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1.
Am Heart J ; 165(4): 591-9, 2013 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-23537977

RESUMO

BACKGROUND: During percutaneous coronary intervention (PCI) performed in the emergent setting of ST-segment elevation myocardial infarction (STEMI), uncertainty about patients' ability to comply with 12 months dual antiplatelet therapy after drug-eluting stenting is common, and thus, selective bare-metal stent (BMS) deployment could be an attractive strategy if this achieved low target vessel revascularization (TVR) rates in large infarct-related arteries (IRAs) (≥3.5 mm). METHODS AND RESULTS: To evaluate this hypothesis, among 1,282 patients with STEMI who underwent PCI during their initial hospitalization, we studied 1,059 patients (83%) who received BMS, of whom 512 (48%) had large IRAs ≥3.5 mm in diameter, 333 (31%) had IRAs 3 to 3.49 mm, and 214 (20%) had IRAs <3 mm. At 1 year, TVR rate in patients with BMS was 5.8% (2.2% with large BMS [≥3.5 mm], 9.2% with BMS 3-3.49 mm [intermediate], and 9.0% with BMS <3.0 mm [small], P < .001). The rates of death/reinfarction among patients with large BMS compared with intermediate BMS or small BMS were lower (6.6% vs 11.7% vs 9.0%, P = .042). Among patients who received BMS, the independent predictors of TVR at 1 year were the following: vessel diameter <3.5 mm (odds ratio [OR] 4.39 [95% CI 2.24-8.60], P < .001), proximal left anterior descending coronary artery lesions (OR 1.89 [95% CI 1.08-3.31], P = .027), hypertension (OR 2.01 [95% CI 1.17-3.438], P = .011), and prior PCI (OR 3.46 [95% CI 1.21-9.85], P = .02). The predictors of death/myocardial infarction at 1 year were pre-PCI cardiogenic shock (OR 8.16 [95% CI 4.16-16.01], P < .001), age ≥65 years (OR 2.63 [95% CI 1.58-4.39], P < .001), left anterior descending coronary artery culprit lesions (OR 1.95 [95% CI 1.19-3.21], P = .008), female gender (OR 1.93 [95% CI 1.12-3.32], P = .019), and American College of Cardiology/American Heart Association lesion classes B2 and C (OR 2.17 [95% CI 1.10-4.27], P = .026). CONCLUSION: Bare-metal stent deployment in STEMI patients with IRAs ≥3.5 mm was associated with low rates of TVR. Their use in this setting warrants comparison with second-generation drug-eluting stenting deployment in future randomized clinical trials.


Assuntos
Infarto do Miocárdio/terapia , Stents , Idoso , Angiografia Coronária , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/mortalidade , Prognóstico , Recidiva , Medição de Risco , Resultado do Tratamento
2.
Am J Cardiol ; 107(6): 863-70, 2011 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-21376928

RESUMO

In patients with acute coronary syndromes undergoing percutaneous coronary intervention (PCI), the diagnosis of periprocedural myocardial infarction is often problematic when the pre-PCI levels of cardiac troponin T (TnT) are elevated. Thus, we examined different TnT criteria for periprocedural myocardial infarction when the pre-PCI TnT levels were elevated and also the associations between the post-PCI cardiac marker levels and outcomes. We established the relation between the post-PCI creatine kinase-MB (CKMB) and TnT levels in 582 patients (315 with acute coronary syndromes and 272 with stable coronary heart disease). A post-PCI increase in the CKMB levels to 14.7 µg/L (3 × the upper reference limit [URL] in men) corresponded to a TnT of 0.23 µg/L. In the 85 patients with acute coronary syndromes and normal CKMB, but elevated post peak TnT levels before PCI (performed at a median of 5 days, interquartile range 3 to 7), the post-PCI cardiac marker increases were as follows: 21 (24.7%) with a ≥ 20% increase in TnT, 10 (11.8%) with an CKMB level >3 × URL, and 12 (14%) with an absolute TnT increase of >0.09 µg/L (p <0.005 for both). In the patients with stable coronary heart disease and post-PCI cardiac markers > 3× URL compared to those without markers elevations, the rate of freedom from death or nonfatal myocardial infarction was 88% for those with TnT elevations versus 99% (p <0.001, log-rank) and 84% for those with CKMB elevations versus 98% (p <0.001, log-rank). Of the patients with acute coronary syndromes, the post-PCI marker levels did not influence the outcomes. In conclusion, in patients with acute coronary syndromes and elevated TnT levels undergoing PCI several days later, ≥20% increases in TnT were more common than absolute increments in the TnT or CKMB levels of >3× URL. Also, periprocedural cardiac marker elevations in patients with acute coronary syndromes did not have prognostic significance.


Assuntos
Síndrome Coronariana Aguda/sangue , Infarto do Miocárdio/diagnóstico , Troponina T/sangue , Síndrome Coronariana Aguda/mortalidade , Angioplastia Coronária com Balão , Biomarcadores/sangue , Distribuição de Qui-Quadrado , Doença das Coronárias/sangue , Doença das Coronárias/mortalidade , Creatina Quinase/sangue , Feminino , Taxa de Filtração Glomerular , Humanos , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/mortalidade , Infarto do Miocárdio/terapia , Inibidores da Agregação Plaquetária/administração & dosagem , Estudos Prospectivos , Estatísticas não Paramétricas
3.
J Clin Neurosci ; 11(1): 25-30, 2004 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-14642361

RESUMO

This is an appraisal of the varied clinical presentation and the neural substrate for akinetic mutism following stroke. The diagnosis is important as akinetic mutism is often misdiagnosed as depression, delirium and locked-in-syndrome. This is a descriptive study of eight selected patients with akinetic mutism following infarction/haemorrhage in different regions of the brain with characteristic syndromes. They involved the critical areas namely, the frontal (cingulate gyrus, supplementary motor area and dorso-lateral border zone), basal ganglia (caudate, putamen), the mesencephalon and thalamus. The disorders of speech and communication took different forms. The speech disorder included verbal inertia, hypophonia, perseveration, softened and at times slurred. The linguistic disturbances were fluent, non-fluent, anomia and transcortical (motor, mixed) aphasias. The findings were related to what is known about the neuroanatomic location of the lesions and the role of the frontal-subcortical circuitry in relation to behaviour. Akinetic mutism could be explained by damage to the frontal lobe and or interruption of the complex frontal subcortical circuits.


Assuntos
Afasia Acinética/etiologia , Acidente Vascular Cerebral/complicações , Adulto , Idoso , Afasia Acinética/patologia , Encéfalo/patologia , Feminino , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Pessoa de Meia-Idade , Exame Neurológico , Tomografia Computadorizada por Raios X/métodos
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