Person: Vivas Balcones, Luis David
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First Name
Luis David
Last Name
Vivas Balcones
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Medicina
Area
Medicina
Identifiers
4 results
Search Results
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Item Apical ballooning syndrome and previous coronary artery disease: a novel relationship(International Journal of Cardiology, 2008) Núñez Gil, Iván Javier; García Rubira, Juan Carlos; Fernández Ortiz, Antonio Ignacio; Vivas Balcones, Luis David; Gonzalez, Juan José; Luaces Méndez, María; Macaya Miguel, CarlosApical transient left ventricular diskynesia is a recently described entity able to imitate acute coronary syndrome. The presence of previous coronary artery disease (CAD) is an exclusion criterion for this diagnosis in several studies. We report the case of a sixty-three year-old-caucasian man with previously known CAD, left anterior descending artery (LAD) stented-disease, presenting in the emergency room with angina and ST-segment elevation. A coronariography was urgently performed. No new coronary lesions could be demonstrated. LAD-placed stents were patent and showed no change in their angiographic appearance. Left ventriculogram demonstrated apical diskynesia (Takotsubo-like). Complete and rapid resolution of left ventricular dysfunction was echocardiographycally displayed seven days later. Months after, coronary lesions increased associated with new acute coronary syndromes and new revascularization procedures were required. The present case supports the idea that CAD and apical transient diskynesia could coexist in the same patient, arising further questions about the pathophysiology, prognosis and management of the latter.Item Prognostic value of first fasting glucose measurement compared with admission glucose level in patients with acute coronary syndrome(Revista Española de Cardiología, 2008) Vivas Balcones, Luis David; García Rubira, Juan Carlos; González Ferrer, Juan José; Núñez Gil, Ivan Javier; Del Prado, Nayade; Fernández Ortiz, Antonio; Macaya, CarlosEstudio observacional unicéntrico que analizó 547 pacientes consecutivos ingresados por un síndrome coronario agudo. Se evaluaron los niveles de glucemia en varios puntos como fueron durante el ingreso y la primera glucemia en ayunas. El estudio concluyó que es la primera glucemia en ayunas y no al ingreso el parámetro que se relaciona con un factor de riesgo independiente de eventos cardiovasculares (muerte o reinfarto) durante la hospitalización.Item Influence of HbA1c levels on platelet function profiles associated with tight glycemic control in patients presenting with hyperglycemia and an acute coronary syndrome. A subanalysis of the CHIPS Study ("Control de HIperglucemia y Actividad Plaquetaria en Pacientes con Síndrome Coronario Agudo")(Journal of Thrombosis and Thrombolysis, 2013) Vivas Balcones, Luis David; García Rubira, Juan Carlos; Bernardo, Esther; Angiolillo, Dominick J.; Martín, Patricia; Calle Pascual, Alfonso Luis; Núñez Gil, Iván; Macaya Miguel, Carlos; Fernández Ortiz, Antonio IgnacioPatients with hyperglycemia, an acute coronary syndrome and poor glycemic control have increased platelet reactivity and poor prognosis. However, it is unclear the influence of a tight glycemic control on platelet reactivity in these patients. This is a subanalysis of the CHIPS study. This trial randomized patients with hyperglycemia to undergo an intensive glucose control (target blood glucose 80-120 mg/dL), or conventional glucose control (target blood glucose <180 mg/dL). We analyzed platelet function at discharge on the subgroup of patients with poor glycemic control, defined with admission levels of HbA1c higher than 6.5%. The primary endpoint was maximal platelet aggregation following stimuli with 20 μM ADP. We also measured aggregation following collagen, epinephrine, and thrombin receptor-activated peptide, as well as P2Y12 reactivity index and surface expression of glycoprotein IIb/IIIa and P-selectin. A total of 67 patients presented HbA1c ≥ 6.5% (37 intensive, 30 conventional), while 42 had HbA1c < 6.5% (20 intensive, 22 conventional). There were no differences in baseline characteristics between groups. At discharge, patients with HbA1c ≥6.5% had significantly reduced MPA with intensive glucose control compared with conventional control (46.1 ± 22.3 vs. 60.4 ± 20.0%; p = 0.004). Similar findings were shown with other measures of platelet function. However, glucose control strategy did not affect platelet function parameters in patients with HbA1c < 6.5%. Intensive glucose control in patients presenting with an acute coronary syndrome and hyperglycemia results in a reduction of platelet reactivity only in the presence of elevated HbA1c levels.Item Circadian variations of infarct size in acute myocardial infarction(Heart, 2011) Suárez Barrientos, Aida; López Romero, Pedro; Vivas Balcones, Luis David; Castro Ferreira, Francisco; Núñez Gil, Ivan; Franco, Eduardo; Ruiz Mateos, Borja; García Rubira, Juan Carlos; Fernández Ortiz, Antonio Ignacio; Macaya Miguel, Carlos; Ibanez, BorjaBackground: The circadian clock influences a number of cardiovascular (patho)physiological processes including the incidence of acute myocardial infarction. A circadian variation in infarct size has recently been shown in rodents, but there is no clinical evidence of this finding. Objective: To determine the impact of time-of-day onset of ST segment elevation myocardial infarction (STEMI) on infarct size. Methods: A retrospective single-centre analysis of 811 patients with STEMI admitted between 2003 and 2009 was performed. Infarct size was estimated by peak enzyme release. The relationship between peak enzyme concentrations and time-of-day were characterised using multivariate regression splines. Time of STEMI onset was divided into four 6-hour periods in phase with circadian rhythms. Results: Model comparisons based on likelihood ratio tests showed a circadian variation in infarct size across time-of-day as evaluated by peak creatine kinase (CK) and troponin-I (TnI) concentrations (p=0.015 and p=0.012, respectively). CK and TnI curves described similar patterns across time, with a global maximum in the 6:00-noon period and a local minimum in the noon-18:00 period. Infarct size was largest in patients with STEMI onset in the dark-to-light transition period (6:00-noon), with an increase in peak CK and TnI concentrations of 18.3% (p=0.031) and 24.6% (p=0.033), respectively, compared with onset of STEMI in the 18:00-midnight period. Patients with anterior wall STEMI also had significantly larger infarcts than those with STEMI in other locations. Conclusions: Significant circadian oscillations in infarct size were found in patients according to time-of-day of STEMI onset. The infarct size was found to be significantly larger with STEMI onset in the dark-to-light transition period (6:00-noon). If confirmed, these results may have a significant impact on the interpretation of clinical trials of cardioprotective strategies in STEMI