The Falcon(TM) eccentric coronary balloon angioplasty catheter:A randomized safety and efficacy study

Percutaneous coronary angioplasty (PTCA) is usually performed using concentric shaped balloon catheters with the guidewire passing through the center of the shaft. The Falcon(TM) balloon catheter features a guide wire lumen on the outside of the balloon so that an eccentric balloon catheter profile is obtained concentrating the dilating force on the wire supported side, allowing lower inflation pressures and potentially causing less vessel injury. The aim of this study was to evaluate the safety and efficacy of this new balloon catheter in patients with stable and unstable angina. In 95 prospectively randomized patients, 57 lesions were dilated with a concentric balloon and 51 with the eccentric balloon. Technical success in the two groups was similar (73.3% vs. 74.5% control vs. Falcon respectively). Procedural success was 96.5% vs. 96.1% in the control and Falcon groups respectively. The mean increase in minimum luminal diameter (MLD) was 1.01 +/- 0.41 mm in the control vs 0.85 +/- 0.45 mm in Falcon (p = 0.053). There was an increase in type A dissections in the Falcon group 18 (36.75%) vs. 10 (19.23%) in the control group (p = 0.07) with no difference in stent implantation, myocardial infarction, CABG or death between the two groups. All patients with a technically successful PTCA were followed-up. Seventeen (43.6%) in the control and 11 (32.4%) in the Falcon had repeat coronary angiography (p = 0.38), 12 (30.8%) vs. 7 (20.6%) had repeat PTCA (p = 0.37) and time to PTCA was 116 +/- 70 days vs. 154 +/- 103 days respectively (p = 0.36). The Falcon performed technically as well as the concentric balloons. Despite a smaller MLD and increase in Type A dissections there was no associated increase in complications or reintervention for restenosis. Further investigation is required to evaluate the role of this mechanism of dilatation in restenosis

Plasma angiotensin-converting enzyme activity and left ventricular dilation after myocardial infarction

Background Left ventricular dilation after acute myocardial infarction (MI) is mainly determined by infarct size. In addition, this detrimental structural adaptation seems to be augmented in patients with the ACE DD genotype. The ACE DD genotype is associated with increased ACE activity. The aim of the present study was to evaluate whether ACE activity per se may carry prognostic significance far subsequent left ventricular dilation as assessed by echocardiography during 1-year follow-up after acute MI. Methods and Results Left ventricular end-systolic and end-diastolic volume indexes were assessed by two-dimensional echocardiography. In 102 consecutive patients, plasma ACE activity was determined 3.7 +/- 0.1 hours after the onset of MI. In 64 of these patients, left ventricular volume indexes obtained at baseline and 1 year after MI were used for the present analysis. Patients were divided into a group having low ACE activity (less than or equal to 12 IU/L, n = 15) and a group having high ACE activity (>12 IU/L, n = 49). Infarct size was a significant predictor of the increase in left ventricular volume indexes (P = .0001) in these patients. Multivariate regression analysis, after correction for infarct size, demonstrated that elevated plasma ACE activity is a significant predictor of the increase in left ventricular end-diastolic and end-systolic volume indexes (P = .0006 and P = .02, respectively) 1 year after RI. Conclusions Elevated plasma ACE activity determined soon after the onset of MI may be a significant predictor of the development of left ventricular dilation and may identify patients at risk

Plasma semicarbazide-sensitive amine oxidase is elevated in patients with congestive heart failure

Objective: Semicarbazide-sensitive amine oxidase (SSAO) is present in various mammalian tissues, especially in vascular smooth muscle cells, but also in plasma. The enzyme has been suggested to play a role in vascular endothelial damage through conversion of amines into cytotoxic aldehydes, ammonia and hydrogen peroxide. Endothelial dysfunction is present in diabetes mellitus (DM) and congestive heart failure (CHF). Elevated plasma SSAO activities have been reported in patients with DM, bur no data on patients with CHF are as yet available. Methods and Results: Plasma SSAO was measured in 271 patients with CHF and compared to values in 77 controls. SSAO was found to be elevated in patients with CHF compared to controls (589 +/- 252 vs. 355 +/- 114 mU/l; P <0.0001). Plasma SSAO was higher in NYHA class III/IV than in class III (662 +/- 288 vs. 555 +/- 226 mU/l; P = 0.004) and also higher in patients with concomitant DM than in those without (706 +/- 248 vs. 557 +/- 245 mU/l; P <0.0001). Plasma SSAO correlated with plasma atrial natriuretic peptide (r = 0.421 P <0.0001), with plasma norepinephrine (r = 0.27: P <0.0001) and with left ventricular ejection fraction (r = -0.13; P = 0.0162). Multiple regression analysis showed atrial natriuretic peptide, norepinephrine, DM and cardiothoracic ratio to be the main determinants of plasma SSAO. Conclusion: The finding of elevated plasma SSAO in CHF, increasing with severity of the disease and with the concomitant presence of DM, supports the suggestion that SSAO may be involved in the pathogenesis of vascular endothelial damage. Plasma SSAO may be a useful parameter in assessing severity of CHF and in prognostic evaluation. Pharmacologic manipulation of SSAO activity might be an interesting new concept for prevention of vascular endothelial damage in various vascular disease entities