VANQWISH: risk stratification of non Q-wave myocardial infarction.
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Biomedical subjects
Publications and source records attributed to J D Talley.
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BACKGROUND: Experimental and clinical observations suggest that lowering serum lipid levels may reduce the risk of restenosis after coronary angioplasty. We report the results of a prospective, randomized, double-blind trial evaluating whether lowering lipid levels with lovastatin can prevent or delay restenosis after angioplasty. METHODS: Seven to 10 days before angioplasty, we randomly assigned eligible patients to receive lovastatin (40 mg orally twice daily) or placebo. Patients who underwent successful, complication-free, first-time angioplasty of a native vessel (the index lesion) continued to receive therapy for six months, when a second coronary angiogram was obtained. The primary end point was the extent of restenosis of the index lesion, as assessed by quantitative coronary arteriography. Of 404 patients randomly assigned to study groups, 384 underwent angioplasty; 354 of the procedures were successful, and 321 patients underwent angiographic restudy at six months. RESULTS: At base line, the patients in the lovastatin group (n = 203) and the placebo group (n = 201) were similar with respect to demographic clinical, angiographic, and laboratory characteristics. At base line the mean (+/- SD) degree of stenosis, expressed as a percentage of the diameter of the vessel, was 64 +/- 11 percent in the lovastatin group, as compared with 63 +/- 11 percent in the placebo group (P = 0.22). Despite a 42 percent reduction in the serum level of low-density lipoprotein cholesterol in the lovastatin group, after six months of treatment the amount of stenosis seen in the second angiogram was 46 +/- 20 percent in the placebo group, as compared with 44 +/- 21 percent in the lovastatin group (P = 0.50). Similarly, there were no significant differences in minimal luminal diameter or other measures of restenosis. A trend was noted toward more myocardial infarctions in the lovastatin group, as a result of acute vessel closure or restenosis at the site of angioplasty, but there were no other important differences between the two groups in the frequency of fatal or nonfatal events at six months. CONCLUSIONS: Treatment with high-dose lovastatin initiated before coronary angioplasty does not prevent or delay the process of restenosis in the first six months after the procedure.
A prospective randomized trial was performed to detect technical and clinical differences of 7F compared to 8F guiding catheters (GC) used in elective coronary angioplasty (PTCA). One hundred and fifteen patients undergoing elective PTCA with standard balloon dilatation catheters were randomized to 7F (55 pts) or 8F (58 pts) guiding catheters. The endpoints were primarily coronary artery and peripheral vascular complications; and secondarily, technical details and quantitative and qualitative angiographic quality. There was no difference between 7F or 8F GC for development of coronary or peripheral vascular complications. With 7F GC there was less blood loss (Hct, 3.5 +/- 3.4% vs. 6.5 +/- 9.6%, P = .033), and less contrast medium (160 +/- 88 mL vs. 200 +/- 119 mL, P = .049) used. Angiographic quality was similar, although visualization of lesions in the left anterior descending coronary artery in the left anterior oblique projection was improved with the 8F GC. There is no advantage of 7F GC for the prevention of coronary or peripheral vascular complications, although there was less blood loss and contrast medium used with the 7F systems.
To assess by serial quantitative angiography, the significance of clinical and angiographic variables that affect the progression of coronary artery disease (CAD). Progression of disease by sequential angiography is unpredictable and the role of clinical risk factors controversial. Various intervention trials have demonstrated less progression and even regression in hyperlipidemic patients. Correlates of progression have included a younger age, unstable angina, and greater involvement of the coronary arteries, with few studies looking at angiographic features of individual lesions. Serial angiograms on 74 patients were analyzed by computer assisted quantitative angiography using absolute measurements. A total of 99 diseased segments were analyzed for progression defined as an absolute reduction of 20% in luminal cross-sectional area. A preliminary correlation coefficient was calculated for each of the clinical and angiographic variables to detect any association with progression, and the odds ratio determined. The presence of any of the clinical risk factors-diabetes, hypertension, serum cholesterol, smoking, and a family history of coronary disease could not predict progression. The use of beta blockers was three times less likely to be associated with progression (odds ratio 0.33). While the presence of distal disease was associated with progression of a more proximal lesion (odds ratio 2.4), eccentricity, branch point location, lesion length, calcification, thrombus, or the presence of collaterals did not influence progression of disease in an individual segment. In conclusion, the presence of any of the clinical risk factors could not predict progression of disease in an individual coronary segment as determined by serial quantitative angiography, and the use of beta blockers and the absence of coexistent distal disease was associated with less progression of disease in an individual coronary segment. This may be related to changes in wall stress, reduced platelet interactions, and the integrity and permeability of the vascular endothelium to lipids.
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BACKGROUND: This study was performed to determine the safety and potential efficacy of an intravenous perfluorochemical emulsion (Fluosol) as an adjunct reperfusion therapy aimed at preventing reperfusion injury for patients with acute myocardial infarction. METHODS AND RESULTS: Patients (430) were randomized in a prospective open-labeled study, 213 to receive Fluosol and 217 to receive no Fluosol, along with 100 mg of tissue-type plasminogen activator given over 3 hours. Major end points included global ejection fraction, regional wall motion analysis, infarct size as measured by tomographic thallium imaging, and a composite clinical outcome measure. Baseline patient and angiographic characteristics were similar in the two groups. No significant difference in global ejection fraction (52% without Fluosol, 51% with Fluosol) or regional wall motion (-2.4 SD/chord with Fluosol, -2.2 SD/chord without Fluosol) was demonstrated in patients receiving Fluosol versus those not receiving Fluosol, nor was there a significant difference in thallium infarct size. Although Fluosol-treated patients with anterior infarction had an insignificantly lower mean infarct size (18.7% of the left ventricle) compared with patients with anterior infarction not treated with Fluosol (21.2% of left ventricle), this trend was not evident in the median infarct size values (22% versus 17%), left ventricular ejection fraction values (46% without Fluosol, 47% with Fluosol), or regional wall motion (-2.5 SD/chord in both groups). Rates of death and stroke were no different in the two groups; however, patients who received Fluosol experienced less recurrent ischemia. Patients receiving intravenous Fluosol had more transient congestive heart failure and pulmonary edema, perhaps because of necessary fluid administration. There was no difference in hemorrhagic complications between the two study groups. CONCLUSIONS: When given with a thrombolytic agent, Fluosol was not associated with improvement in ventricular systolic function, reduction in thallium infarct size, or overall clinical outcome. Fluosol was, however, associated with a reduction in ischemic complications and with an increase in pulmonary edema and congestive heart failure.
BACKGROUND: Aortic counterpulsation has been observed to reduce the rate of reocclusion of the infarct-related artery after patency has been restored during acute myocardial infarction in observational studies. To evaluate the benefit-to-risk ratio of aortic counterpulsation during the early phase of myocardial infarction, a multicenter randomized clinical trial was performed. METHODS AND RESULTS: Patients who had patency restored during acute cardiac catheterization within the first 24 hours of onset of myocardial infarction were randomly assigned to aortic counterpulsation for 48 hours versus standard care. Intravenous heparin was used similarly in both groups and was continued for a median (25th, 75th percentile) of 5 (2,7) days. A total of 182 patients were enrolled; 96 were assigned to aortic counterpulsation and 86 to standard care. Repeat cardiac catheterization was performed at a median of 5 (4,6) days after randomization in 89% of patients assigned to aortic counterpulsation and in 90% of control patients. Patients randomized to aortic counterpulsation had similar rates of severe bleeding complications (2% versus 1%), number of units of blood transfused (mean, 1.3 +/- 2.6 versus 0.9 +/- 1.8 units), and vascular repair or thrombectomy (5% versus 2%) compared with patients treated in a conventional manner. Patients randomized to aortic counterpulsation had significantly less reocclusion of the infarct-related artery during follow-up compared with control patients (8% versus 21%, P < .03). In addition, there was a significantly lower event rate in patients assigned to aortic counterpulsation in terms of a composite clinical end point (death, stroke, reinfarction, need for emergency revascularization with angioplasty or bypass surgery, or recurrent ischemia): 13% versus 24%, P < .04. CONCLUSIONS: This randomized trial showed that careful use of prophylactic aortic counterpulsation can prevent reocclusion of the infarct-related artery and improve overall clinical outcome in patients undergoing acute cardiac catheterization during myocardial infarction.