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Is lipoprotein(a) a  risk factor for ischemic stroke and venous thromboembolism?
AbstractThe structural similarity with plasminogen as well as thrombogenic and atherogenic in vitro functions raise the question if lipoprotein(a) (Lp(a)) is a  risk factor for venous thromboembolism (VTE) and ischemic stroke. Numerous case–control and prospective studies using different cut-off values to define high Lp(a) generated conflicting evidence for both VTE and ischemic stroke. Several meta-analyses demonstrated independent associations of elev ated Lp(a) with a history of VTE or ischemic stroke. However, the evidence of prospective studies for associations of Lp(a) with incident stroke or recurrent VTE remain...
Source: Clinical Research in Cardiology Supplements - April 1, 2019 Category: Cardiology Source Type: research

Lipoprotein(a) apheresis in patients with peripheral arterial disease: rationale and clinical results
AbstractPatients with symptomatic peripheral arterial disease (PAD) are at a  very high risk of cardiovascular morbidity and mortality. Elevated lipoprotein(a) levels have been shown to be a risk factor for coronary artery disease (CAD) and stroke. More recently elevated lipoprotein(a) levels have also been demonstrated to be associated with prevalent and incident PAD, and even may be a stronger risk factor for PAD compared with CAD. Lipoprotein apheresis is currently the only efficient way to lower lipoprotein(a) levels. Lipoprotein(a) apheresis has been shown to reduce major coronary events in patients with CAD. There...
Source: Clinical Research in Cardiology Supplements - April 1, 2019 Category: Cardiology Source Type: research

Lipoprotein(a) and proprotein convertase subtilisin/kexin type  9 inhibitors
AbstractLipoprotein(a) (Lp(a)) is an internationally accepted independent atherogenic risk factor. Details about its synthesis, many aspects of composition and clearance from the bloodstream are still unknown. LDL receptor (LDLR) (and probably other receptors) play a  role in the elimination of Lp(a) particles. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors increase the number of available LDLRs and in this way very effectively reduce the LDL cholesterol (LDL-C) concentrations. As shown in controlled studies using PCSK9 inhibitors, Lp(a) leve ls are decreased by 20 to 30%, though in some patients no eff...
Source: Clinical Research in Cardiology Supplements - April 1, 2019 Category: Cardiology Source Type: research

Lipoprotein apheresis is an optimal therapeutic option to reduce increased Lp(a) levels
AbstractBackgroundLipoprotein(a) (Lp(a)) is a  genetic risk factor for cardiovascular disease (CVD) and is associated with the induction and sustaining of atherosclerotic cardiovascular diseases (ASCVD). Since 2008 Lp(a) along with progressive CVD has been approved as an indication for regular lipoprotein apheresis (LA) in Germany. The German Lipoprotein Apheresis Registry (GLAR) has been initiated to provide statistical evidence for the assessment of extracorporeal procedures to treat dyslipidemia for both LDL-cholesterol (LDL-C) and Lp(a). The GLAR now allows prospective investigations over a 5-year period about annual...
Source: Clinical Research in Cardiology Supplements - April 1, 2019 Category: Cardiology Source Type: research

Lipoprotein(a) —antisense therapy
AbstractElevated levels of lipoprotein(a) (Lp(a)) contribute to the risk of early and severe cardiovascular disease (CVD) and Lp(a) is acknowledged as a  risk factor to be included in risk assessment. The established lipid-modifying medical therapies do not lower Lp(a) except niacin but no data of endpoint trials are available. Of the new lipid-modifying drugs a few have some impact on Lp(a). Whether the Lp(a) lowering effect contributes to the re duction of CVD events would have to be shown in Lp(a) dedicated trials. None of the available agents is indicated to lower Lp(a). Lipoprotein apheresis lowers levels of Lp(a) s...
Source: Clinical Research in Cardiology Supplements - April 1, 2019 Category: Cardiology Source Type: research

Prediction of cardiovascular risk by Lp(a) concentrations or genetic variants within the LPA gene region
AbstractIn the middle of the 1990s the interest in Lp(a) vanished after a  few badly performed studies almost erased Lp(a) from the map of biological targets. However, since roughly 10 years the interest has begun to grow again mainly for two reasons: first, genetic studies using easily accessible and high-throughput techniques for genotyping of single-nucleotide polym orphisms (SNPs) have allowed large studies in patients with cardiovascular disease and controls to be performed. This strengthened the earlier findings on a copy number variation in theLPA gene and its association with cardiovascular outcomes. Second, new...
Source: Clinical Research in Cardiology Supplements - April 1, 2019 Category: Cardiology Source Type: research

Lipoprotein(a) —an interdisciplinary challenge
AbstractLipoprotein(a) (Lp(a)) is an internationally recognized atherogenic risk factor which is inherited and not changed by nutrition or physical activity. At present, only proprotein convertase subtilisin/kexin type  9 (PCSK9) inhibitors may modestly decrease its concentration (but not in all patients)—leading to a certain decrease in cardiovascular events (CVE) in controlled studies. However, at present an elevation of Lp(a) is not a generally accepted indication for their use. More effective is lipoprote in apheresis (LA) therapy with respect to both lowering Lp(a) levels and reduction of CVE. In the future, an a...
Source: Clinical Research in Cardiology Supplements - April 1, 2019 Category: Cardiology Source Type: research

Lipoprotein(a) and mortality —a high risk relationship
AbstractLipoprotein(a) (Lp(a)) is an independent cardiovascular risk factor playing a  causal role for atherosclerotic cardiovascular disease (ASCVD). Early or progressive ASCVD or a familial predisposition are key findings which can be associated with Lp(a)-hyperlipoproteinemia (Lp(a)-HLP). The German guideline for the indication of lipoprotein apheresis in patients with Lp(a)-HLP has proved to be of value to identify patients at highest risk, using the composite of a Lp(a) threshold>60  mg/dl (>120  nmol/l) and clinical ASCVD progression despite effective LDL-C lowering therapy. In particular for such patien...
Source: Clinical Research in Cardiology Supplements - April 1, 2019 Category: Cardiology Source Type: research

Lipoprotein(a)
(Source: Clinical Research in Cardiology Supplements)
Source: Clinical Research in Cardiology Supplements - April 1, 2019 Category: Cardiology Source Type: research

Lipoprotein(a) apheresis in patients with peripheral arterial disease: rationale and clinical results
AbstractPatients with symptomatic peripheral arterial disease (PAD) are at a  very high risk of cardiovascular morbidity and mortality. Elevated lipoprotein(a) levels have been shown to be a risk factor for coronary artery disease (CAD) and stroke. More recently elevated lipoprotein(a) levels have also been demonstrated to be associated with prevalent and incident PAD, and even may be a stronger risk factor for PAD compared with CAD. Lipoprotein apheresis is currently the only efficient way to lower lipoprotein(a) levels. Lipoprotein(a) apheresis has been shown to reduce major coronary events in patients with CAD. There...
Source: Clinical Research in Cardiology Supplements - March 14, 2019 Category: Cardiology Source Type: research

Lipoprotein(a) —antisense therapy
AbstractElevated levels of lipoprotein(a) (Lp(a)) contribute to the risk of early and severe cardiovascular disease (CVD) and Lp(a) is acknowledged as a  risk factor to be included in risk assessment. The established lipid-modifying medical therapies do not lower Lp(a) except niacin but no data of endpoint trials are available. Of the new lipid-modifying drugs a few have some impact on Lp(a). Whether the Lp(a) lowering effect contributes to the re duction of CVD events would have to be shown in Lp(a) dedicated trials. None of the available agents is indicated to lower Lp(a). Lipoprotein apheresis lowers levels of Lp(a) s...
Source: Clinical Research in Cardiology Supplements - March 10, 2019 Category: Cardiology Source Type: research

Prediction of cardiovascular risk by Lp(a) concentrations or genetic variants within the LPA gene region
AbstractIn the middle of the 1990s the interest in Lp(a) vanished after a  few badly performed studies almost erased Lp(a) from the map of biological targets. However, since roughly 10 years the interest has begun to grow again mainly for two reasons: first, genetic studies using easily accessible and high-throughput techniques for genotyping of single-nucleotide polym orphisms (SNPs) have allowed large studies in patients with cardiovascular disease and controls to be performed. This strengthened the earlier findings on a copy number variation in theLPA gene and its association with cardiovascular outcomes. Second, new...
Source: Clinical Research in Cardiology Supplements - March 10, 2019 Category: Cardiology Source Type: research

Is lipoprotein(a) a  risk factor for ischemic stroke and venous thromboembolism?
AbstractThe structural similarity with plasminogen as well as thrombogenic and atherogenic in vitro functions raise the question if lipoprotein(a) (Lp(a)) is a  risk factor for venous thromboembolism (VTE) and ischemic stroke. Numerous case–control and prospective studies using different cut-off values to define high Lp(a) generated conflicting evidence for both VTE and ischemic stroke. Several meta-analyses demonstrated independent associations of elev ated Lp(a) with a history of VTE or ischemic stroke. However, the evidence of prospective studies for associations of Lp(a) with incident stroke or recurrent VTE remain...
Source: Clinical Research in Cardiology Supplements - March 4, 2019 Category: Cardiology Source Type: research

Lipoprotein(a) and proprotein convertase subtilisin/kexin type  9 inhibitors
AbstractLipoprotein(a) (Lp(a)) is an internationally accepted independent atherogenic risk factor. Details about its synthesis, many aspects of composition and clearance from the bloodstream are still unknown. LDL receptor (LDLR) (and probably other receptors) play a  role in the elimination of Lp(a) particles. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors increase the number of available LDLRs and in this way very effectively reduce the LDL cholesterol (LDL-C) concentrations. As shown in controlled studies using PCSK9 inhibitors, Lp(a) leve ls are decreased by 20 to 30%, though in some patients no eff...
Source: Clinical Research in Cardiology Supplements - March 4, 2019 Category: Cardiology Source Type: research