Mar Martinez Quesada

Dr. Mar Martinez Quesada


Research Focus & Metrics

Academic Career Length

22Years (2005-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 April 2005 in Revista Española de Cardiología (English Edition)
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Journal Article
Closed access
MQMar Martinez Quesada
Mar Martinez Quesada
FBFrancisco Trujillo Berraquero
Francisco Trujillo Berraquero
MDManolo Almendro Delia
Manolo Almendro Delia
RURafael Hidalgo Urbano
Rafael Hidalgo Urbano
JFJosé M. Cruz Fernández
José M. Cruz Fernández

12 April 2024 in Journal of Clinical Medicine
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Journal Article
Open access
PDF file
MOMaría Rosa Fernández Olmo
María Rosa Fernández Olmo
MBMagdalena Carrillo Bailen
Magdalena Carrillo Bailen
MQMar Martinez Quesada
Mar Martinez Quesada
CMCarmen Rus Mansilla
Carmen Rus Mansilla
MTMiriam Martin Toro
Miriam Martin Toro
Alberto CorderoAlberto Cordero
Alberto Cordero
Background: Lipoprotein(a) [Lp(a)] is a proatherogenic particle associated with increased cardiovascular risk. It is mainly genetically determined; so, the aim of our study is to evaluate the levels of Lp(a) in the relatives of a prospective cohort of patients who have suffered from an acute coronary syndrome (ACS) with Lp(a) ≥ 50 mg/dL. Methods: We conducted a multicenter prospective study, in which consecutive patients who had suffered from an ACS and presented Lp(a) ≥ 50 mg/dL and their first-degree relatives were included. Results: We included 413 subjects, of which 56.4% were relatives of the patients. Family history of early ischemic heart disease was present in 57.5%, and only 20.6% were receiving statin treatment. The family cohort was younger (37.5 vs. 59.1 years; p < 0.001), and 4% had ischemic heart disease and fewer cardiovascular risk factors. Mean Lp(a) levels were 64.9 mg/dL, 59.4% had levels ≥ 50 mg/dL, and 16.1% had levels ≥ 100 mg/dL. When comparing the patients with respect to their relatives, the mean level of Lp(a) was lower but without significant differences regarding the levels of LDLc, ApoB, and non-HDL. However, relatives with Lp(a) ≥ 50 mg/dL, had values similar to the group of patients with ACS (96.8 vs. 103.8 mg/dL; p = 0.18). No differences were found in Lp(a) levels in relatives based on the other lipid parameters. Conclusions: Overall, 59.4% of the first-degree relatives of patients who suffered from an ACS with Lp(a) ≥ 50 mg/dL also had elevated levels. Relatives with elevated Lp(a) had similar levels as patients.