Quantitative Coronary Dimensions and Restenosis After Directional Atherectomy or Balloon Angioplasty

Coronary artery dimensions were evaluated in 42 patients (52 lesions) undergoing directional atherectomy of primary atheromatous lesions in native coronary arteries between October 1989 and April 1991, Dimensions were compared with a cohort of 162 patients (213 lesions) undergoing percutaneous transluminal coronary angioplasty of similar lesions between March 1984 and April 1988. Computer-assisted quantitative angiography was performed for paired near-orthogonal views (captured during diastole) of each treated lesion; image pairs taken prior to, immediately following, and 6 months after coronary intervention were studied. Although coronary dimensions were equivalent for the two treatment groups before therapy, the immediate posttreatment minimal lumen diameter was significantly larger after atherectomy than angioplasty (2.24 ± 0.53 mm vs 1.52 ± 0.34 mm, P < 0.01). Despite this, coronary dimensions were similar in the two groups at follow-up angiography. Several dichotomous definitions of restenosis were tested using these quantitative data. Restenosis rates were similar for the two treatments using most definitions, but those definitions based on loss of relative or absolute lumen dimensions resulted in higher rates of restenosis following atherectomy. These data demonstrate that: (1) directional coronary atherectomy can achieve greater initial gain in luminal dimensions than angioplasty; (2) the loss in vessel dimensions within 6 months (late loss) is greater after atherectomy than after angioplasty; and (3) restenosis definitions rely on relative or absolute loss of initial luminal gain favor of angioplasty. (J Interven Cardiol 1996;9:121–127)     

Synthesis of HC toxin and related cyclopeptides containing the (L-Ala-D-Ala-L-Ada-D-Pro) sequence

In studies leading to HC toxin synthesis, a phytotoxic cyclic tetrapeptide with the sequence cyclo (L-Ala-D-Ala-L-Aoe-D-Pro), we have determined optimal conditions for the cyclization which constitutes one of the most important steps in the synthesis of the toxin. All four possible sequences containing an optically active precursor, i.e. L-Ada = (2 S)-2-amino-9-decenoic acid instead of Aoe, have been prepared and subjected to cyclization. Owing to the differences in racemization risk during activation of the terminal carboxyl aminoacid different cyclization procedures have been applied. Cyclopeptide yields and selectivity between cyclomonomer and dimer both containing the title sequence are mainly controlled by the linear precursor sequence. The cyclic tetrapeptide is only obtained with D-proline in the C-terminal position, the best yield reached by the -ONSu activation method. Starting from the peptide, the (9S, 9R) HC toxin epimer on the epoxidic carbon atom has been further synthesized in two steps.     

Ultrasonic detection of nonopaque renal calculi

Four patients with 5 nonopaque renal calculi composed of uric acid were examined by ultrasound. The calculi varied in size from a 1.5 X 1.5-cm intrapelvic stone to a staghorn calculus measuring 4 cm. All stones were satisfactorily imaged by ultrasound, allowing a diagnosis of nephrolithiasis to be made with confidence in each case. In 2 patients with poor excretion on urography, the diagnosis was not suspected prior to the ultrasound examination. The authors feel that ultrasound has great potential value in the investigation of nonopaque filling defects of the renal pelvis and in patients with urographic nonvisualization who have a high risk of uric acid lithiasis.     

The metabolism of dimethylformamide and dimethylacetamide

N-Methylformamide has been isolated and identified in rat urine as a metabolite of dimethylformamide when the latter is administered to rats sc. N-Methylacetamide and acetamide have been isolated and identified in rat urine following sc doses of dimethylacetamide. In vitro studies with liver homogenates and enhancement of demethylation when N-demethylase was induced by phenobarbital in the liver support demethylation as a metabolic pathway for these substituted amides.