Estratégia Fármaco-Invasiva no Infarto do Miocárdio: Análise Descritiva, Apresentação de Sintomas Isquêmicos e Preditores de Mortalidade / Pharmaco-invasive Strategy in Myocardial Infarction: Descriptive Analysis, Presentation of Ischemic Symptoms and Mortality Predictors

Resumo Fundamento O infarto do miocárdio com elevação do segmento-ST (IAMCSST) é definido por sintomas acompanhados por alterações típicas do eletrocardiograma. Entretanto, a caracterização dos sintomas isquêmicos não é clara, principalmente em subgrupos, como mulheres e idosos. Objetivos Analisar a tipificação dos sintomas isquêmicos, métricas temporais e observar a ocorrência de desfechos intra-hospitalares, em análise dos escores preditivos, em pacientes com IAMCSST, em estratégia fármaco-invasiva. Métodos Estudo envolvendo 2.290 pacientes. Tipos de apresentações clínicas pré-definidas: dor típica, dor atípica, dispnéia, sincope. Medimos o tempo entre o início dos sintomas à demanda pelo atendimento e o intervalo entre a chegada à unidade-médica e trombólise. Odds-ratios (OR; IC-95%) foram estimadas em modelo de regressão. Curvas ROCs foram construídas para preditores de mortalidade. Nível de significância adotado (alfa) foi de 5%. Resultados Mulheres apresentaram alta prevalência de sintomas atípicos; maior tempo entre o início dos sintomas e a procura por atendimento; atraso entre a chegada ao pronto-socorro e a fibrinólise. A mortalidade hospitalar foi de 5,6%. Predição de risco pela classificação Killip-Kimball: AUC: [0,77 (0,73-0,81)] em classe ≥II. Subgrupos estudados [OR (IC-95%)]: mulheres [2,06 (1,42-2,99); p=0,01]; insuficiência renal crônica [3,39 (2,13-5,42); p<0,001]; idosos [2,09 (1,37-3,19) p<0,001]; diabéticos [1,55 (1,04-2,29); p=0,02]; obesos 1,56 [(1,01-2,40); p=0,04]; acidente vascular cerebral prévio [2,01 (1,02-3,96); p=0,04] correlacionaram-se com maiores taxas de mortalidade. Conclusão Apesar das mais altas taxas de mortalidade em alguns subgrupos, disparidade significativa persiste nas mulheres, com atrasos no reconhecimento dos sintomas e trombólise imediata. Destaca-se a aplicabilidade do escore Killip-Kimball na predição, independentemente da apresentação clínica.

Abstract Background ST-segment elevation myocardial infarction (STEMI) is defined by symptoms accompanied by typical electrocardiogram changes. However, the characterization of ischemic symptoms is unclear, especially in subgroups such as women and the elderly. Objectives To analyze the typification of ischemic symptoms, temporal metrics and observe the occurrence of in-hospital outcomes, in the analysis of predictive scores, in patients with STEMI, in a drug-invasive strategy. Methods Study involving 2,290 patients. Types of predefined clinical presentations: typical pain, atypical pain, dyspnea, syncope. We measured the time between the onset of symptoms and demand for care and the interval between arrival at the medical unit and thrombolysis. Odds-ratios (OR; CI-95%) were estimated in a regression model. ROC curves were constructed for mortality predictors. The adopted significance level (alpha) was 5%. Results Women had a high prevalence of atypical symptoms; longer time between the onset of symptoms and seeking care; delay between arrival at the emergency room and fibrinolysis. Hospital mortality was 5.6%. Risk prediction by Killip-Kimball classification: AUC: [0.77 (0.73-0.81)] in class ≥II. Subgroups studied [OR (CI-95%)]: women [2.06 (1.42-2.99); p=0.01]; chronic renal failure [3.39 (2.13-5.42); p<0.001]; elderly [2.09 (1.37-3.19) p<0.001]; diabetics [1.55 (1.04-2.29); p=0.02]; obese 1.56 [(1.01-2.40); p=0.04]: previous stroke [2.01 (1.02-3.96); p=0.04] correlated with higher mortality rates. Conclusion Despite higher mortality rates in some subgroups, significant disparity persists in women, with delays in symptom recognition and prompt thrombolysis. We highlight the applicability of the Killip-Kimball score in prediction, regardless of the clinical presentation.

Estatinas y accidente cerebrovascular: posibles mecanismos de acción de la protección neurovascular / Statins and stroke: potential mechanisms for neurovascular protection

Resumen. Como la esperanza de vida media de los seres humanos está aumentando en todo el mundo, el accidente cerebrovascular isquémico se ha convertido en una de las causas más importantes de morbimortalidad, especialmente en los países emergentes. Se ha establecido un descenso significativo en las tasas del primer accidente cerebrovascular y del accidente cerebrovascular recurrente con el uso de estatinas en ensayos clínicos grandes y en metaanálisis y revisiones sistemáticas. Curiosamente, los estudios de observación describieron que los niveles de colesterol estaban sólo débilmente asociados al accidente cerebrovascular isquémico, lo que sugiere que debe haber otros posibles mecanismos implicados en la protección vascular. De hecho, más allá de los cambios en los lípidos, se han propuesto algunas propiedades de estos medicamentos relativas a la inflamación, hemostasia, función endotelial, estabilización de las placas de ateroma y, más recientemente, a la movilización de las células endoteliales. Asimismo, un metaanálisis reciente también puso de manifiesto que las estatinas reducen la presión arterial sistólica y diastólica. En general, todos estos beneficios pueden contribuir a la prevención de los accidentes cerebrovasculares mediante el uso de estatinas (AU)

Summary. As the average human lifespan is increasing worldwide, ischemic stroke became one of the most important causes of mortality and morbidity, particularly in emerging countries. Significant decrease in the rates of first and recurrent stroke using statins has been established in large clinical trials and in systematic reviews and meta-analyses. Interestingly, observational studies reported that cholesterol levels were only weakly associated with ischemic stroke, suggesting that other potential mechanisms for vascular protection should be implicated. Indeed, beyond lipid changes, some properties of these drugs, related to inflammation, hemostasis, endothelial function, plaque stabilization, and more recently, to the mobilization of endothelial cells, have been proposed. In addition, recent meta-analysis also revealed that statins decrease systolic and diastolic blood pressure. Taken together, all these benefits can contribute for stroke prevention by statins (AU)

Reduction in C-reactive protein and LDL cholesterol and cardiovascular event rates after initiation of rosuvastatin: a prospective study of the JUPITER trial.

BACKGROUND: Statins lower high-sensitivity C-reactive protein (hsCRP) and cholesterol concentrations, and hypothesis generating analyses suggest that clinical outcomes improve in patients given statins who achieve hsCRP concentrations less than 2 mg/L in addition to LDL cholesterol less than 1.8 mmol/L (<70 mg/dL). However, the benefit of lowering both LDL cholesterol and hsCRP after the start of statin therapy is controversial. We prospectively tested this hypothesis. METHODS: In an analysis of 15 548 initially healthy men and women participating in the JUPITER trial (87% of full cohort), we prospectively assessed the effects of rosuvastatin 20 mg versus placebo on rates of non-fatal myocardial infarction, non-fatal stroke, admission for unstable angina, arterial revascularisation, or cardiovascular death (prespecified endpoints) during a maximum follow-up of 5 years (median 1.9 years), according to on-treatment concentrations of LDL cholesterol (>/=1.8 mmol/L or <1.8 mmol/L) and hsCRP (>/=2 mg/L or <2 mg/L). We included all events occurring after randomisation. This trial is registered with ClinicalTrials.gov, number NCT00239681. FINDINGS: Compared with placebo, participants allocated to rosuvastatin who achieved LDL cholesterol less than 1.8 mmol/L had a 55% reduction in vascular events (event rate 1.11 vs 0.51 per 100 person-years; hazard ratio [HR] 0.45, 95% CI 0.34-0.60, p<0.0001), and those achieving hsCRP less than 2 mg/L a 62% reduction (event rate 0.42 per 100 person-years; HR 0.38, 95% CI 0.26-0.56, p<0.0001). Although LDL cholesterol and hsCRP reductions were only weakly correlated in individual patients (r values <0.15), we recorded a 65% reduction in vascular events in participants allocated to rosuvastatin who achieved both LDL cholesterol less than 1.8 mmol/L and hsCRP less than 2 mg/L (event rate 0.38 per 100 person-years; adjusted HR 0.35, 95% CI 0.23-0.54), versus a 33% reduction in those who achieved one or neither target (event rate 0.74 per 100 person-years; HR 0.67, 95% CI 0.52-0.87) (p across treatment groups <0.0001). In participants who achieved LDL cholesterol less than 1.8 mmol/L and hsCRP less than 1 mg/L, we noted a 79% reduction (event rate 0.24 per 100 person-years; HR 0.21, 95% CI 0.09-0.52). Achieved hsCRP concentrations were predictive of event rates irrespective of the lipid endpoint used, including the apolipoprotein B to apolipoprotein AI ratio. INTERPRETATION: For people choosing to start pharmacological prophylaxis, reduction in both LDL cholesterol and hsCRP are indicators of successful treatment with rosuvastatin.