Experimental pharmacology indicates that prenalterol is a selective beta 1-adrenoceptor activator. In 5 normal individuals, 15 minutes after the drug (infused at a dose of 15 micrograms/kg over 5 min) the following circulatory changes were seen: a) increase of cardiac index (+31%), heart rate, stroke index, systolic aortic pressure, left and right ventricular mean rate of ejection and mean rate of the pressure rise in either ventricle during the pre-ejection phase; b) reduction of systemic vascular resistance (-18%), appearance, built-up and disappearance times in the left ventricular dye dilution curves. Pulmonary systolic, diastolic and wedge pressures and vascular resistance did not vary consistently. The circulatory effects persisted almost unchanged 30 minutes after the infusion. In a group of 5 patients with heart failure due to primary congestive cardiomyopathy, refractory to conventional therapy, the haemodynamic response to prenalterol (infused at a dose of 30 micrograms/kg over 5 min) was qualitatively similar to that of normal subjects in 3 cases. In 2 other patients cardiac performance deteriorated. The reasons for this paradoxical effect were not identified. These preliminary results suggest that prenalterol is a potent selective inotropic agent in man, that may assist in the therapeutic management of refractory heart failure due to congestive cardiomyopathy. However, careful haemodynamic monitoring is advisable for its use in this dysfunction until broader clinical experience can be accumulated.

The effect of stent coatings in preventing early thrombotic occlusion remains to be proved. The purpose of this study was to evaluate the safety and efficacy of the Carbostent™, a new coronary stent with a nonthrombogenic coating (Carbofilm™), in 110 consecutive patients (73.6% men, mean age 61 ± 9 years) who met prespecified clinical and angiographic inclusion criteria and were treated with aspirin monotherapy after stenting. Stable angina (75.5%), unstable angina (18.2%), and silent ischemia (6.3%) were clinical indications for coronary revascularization. Patients received 10,000 U of heparin and no IIb/IIIa inhibitors or postprocedural heparin. Complex lesion characteristics (B2, C) were present in 39 out of 129 (30.2%) lesions. Mean lesion length was 15.6 ± 7.4 mm, and 32% of the lesions were >15 mm (range 16–52 mm). Small coronary vessels (<3.0 mm) were treated in 28% of the cases. A total of 165 Carbostent™ were used in 129 coronary lesions of the 110 patients. Single‐vessel stenting was performed in 97 (88%) patients and multivessel stent placement in 13 (12%) patients. The mean length of the stented segment was 21 ± 13 mm (range 9–95 mm). Procedural and clinical success was achieved in all patients. At 1‐month follow‐up, there were no stent thrombosis or other major adverse cardiac events. We observed 2 (1.8%) non‐Q‐wave myocardial infarctions and 2 (1.8%) vascular complications. This study indicates that the Carbostent™ may prevent stent thrombosis in selected patients treated with aspirin only. A randomized study comparing aspirin alone versus combined ticlopidine and aspirin after Carbostent™ implantation will be needed to confirm these results. Cathet Cardiovasc Intervent 2002;55:150–156. © 2002 Wiley‐Liss, Inc.

Worse outcomes have been observed in women after PTCA. The present study was undertaken to compare clinical and angiographic results of coronary stenting among women and men. We retrospectively analyzed acute and 6-month results in a consecutive series of 940 men and 160 women undergoing coronary stent implantation between May 1992 and January 1998. Women were older (63 vs. 57 years; P = 0.001), more often hypertensive (46.9% vs. 31.4%; P < 0.001) and diabetic (13.2% vs. 8.3%; P = 0.05), and less often smokers than men (32.5% vs. 70.5%; P < 0.001). A previous history of Q-wave MI was less frequently present in women (28.2% vs. 40.2%; P = 0.003) who more often underwent coronary revascularization because of unstable angina (37.5% vs. 27.1%; P = 0.027). No difference was observed in coronary artery disease extension, lesion complexity, and stented vessel between the sexes. Bailout stenting was more frequently needed in women (28% vs. 17.8%; P = 0.001). No difference was observed in the number of stent implanted per vessel and per patient and average maximal inflation pressure used for stent postdilation. However, a smaller final balloon size was used in women. Procedural and clinical success was achieved in 94.4% and 92.5% of women and 96.7% and 94.5% of men (P = NS), respectively, without differences regarding in-hospital major adverse cardiac events. Bleeding complications occurred more often in women when anticoagulation was used (OR = 2.87; 95% CI = 1.38-5.74). At 6-month clinical follow-up, TLR was similar between the sexes and event-free survival was 75.5% in women and 81.5% in men (P = NS). Angiographic follow-up, performed in 71% of the patients, showed that restenosis was 64% higher in women (OR = 1.64; 95% CI = 1.02-2.61). Despite older age, higher incidence of comorbidities, and more unstable presentation, women treated with coronary stenting showed acute and mid-term clinical results similar to those observed in men. However, they were significantly more likely to develop angiographic restenosis.

BACKGROUND:Oxidative stress is present in cardiovascular diseases (CVDs), and hyperhomocysteinemia, an independent risk factor for these diseases, may play a role by inducing production of oxygen free radicals.METHODS:To evaluate the possible role of homocysteine (Hcy) in inducing oxidative stress in coronary artery disease (CAD), plasma Hcy was measured in 68 consecutive cardiovascular patients, and plasma malondialdehyde (MDA), both free and total (free + bound), was measured in 40 patients with CAD (18 with chronic stable angina and 22 with unstable angina). As controls, we tested 70 healthy volunteers. Hcy was measured by an immunoenzymatic method and MDA, an index of lipid peroxidation, by gas chromatography-mass spectrometry.RESULTS:Plasma Hcy concentrations were significantly higher in cardiovascular patients than in controls (10.2 vs 8.9 micromol/L; P <0.0002), with no significant difference between values in the stable and unstable angina subgroups. Similarly, total MDA was significantly higher in the CAD group than in the controls (2.6 vs 1.3 micromol/L; P <0.00001), again with no significant difference between stable and unstable angina patients. By contrast, free MDA, which was significantly higher in the CAD patients than the controls (0.4 vs 0.2 micromol/L; P < 0.00001), was also significantly higher in the unstable than in the stable angina group (0.5 vs 0.3 micromol/L; P <0.03). However, no correlation was observed among Hcy and free and total MDA.CONCLUSIONS:Our findings show that a moderate increase of Hcy is associated with CVD but that Hcy at the detected values cannot be considered completely responsible for oxidative damage. That lipid peroxidation is involved in CAD is shown by our observation of significantly increased plasma free and total MDA concentrations compared with controls. Moreover, free MDA values discriminated between unstable and chronic stable angina, and could thus represent a new diagnostic tool.