RESUMEN
Adjunctive balloon dilatation strategy has been shown to improve optimal stent deployment. As improvements in current stent designs evolve, less adjunctive balloon dilatation may be needed. However, few data currently exist to support this practice. We evaluated 88 native coronary lesions treated with single stent implantation (Nir, Tristar or S670). Serial intravascular ultrasound was performed after successful stent deployment and again after adjunctive balloon dilatation. To investigate further the precise expansion characteristics of the stents, serial volumetric intravascular ultrasound analyses were performed in 40 patients with automated pullback. After adjunctive balloon dilatation, minimal stent area increased significantly, from 6.4 +/- 2.1 to 7.4 +/- 2.2 mm(2) (p <0.001). Volumetric analysis showed a corresponding increase in stent volume index (6.6 +/- 1.8 to 7.5 +/- 2.0 mm(3)/mm, p <0.001). In the analysis of cross sections at 0.5-mm axial intervals, the percentage of cross sections, where stent area was > or =80% of the average reference lumen area, increased from 51% to 78% (p <0.001). Similarly, the percentage of cross sections, where stent area was > or =90% of the average reference lumen area, increased from 29% to 56% (p <0.001) with postdilatation. Postdeployment high- pressure balloon dilatation improved minimal stent area and volumetric expansion throughout the stented segment.
Asunto(s)
Angioplastia Coronaria con Balón , Enfermedad Coronaria/terapia , Stents , Enfermedad Coronaria/diagnóstico por imagen , Femenino , Humanos , Masculino , Persona de Mediana Edad , Resultado del Tratamiento , UltrasonografíaRESUMEN
A 73-year-old woman was admitted to St. Margaret's Hospital with a history of an acute anteroseptal infarction, a loud cardiac murmur, and low cardiac output. Cardiac catheterization revealed a large, high ventricular septal defect and normal coronary arteries. Despite successful closure of the ventricular septal rupture, death occurred in the operating room due to severe right ventricular dysfunction. Although this patient had normal major coronary arteries, a ventricular septal rupture developed, which was probably caused by spasm or isolated atherosclerotic disease of a large septal perforator.
RESUMEN
In order to evaluate the usefulness of thallium-201 (201TI) myocardial scintigraphy in delineating the location and size of prior myocardial infarction, 32 patients were evaluated at a mean of 7 +/- 2 months after infarction with a 12-lead ECG, resting 201TI myocardial scintigram, biplane left ventriculogram and coronary angiograms. From the left ventriculogram, asynergy was quantified as percent abnormally contracting segment (% ACS), the percent of end-diastolic circumference which was either akinetic or dyskinetic. Using a computerized planimetry system, we expressed 201TI perfusion defects as a percentage of total potential thallium uptake. Of 21 patients with ECG evidence of prior transmural infarction, a 201TI defect was present in 20 (95%), and angiographic asynergy was present in all 21 (100%). The site of prior infarction by ECG agreed with the 201TI defect location in 24 of 32 patients (75%) and with site of angiographic asynergy in 23 of 32 patients (72%). Scintigraphic defects were present in only four of 10 patients (40%) with ACS less than or equal to 6%, but scintigraphic defects were found in 20 to 22 patients (91%) with ACS greater than 6% (p less than 0.01). Thallium defect size correlated marginally with angiographic left ventricular ejection fraction (r = -0.60) but correlated closely with angiographic % ACS (r = 0.80). Thallium defect size was similar among patients with one-, two-, or three-vessel coronary artery disease (greater than or equal to 70% stenosis), but thallium defect size was larger in patients with electrocardiographic evidence of transmural infarction (p less than 0.01) or pulmonary capillary wedge pressure greater than 12 mm Hg (p less than 0.001). Thus, resting 201TI myocardial scingigraphy is useful in localizing and quantifying the extent of prior myocardial infarction, but is insensitive to small infarcts (ACS less than 6%).