Coronary artery spasm after percutaneous transluminal coronary angioplasty: pathophysiology and clinical consequences.
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
T A Fischell
Publications and source records attributed to T A Fischell.
Ex-vivo results using a new pullback atherectomy catheter (PAC).
In order to evaluate the feasibility of performing definitive atheromatous plaque removal using a novel retrograde cutting (Pullback) atherectomy catheter, pullback atherectomy was performed in 13 severely diseased cadaveric superficial femoral arteries. All experiments were performed using cadaver tissue either mounted in a perfusion/mounting chamber (n = 10) or left in situ (n = 3). In general, a single cut was made with each of three sequentially larger atherectomy catheters (2.5 mm, 3.0 mm, and then 3.5 mm devices). The results were evaluated by angiography and by light microscopy. Nine of the 13 experiments were performed in totally occluded vessels. The mean pre-atherectomy stenosis (all specimens) was 95 +/- 3%, with a final mean postatherectomy stenosis of 21 +/- 5%. There was one vessel performation. We conclude from these preclinical studies that retrograde atherectomy with the Pullback Atherectomy Catheter is a feasible means of performing definitive atherectomy. Despite the promising potential of retrograde atherectomy, little can be said with certainty about the clinical utility of such a device at this early stage.
Arteriosclerosis↗
Determinants of smooth muscle injury during balloon angioplasty.
To study the determinants of smooth muscle injury during balloon angioplasty, we conducted a series of experiments to examine the effects of degree of arterial stretching, duration of balloon inflation, and arterial precontraction on smooth muscle injury after balloon angioplasty in isolated, perfused whole-vessel segments of rabbit aortas and dog carotid arteries. Freshly dissected rabbit thoracic aortas and dog carotid arteries were mounted in a muscle bath-perfusion chamber and perfused at 80 mm Hg. The proximal half of each aorta was dilated with a 5-mm (41 +/- 6% stretch), 6-mm (64 +/- 6% stretch), or 8-mm (97 +/- 9% stretch) balloon angioplasty catheter, and the uninjured half of each vessel served as the control. The vasoconstrictor behavior of the dilated segment was then assessed by dose-response testing; long-axis, ultrasonic imaging combined with computerized edge-detection image processing was used to measure changes in segmental internal vessel diameters that were induced by phenylephrine. A similar series of experiments was performed in dog carotid arteries with 5-mm balloon catheters (42 +/- 2% stretch) to compare the susceptibility to smooth muscle injury between elastic (aortic) and muscular (carotid) arteries. Additional experiments were performed to determine the roles of prolonged (30 minutes) balloon inflation and arterial precontraction on smooth muscle injury after balloon angioplasty. In rabbit aortas, the dilated arterial segments demonstrated normal reactivity to phenylephrine after dilatation with 5- and 6-mm balloons (p = NS versus control). Severe smooth muscle injury (histopathologically) with "arterial paralysis" was observed after severe stretch (8-mm balloon) and after 5-mm balloon dilatation (46 +/- 5% stretch) in precontracted vessels. Prolonged balloon inflations did not impair aortic vasoconstrictor behavior. Dog carotid (muscular) arteries demonstrated angioplasty-induced smooth muscle injury with less severe degrees of stretch (47-52% stretch). Geometric modeling suggests that medial stretching during balloon angioplasty of diseased vessels in vivo is in the range of 15-41%.(ABSTRACT TRUNCATED AT 400 WORDS)
Angioplasty, Balloon↗
Evidence for altered epicardial coronary artery autoregulation as a cause of distal coronary vasoconstriction after successful percutaneous transluminal coronary angioplasty.
To determine whether vasoconstriction distal to the site of successful percutaneous transluminal coronary angioplasty (PTCA) is a result of altered autoregulation in a hypoperfused coronary artery, we examined the association of this distal vasoconstriction with lesion severity in 20 patients. Lesion severity was classified as moderate, severe or critical (greater than 1.0, 0.5-1.0, and less than 0.5 mm, respectively). Quantitative coronary measurements were made at 3, 15, and 30 min after PTCA, and then after intracoronary (IC) nitroglycerin, in coronary segments distal to the dilated lesion (distal) and in a nonmanipulated vessel (control). Coronary vasoconstriction in the Distal segment after PTCA correlated with lesion severity, with 14 +/- 4%, 28 +/- 2%, and 41 +/- 5% vasoconstriction (vs. IC nitroglycerin, 30 min after PTCA) in the moderate, severe and critical lesion severity subgroups, respectively (P less than 0.01 for critical or severe vs. moderate). This vasoconstriction was significantly greater than that observed in the corresponding control segment for patients with severe (P less than 0.01), and critical (P less than 0.001) lesions. These findings suggest that hypoperfused human epicardial coronary arteries "reset" their autoregulatory responsiveness and that distal vasoconstriction after PTCA is the result of this altered autoregulation. These findings have clinical implications concerning the etiology, prophylaxis and treatment of coronary spams after PTCA and coronary bypass surgery.
Angiography↗
Occlusive coronary-artery spasm as a cause of acute myocardial infarction after coronary-artery bypass grafting.
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Coronary Artery Bypass↗
Endothelium-dependent arterial vasoconstriction after balloon angioplasty.
To determine whether balloon angioplasty can provoke arterial vasoconstriction independent of platelet aggregation and neurogenic input, we studied the spontaneous vasomotor effects of balloon dilatation in isolated, perfused whole-vessel segments of rabbit aorta and pig carotid artery. Freshly dissected rabbit thoracic aortas were mounted in a muscle bath-perfusion chamber, perfused with physiologic saline solution at 70 mm Hg, and allowed to equilibrate. The proximal or distal half of the aortas were dilated with either a "large" (5 mm, 31-51% stretch beyond relaxed diameter) or a "small" (4 mm, 5-16% stretch) balloon angioplasty catheter with the other half of the vessel serving as the control. A similar series of experiments were performed in pig carotid arteries using "large" (6 or 8 mm, 48-90% stretch) balloon catheters. The spontaneous vasomotor effects of balloon angioplasty were examined with long-axis, high-frequency ultrasonic imaging combined with computerized edge detection image processing to measure changes in segmental internal vessel diameters. Additional experiments were carried out in rabbit aortas to determine the roles of the endothelium, extracellular calcium, indomethacin, ibuprofen, and calcium-channel blockade in modulating angioplasty-induced vasoconstriction. Significant arterial vasoconstriction was observed in the balloon angioplasty segments after dilatation with 5-mm balloons but not with 4-mm balloons. After dilatation with 5-mm balloons, the angioplasty segments' cross-sectional areas decreased by an average of 31% versus 4% for the nondilated (control) segments (p less than 0.0001). Similar postangioplasty vasoconstriction was observed in the pig carotid arteries (decrease in minimal vessel cross-sectional area of 41% [angioplasty segment] versus 2% [control segment]) (p less than 0.005). This angioplasty-induced vasoconstriction was prevented by endothelial denudation before angioplasty, removal of extracellular calcium, and pretreatment with indomethacin or ibuprofen. The vasoconstriction was only partially inhibited by calcium channel blockade with verapamil. These findings demonstrate that stretch-pressure-induced arterial vasoconstriction may occur after balloon angioplasty, independent of platelet aggregation and neurogenic input. This angioplasty-induced vasoconstriction appears to be mediated by an endothelially derived cyclooxygenase product(s).
Angioplasty, Balloon↗
Effects of acetylcholine on epicardial coronary arteries after cardiac transplantation without angiographic evidence of fixed graft narrowing.
The coronary response to acetylcholine was evaluated in 10 patients who had had cardiac transplantation 1 to 8 years earlier and in 4 patients who did not undergo transplantation. All 14 patients had no angiographic evidence of fixed coronary arterial narrowing. Acetylcholine was infused in 10-fold increasing concentrations (10(-6) to 10(-2) M) into the midpoint of the left anterior descending coronary artery by an infusion catheter. Administration was terminated when either vasoconstriction was noted at fluoroscopy or when the maximal acetylcholine concentration was reached. Vascular responses were evaluated by quantitative angiography. All 14 patients had a decrease in coronary lumen size in response to acetylcholine. The mean percentage of vasoconstriction was 37 +/- 24% (p less than 0.001). Combined infusion of nifedipine and the maximal vasoconstricting dose of acetylcholine did not result in a significant reversal of coronary vasoconstriction in all 10 cardiac transplantation patients. It was concluded that acetylcholine is a potent coronary vasoconstrictor in patients who had cardiac transplantation and possibly lacks vasodilating effects in most normal patients without angiographic evidence of coronary artery disease, thus suggesting that acetylcholine might not be a suitable pharmacologic agent for testing endothelial cell integrity.
Acetylcholine↗
Transesophageal two-dimensional echocardiography and color Doppler flow velocity mapping in the evaluation of cardiac valve prostheses.
To determine the value of transesophageal ultrasound in the assessment of cardiac valve prostheses, 14 patients with clinically suspected mitral prosthesis malfunction were studied by transthoracic and transesophageal two-dimensional imaging as well as by color Doppler flow velocity mapping (color Doppler). Patients underwent left ventricular angiography (n = 13), surgery (n = 11), or both angiography and surgery (n = 10). Nine patients had only mitral valve replacement, four patients had both mitral and aortic valve replacement, and one patient had mitral, aortic, and tricuspid valve replacement. There were 16 biological and four mechanical prostheses. The degree of mitral regurgitation was graded by both transthoracic and transesophageal color Doppler according to the area of the regurgitant jet visualized and was compared with a three-point classification of mitral regurgitation by left ventricular angiography judged by observers blinded to the echocardiographic results. All transesophageal studies were performed without complication and were well tolerated. The pathological morphology of the mitral prosthesis was additionally or more clearly visualized by transesophageal two-dimensional imaging and subsequently proven at surgery in three patients with flail leaflets and one patient with a vegetation compared with images obtained by the transthoracic approach. Valvular regurgitation was graded by the transthoracic approach as absent in four patients, mild in two patients, moderate in five patients, and severe in only three patients. The transesophageal assessment showed absence of mitral regurgitation in two patients, moderate regurgitation in two patients, and severe regurgitation in 10 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Coronary artery vasoconstriction routinely occurs after percutaneous transluminal coronary angioplasty. A quantitative arteriographic analysis.
To determine whether percutaneous transluminal coronary angioplasty (PTCA) increases coronary artery luminal dimensions by stretching and injuring ("paralyzing") the smooth muscle of the arterial wall, we prospectively analyzed spontaneous changes and then intracoronary nitroglycerin-induced changes in segmental coronary artery diameters during the first 30 minutes after uncomplicated single-vessel PTCA in 10 patients. Five additional patients received intravenous nitroglycerin throughout the procedure to determine whether nitroglycerin could prevent vasoconstriction after PTCA. All of the patients were maintained on oral doses of diltiazem and aspirin at the time of the study. Coronary arteriography was performed at 2, 5, 15, and 30 minutes after PTCA and then 3 minutes after 300 micrograms i.c. nitroglycerin. Quantitative measurements (computerized edge-detection) were performed at each time, in coronary segments centered in the dilated segment, distal to the dilated segment, and in a control vessel not manipulated with the balloon catheter or guidewire. Progressive vasoconstriction (defined as a loss of diameter that was reversed by intracoronary nitroglycerin) was observed after PTCA in the dilated and distal segments (10 of 10 patients) but not in the control segment. The vasoconstriction in the dilated segment at 30 minutes (mean, 30 +/- 4%) was highly statistically significant compared with vasoconstriction at 2 and 5 minutes after PTCA (p less than 0.001) and compared with the control segment at 30 minutes (p less than 0.005). There was no significant loss of diameter after PTCA in the dilated segment in the five patients who received intravenous nitroglycerin. In conclusion, 1) spontaneous coronary artery vasoconstriction after PTCA occurs routinely at and distal to the site of balloon dilatation despite pretreatment with aspirin and calcium channel blockers; 2) coronary artery vasoconstriction after PTCA is rapidly reversed by intracoronary nitroglycerin and can be prevented by the continuous administration of intravenous nitroglycerin during and after the procedure; 3) these results are incompatible with the hypothesis that PTCA improves coronary luminal dimensions by arterial "paralysis"; and 4) these findings have implications concerning the etiology and prophylaxis of abrupt vessel closure after PTCA.
Aged↗
Long-term follow-up after surgical correction of Wolff-Parkinson-White syndrome.
The long-term efficacy of surgical correction of Wolff-Parkinson-White syndrome was evaluated in 45 consecutive patients. Before surgery, 42 patients had reciprocating tachycardia and 12 had atrial fibrillation. The principal operative procedure was endocardial incision in 42 patients, endocardial cryoablation in 2 patients and epicardial cryoablation without dissection of the atrioventricular (AV) fat pad in 1 patient. Two patients had perioperative complications. One patient had bleeding that necessitated reoperation, and one had a right cerebral stroke with subsequent clearing of neurologic deficit. At postoperative electrophysiologic study, only the patient who underwent epicardial cryoablation had conduction over an accessory connection. Two others had intermittent delta waves in the early postoperative period but no accessory connection conduction at electrophysiologic study. During a mean follow-up of 3.1 years, the patient with ineffective cryoablation had recurrent orthodromic tachycardia, and one other patient had late recurrence of delta waves without arrhythmias. Four other patients had frequent palpitation, which was caused by premature ventricular complexes in three and sinus tachycardia in one. Seventeen patients had occasional "skipped beats" without recurrence of tachyarrhythmias. Twelve of 13 patients whose arrhythmias limited employment before surgery returned to work after surgery. By actuarial analysis at 1, 2 and 3 years, all patients were alive and 98% were free from tachyarrhythmias. Surgical correction of Wolff-Parkinson-White syndrome provides excellent long-term results with low morbidity. Patients who are disabled by arrhythmias return to work after successful surgery. Delta waves may persist or recur without return of arrhythmias. Minor postoperative episodes of palpitation are common and do not correlate with tachyarrhythmias.
Endocardium↗
Use of two-dimensional ultrasonic imaging to measure pharmacologically induced vasomotion in rabbit aorta.
We have developed a novel method combining two-dimensional ultrasonic imaging and computerized edge detection to study the vasomotor responses of isolated arterial vessels to various pharmacological agents. Using this in vitro system, we studied the contraction and relaxation of rabbit aorta, respectively, to phenylephrine and acetylcholine. Quantification of these drug-induced changes in vessel wall diameter was achieved by computerized edge detection processing of the two-dimensional ultrasonic vessel wall images. Resolution of this imaging system was determined to be +/- 0.27 mm. Dose-response curves obtained via this new method showed a high degree of correlation with data obtained by classical tissue bath techniques using ring segments. Two-dimensional ultrasonic imaging combined with computerized edge detection is a new and sensitive method to study vasoreactivity of whole, isolated arterial vessels to pharmacological agents.
Acetylcholine↗
Comparative effectiveness of intravascular stents in resisting arterial vasoconstriction: evaluation with use of intact elastic (rabbit aorta) and muscular (dog carotid) arteries in an ex vivo model.
PURPOSE: The ability of three different intravascular stents (Gianturco-Roubin, Palmaz-Schatz, and CV Rad), and two different metals (stainless steel and tantalum) to resist vasoconstriction was evaluated in an intact artery ex vivo model. MATERIALS AND METHODS: Stents were deployed in 21 rabbit thoracic aortae and five dog carotid arteries, which were constricted with phenylephrine and serotonin, respectively. Vasoconstriction was measured with the use of high-frequency ultrasonic imaging. RESULTS: The maximal vasoconstriction of the control segment was 37.7% +/- 2.6 with rabbit aortae and 36.3% +/- 4.1 with dog carotid arteries, while the average maximal constriction for all segments in which stents were placed was 5.7% +/- 1.1 (P < .01). The maximal constriction of the Gianturco-Roubin stainless steel stent was 9.4% +/- 2.7 versus 7.9% +/- 1.6 with the tantalum version (P = .65). Both designs showed somewhat greater constriction compared with either the Palmaz-Schatz (3.3% +/- 0.9) or the CV Rad (1.4% +/- 1.1) stents. CONCLUSIONS: Although all of the stents tested substantially resist arterial vasoconstrictive forces, the Palmaz-Schatz and CV Rad stents resist vasoconstriction to a greater degree than the Gianturco-Roubin stents. Tantalum and stainless steel stents of the same design (Gianturco-Roubin) appear similar in their ability to resist vasoconstrictive forces.
Animals↗
Dose and dose rate effects of beta-particle emitting radioactive stents in a porcine model of restenosis.
BACKGROUND: Radioactive stents have been proposed as a means to prevent in-stent restenosis by inhibiting intimal proliferation with continuous low-dose irradiation. OBJECTIVES: The purpose of this study is to determine the effects of cumulative dose and dose-rate delivery on neointimal formation using 32P and 90Y beta-particle emitting radioactive stents in a porcine coronary model of restenosis. METHODS AND MATERIALS: We compared the late histologic results of 0.25 to 32.0 microCi 90Y (half-life 64 hours) (n = 64 stents) and 0.1 to 57.6 microCi 32P (half-life 14.3 days) (n = 55 stents) Beta-particle emitting radioactive stents with non-radioactive (n = 40) stents in a porcine coronary model of restenosis. A computer-based dosimetry modeling program was used to determine the 28 day cumulative dose and dose-rate delivery for the beta-particle emitting radioactive stents at a distance of 0.1 mm from the stent surface. RESULTS: Continuous low dose-rate (1 to 5 cGy/hr) radiation delivery for > 2 weeks via a 0.1 to 0.5 microCi 32P radioactive stent effectively reduced in-stent neointimal hyperplasia at 90 days. Cumulative doses of > 55 Gy induced severe adventitial fibrosis, microvascular damage and promoted the formation of a matrix-rich neointima. Delayed vascular repair was evident at focal regions within the body of radioactive stents that delivered cumulative doses of > or = 140 Gy at 28 days and cumulative doses of 1,100 Gy at 90 days. CONCLUSIONS: These data may be useful in predicting safe and effective dose and dose rate delivery for beta-particle emitting radioactive stents.
Animals↗
Chronic stimulation via percutaneously inserted epidural electrodes.
Thirty-one patients suffering from intractable pain associated with chronic low back syndrome, cancer, and other disorders have been studied after an average of 6 months of treatment by electrical stimulation of the spinal cord applied using electrodes inserted through a Touhy needle into the epidural space. As judged by three different subjective rating methods, epidrual stimulation successfully relieved otherwise intractable chronic pain in from 23 to 26 of the 31 patients. Reported improvements in the ability to perform various everyday activities, and elimination of drug usage by many patients, corroborated this finding.
Adult↗
Chronic dorsal column stimulation via percutaneously inserted epidural electrodes. Preliminary results in 31 patients.
31 patients suffering from intractable pain associated with chronic low back syndrome, terminal cancer, and other disorders have been studied after an average 6 months' treatment by electrical stimulation of the spinal cord applied via electrodes inserted through a Tuohy needle into the epidural space. As judged by three different subjective rating methods, epidural stimulation successfully relieved otherwise intractable chronic pain in from 23 to 26 of the 31 patients. Reported improvements in the ability to perform various everyday activities, and elimination of drug usage by many patients, corroborate this finding. The side effects of stimulation, both as reported subjectively and as measured objectively by sensory testing, were not clinically significant. Spontaneous electrode displacements, leading to loss of analgesia and requiring minor surgery for repositioning, were encountered frequently, as were lead wire failures necessitating replacement. The partially implanted, externally powered stimulation system presently in use also suffers from problems of reliability and convenience to the patient.
Electric Stimulation Therapy↗