|Year : 2004 | Volume
| Issue : 2 | Page : 36-38
|Date of Web Publication||22-Jun-2010|
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
. Cardiovascular news. Heart Views 2004;5:36-8
One-year outcome of pre-hospital thrombolysis for acute myocardial infarction: The french experience
Limited data are available on the impact of prehospital thrombolysis (PHT) in the "real-world" setting. Of 443 intensive care units in France, 369 (83%) prospectively collected all cases of infarction (?? 48 hours of symptom onset) in November 2000; 1922 patients (median age, 67 years; 73% men) with ST-segment-elevation infarction were included, of whom 180 (9%) received intravenous thrombolysis before hospital admission (PHT). Patients with PHT were younger than those with in-hospital thrombolysis, primary percutaneous interventions, or no reperfusion therapy. Median time from symptom onset to hospital admission was 3.6 hours for PHT, ?? 3.5 hours for in-hospital lysis, 3.2 hours for primary percutaneous interventions, and 12 hours for no reperfusion therapy.
In-hospital death was 3.3% for PHT, 8.0% for in-hospital lysis, 6.7% for primary percutaneous interventions, and 12.2% for no reperfusion therapy. One-year survival was 94%, 89%, 89%, and 79%, respectively. In a multivariate analysis of predictors of 1-year survival, PHT was associated with a 0.49 relative risk of death (95% CI, 0.24 to 1.00; P=0.05). When the analysis was limited to patients receiving reperfusion therapy, the relative risk of death for PHT was 0.52 (95% CI, 0.25 to 1.08; P=0.08). In patients with PHT admitted in 3.5 hours, in-hospital mortality was 0% and 1-year survival was 99%.
The study concluded that the 1-year outcome of patients treated with PHT compares favorably with that of patients treated with other modes of reperfusion therapy; this favorable trend persists after multivariate adjustment. Patients with PHT admitted very early have a very high 1-year survival rate.
Effect of 600 mg loading with Clopidogrel in patients with CAD with and without Chronic Clopidogrel Therapy
It is not known whether further suppression of platelet function can be achieved with clopidogrel beyond that provided by currently recommended loading and maintenance doses. Investigators performed a prospective study comparing the antiplatelet effects of a 600-mg loading dose of clopidogrel given to patients with and without chronic clopidogrel therapy.
Those eligible for this prospective study were aspirin-treated patients with suspected or documented coronary artery disease admitted to hospital for coronary angiography. Two series of 20 consecutive patients each were assessed in this study. The first series included patients who had never received clopidogrel (first-use group); the second series included patients on chronic therapy with a daily dose of 75 mg clopidogrel for 1 month (chronic therapy group). Blood samples were drawn before and 6 hours after oral administration of 600 mg clopidogrel for aggregometry and flow cytometry studies.
In the first-use group, loading with 600 mg clopidogrel inhibited ADP 5 μmol/L-induced platelet aggregation from 90±9% to 51±19% (P<0.001). In the chronic therapy group, loading with 600 mg clopidogrel yielded further inhibition of ADP 5 μmol/L-induced platelet aggregation in addition to that achieved by the maintenance dose of 75 mg/d, from 52±14% to 33±12% (P<0.001). In both groups, 600 mg clopidogrel loading significantly inhibited ADP-induced expression of glycoprotein IIb/IIIa and P-selectin receptors.
The study concluded that further platelet inhibition can be achieved with clopidogrel in addition to that provided by currently recommended loading and maintenance doses. Higher doses may be warranted after assessment of their clinical efficacy and safety.
Medical costs and quality of life 10 to 12 years after randomization to angioplasty or bypass surgery for multivessel CAD
Coronary bypass surgery (CABG) and angioplasty (PTCA) have been compared in several randomized trials, but data about long-term economic and quality-of-life outcomes are limited.
Cost and quality-of-life data were collected prospectively from 934 patients who were randomized in the Bypass Angioplasty Revascularization Investigation (BARI) and followed up for 10 to12 years. CABG had 53% higher costs initially, but the gap closed to < 5% during the first 2 years; after 12 years, the mean cumulative cost of CABG patients was $123 000 versus $120 750 for PTCA, yielding a cost-effectiveness ratio of $14 300/life-year added.
CABG patients experienced significantly greater improvement in their physical functioning for the first 3 years but not in later follow-up. Recurrent angina substantially reduced all quality-of-life measures throughout follow-up. Cumulative costs were significantly higher among patients with diabetes, heart failure, and comorbid conditions and among women; costs also were increased by angina, by the number of revascularization procedures, and among patients who died.
Early differences between CABG and PTCA in costs and quality of life were no longer significant at 10 to 12 years of follow-up. CABG was cost-effective as compared with PTCA for multivessel disease.
Non-invasive measurement of systemic endothelial dysfunction predicts cardiac events in patients with acute coronary syndrome
Endothelial vasodilator dysfunction may serve as a marker integrating the vascular risk of an individual; however, whether systemic vasodilator function predicts disease progression and cardiovascular event rates in patients with manifest acute coronary syndromes (ACS) is unknown.
In 198 patients with angiographically documented ACS, forearm blood flow (FBF) responses to acetylcholine (ACH; 10 to 50 μg/min) and sodium nitroprusside (SNP; 2 to 8 μg/min) were measured by venous occlusion plethysmography before hospital discharge within 5 days of an episode of an ACS. Cardiovascular events (cardiovascular death, myocardial infarction, and ischemic stroke) served as outcome variables over a mean follow-up period of 47.7±15.1 months.
Patients who experienced cardiovascular events during follow-up (n=31) had a significantly reduced vasodilator response to ACH (P<0.05) and SNP (P<0.05). By multivariate analysis, vasodilator response to ACH and elevated troponin T serum levels were the only significant (P<0.05) independent predictors of a poor prognosis, even after adjustment for traditional cardiovascular risk factors, concurrent medication, invasive treatment strategy, and C-reactive protein serum levels.
Recovery of endothelium-dependent vasoreactivity as assessed by repeated FBF assessment 8 weeks after the index measurement after the ACS predicted further event-free survival in a subset of 78 patients.
Systemic endothelium-dependent vasoreactivity predicts recurrence of instability and cardiovascular event rates in patients with ACS. Furthermore, the recovery of systemic endothelial function is associated with event-free survival. Assessment of systemic vasoreactivity, measured by a minimally invasive test, provides important prognostic information in addition to that derived from traditional risk factor assessment in patients with ACS.
Left ventricular remodeling and heart failure in diabetic patients treated with primary angioplasty for acute myocardial infarction
Diabetes mellitus has been recognized as a strong predictor of heart failure (HF) in patients with acute myocardial infarction (AMI). However, considerable controversy exists regarding the pathogenetic mechanisms of HF after AMI in diabetic patients. Researchers hypothesized that the increased incidence of HF in diabetic patients was associated with a greater propensity for left ventricular (LV) remodeling.
A series of 325 patients (42 diabetics) with AMI successfully treated with primary angioplasty underwent serial 2D echocardiography from admission to 1 and 6 months and 6-month angiography. No significant difference was found between diabetics and nondiabetics regarding baseline clinical, angiographic, and echocardiographic characteristics, as well as 6-month restenosis and reocclusion rates.
At 6 months, a similar incidence of LV remodeling was observed in diabetics and nondiabetics (33% versus 25%; P=0.234), with similar patterns of changes in LV volumes and LV global and regional systolic function. At 5 years, the incidence of HF was higher in the diabetics (43% versus 20%, P=0.001). Diabetes was found to be an independent predictor of HF at 5 years (hazard ratio, 1.8; P=0.0366). However, LV remodeling was predictive of HF in the nondiabetics (P=0.023) but not in the diabetics (P=0.123). In a subgroup of patients, higher LV chamber stiffness (as assessed by echocardiography) was detected in the diabetics with HF.
The more frequent progression to HF in the diabetics after AMI is not explained by a greater propensity for LV remodeling. Other factors, such as diastolic dysfunction, may play a role.
Balloon dilation of severe aortic stenosis in the fetus may prevent hypoplastic left heart syndrome
Preventing the progression of fetal aortic stenosis (AS) to hypoplastic left heart syndrome (HLHS) requires identification of fetuses with salvageable left hearts who would progress to HLHS if left untreated, a successful in utero valvotomy, and demonstration that a successful valvotomy promotes left heart growth in utero. Fetuses meeting the first criterion are undefined, and previous reports of fetal AS dilation have not evaluated the impact of intervention on in utero growth of left heart structures.
Investigators at Boston Children's Hospital and Harvard Medical School offered fetal AS dilation to 24 mothers whose fetuses had AS.
At least 3 echocardiographers assigned a high probability that all 24 fetuses would progress to HLHS if left untreated. Twenty (21 to 29 weeks' gestation) underwent attempted AS dilation, with technical success in 14. Ideal fetal positioning for cannula puncture site and course of the needle (with or without laparotomy) proved to be necessary for procedural success.
Serial fetal echocardiograms after intervention demonstrated growth arrest of the left heart structures in unsuccessful cases and in those who declined the procedure, while ongoing left heart growth was seen in successful cases. Resumed left heart growth led to a 2-ventricle circulation at birth in 3 babies.
Fetal echocardiography can identify midgestation fetuses with AS who are at high risk for developing HLHS. Timely and successful aortic valve dilation requires ideal fetal and cannula positioning, prevents left heart growth arrest, and may result in normal ventricular anatomy and function at birth.
Maternal calcium intake and offspring blood pressure
Few data exist on the intergenerational influence of calcium intake during pregnancy on offspring blood pressure.
As part of the ongoing US prospective cohort study Project Viva, we analyzed 4091 Dinamap blood pressure measurements from 936 six-month-old infants whose mothers had completed food frequency questionnaires during the second trimester of pregnancy. We used mixed models to estimate effects of maternal calcium intake on offspring systolic blood pressure. Mean±SD daily total maternal calcium intake was 1494±523 mg, consisting of 1230±486 mg from foods and 264±191 mg from supplements. Mean±SD 6-month blood pressure was 89.9±12.9 mm Hg. From bottom to top quartile of dietary calcium from foods adjusted for energy intake and measurement conditions, mean infant systolic blood pressures were 91.0, 90.2, 90.9, and 90.2 mm Hg (trend P=0.62). From calcium supplements only, the values were 91.5, 90.2, 90.4, and 88.4 mm Hg (trend P=0.006).
After further adjustment for demographic, anthropometric, dietary, social, and economic variables, the decrease in 6-month systolic blood pressure was -3.0 mm Hg (95% CI, -4.9 to -1.1) for each 500-mg increment of maternal supplemental calcium intake during pregnancy. We did not find evidence of effect modification by maternal vitamin D or potassium intake or by infant body mass index. First-trimester calcium intake was not associated with offspring blood pressure.
These observational data suggest that supplementing maternal midgestational calcium intake may lower offspring blood pressure, thus helping to prevent hypertension in the next generation.
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