957-108 Does Reperfusion Induced by Angioplasty Confer the Same Benefit as Thrombolysis in Terms of Late Potentials?

Angioplasty or thrombolysis (T) during acute myocardial infarction (MI) are two effective methods for achieving reperfusion, but whether reperfusion induced by angioplasty confers the same protection against the presence of late potentials on signal-averaged electrocardiography (SAE) as that induced by T remains debated. We studied retrospectively 102 consecutive Pts with successful reperfusion (TIMI grade 3 patency in acute phase), obtained by T, primary angioplasty (P), or rescue angioplasty (R) during the first 6 hours of MI. T Pts all had angiography at 90min to prove reperfusion. All had SAE >6 days later. Late potentials were defined as, ≥2 of the following criteria: QRS >120msec, RMS40 <20μV, LAS> 38msec. Results are (mean±SD):TPRPnumber of Pts354027Age (years)59.9±1160.5±1453±13<0.04% males868593NS% anterior545846NSTime to treatment (min)169±72212±79171±76NSTime to reperfusion (min)285±75*261±90280±98NSEjection fraction°(%)53±845±1546±14NS% Late potentials431011<0.001*time to 90min angiography with proven reperfusion°radionuclide left ventricular ejection fraction at dischargeThus, after MI, the prevalence of late potentials appears lower when acute reperfusion is obtained by angioplasty rather than by thrombolysis. This difference does not appear related to differences in time to treatment, time to reperfusion, left ventricular function or other patient characteristics

Myocardial Infarction in a 29-Year-Old Woman Leads to Diagnosis and Treatment of a Rare Disease

International audienceCase Presentation: A 29-year-old woman without history of cardiac disease or risk factors sought treatment for sudden onset of chest pain radiating down the back, jaw, and arms, complicated by discomfort in the orthostatic position and severe headache. She had a history of epistaxis since childhood as well as familial history of epistaxis via her mother. BMI was 22 kg/m2, and electrocardiography showed ST segment depression in V1V2 precordial leads and T-wave inversion in inferior leads. Troponin was elevated at 3,700 ng/L (normal, < 34 ng/L), with a peak of 11,115 ng/L

Blood transfusion, bleeding, anemia, and survival in patients with acute myocardial infarction: FAST-MI registry

International audienceBackground An association between transfusion during index hospitalization and increased subsequent mortality has been reported in acute myocardial infarction (AMI). Whether this reflects the prognostic role of transfusion per se, or the impact of the index event leading to transfusion, remains unclear. We sought to evaluate the impact of transfusion on mortality in patients with AMI. Methods Using the nationwide FAST-MI 2005 AMI registry, we recorded anemia on admission, Thrombolysis in Myocardial Infarction major or minor bleeding, and transfusions during hospital stay. Multivariable analyses were performed to identify independent predictors of in-hospital and 5-year mortality. Cohorts of patients matched for propensity to receive transfusion were compared. Results Among 3541 patients with AMI, 827 (23.4%) had anemia on admission, 114 (3.2%) had minor or major bleeding, and 151 (4.3%) underwent transfusion. After multivariable analysis, both anemia and bleeding were independently associated with 5-year mortality (hazard ratio [HR] 1.4, 95% CI 1.2-1.6 and HR 1.4, 95% CI 1.1-1.8, respectively), whereas transfusion did not appear to be an independent predictor (HR 1.1, 95% CI 0.8-1.5). Mortality at 5 years did not differ between cohorts matched for propensity to receive transfusion. Conclusions In this cohort, anemia on admission and bleeding during hospitalization were both associated with increased 5-year mortality in patients with myocardial infarction. Conversely, transfusion per se was not associated with lower survival. Further work is needed to clarify the optimal transfusion strategy in patients with bleeding or anemia and myocardial infarction

Trends in Cardiovascular Disease Risk Factor Prevalence and Estimated 10-Year Cardiovascular Risk Scores in a Large Untreated French Urban Population: The CARVAR 92 Study

<div><p>Background</p><p>Surveys measuring effectiveness of public awareness campaigns in reducing cardiovascular disease (CVD) incidence have yielded equivocal findings. The aim of this study was to describe cardiovascular risk factors (CVRFs) changes over the years in an untreated population-based study.</p><p>Methods</p><p>Between 2007 and 2012, we conducted a screening campaign for CVRFs in men aged 40 to 65 yrs and women aged 50 to 70 yrs in the western suburbs of Paris. Data were complete for 20,324 participants of which 14,709 were untreated.</p><p>Results</p><p>The prevalence trend over six years was statistically significant for hypertension in men from 25.9% in 2007 to 21.1% in 2012 (p=0.002) and from 23% in 2007 to 12.7% in 2012 in women (p<0.0001). The prevalence trend of tobacco smoking decreased from 38.6% to 27.7% in men (p=0.0001) and from 22.6% to 16.8% in women (p=0.113). The Framingham 10-year risk for CVD decreased from 13.3 ± 8.2 % in 2007 to 11.7 ± 9.0 % in 2012 in men and from 8.0 ± 4.1 % to 5.9 ± 3.4 % in women. The 10-year risk of fatal CVD based on the European Systematic COronary Risk Evaluation (SCORE) decreased in men and in women (p <0.0001).</p><p>Conclusions</p><p>Over a 6-year period, several CVRFs have decreased in our screening campaign, leading to decrease in the 10-year risk for CVD and the 10-year risk of fatal CVD. Cardiologists should recognize the importance of community prevention programs and communication policies, particularly tobacco control and healthier diets to decrease the CVRFs in the general population.</p></div

Cardiovascular risk factors and estimated 10-year risk for CVD and fatal CVD in adjusted model (population C) (N = 6,504).

<p>*Mean ± SD</p><p>Population C represented the age- and sex-adjusted untreated population.</p><p>Linear trends were verified using the Cochran-Armitage trend test for linearity for categorical data (diabetes, hypertension, high LDL-C, obesity, current smokers), and regression lines for parametric data (10-year risk of fatal CVD and 10-year risk of CVD).</p><p>CVD = cardiovascular disease; LDL-C = low-density lipoprotein-cholesterol</p><p>Cardiovascular risk factors and estimated 10-year risk for CVD and fatal CVD in adjusted model (population C) (N = 6,504).</p

Cardiovascular risk factors and estimated 10-year risk for CVD and fatal CVD between 2007 and 2012 in population B.

<p>Cardiovascular risk factors and estimated 10-year risk for CVD and fatal CVD between 2007 and 2012 in population B.</p

Characteristics of the participants in population A.

<p>Population A consisted of the total participants who presented to the medical visit and for whom data were complete.</p><p>Characteristics of the participants in population A.</p

Cardiovascular risk factors and estimated 10-year risk for CVD and fatal CVD in population B (N = 14,709).

<p>*Mean ± SD</p><p>Population B consisted of the total participants who presented to the medical visit and for whom data were complete and who were not taking any antihypertensive or lipid-lowering agents or drug treatment for diabetes</p><p>Linear trends were verified using the Cochran-Armitage trend test for linearity for categorical data (diabetes, hypertension, high LDL-C, obesity, current smokers), and regression lines for parametric data (10-year risk of fatal CVD and 10-year risk of CVD)</p><p>CVD = cardiovascular disease; LDL-C = low-density lipoprotein-cholesterol</p><p>Cardiovascular risk factors and estimated 10-year risk for CVD and fatal CVD in population B (N = 14,709).</p

Cardiovascular risk factors and estimated 10-year risk for CVD and fatal CVD between 2007 and 2012 (adjusted model).

<p>Cardiovascular risk factors and estimated 10-year risk for CVD and fatal CVD between 2007 and 2012 (adjusted model).</p