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Biomedical subjects

M C Fishbein

Publications and source records attributed to M C Fishbein.

At least 109 records · Page 6Linked to original sources
PubMed1996

Reentrant wave fronts in Wiggers' stage II ventricular fibrillation. Characteristics and mechanisms of termination and spontaneous regeneration.

The mechanisms of Wiggers' stage II ventricular fibrillation (VF) are poorly understood. Using computerized mapping techniques, we studied the patterns of activation during Wiggers' stage II VF in 13 open-chest dogs. In 7 of the 13 dogs, the right ventricular Purkinje fibers and adjacent subendocardial myocytes were ablated with Lugol solution. VF was induced electrically, and 3 to 5 seconds of data were obtained beginning approximately 2.5 seconds after the onset of VF. Dynamic displays of the activation patterns and isochronal maps revealed the presence of reentrant wave fronts in 17 of 33 runs of VF in ablated ventricles and in 12 of 45 runs of VF in intact ventricles. The incidence of reentry was not different between the subendocardium-ablated group versus the nonablated group (1.7 +/- 1.6 versus 1.2 +/- 1.6 rotations per episode of VF, P = .19). There were no differences in the core size (25 +/- 19 versus 29 +/- 18 mm2), life span (3.4 +/- 1.1 versus 3.2 +/- 1.2 rotations), or cycle length (111 +/- 12 versus 107 +/- 8 ms) in ablated ventricles versus intact ventricles, respectively. The core was unstable as it meandered within the mapped area displacing the entire reentrant wave front. In all episodes, the reentrant wave fronts were spontaneously initiated by an interaction between two propagating wave fronts roughly perpendicular to each other. The second wave front met the tail of the first wave front 69 +/- 11 ms (range, 40 to 90 ms) after its latest activation, indicating that the interaction occurred during a vulnerable period. The reentrant wave fronts terminated spontaneously (n = 7), as the result of interference by an invading wave front (n = 19 or meandered off the mapped region (n = 3). We conclude the following: (1) Reentrant activities with short life spans and meandering cores are present during Wiggers' stage II VF in dogs. (2) New reentrant wave fronts are generated when one wave front interacts with another wave front during its vulnerable period. (3) The reentrant wave fronts terminate spontaneously or as the result of interference. (4) Chemical subendocardial ablation does not affect the incidence, life span, cycle length, or core size of the reentrant wave fronts.

Animals↗
PubMed1996

Isolated coronary artery transplantation in pigs: a new model to study transplantation arteriosclerosis and humoral rejection.

BACKGROUND: Graft atherosclerosis is a major cause of death after heart transplantation; its causes are multifactorial and poorly understood. To determine whether specific sensitization to coronary artery antigens is a contributing factor, we developed an isolated coronary artery allotransplantation model in pigs. METHODS: Of 46 Yucatan minipigs, 32 received a segment from a farm pig coronary artery into the common carotid artery (coronary allograft group) and 14 had a left to right common carotid artery autotransplant (carotid autograft group). No immunosuppressive drugs were given; all pigs received heparin for 5 days. We examined patency rates, histologic changes, and endothelial deposition of immunoglobulin G and M. RESULTS: In the coronary allograft group, patency rates were 100% (11 of 11) at 1 to 29 days, 20% (2 of 10) at 30 to 89 days, and 0% (0 of 11) after 90 days (overall 40.6%, 13 of 32). Histologic findings included endothelial cell hyperplasia, intimal proliferation, medial necrosis, adventitial inflammation, and ultimately luminal thrombosis. Deposition of immunoglobulin G and M was examined in the patent grafts and was seen in 90.9% (10 of 11) of grafts from days 1 to 29 and in the two patent but partially occluded grafts at 41 and 56 days. All carotid autografts except one (92.8%, 13 of 14) were patent up to 140 days and showed no or mild focal intimal thickening with normal media and adventitia. Deposition of immunoglobulin could not be detected in the autograft group. CONCLUSIONS: In this pig model of coronary artery allotransplantation, typical histologic findings of graft atherosclerosis are produced. Deposition of immunoglobulin G and M occurs early and is associated with endothelial cell hyperplasia and intimal proliferation. This model may be useful for the study of graft atherosclerosis and assessment of interventions designed to halt its progression.

Animals↗
PubMed1995

VCL, an antagonist of the platelet GP1b receptor, markedly inhibits platelet adhesion and intimal thickening after balloon injury in the rat.

BACKGROUND: Arterial injury is immediately followed by platelet adhesion at the site of injury, a process that requires the interaction of subendothelial von Willebrand factor with the platelet GP1b receptor. VCL, a recombinant von Willebrand factor GP1b binding domain, inhibits platelet binding to von Willebrand factor. The aim of this study was to determine whether VCL inhibits platelet adhesion at the site of arterial injury and affects neointimal thickening after injury in rats. METHODS AND RESULTS: Sprague-Dawley rats were randomized to receive VCL, 4 mg/kg bolus followed by a continuous infusion of 2 mg.kg-1.h-1 for 72 hours, or an identical volume of saline. Balloon injury of the femoral artery was performed 15 minutes after the initial bolus injection of VCL. Scanning electron microscopy performed 1 and 3 days after injury indicated that VCL-treated rats had > 80% reduction in the number of platelets adherent to the vessel wall at the site of injury compared with controls (P < .003). Histological examination at day 14 showed that, compared with controls, VCL-treated rats had a 60% reduction in the intima-media ratio (0.21 +/- 0.03 versus 0.53 +/- 0.06, P = .001) and a reduced luminal area stenosis (12 +/- 3% versus 38 +/- 10%, P = .04). At 28 days after injury, there was no rebound of neointimal thickening in VCL-treated rats (intima-media ratio, 0.19 +/- 0.04; luminal stenosis, 17 +/- 5%). The difference between VCL-treated rats and control rats persisted but was attenuated (intima-media ratio, 0.19 +/- 0.04 versus 0.28 +/- 0.1, P = .162; luminal stenosis, 17 +/- 5% versus 31 +/- 5%, P = .058) as neointimal thickening regressed in untreated rats. With the use of proliferating cell nuclear antigen immunohistochemistry on day 3, VCL had no effect on smooth muscle cell (SMC) proliferation. CONCLUSIONS: Antagonism of the platelet GP1b receptor by VCL profoundly decreased platelet deposition at the site of balloon injury in the rat femoral artery. This effect was associated with a persistent reduction in neointimal thickening. The lack of effect of VCL on SMC proliferation suggests that the decrease in neointimal thickening may have been mediated through inhibition of SMC migration and/or modulation of the extracellular matrix.

Angioplasty, Balloon↗
PubMed1995

Absence of lethal reperfusion injury after 3 hours of reperfusion. A study in a single-canine-heart model of ischemia-reperfusion.

BACKGROUND: Whether reperfusion can cause necrosis of previously viable myocytes (lethal reperfusion injury) remains controversial. Numerous studies examined the ability of various agents to prevent or limit reperfusion injury, but the results were contradictory. In a single-canine-heart model of ischemia-reperfusion, we previously demonstrated that 5 minutes of reperfusion does not increase the transmural extent of necrosis. Since the 5-minute period of reperfusion is considered by some to be too short for the full manifestation of reperfusion injury, we reexamined the issue of lethal reperfusion injury using a modification of the single-heart model of ischemia-reperfusion that allowed extending the reperfusion period to 3 hours. METHODS AND RESULTS: In anesthetized, open-chest dogs, the distal half of the left anterior descending coronary artery (LAD) segment between the last diagonal branch and the apex was perfused via a shunt from the left carotid artery. The shunt was closed for periods of 90 to 180 minutes, depending on the ECG severity of ischemia, and reperfused for 3 hours. While the distal region was perfused from the carotid artery, the LAD was occluded proximal to the last diagonal branch for the same period of time as the distal region had been earlier. The time of occlusion was chosen such that the end of the occlusion period coincided with the end of the experiment. Thus, both regions of the LAD territory were subjected to identical periods of ischemia, but only the distal region was reperfused. At the end of the experiment, the boundary between the proximal (nonreperfused) and distal (reperfused) area was delineated by blue dye, and the heart was arrested, cut into slices 1 cm thick parallel to the LAD, and placed in triphenyltetrazolium chloride. The epicardial edges of necrosis in the reperfused and the nonreperfused regions were examined for any shift that might suggest a difference in the transmurality of necrosis. The areas of necrotic and viable myocardium were measured by planimetry within 1 cm on either side of the boundary. In all 14 dogs, the epicardial edges of necrosis ran as a single line across the boundary, and no shift was present. There was also no difference in the transmurality of necrosis between the reperfused and nonreperfused regions (64.9 +/- 20.7% versus 66.1 +/- 17.0% of left ventricular wall thickness, respectively, P = .32 by paired t test). CONCLUSIONS: In a single-canine-heart model of ischemia-reperfusion, there was no evidence of lethal reperfusion injury after 3 hours of reperfusion.

Animals↗
PubMed1995

Permanent pacemaker for rejection episodes after heart transplantation: a poor prognostic sign.

BACKGROUND: The development of arrhythmias early or late after heart transplantation has been associated with acute and chronic rejection. This study aims to document the importance of this relationship and its value as a prognostic sign in those patients who required a permanent pacemaker for rejection episodes. METHODS: A retrospective analysis of 158 orthotopic heart transplantations performed in 157 patients between December 1988 and April 1995 was done. The clinical course and the outcome of 6 patients who underwent insertion of a permanent pacemaker for bradyarrhythmias caused by acute or chronic allograft rejection were compared with the course and outcome of 9 patients who had pacemaker placement as a result of sinus node dysfunction not associated with rejection. RESULTS: The mortality rate was 100% for patients whose indication for permanent pacing was severe acute or chronic rejection. Conversely, 8 of the 9 patients who underwent pacemaker placement for sinus node dysfunction not associated with rejection are long-term survivors; the one late death was due to a noncardiac cause. CONCLUSIONS: We observed a strong relationship between bradyarrhythmias requiring a permanent pacemaker and severe acute or chronic allograft rejection. This association suggests a poor prognosis and indicates that these patients should be managed aggressively. Such management includes close immunologic surveillance for cellular and humoral rejection, increased frequency of endomyocardial biopsies and coronary angiography, and early consideration for retransplantation.

Acute Disease↗
PubMed1995

Heart transplantation for Chagas' cardiomyopathy.

We present 2 patients who underwent orthotopic heart transplantation for end-stage Chagas' cardiomyopathy. Despite immunosuppressive therapy, postoperative prophylaxis with nifurtimox appeared to prevent Trypanosoma cruzi reactivation. Neither patient has shown signs of Chagas' myocarditis, and both are clinically well 12 and 72 months after transplantation. The successful outcome of our patients suggests that heart transplantation is a reasonable therapeutic option in patients with end-stage Chagas' cardiomyopathy.

Adult↗
PubMed1995

Cellular mechanisms of ventricular bipolar electrograms showing double and fractionated potentials.

OBJECTIVES: This study sought to determine the types of trans-membrane action potentials associated with bipolar electrograms that show double and fractionated potentials. BACKGROUND: The cellular correlates of ventricular bipolar electrograms showing double potentials and fractionated low amplitude potentials remain poorly defined. METHODS: A bipolar electrogram (1-cm interelectrode distance [6F, USCI]) and two transmembrane action potentials (within 1 mm of each pole) were recorded simultaneously in 12 isolated canine right ventricular endocardial preparations (2 x 1 cm, 2 mm thick). The long axis of the bipolar electrode was parallel to the long axis of the superficial endocardial fibers, and the recordings were made at 40 to 500 Hz. RESULTS: The following phenomena were associated with double potentials: 1) an increase in conduction time between the two poles of the bipole during a) the propagation of premature action potentials (7 of 12 tissues in 4 mmol/liter extracellular potassium ion concentration [K+]o); b) rapid pacing and premature stimuli (3 of 6 in 9 mmol/liter [K+]o); and c) the propagation of slow responses induced by barium chloride (4 mmol/liter). There was a positive correlation between conduction time (CT) and interspike interval (IPI) of the double potential (IPI [ms] = 0.5 x CT [ms] + 35) during early afterdepolarizations induced by barium chloride (4 mmol/liter) superfusion (three of six tissues). The following events were associated with fractionated electrograms: 1) propagation of induced graded responses (six tissues) in 4 mmol/liter [K+]o; 2) induced reentry at cycle lengths of 140 to 170 ms in 9 mmol/liter [K+]o (four of six tissues); and 3) asynchronous afterdepolarizations induced by 4 mmol/liter barium chloride (four of six tissues). CONCLUSIONS: Endocardial double potentials and fractionated electrograms seen on clinically used bipolar electrodes occur under conditions of slowed or discontinuous conduction and induced reentry and during asynchronous automatic firing initiated by afterdepolarizations. Caution must be exercised in interpreting such bipolar electrograms because more than one type of cellular action potential may cause these abnormal electrographic results.

Action Potentials↗
PubMed1995

Influence of vein valves in the development of arteriosclerosis in venoarterial grafts in the rabbit.

Coronary saphenous vein grafts in human beings have a more limited long-term patency rate than internal thoracic artery grafts, primarily because of more rapid development of arteriosclerosis. The factors responsible for this increased susceptibility are not completely understood. To test the hypothesis that vein valves may influence this process, we studied 48 hypercholesterolemic rabbits with jugular vein grafts interposed into the carotid arterial circulation. In 24 animals (group A), the vein segments did not contain a vein valve. In the other 24 animals (group B), a vein valve was present. Both groups were further divided in four subgroups of six to be put to death at 2, 4, 6, and 8 weeks after the operation. All animals were fed a 2% cholesterol diet. At postmortem examination, alternate 2 mm sections were either stained with hematoxylin and eosin for histologic and morphometric studies or frozen in liquid nitrogen for immunohistochemistry and in situ hybridization studies. Proliferating cell nuclear antigen immunostaining was used to study cell proliferation. Wall thickness of vein grafts increased with time. During the first 2 weeks intimal and medial thickening was primarily due to an increase in numbers of cells. Between 2 and 6 weeks further intimal and medial thickening occurred, but without additional increase in cell numbers. After 6 weeks, foam cells and lipid deposits started to appear. By 8 weeks, changes identical to those seen in arteriosclerotic plaques in human beings were evident. These changes developed sooner and with more intensity in group B animals (p < 0.01 to 0.001), and they developed faster and with more severity in segments of vein located distal to the valve than in the segments located proximal to the valve (p < 0.001). This is the first controlled experiment demonstrating that the presence of valves in the vein segments is associated with augmented and accelerated intimal changes leading to vein atheromatosis.

Animals↗
PubMed1995

Survival of acute intestinal infarction after cardiac transplantation.

We report the case of a 52-year-old male who underwent total orthotopic heart transplantation for end-stage ischemic cardiomyopathy. The postoperative course was complicated by acute intestinal infarction which was diagnosed after surgical exploration, and treated with a subtotal colectomy with Brooke ileostomy and closure of the distal sigmoid three days posttransplant. The patient survived with nutritional support and broad antibiotic prophylaxis. Review of the literature on acute abdominal complications after operations involving cardiopulmonary bypass suggests that such complications are usually fatal. Detection and diagnosis may be obscured and treatment complicated by immunosuppression after cardiac transplantation. Because of the poor prognosis without appropriate management, a high level of suspicion, early and aggressive diagnostic measures, and swift surgical intervention are essential to survival.

Colon↗
PubMed1995

Effects of chemical subendocardial ablation on activation rate gradient during ventricular fibrillation.

The mechanism by which an endocardial-epicardial activation rate gradient develops after 1 or 2 min of sustained ventricular fibrillation is unknown. We recorded from electrodes on the epicardium and from hook electrodes in the endocardium in three open-chest control dogs during prolonged ventricular fibrillation. The same recordings were also made in seven dogs after right ventricular subendocardial ablation with Lugol solution and in three dogs after substitution of air for the cavitary blood. The effects of these interventions, i.e., Lugol ablation (n = 2) and the exposure to air (n = 2), on the subendocardial Purkinje fiber transmembrane action potential properties were also evaluated in vitro using microelectrode recording techniques. The in vivo studies showed a significant endocardial-epicardial rate gradient in the control dogs and in dogs that had air substituted for the cavitary blood. In comparison, in dogs that underwent chemical subendocardial ablation, the activation cycle lengths for the endocardium and epicardium were not significantly different. The in vitro studies showed that subendocardial Purkinje fiber action potentials could still be recorded for up to 10 min of exposure to air. In comparison, in the tissues subjected to chemical ablation, no transmembrane action potentials could be recorded from either the Purkinje fibers or superficial ventricular muscle cells. We conclude that the development of an endocardial-epicardial activation rate gradient during prolonged ventricular fibrillation depends on the presence of intact subendocardial Purkinje fibers and ventricular myocytes. The retained cavitary blood is not responsible for the development of the rate gradient.

Animals↗
PubMed1995

Genetic determination of cartilaginous metaplasia in mouse aorta.

Calcification frequently occurs in atherosclerotic plaques in humans, but the cellular and genetic factors contributing to this pathological trait are unknown. We previously reported that the arterial calcification among inbred strains is genetically determined, and we now report that cartilaginous metaplasia, associated with the presence of arterial chondrocytes that express type II collagen, may underlie this calcification. Both uncalcified and calcified cartilaginous metaplasia were often colocalized with aortic atheromatous lesions and calcification, and clear genetic differences were observed in the occurrence of aortic cartilaginous metaplasia among inbred strains. Analysis of a genetic cross between strains C57BL/6J (exhibiting aortic cartilaginous metaplasia) and C3H/HeJ (no aortic cartilaginous metaplasia) revealed a recessive inheritance pattern; thus, F1 mice were entirely devoid of cartilaginous metaplasia, in common with the C3H/HeJ parental strain. Analyses of an F2 cross and a set of recombinant inbred strains derived from parental strains C57BL/6J and C3H/HeJ were consistent with a major gene effect exhibiting incomplete penetrance. The occurrence of aortic calcification was correlated with the occurrence of cartilaginous metaplasia in these genetic crosses, suggesting a link between the traits. Finally, we observed widespread calcified cartilaginous metaplasia within spontaneous atherosclerotic lesions in mice targeted for a null mutation in the apoE gene, suggesting that cartilaginous metaplasia is a potential pathway for artery wall calcification associated with the atherosclerotic plaque.

Animals↗
PubMed1995

Interaction between strong electrical stimulation and reentrant wavefronts in canine ventricular fibrillation.

This study was designed to test the hypothesis that the effects of a strong electrical stimulus on reentrant wavefronts in ventricular fibrillation (VF) are dependent on the timing of the stimulus. We studied six open-chest dogs by computerized mapping techniques. A plaque electrode array with up to 509 bipolar electrodes was placed on the right ventricular epicardium. The interelectrode distance was 1.6 mm, and the interpolar distance was 0.5 mm. After eight baseline pacing stimuli (S1) with cycle lengths of 300 ms, a strong premature stimulus (S2) (73 +/- 10 mA) was given to induce VF. In subsequent episodes, a second strong premature stimulus (S3) was given at progressively longer S2-S3 intervals in 20-ms increments. The results showed that, at baseline, the S2 consistently induced figure-eight reentry and VF. The VF cycle length immediately after the S2 averaged 108 +/- 17 ms. The S3 resulted in one of the following responses: (1) termination of reentry and VF; (2) induction of different reentrant wavefronts or a focal pattern of repetitive activation; or (3) persistence of the same figure-eight reentry. The intervals between the S3 and the immediately preceding activation at the site of the S3 (the recovery intervals) were 39 +/- 12 ms (range, 20 to 60 ms) and 61 +/- 20 ms (range, 30 to 90 ms) for response patterns 1 and 2, respectively. The recovery intervals associated with response pattern 3 were either < or = 30 ms (22 +/- 8 ms) or > or = 80 ms (94 +/- 15 ms). The differences among these four intervals were significant (P < .001). We conclude that the effects of strong electrical stimulation on the reentrant wavefronts in VF are dependent on the recovery interval since the previous local activation. A protective zone occurred between 20 and 60 ms, during which time a strong electrical stimulus could terminate reentry and abort VF. This zone was followed by a vulnerable period during which new activation wavefronts could be induced. If a strong electrical stimulus was given shortly after or sufficiently long after the previous local activation, the same figure-eight reentrant pattern continued.

Animals↗
PubMed1994

High intensity, low frequency catheter-delivered ultrasound dissolution of occlusive coronary artery thrombi: an in vitro and in vivo study.

OBJECTIVES: This study assessed the efficacy of a new high intensity, low frequency therapeutic coronary ultrasound catheter for thrombus dissolution in vitro and in vivo in canine coronary arteries. BACKGROUND: Therapeutic ultrasound has been shown to dissolve thrombi in vitro and in peripheral arteries in vivo. There have been no previous studies on in vivo coronary thrombus dissolution by ultrasound. METHODS: In vitro, we exposed 1- to 4-h old human blood clots for 3 min to pulsed-wave ultrasound. Clot dissolution under various conditions was evaluated. In vivo occlusive coronary thrombi were induced in 18 dogs. RESULTS: In vitro irrigation alone (10 ml/min of normal saline solution) and ultrasound alone each contributed to a reduction of clot weight by 47.1 +/- 11.4 mg and 84.6 +/- 25.6 mg, respectively, after 3 min (p < 0.001). Ultrasound plus irrigation resulted in a reduction of clot weight by 216.5 +/- 31.5 mg after 3 min (p < 0.001). The magnitude of clot dissolution was considerably amplified when ultrasound energy was combined with irrigation, probably because of cavitational effects. In vivo, in three dogs mechanical passage of the unactivated probe failed to recanalize the artery, and the arteries remained thrombotically occluded. After passage of the activated ultrasound probe, angiography revealed widely patent coronary arteries in 13 of 15 dogs and partial recanalization with filling defects indicative of residual thrombus in 2 of 15 dogs. Three of 15 coronary arteries were histologically free of residual thrombi. Mural thrombi extending to < or = 10% of the vessel circumference were seen in 10 of 15 dogs. Residual thrombi > or = 50% of the vessel circumference were found in two cases. There was no histologic evidence of ultrasound-mediated vessel damage. CONCLUSIONS: Catheter-delivered therapeutic ultrasound effectively dissolves clots in vitro and in canine coronary arteries in vivo. Thus, therapeutic catheter-delivered ultrasound has the potential to serve as an adjunct or alternative treatment for thrombus-mediated coronary ischemic syndromes or myocardial infarction.

Animals↗
PubMed1994

High stress regions in saphenous vein bypass graft atherosclerotic lesions.

OBJECTIVES: Our aim was to test the hypothesis that maximal stresses in saphenous vein atherosclerotic stenoses are greater than those in native coronary artery stenoses. BACKGROUND: The patency of coronary artery saphenous vein bypass grafts decreases with time, usually because of thrombosis. Plaque rupture has been described as one mechanism of vein graft thrombosis. METHODS: Twenty-six nonruptured human lesions were studied. Fourteen lesions were from native coronary arteries, and 12 were from saphenous vein bypass grafts placed a mean +/- SD of 9.8 +/- 3.3 years before pathologic study. The finite element method was used to determine the distribution of stress in the lesion, using estimates of material properties from previous measurements of human tissues. RESULTS: Maximal circumferential stresses were significantly higher in the saphenous vein lesions (median 352 kPa [interquartile range 161 to 475]) than in the coronary artery lesions (median 104 kPa [interquartile range 75 to 185]) (p = 0.05). Thin-walled cylinder formulations predict that stresses are proportional to the radius of the vessel and inversely proportional to the minimal wall thickness. In this study, there was a good correlation between the maximal stress in the 26 lesions and the ratio of the square root of lumen area to minimal fibrous cap thickness (r = 0.83, p < 0.001). CONCLUSIONS: Maximal circumferential tensile stresses in saphenous vein bypass graft stenoses are higher than in native coronary artery atherosclerotic stenoses. These data suggest that strategies that decrease stresses in bypass graft atherosclerotic lesions, such as prevention of lipid accumulation, could reduce the probability of plaque rupture in bypass grafts.

Arteriosclerosis↗
PubMed1994

Catheter-delivered high intensity, low frequency ultrasound induces vasodilation in vivo.

This study investigated the effect of intravascular high intensity, low frequency catheter-delivered ultrasound on vasomotor behaviour in vivo. Catheter-delivered therapeutic ultrasound induces endothelium-independent vasodilation in vitro. To study this effect in vivo we analysed the angiograms of canine coronaries and human femoropopliteal arteries before and after ultrasound exposure. Vasomotor behaviour was studied using a computer edge detection program. We analysed the angiograms of: (1) eight canine left coronary arteries before and after ultrasound; (2) eight canine left coronaries only subjected to serial angiograms, and three canine left coronary arteries of two dogs after passing the unactivated ultrasound probe down the coronary artery infusing saline at a rate of 10-20 ml.min-1, which served as controls, and (3) eight angiographically normal human arterial sites proximal to occlusions in eight femoropopliteal arteries of patients undergoing ultrasound angioplasty for peripheral vascular disease. Vessel diameter of canine coronaries after ultrasound exposure increased from 2.3 +/- 0.3 mm to 2.8 +/- 0.3 mm (21 +/- 2.3%) (P < 0.01). There was no change in vascular diameter in controls after multiple angiograms (2.4 +/- 0.3 mm vs 2.5 +/- 0.2 mm (4.2 +/- 0.2%) (P = ns). Average vessel diameter after passage of the unactivated probe with saline infusion decreased in the left anterior descending coronary artery from 3.66 mm to 3.13 mm, and in the left circumflex coronary artery from 2.88 mm to 2.62 mm. Vessel diameter in human femoropopliteal arteries increased from 3.2 +/- 0.2 mm to 3.6 +/- 0.5 mm or by 14.3 +/- 2.9% respectively (P < 0.01) after exposure to ultrasound energy.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty↗
PubMed1994

Pathology of atheromatous lesions in inbred and genetically engineered mice. Genetic determination of arterial calcification.

We report comprehensive pathological studies of atheromatous lesions in various inbred mouse strains fed a high-fat, high-cholesterol diet and in two genetically engineered strains that develop spontaneous lesions on a low-fat chow diet. Coronary and aortic lesions were studied with respect to anatomic locations, lesion severity, calcification, and lipofuscin deposition. Surprisingly, the genetic determinants for coronary fatty lesion formation differed in part from those for aortic lesion development. This suggests the existence of genetic factors acting locally as well as systematically in lesion development. We used immunohistochemical analyses to determine the cellular and molecular compositions of the lesions. The aortic lesions contained monocyte/macrophages, lipid, apolipoprotein B, serum amyloid A proteins, and immunoglobulin M and showed expression of vascular cell adhesion molecule-1 and tumor necrosis factor-alpha, all absent in normal arteries. In certain strains, advanced lesions developed in which smooth muscle cells were commonly observed. The lesions in mice targeted for a null mutation in the apolipoprotein E gene were much larger, more widely dispersed, and more fibrous, cellular, and calcified in nature than the lesions in laboratory inbred strains. When apolipoprotein A-II transgenic mice were maintained on a low-fat chow diet, the lesions in these mice were relatively small and located in the very proximal regions of the aorta. There were clear differences in the occurrence of arterial wall calcification among genetically distinct inbred mouse strains, indicating for the first time a genetic component in this clinically significant trait. Analysis of a genetic cross indicated a complex pattern of calcification inheritance with incomplete penetrance.

Animals↗
PubMed1994

Use of therapeutic ultrasound in percutaneous coronary angioplasty. Experimental in vitro studies and initial clinical experience.

BACKGROUND: Previous studies have shown the feasibility of peripheral arterial ultrasound angioplasty. METHODS AND RESULTS: In this report, we describe the use of percutaneous therapeutic ultrasound for coronary angioplasty. In vitro, 11 postmortem, atherosclerotically occluded coronary arteries were obtained to assess catheter-delivered ultrasound for arterial recanalization as well as for assessment of the size of particulate debris. Clinically, coronary ultrasound angioplasty was performed in 19 patients (mean age, 56 years) to assess safety and feasibility for the treatment of obstructive coronary atherosclerosis. Three patients with unstable angina and 16 with exercise-induced myocardial ischemia were treated with a prototype 4.6F coronary catheter ultrasound ablation device with a 1.7-mm diameter ball tip. The ultrasound coronary catheter delivered ultrasound energy at 19.5 kHz, with a power output of 16 to 20 W at the transducer. Energy is delivered in a pulsed mode with a 50% duty cycle of 30 milliseconds. Patients were treated for a mean of 493 seconds (range, 130 to 890) with intracoronary ultrasound ablation. All lesions were treated with adjunctive balloon angioplasty. All 11 postmortem coronary occlusions were recanalized, and 99% of the particulates generated were < 10 microns in diameter. We found that after ultrasound, mean (+/- SD) coronary arterial stenosis fell from 80 +/- 12% to 60 +/- 18% (P < .001) and to 26 +/- 11% (P < .001) after adjunctive balloon angioplasty. Mean pressures required to achieve full balloon inflation were 2.7 atm (range, 1 to 5.5) with a median of 3.0-mm balloon size (2.5 to 3.5). No ultrasound-related complications were identified. CONCLUSIONS: Intracoronary ultrasound plaque ablation appears to be safe. Our findings suggest that catheter-delivered high-intensity, low-frequency ultrasound may be useful for lesion debulking and enhancing arterial distensibility, allowing balloon dilation at relatively low pressures.

Angioplasty, Balloon, Coronary↗