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1.
J Cardiovasc Med (Hagerstown) ; 16(3): 156-62, 2015 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-24566391

RESUMO

AIM: To assess serum levels of the plaque calcification regulators osteoprotegerin (OPG) and Matrix Gla-proteins (MGP) in individuals with stable angina and acute myocardial infarction submitted to coronary angiography and their relation to coronary artery disease burden. METHODS: The study included 40 individuals affected by ST-elevation myocardial infarction (STEMI) and 40 individuals with stable angina who all underwent coronary angiography, with evaluation of the extent of coronary artery disease by Syntax Score calculation and measurement of serum OPG and MGP levels. Osteoporosis was excluded by femoral and vertebral computerized bone mineralometry. RESULTS: Serum OPG and MGP levels were respectively 3.87 ±â€Š1.07 pmol/l and 6.80 ±â€Š2.43 nmol/l in the stable angina group, 7.57 ±â€Š1.5 pmol/l and 7.18 ±â€Š1.93 nmol/l in the STEMI group (P < 0.01 and P = 0.33, respectively). Pearson correlation coefficient for OPG and Syntax Score, MGP and Syntax score was respectively 0.79 (P < 0.01) and 0.18 (P = 0.22) in the stable angina group, -0.03 (P = 0.43) and 0.10 (P = 0.5) in the STEMI group.Serum OPG and MGP levels were respectively 5.52 ±â€Š1.02 pmol/l and 7.56 ±â€Š1.42 nmol/l in diabetics, 4.3 ±â€Š0.8 pmol/l and 6.52 ±â€Š1.14 nmol/l in nondiabetics (P < 0.05; P < 0.05). CONCLUSION: OPG, in a relatively small group of patients with stable angina, correlates proportionally with the extent of coronary artery disease (CAD), as evaluated by the Syntax Score. Higher serum OPG levels can be observed in individuals with STEMI regardless of CAD burden. As for MGP, a potential role as marker of plaque calcification remains unproven.


Assuntos
Angina Estável/sangue , Proteínas de Ligação ao Cálcio/sangue , Proteínas da Matriz Extracelular/sangue , Infarto do Miocárdio/sangue , Osteoprotegerina/sangue , Idoso , Angina Estável/diagnóstico por imagem , Biomarcadores/sangue , Densidade Óssea , Calcinose , Angiografia Coronária , Doença da Artéria Coronariana/sangue , Doença da Artéria Coronariana/diagnóstico por imagem , Angiopatias Diabéticas/sangue , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/diagnóstico por imagem , Proteína de Matriz Gla
2.
Congenit Heart Dis ; 7(5): E78-81, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22471727

RESUMO

Tetralogy of Fallot is the most common cyanotic congenital heart defect and accounts for about 5% of all congenital cardiopathies. The definitive treatment modality for tetralogy of Fallot is reparative surgery, which is recommended to be performed by the time of diagnosis. Without surgical repair, most patients would die during their childhood. In the past, survival data indicated that 66% of persons with tetralogy of Fallot not surgically treated lived until the age of 1, 49% lived until the age of 3, and 24% lived until the age of 10. We now present a rare case of a man with unrepaired tetralogy of Fallot who survived until the age of 85. He presented to our emergency room for dyspnea and palpitations due to a new-onset high-frequency atrial fibrillation and acute heart failure; transthoracic echocardiography showed the presence of tetralogy of Fallot. By consulting the scientific literature, we can say that this is the second patient who survived more than 80 years without surgical intervention.


Assuntos
Tetralogia de Fallot/complicações , Idoso de 80 Anos ou mais , Fibrilação Atrial/etiologia , Progressão da Doença , Ecocardiografia , Humanos , Hipertensão Pulmonar , Masculino , Insuficiência da Valva Mitral/etiologia , Edema Pulmonar/etiologia , Tetralogia de Fallot/diagnóstico , Tetralogia de Fallot/terapia , Resultado do Tratamento , Obstrução do Fluxo Ventricular Externo/etiologia
3.
J Cardiol Cases ; 5(3): e143-e146, 2012 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30532925

RESUMO

We report a case of a 66-year-old Caucasian male who presented to our department with unstable angina in July 2011. He had a medical history of trivessel coronary artery disease and underwent several percutaneous coronary interventions (2003, 2004, and 2006). The latest coronary angiography, performed in January 2011, showed mild intimal hyperplasia within the proximal left anterior descending segment, treated with a sirolimus-eluting stent in 2003. On admission, electrocardiogram was positive for a recent acute coronary syndrome, so the patient underwent coronary angiography, which showed proximal left anterior descending stent thrombosis, occurred eight years after drug-eluting stent implantation. Intravascular ultrasound revealed a soft plaque rupture within the stented segment, which was the cause of stent thrombosis. So the lack of endothelialization over stent struts is not the only mechanism determining acute coronary syndromes late after stent implantation. In-stent neoatherosclerosis, frequently disregarded, is another possible actor especially of very late thrombotic events. However, the pathogenesis of this phenomenon has not been clearly established.

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