Rotational ablation of coronary artery lesions using single, large burrs.

Previous clinical use of the Rotablator in coronary artery disease has involved a sequential increase in burr sizes up to 2 mm in diameter and has often utilized balloon adjunct to achieve an optimal result. We report our experience and describe our technique using a single, large burr (2.25, 2.5, or 2.75 mm diameter) without balloon assistance. The burr size was selected to approximate 70-90 percent of the apparent normal lumen diameter. Thirty-one patients with 36 lesions of complex morphology (eccentric, irregular, calcified, ulcerated, at bends, at bifurcations, completely occluded, as well as balloon failures) were successfully treated with the Rotablator. Results were assessed by computerized quantitative angiography. The percent diameter stenosis (mean +/- SD) for the group was reduced from 69.8 +/- 11.3% to 30.9 +/- 10% (p less than 0.001). The mean absolute diameter stenosis increased from 0.9 +/- 0.3 mm to 2.2 +/- 0.3 mm (p less than 0.001). Angiographically visible dissections were seen in 4 patients and were uncomplicated in 2. One patient had a non-Q-wave myocardial infarction. A fourth patient had a presumed acute occlusion 36 hr after the procedure, necessitating emergency bypass surgery, but without Q waves on the electrocardiogram or wall-motion abnormalities on the echocardiogram. Nitroglycerin was infused through the Rotablator catheter and has considerably lowered the degree and frequency of spasm. No other acute complications occurred. The mean procedure time using a single burr was shorter than when multiple burrs were used: 56.5 vs. 97.3 min, respectively (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Rotablator induced "shave" of intraluminal cap exposing intramural plaque crater.

A patient with recent onset of unstable angina was found to have a severe, eccentric stenosis of the proximal left anterior descending coronary artery. Rotational atherectomy was performed. After the first passage of the burr across the stenosis, an intraplaque crater was angiographically visualized. It is hypothesized that the patient's clinical presentation may be attributed to plaque rupture and formation of an intraplaque crater which was sealed by a fibrous cap. This cap was "shaved" by the rotating burr, exposing the crater. Adjunctive balloon dilatation expanded the true lumen and compressed the crater.

Treatment of symptomatic peripheral atherosclerotic disease with a rotational atherectomy device.

Narrowings 70 to 90% in diameter in 3 iliac, 4 superficial femoral and 2 popliteal arteries were crossed and atherectomized successfully in 6 patients using the Squibb Rotablator under angiographic guidance during surgical bypass procedures on these arteries. The Rotablator consists of a 1.25 to 4.5 mm diameter oblong burr with tiny diamond blades mounted on a flexible shaft, which tracks over a spring-tip guidewire and rotates at speeds greater than 120,000 rpm. All stenoses were reduced to less than or equal to 50% of the normal luminal diameter. No significant complications occurred. Of the 6 patients having the atherectomy procedure, 5 were reevaluated by duplex Doppler measurements 1.5 to 5.5 (mean 3.5) months after atherectomy and found to be patient with only mild residual flow disturbance. Repeat follow-up by angiography after a mean of 5.2 months, however, showed only 3 (37%) of the atherectomized segments in 3 patients to still be patent. All were symptomatically improved. Of the effluent particles analyzed, 90% were less than 8 microns in size, while only 5% reached 250 microns. With improvements in technique, the largest particles were 150 to 180 microns, constituting only 1.4% of effluent debris. Samples of the effluent from 2 patients were injected in vivo into the left coronary system of 2 pigs. There were no acute hemodynamic or electrocardiographic complications or pathologic evidence of muscle necrosis or vascular thrombosis 18 to 48 hours later. These preliminary results with respect to feasibility and safety of the Rotablator are promising.

Effect of nifedipine on exercise-induced left ventricular dysfunction and myocardial hypoperfusion in stable angina.

To assess the effects of nifedipine on left ventricular function and regional myocardial perfusion, exercise radionuclide ventriculography was performed in 15 men (median age 59 years) and exercise thallium-201 scintigraphy was done in 11 of them, before and 90 minutes after the oral administration of 20 mg of nifedipine. All patients had stable angina and angiographically proved coronary artery disease without evidence of spasm. Exercise tolerance after administration of nifedipine increased from 343 +/- 42 seconds to 471 +/- 50 seconds (p less than 0.01), whereas the peak exercise double product remained essentially unchanged (difference not significant). Ejection fraction improved significantly at rest (from 49 +/- 3.6% to 52 +/- 3.3%, p less than 0.05) and at peak exercise (42 +/0 3.3% to 47 +/- 3.7%, p less than 0.05). Nifedipine also resulted in an improved segmental wall motion score (4.3 +/- 2.3 to 3.0 +/- 2.3, p less than 0.05; 0 = normal and 4 = worst degree of dysfunction). The ejection fraction increased by more than 5% in one third of the patients at rest, and in more than half of the patients at peak exercise. Improved exercise myocardial perfusion occurred in 5 of 11 patients (45%) and in 7 of 28 segments (25%) with reversible hypoperfusion. Thus, nifedipine produces significant improvement in global and regional left ventricular function in patients with coronary artery disease and stable angina. This may be accounted for, at least in part, by improvement in myocardial perfusion.

Comparison of cold pressor and exercise radionuclide angiocardiography in coronary artery disease.

To investigate the role of the cold pressor test (CPT) with radionuclide angiocardiography in the diagnosis of coronary artery disease (CAD), we performed angiocardiography in 52 patients (18 with angiographically normal coronary arteries and 34 with CAD) during the resting state, CPT, and supine bicycle exercise (EX). In normal subjects, left ventricular ejection fraction (EF) was unchanged between rest (58 +/- 9%) and CPT (59 +/- 9%, p = ns), but increased during maximal EX (69 +/- 9%, p less than 0.01). In CAD patients, EF fell from 55 +/- 9% at rest to 49 +/- 9% during CPT (p less than 0.01), and to 53 +/- 11% during EX (p = ns vs. rest). Twenty-seven CAD patients (79%) developed new or worsening areas of dyssynergy during CPT, vs. 25 patients (73%) during EX. Thus, the cold pressor test with radiocardiography appears to be a useful noninvasive test for the diagnosis and functional evaluation of CAD, particularly in patients unable to perform a satisfactory exercise test.

Effects of digoxin on left ventricular function in coronary artery disease patients.

To assess whether digitalis modifies or prevents the deterioration of the left ventricular ejection fraction and wall motion during acute ischemia, we performed gated blood pool radionuclide ventriculograms in 15 patients with angiographically documented coronary artery disease. All patients were studied in the resting state and during maximal supine bicycle exercise, both before and 1 hour after 1 mg intravenous digoxin. There was no significant difference, pre-digoxin vs post-digoxin, in exercise tolerance (415 +/- 84 vs 418 +/- 107 seconds), number of segments with abnormal resting wall motion (12 vs 11) or exercise wall motion (21 vs 19). Ten patients developed angina during the same exercise load, irrespective of digoxin administration. Twelve patients had subnormal left ventricular ejection fraction during exercise pre-digoxin, vs 13 patients post-digoxin (P = ns). In the resting state, the left ventricular ejection fraction was higher after digoxin (53 +/- 14% pre vs 58 +/- 14% post, P less than 0.05). During exercise, however, the left ventricular ejection fraction was not significantly improved after digoxin (50 +/- 16% pre vs 53 +/- 17% post, P = ns). These data indicate that although acute administration of digoxin improves the resting left ventricular function, it does not improve exercise tolerance to angina. Furthermore, intravenous digoxin does not appear to prevent the deterioration of left ventricular wall motion and ejection fraction during exercise induced ischemia.