Refractory no-reflow successfully treated with local infusion of high-dose adenosine and verapamil--a case report.

No-reflow is an unpredictable complication following percutaneous coronary intervention. No-reflow is associated with myocardial ischemia and infarction and increased mortality. A case of refractory no-reflow is described that was rapidly and successfully treated with multiple infusions of high doses of verapamil and adenosine applied directly at the site of no-reflow through a perfusion catheter.

Incidence of thrombocytopenia following coronary stent placement using abciximab plus clopidogrel or ticlopidine.

The incidence of thrombocytopenia with ticlopidine and clopidogrel when used in conjunction with abciximab has not been systematically addressed. We evaluated the rate of thrombocytopenia in patients undergoing intracoronary stent implantation receiving bolus plus infusion of abciximab and either ticlopidine or clopidogrel. We noted an incidence of 24% with the combination of 300-mg clopidogrel and abciximab. Other doses of ticlopidine (250 and 500 mg) and clopidogrel (75 mg) did not result in a statistically significant increase in thrombocytopenia over that of the 2.5%-5.2% reported incidence with abciximab alone. Length of hospital stay was 2.3 vs. 6.4 days in those developing thrombocytopenia (P = 0.06). Four (25%) developed thrombocytopenia requiring blood transfusion. Eight (50%) had no sequelae. The combination of 300-mg clopidogrel and abciximab results in a significant increase in the incidence of thrombocytopenia. This is an important clinical observation that merits further study.

Origins of breath nitric oxide in humans.

STUDY OBJECTIVES: Nitric oxide (NO) exists in the human breath, but little is known about its site of origin or enzyme source. The aims of this study were to locate the main site of NO release into human breath and to decide whether the inducible isoform of NO synthase (iNOS) and nasal bacteria contribute to breath NO. DESIGN: Using a chemiluminescence assay, NO levels were measured in air exhaled from the nose, mouth, trachea, and distal airway. The susceptibility of breath NO to treatment with a topical corticosteroid (to inhibit iNOS; intranasal beclomethasone dipropionate for 2 weeks) and with antibiotics (systemic amoxicillin plus clavulanic acid and intranasal bacitracin zinc, 5 to 10 days) was also tested. PARTICIPANTS: Twenty-one healthy subjects, 9 intubated patients, and 7 patients undergoing bronchoscopy. All subjects were nonsmokers free of pneumonia, rhinitis, and bronchitis. MEASUREMENTS AND RESULTS: Breath NO levels, collected in the gas sampling bags, were greater (p < 0.05) in the nose (25 +/- 2 parts per billion [ppb]) than in the mouth (6 +/- 1 ppb), trachea (3 +/- 1 ppb), or distal airway (1 +/- 2 ppb). Similar results were obtained when NO was sampled directly by cannula from nose or mouth during resting breathing. Nasal breath NO signal increased sharply during 30 s of breath-holding. Beclomethasone, but not antibiotics, decreased nasal NO levels without changing oral breath NO. CONCLUSIONS: Most NO in normal human breath derives locally from the nose where it can reach high levels during breath-holding. NO is synthesized, at least in part, by a steroid-inhibitable, nonbacterial, NO synthase, presumably iNOS.