contributes to the creation of the atherogenic lipoprotein profile. Conversely, decreased serum concentration of LDL1 suggests, that the LDL1 subfraction does not contribute to the creation of an atherogenic lipoprotein profile of specific individuals, i.e., those who survived a stroke. MATERIALS AND METHODS: A quantitative analysis of serum lipoproteins in a group of stroke patients, and in a group of healthy normolipidemic volunteers, without signs of clinically manifested impairment of the cardiovascular system, was performed. For the analysis of plasma lipoproteins, an innovative electrophoresis method was used, on polyacrylamide gel (PAG) - the Lipoprint LDL system, (Quantimetrix corp., CA, USA). With regard to lipids, total cholesterol and triglycerides in serum were analyzed with an enzymatic CHOD PAP method (Roche Diagnostics, FRG). A new parameter, the score for anti-atherogenic risk (SAAR), was calculated as the ratio between non-atherogenic to atherogenic serum lipoproteins in examined subjects. RESULTS: An atherogenic lipoprotein profile phenotyp B was identified in the individuals who survived a stroke. There were increased concentrations of total cholesterol, triglycerides (p<0.001), and atherogenic lipoproteins: VLDL (p<0.001), total LDL, LDL2 (p<0.0001) and LDL3-7 (p<0.01), in the group of stroke patients, compared to the control group. The LDL1 subfraction, like HDL, was decreased and did not contribute to the formation of the atherogenic lipoprotein spectrum in stroke-surviving individuals. Therefore, it can be assumed that the LDL1 subfraction is not an atherogenic part of the LDL family, which was usually considered to be an atherogenic lipoprotein part of the lipoprotein spectrum. Decreased SAAR values - score of anti-atherogenic risk, was confirmed in the stroke surviving individuals, compared to the controls, with high statistical significance (p<0.0001). CONCLUSIONS: The advantages of this new method include: (i) Identification of an atherogenic and a non-atherogenic lipoprotein profile, in the serum of examined individuals. (ii) Identification of an atherogenic normopidemic lipoprotein profile; phenotype B in subjects who survived a stroke. (iii) Introduction of new risk measure, the score for anti-atherogenic risk (SAAR), to estimate the atherogenic risk of examined individuals. (iv) Declaration of an atherogenic lipoprotein profile is definitive when small dense LDL are present in serum. It is valid for hyperlipidemia and for normolipidemia as well. (v) Selection of optimal therapeutic measures, including removal of atherogenic lipoproteins, as a part of a complex therapeutic approach, and the secondary prevention of a relapsing ischemic cerebral-vascular event.
Asunto(s)
Aterosclerosis/metabolismo , Hiperlipidemias/metabolismo , Lipoproteínas/sangre , Accidente Cerebrovascular/metabolismo , Anciano , Anciano de 80 o más Años , Aterosclerosis/epidemiología , Colesterol/sangre , HDL-Colesterol/sangre , LDL-Colesterol/sangre , VLDL-Colesterol/sangre , Femenino , Humanos , Hiperlipidemias/epidemiología , Masculino , Persona de Mediana Edad , Proyectos Piloto , Medición de Riesgo/métodos , Factores de Riesgo , Accidente Cerebrovascular/epidemiología , Sobrevivientes/estadística & datos numéricos , Triglicéridos/sangreRESUMEN
OBJECTIVE: The HDL family forms a protective part of plasma lipoproteins. It consists of large HDL, intermediate HDL, and small HDL subclasses. The large HDL and intermediate HDL subclasses are considered anti-atherogenic parts of the HDL family. The atherogenicity of the small HDL subclass is currently the subject of much discussion. In the patient group with the diagnosis of cardiovascular disease (arterial hypertension, coronary heart disease) and in individuals with a non-atherogenic hypercholesterolemia, a type of lipoprotein profile (either a non-atherogenic phenotype A, or an atherogenic phenotype B) was identified, and a concentration of small dense LDL (sdLDL) was analyzed. The aim of this study was to identify the major representative of the HDL subclasses in the individuals with cardiovascular diseases, who had an atherogenic lipoprotein phenotype B, and in the individuals with the diagnosis of non-atherogenic hyper-betalipoproteinemia LDL1,2, who had a non-atherogenic lipoprotein phenotype A. METHODS: Identification of the specific lipoprotein phenotype and a quantitative analysis of small dense LDL was performed by an electrophoresis method on polyacrylamide gel (PAG), using the Lipoprint LDL system. For a quantitative analysis of HDL subclasses, i.e., large HDL, intermediatete HDL, and small HDL, in subjects with newly diagnosed cardiovascular diseases (arterial hypertension and coronary heart disease), and in subjects with a non-atherogenic hypercholesterolemia (hyper-betalipoproteinemia LDL1,2), we used an innovative electrophoresis method on polyacrylamide gel (PAG), the Lipoprint HDL system. With regard to lipids, total cholesterol and triglycerides in plasma were analyzed by an enzymatic CHOD PAP method. A control group consisted of a group of healthy normolipidemic volunteers without signs of clinically manifested impairment of the cardiovascular system. RESULTS: In the patient group with the diagnosis of arterial hypertension (p<0.0002) and coronary heart disease (p<0.0001), (both are classified as cardiovascular diseases), the large HDL subclass was significantly decreased and the small HDL subclass was increased (p<0.0001). The concentration of the intermediate HDL subclass did not differ from that of the control group. These results were in accordance with an atherogenic lipoprotein phenotype B in individuals with the diagnosis of cardiovascular diseases, where, using a Lipoprint LDL analysis, a high concentration of atherogenic small dense LDL (p<0.0001) was found. Thus, it seems that the small HDL subclass represents an atherogenic part of the HDL family. Conversely, an increased concentration of total HDL (p<0.0001), large HDL (p<0.005), and intermediate HDL subclasses (p<0.0001) was found in a group of subjects with a non-atherogenic hyper-betalipoproteinemia LDL1,2.The concentration of the small HDL subclass did not differ from that of the control group. In this non-atherogenic lipoprotein profile, only traces of atherogenic small dense LDL were identified. CONCLUSIONS: The advantages of this new method includes: (i) Identification of ten HDL subfractions with Lipoprint HDL analysis (large HDL1-3, intermediate HDL 4-7, and small HDL 8-10) . (ii) Discovery of a high concentration of small HDL in plasma lipoproteins in patients with cardovascular diseases with an atherogenic lipoprotein phenotype B, confirms that the atherogenic subclass of HDL family is attributable to small HDL. (iii) Presence of a low concentration of small HDL in non-atherogenic hypercholesterolemia also confirms the atherogenic characteristics of the small HDL subclass per se. (iv) Presence of small dense LDL is definitive to diagnose an atherogenic lipoprotein profile. It is valid for hyperlipidemia and for normolipidemia as well.