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Biomedical subjects

L W Gimple

Publications and source records attributed to L W Gimple.

At least 37 records · Page 2Linked to original sources
PubMed1996

Arterial thrombin activity after angioplasty in an atherosclerotic rabbit model: time course and effect of hirudin.

BACKGROUND: A 2-hour infusion of the direct thrombin inhibitor hirudin at the time of balloon angioplasty limits restenosis in the focally atherosclerotic rabbit. Although short-term administration of hirudin may have a prolonged biological effect, the effect of hirudin on vessel thrombin activity has not been previously studied in an animal model of angioplasty. We hypothesized that a short intravenous infusion of hirudin would result in prolonged inhibition of arterial wall-associated thrombin activity (ATA) after angioplasty. METHODS AND RESULTS: Sixty-one rabbits received recombinant hirudin (r-hirudin)(1 mg/kg bolus plus 1 mg x kg(-1) x h(-1)x2hours) or bolus heparin (controls, 150 U/kg) intravenously at the time of femoral balloon angioplasty. ATA was measured through exposure of arterial segments ex vivo to fibrinogen and conducting an assay for fibrinopeptide A (FPA). ATA was low in nonballooned, atherosclerotic vessels (FPA=0.5+/-0.3 ng x mL(-1) x mg(-1)) but increased significantly at 24 hours after angioplasty in the heparin group (3.7+/-0.9 ng x mL(-1) x mg(-1), P<.01 versus baseline, n=9) but not in the hirudin group (FPA = 1.4+/-0.3; P=NS versus baseline, P<.02 versus heparin controls, n=8). The time course of ATA after angioplasty was assessed in 44 rabbits. Thrombin activity peaked at 48 hours and declined to baseline at 72 hours and 7 days. FPA values between the heparin and r-hirudin groups were similar at these later time points. CONCLUSIONS: A 2-hour intravenous infusion of r-hirudin suppressed ATA measured 24 hours after angioplasty in the focally atherosclerotic rabbit. This prolonged biological effect may account, in part, for the reduction in restenosis seen in this model.

Angioplasty, Balloon↗
PubMed1996

Effect of thrombin inhibition with desulfatohirudin on early kinetics of cellular proliferation after balloon angioplasty in atherosclerotic rabbits.

BACKGROUND: Thrombin may have a pivotal role in restenosis after angioplasty. Hirudin, a potent thrombin inhibitor, reduces luminal narrowing by plaque after angioplasty in a rabbit model of atherosclerosis. Because cellular proliferation is believed to be an important mechanism for restenosis and thrombin has been shown to be a potent smooth muscle cell mitogen in vitro, we hypothesized that the mechanism of the effect of hirudin on limiting luminal narrowing by plaque occurs via inhibition of cellular proliferation. METHODS AND RESULTS: Femoral atherosclerosis was induced in 108 rabbits, and balloon angioplasty was performed. At angioplasty, group 1 rabbits (n=38) were treated with a 2-hour infusion of hirudin, and group 2 rabbits (n=41) were treated with heparin. Group 3 rabbits (n=29) were treated with hirudin (n=15) or heparin (n=14) and killed at 7 or 28 days to determine cross-sectional area narrowing by plaque and cellular proliferation with the use of bromodeoxyuridine labeling. At 29, 71, or 167 hours after angioplasty, group 1 and 2 rabbits were injected with 3H-thymidine and killed 1 hour later, and labeling indexes were determined. A significant increase in the index of 3H-thymidine-labeled nuclei was observed in the intima of "ballooned" arteries compared with "nonballooned" atherosclerotic arteries at both 30 hours (0.06+/-0.05 versus 0.01+/-0.01, P<.01) and 72 hours (0.10+/-0.06 versus 0.004+/-0.004, P<.01). By 7 days, the index of labeled cells was similar to baseline (0.04+/-0.03 versus 0.01+/-0.01, P=.12). Hirudin had no effect on the 3H-thymidine labeling indexes at any of the time points studied despite the fact that hirudin treatment in group 3 rabbits resulted in less cross-sectional area narrowing by plaque at both 7 and 28 days after angioplasty (41+/-16 versus 24+/-12 at 7 days and 60+/-21 versus 44+/-17 at 28 days, heparin versus hirudin; P<.03). CONCLUSIONS: Balloon angioplasty resulted in a marked increase in cellular proliferation that peaked at 72 hours. A 2-hour infusion of hirudin failed to reduce early 3H-thymidine labeling, suggesting that inhibition of cell proliferation within the first 7 days after angioplasty is not the predominant mechanism by which hirudin exerts its effect on limiting luminal narrowing by plaque 28 days after balloon angioplasty in this animal model.

Angioplasty, Balloon↗
PubMed1996

Thrombin and vascular smooth muscle cell proliferation: implications for atherosclerosis and restenosis.

Despite long-standing knowledge about the relationship between thrombosis and atherosclerosis, the specific role of thrombin in modulating atherosclerosis and the response to vascular injury is not well understood. Thrombin receptor stimulation in vitro signals many cellular events that are associated with the response to vascular injury (atherosclerosis) in vivo. Proliferation of smooth muscle cells (SMCs) is an important component of the response to vascular injury. We have previously shown that human alpha-thrombin and the 14-amino acid human thrombin receptor-activating peptide (huTRAP-14) stimulate proliferation of cultured rat aortic SMCs. However, thrombin-induced SMC proliferation demonstrates delayed kinetics relative to platelet-derived growth factor (PDGF-BB, another potent SMC mitogen). Several mechanisms may be responsible for these delayed kinetics in vitro, including production of necessary secondary growth factors and thrombin-induced upregulation of its receptor. In vivo studies have demonstrated that thrombin inhibition limits the response to vascular injury in a hypercholesterolemic rabbit model of focal femoral atherosclerosis. However, this effect does not appear to be mediated by effects on early SMC proliferation. In this discussion, we will address the mechanisms of thrombin-induced SMC proliferation in vitro and apply this knowledge to our understanding of the role of thrombin inhibition in limiting the response to vascular injury in vivo.

Animals↗
PubMed1995

Elevated serum lipoprotein(a) is a risk factor for clinical recurrence after coronary balloon angioplasty.

BACKGROUND: Elevated lipoprotein (Lp) (a) concentrations are associated with coronary artery disease and myocardial infarction. Lp(a) is structurally related to proteins involved in lipid transport, fibrinolysis, coagulation, and cellular mitogenesis and is known to have important physiological interactions with the coagulation and fibrinolytic systems. Because these processes may be important to arterial healing after balloon injury, we hypothesized that elevated Lp(a) concentrations may be associated with recurrence of symptoms and restenosis after balloon angioplasty. METHODS AND RESULTS: We assessed 240 consecutive patients undergoing coronary balloon angioplasty with measurements of Lp(a), total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, apolipoprotein A-I, and apolipoprotein B-100 concentrations from fresh specimens. Patients were evaluated 4 to 6 months after angioplasty for clinical recurrence by repeat angiography if angina had returned or by maximal exercise treadmill testing with thallium imaging if patients remained asymptomatic. Ninety-seven patients (40%) had clinical recurrence; 143 (60%) did not. Patients with recurrence had significantly greater Lp(a) concentrations compared with those without (median, 29 versus 14; P < .0001). Each patient quintile stratified by increasing Lp(a) concentrations had incrementally greater recurrence rates ranging from 27% (lowest quintile) to 60% (highest quintile). By multivariate logistic regression analysis, Lp(a) concentration was the only predictor of recurrence (P < .0001). A subset of frozen, stored serum samples showed a significant decrease in measured Lp(a) concentration over time (mean, 605 days; P < .01). CONCLUSIONS: An elevated Lp(a) concentration was a risk factor for clinical recurrence after percutaneous transluminal balloon coronary angioplasty. Other lipid levels or clinical characteristics were not significantly associated with recurrence. When serum was frozen and stored for a prolonged period, Lp(a) concentration decreased over time.

Angioplasty, Balloon, Coronary↗
PubMed1995

Identification of viable myocardium with contrast echocardiography in patients with poor left ventricular systolic function caused by recent or remote myocardial infarction.

We hypothesized that viable myocardium can be identified in patients with poor left ventricular (LV) systolic function caused by recent or prior infarction using myocardial contrast echocardiography. Accordingly, 39 patients with reduced LV ejection fraction (range 0.10 to 0.40) and recent (n = 30) or remote (n = 9) myocardial infarction were studied. Echocardiography was performed at baseline and at 1 month to assess regional function (1 = normal, 5 = dyskinesia) in 12 segments/patient; the segments were also scored for contrast effect (1 = homogenous, 0.5 = partial, 0 = none) during contrast echocardiography performed in the cardiac catheterization laboratory. Four patients had unsuccessful angioplasty of occluded arteries and were treated medically, 9 were treated medically because of noncritical coronary stenoses (< 80%), and 26 underwent revascularization (16 angioplasty and 10 bypass operation). Twelve segments could not be visualized (2 each in 6 patients), and 30 segments continued to be subserved by totally occluded arteries because of unsuccessful angioplasty in 4 patients. Of the remaining 426 segments, 186 (44%) demonstrated baseline wall motion scores of > or = 3. The best correlate of 1-month wall motion score in these segments was the contrast score (p = -0.62), with better 1-month function noted in segments with more contrast. The overall perfusion status of LV myocardium also correlated (p = -0.59) with global LV systolic function at 1 month. We conclude that myocardial contrast echocardiography can be used during cardiac catheterization to define myocardial segments that are viable in patients with poor LV systolic function caused by recent or remote myocardial infarction.

Adult↗
PubMed1995

Effect of midinfrared holmium: YAG laser angioplasty with and without balloon angioplasty on acute outcome and restenosis in atherosclerotic femoral arteries in rabbits.

BACKGROUND AND OBJECTIVE: Pulsed laser may lessen vascular damage and reduce restenosis. This study examined the acute and chronic effects of midinfrared laser angioplasty with and without balloon angioplasty in atherosclerotic femoral arteries in rabbits. STUDY DESIGN/MATERIALS AND METHODS: Atherosclerosis was induced in arteries by air desiccation and cholesterol feeding. Arteries were assigned to one of four groups: (1) laser angioplasty with a Thullium/Holmium/Chromium:YAG infrared laser (Eclipse), (2) balloon angioplasty, (3) laser followed by balloon angioplasty, and (4) no intervention. Arteries were examined angiographically and histologically at 2 hours and 28 days. RESULTS: Intervention groups had significant initial gain, but this gain was less with laser alone than after balloon or after laser plus balloon. At 2 hours, laser alone caused greater arterial damage and thrombosis compared to controls. At 28 days, arteries treated with laser plus balloon had greater narrowing compared with arteries treated with balloon angioplasty. By multivariate regression analysis, the severity of the pre-intervention stenosis (P = 0.001) and intervention with laser plus balloon (P = 0.01) correlated independently with the severity of luminal narrowing at 28 days. CONCLUSION: Midinfrared Ho:YAG laser angioplasty resulted in substantial acute damage with increased frequency of thrombus formation in this rabbit model. arteries treated with laser alone had suboptimal initial gain and more obstruction by plaque at 28 days compared to nonintervened arteries. The adjunctive use of balloon angioplasty improved initial gain, but correlated with smaller luminal diameters and more severe narrowing by plaque at 28 days.

Angioplasty, Balloon↗
PubMed1995

Thrombin-induced mitogenesis in cultured aortic smooth muscle cells requires prolonged thrombin exposure.

Thrombin has been implicated in vascular smooth muscle cell (VSMC) proliferation after vessel injury. Its proliferative effects, which are mediated via proteolytic activation of a receptor similar or identical to the cloned thrombin receptor (TR), have markedly delayed kinetics. The present study demonstrates that, despite rapid thrombin receptor activation and similar time to S phase entry compared with classic polypeptide growth factors, prolonged thrombin exposure is required to promote maximal VSMC mitogenesis. Flow cytometric analysis of thrombin-stimulated cells revealed that thrombin induced a progressive increase in the growth fraction over 3 days in culture, an effect that was blocked by hirudin even late after thrombin addition. Northern blot hybridization after thrombin stimulation demonstrated that thrombin upregulates TR mRNA expression within 6 h. These findings indicate that VSMC proliferate in response to prolonged thrombin exposure and suggest that the mitogenic delay may involve not only the thrombin-dependent synthesis and activation of newly made TR but also the progressive thrombin-dependent recruitment of cells into the growth fraction.

Animals↗
PubMed1994

Specific factor Xa inhibition reduces restenosis after balloon angioplasty of atherosclerotic femoral arteries in rabbits.

BACKGROUND: Balloon angioplasty of atherosclerotic arteries results in activation of the coagulation cascade. Several coagulation factors, including factor Xa and thrombin, are mitogenic for vascular smooth muscle cells in vitro and thus may play a role in restenosis after balloon angioplasty. Specific inhibition of factor Xa can be achieved with recombinant antistasin (rATS) or tick anticoagulant peptide (rTAP). We hypothesized that inhibition of Xa would limit restenosis after balloon angioplasty in an atherosclerotic rabbit model. METHODS AND RESULTS: Focal femoral atherosclerosis was induced by air desiccation injury and a high-cholesterol diet in 38 New Zealand White rabbits. Recombinant antistasin (n = 20 arteries) or rTAP (n = 14 arteries) was administered by intravenous bolus at the time of balloon angioplasty and followed by a 2-hour infusion; controls (n = 21 arteries) received bolus heparin alone (150 U/kg). Therapeutic prolongation of the activated partial thromboplastin time occurred, and antithrombotic drug levels were achieved in all animals. Luminal diameter in millimeters by quantitative angiography did not differ between treatment groups before (1.1 +/- 0.2 for controls, 1.1 +/- 0.2 for rATS, and 1.1 +/- 0.3 for rTAP) or after balloon angioplasty (1.5 +/- 0.3 for controls, 1.4 +/- 0.2 for rATS, and 1.4 +/- 0.2 for rTAP). At 28 days, treatment with factor Xa inhibitors tended to result in arteries with larger luminal diameter than controls (1.2 +/- 0.3 for rATS, 1.2 +/- 0.3 for rTAP versus 1.0 +/- 0.3 for control, P = .09 by one-way ANOVA). Restenosis, defined as reduction in angiographic luminal diameter (in mm) from 2 hours after angioplasty to 28 days after angioplasty was less in the rATS group than in controls (-0.2 +/- 0.1 versus -0.5 +/- 0.4, P < .001) and tended to be less in the rTAP group (-0.3 +/- 0.2 versus -0.5 +/- 0.4, P = .07). Quantitative histopathological analysis showed less percent cross-sectional area narrowing by plaque in both rATS- and rTAP-treated arteries compared with controls (42 +/- 21%, 47 +/- 18%, and 63 +/- 14%, respectively; P < .01 by one-way ANOVA). CONCLUSIONS: We conclude that a 2-hour infusion of rATS or rTAP reduced angiographic restenosis and resulted in less luminal cross-sectional narrowing by plaque compared with controls.

Angioplasty, Balloon↗
PubMed1994

Microvascular integrity indicates myocellular viability in patients with recent myocardial infarction. New insights using myocardial contrast echocardiography.

BACKGROUND: Patency of the infarct-related artery (IRA) after acute myocardial infarction (AMI) may not reflect the magnitude of tissue perfusion. In animal models of AMI, myocardial cellular necrosis has been associated with extensive capillary damage. Because myocardial contrast echocardiography (MCE) can define the spatial distribution of microvascular perfusion, we hypothesized that it could be used in patients after recent AMI to distinguish myocardial regions that have an intact microvasculature and thus are viable from those without an intact microvasculature and thus are not viable. METHODS AND RESULTS: One hundred five patients with a recent AMI (range, 1 day to 4 weeks; median, 8 days) who were undergoing cardiac catheterization were included in the study. Two-dimensional echocardiography was performed at baseline and repeated 1 month later to assess regional function within the infarct zone (scores of 1 to 5 indicating normal to dyskinetic segments, respectively). MCE was performed in the cardiac catheterization laboratory to assess microvascular perfusion within the infarct bed. A contrast score index was derived by assigning scores to individual segments within the infarct zone (0, 0.5, and 1 denoting no, intermediate, and homogeneous contrast effect, respectively) and deriving the average score within the infarct bed. Revascularization was performed as clinically indicated. Although the baseline wall motion score and the contrast score index were similar in the 90 patients with a patent IRA and the 15 patients with an occluded IRA (median +/- 1 interquartile range, 3 +/- 1 versus 3.5 +/- 1; P = .41), wall motion score 1 month later was significantly better in those with open IRAs compared with those with closed IRAs (2 +/- 2 versus 3 +/- 2, P = .05). In the 90 patients with an open IRA, a strong correlation was noted between wall motion score 1 month later and the contrast score index (rho = -.64, P < .001). On multivariate analysis, the best correlate of the 1-month wall motion score was the contrast score index. CONCLUSIONS: In patients studied in the cardiac catheterization laboratory between 1 day and 4 weeks after AMI, an intact microvasculature as identified by MCE indicates myocardial regions that improve function 1 month later. This study demonstrates that microvascular patency is closely associated with myocardial cellular viability after AMI in humans.

Adult↗
PubMed1994

Intracoronary angiotensin-converting enzyme inhibition improves diastolic function in patients with hypertensive left ventricular hypertrophy.

BACKGROUND: There is increasing recognition of myocardial angiotensin-converting enzyme, which is induced with the development of left ventricular hypertrophy (LVH). The potential physiological significance of subsequent increased angiotensin I to II conversion in the presence of LVH is unclear but has been postulated to cause abnormal Ca2+ handling and secondary diastolic dysfunction. Accordingly, we hypothesized that acute angiotensin-converting enzyme inhibition would result in decreased production of angiotensin II and improved active (Ca(2+)-dependent) relaxation in patients with hypertensive LVH. METHODS AND RESULTS: Intracoronary (IC) enalaprilat was administered to 25 patients with and without LVH secondary to essential hypertension. Indexes of diastolic and systolic LV function were determined from pressure (micromanometer)-volume (conductance) analysis at steady state and with occlusion of the inferior vena cava. Patients were divided into those receiving high- (5.0 mg, n = 15) and low-dose (1.5 mg, n = 10) IC enalaprilat during a 30-minute infusion at 1 mL/min. The high-dose patients were further divided along the median normalized LV wall thickness of 0.671 cm/m2. The time constant of isovolumic relaxation (TauL) was prolonged at baseline in patients receiving high-dose enalaprilat with wall thickness > 0.671 cm/m2 (TauL, 56 +/- 2 versus 44 +/- 2 and 45 +/- 2 milliseconds, respectively, P < .01 by ANOVA) and shortened only in this patient group (TauL, 49 +/- 3 versus 46 +/- 2 and 43 +/- 2 milliseconds, respectively, P < .01 versus baseline and other groups by ANOVA). The improvement in TauL was directly proportional to the degree of LVH (r = .92, P < .001). Although there was a decrease in LV end-diastolic pressure (23 +/- 2 to 15 +/- 1 mm Hg, P < .01) and volume (86 +/- 8 to 67 +/- 9 mL/m2, P < .05) in those patients with a reduction in TauL, this is due to movement down a similar diastolic pressure-volume relation with no change in chamber elastic stiffness (0.023 +/- 0.002 to 0.025 +/- 0.004 mL-1, P = NS). CONCLUSIONS: Intracoronary enalaprilat resulted in an improvement in active (Ca(2+)-dependent) relaxation in those patients with more severe hypertensive LVH. The improvement in active relaxation was directly proportional to the severity of LVH. These results support the hypothesis that the cardiac renin-angiotensin system is an important determinant of active diastolic function in hypertensive LVH.

Adult↗
PubMed1994

Geometric remodeling is not the principal pathogenetic process in restenosis after balloon angioplasty. Evidence from correlative angiographic-histomorphometric studies of atherosclerotic arteries in rabbits.

BACKGROUND: Restenosis after balloon angioplasty of coronary arteries is thought to be a proliferative response of the arterial wall to injury. Recently, it has been suggested that geometric remodeling of the arterial wall, rather than intimal fibromuscular hyperplasia, may be the major pathophysiological mechanism underlying restenosis. In this study, we evaluated the relative contribution of a geometric decrease in arterial size versus neointimal growth to luminal narrowing associated with restenosis after balloon angioplasty of atherosclerotic femoral arteries in rabbits. METHODS AND RESULTS: Focal femoral atherosclerosis was induced by endothelial desiccation injury followed by a 2% cholesterol diet. After 1 month on the high cholesterol diet, the animals were subjected to one of four strategies: (1) balloon angioplasty, (2) balloon angioplasty followed by treatment with the factor Xa inhibitor antistasin, (3) combined laser and balloon angioplasty, or (4) no angioplasty. Animals were killed 2 hours or 28 days after angioplasty, and excised femoral artery segments were prepared for histomorphometric analysis. Angiography was performed serially before and immediately after angioplasty and before the animals were killed. An initial postprocedural gain in luminal diameter at sites of angioplasty was followed by a significant reduction in diameter by angiography and a significant increase in luminal cross-sectional area narrowing by plaque by histomorphometry 28 days after angioplasty compared to adjacent nonangioplastied segments of the same arteries, to nonangioplastied control arteries, or to angioplastied segments of animals treated with the factor Xa inhibitor antistasin. By contrast, the overall arterial size (cross-sectional area bounded by the external elastic lamina) at sites of restenosis was not significantly different from adjacent nonangioplastied segments in the majority of arteries excised at 28 days, and the mean overall arterial size at sites of restenosis was not significantly different from corresponding segments of nonangioplastied control arteries or from angioplastied segments of animals treated with antistasin. In the minority of angioplastied arteries in which the arterial size did change, most got larger. CONCLUSIONS: Geometric remodeling resulting in a decrease in overall cross-sectional arterial size does not appear to be the principal pathogenetic mechanism for restenosis after balloon angioplasty with or without laser in this experimental model.

Angiography↗
PubMed1994

Myocardial viability. Assessment by cardiac scintigraphy.

Myocardial systolic contractile dysfunction can occur despite preservation of myocardial viability, conditions referred to as myocardial 'stunning' or 'hibernation.' Because simple assessment of wall motion does not adequately distinguish nonviable from viable but noncontracting myocardial regions, clinicians require alternate methods to assess whether strategies might be useful. Nuclear imaging techniques can provide relatively precise, clinically relevant information regarding the status of myocardial viability, despite the presence of regional or global systolic dysfunction.

Animals↗
PubMed1993

Exercise thallium-201 scintigraphy after thrombolytic therapy with or without angioplasty for acute myocardial infarction.

Scant data are available concerning the application and results of exercise thallium-201 (Tl-201) scintigraphy after acute myocardial infarction (AMI) treated with thrombolytic therapy. The goals of this study were to determine the ability of exercise Tl-201 scintigraphy to detect inducible ischemia and to identify multivessel coronary artery disease (CAD) in 88 consecutive postinfarction patients who received thrombolytic therapy and underwent both predischarge noninvasive testing and coronary angiography. Exercise-induced Tl-201 redistribution on quantitative scintigraphy was significantly more prevalent than exercise ST-segment depression (48 vs 14%, p < 0.001). Sensitivity and specificity of exercise ST depression alone for identification of multivessel disease was 29 and 96%, respectively. Sensitivity of a remote Tl-201 defect for multivessel CAD detection was 35 and 87%, respectively--not significantly different from values for ST depression alone. When considered as a single variable, the presence of either ST depression or a remote Tl-201 defect was associated with a 58% sensitivity (p < 0.05, compared with either ST depression or Tl-201 redistribution alone), but a somewhat diminished specificity of 78%. There was no difference in extent or severity of angiographic CAD in patients with multivessel CAD with or without inducible ischemia. In conclusion, this study shows that exercise Tl-201 imaging is more sensitive than exercise Tl-201 imaging is more sensitive than exercise ST depression for detection of residual ischemia during submaximal exercise in patients who received thrombolytic therapy for AMI. The combination of the presence of either Tl-201 redistribution or ischemic ST depression was better than either variable alone for identifying patients with multivessel CAD.

Adult↗
PubMed1993

Response of femoral arteries of cholesterol-fed rabbits to balloon angioplasty with or without laser: emphasis on the distribution of foam cells.

Very little is known about the structural composition of the restenotic plaque in evolution. The responses of atherosclerotic femoral arteries of rabbits to balloon angioplasty (BA), thallium/holmium/chromium: YAG infrared laser angioplasty (LA), combined LA and BA, or no angioplasty were compared by blinded quantitative histomorphometry and angiography. The endothelium was injured by nitrogen/air desiccation, and the animals were fed a 2% cholesterol diet for 1 month prior to the angioplasty procedure. Animals were sacrificed 2 hr or 28 days after angioplasty by pressure perfusion with 10% formaldehyde (100 mm Hg), and arterial segments (4-5 cm) were excised bilaterally. The frequency of thrombus was greatest in arteries with LA. Arteries with combined LA and BA had the greatest initial gain in luminal diameter by angiography, but they also had the greatest reduction in luminal diameter from 2 hr to 28 days and the greatest cross-sectional area narrowing by plaque at 28 days. The principal component of the intimal plaques in all groups was fibrous tissue (approximately 90%), with the remainder consisting primarily of "foam cells." By multiple regression analysis, the strongest predictors of cross-sectional area narrowing were contiguity of foam cells between the intima and media, depth of the tear, percentage of foam cells in the plaque, and the intervention of LA followed by BA. The principal predictors of foam cells in the plaque, irrespective of treatment, were also cross-sectional area narrowing, contiguity of foam cells between plaque and media, and the depth of tear. It is suggested that a large proportion of the foam cells of the intima may be derived from foam cells of the media and adventitia rather than from the lumen. These observations may be of particular importance regarding angioplasty in young people where foam cells occupy a significantly greater proportion of the atherosclerotic plaque.

Angioplasty, Balloon↗
PubMed1993

Percutaneous balloon pericardiotomy for the treatment of cardiac tamponade and large pericardial effusions: description of technique and report of the first 50 cases.

OBJECTIVES: This study describes the technique, clinical characteristics and results of the first 50 patients undergoing percutaneous balloon pericardiotomy as part of a multicenter registry. BACKGROUND: Percutaneous balloon pericardiotomy involves the use of a percutaneous balloon dilating catheter to create a nonsurgical pericardial window. METHODS: Patients eligible for percutaneous balloon pericardiotomy had either cardiac tamponade (n = 36) or a moderate to large pericardial effusion (n = 14). In addition to clinical follow-up, serial echocardiograms and chest X-ray films were obtained. RESULTS: The procedure was considered successful in 46 patients after a mean follow-up period of 3.6 +/- 3.3 months. Two patients required an early operation, one for bleeding from a pericardial vessel and one for persistent pericardial catheter drainage. Two patients required a late operation for recurrent tamponade. Minor complications of the procedure included fever in 6 of the first 37 patients (studied before the prophylactic use of antibiotic agents), thoracentesis or chest tube placement in 8 and a small spontaneously resolving pneumothorax in 2. Despite the short-term success of this procedure, the long-term prognosis of the 44 patients with malignant pericardial disease remained poor (mean survival time 3.3 +/- 3.1 months). CONCLUSIONS: Percutaneous balloon pericardiotomy is successful in helping to manage large pericardial effusions, particularly in patients with a malignant condition. It may become the preferred treatment to avoid a more invasive procedure for patients with pericardial effusion and a limited life expectancy.

Aged↗
PubMed1993

Bolus intravenous nitroglycerin predominantly reduces afterload in patients with excessive arterial elastance.

OBJECTIVES: We hypothesized that bolus intravenous nitroglycerin would be an afterload-reducing agent in patients with excessive initial afterload for their level of left ventricular systolic function. Conversely, bolus intravenous nitroglycerin should be a preload-reducing agent in patients without excessive initial afterload. BACKGROUND: Although nitroglycerin has both preload- and afterload-reducing actions, methods to predict its predominant site of action in an individual patient have not been previously described. METHODS: Left ventricular pressure-volume relations were recorded with micromanometer and conductance catheters during bolus injection of intravenous nitroglycerin in 27 patients with both normal left ventricular systolic function and varying degrees of congestive heart failure. Preload was determined by end-diastolic volume, afterload by effective arterial elastance, left ventricular systolic function by end-systolic elastance and coupling of afterload and ventricular function by the ratio of effective arterial elastance to end-systolic elastance (Ea/Ees ratio). An Ea/Ees ratio > 1 was defined as excessive afterload for the level of ventricular function. RESULTS: Patients with an initial Ea/Ees ratio < 1 (Group 1) constituted a group of normotensive patients with intact ventricular function who exhibited a predominant reduction in preload in response to intravenous nitroglycerin. Those with an initial Ea/Ees ratio > 1 and normal or mildly depressed ventricular function (Group 2a) constituted a group of patients, most of whom were hypertensive, who exhibited a predominant afterload reduction. Finally, those with an initial Ea/Ees ratio > 1 and abnormal ventricular function (Group 2b) constituted a group of patients with clinical congestive heart failure who exhibited both preload and afterload reduction but a predominant afterload reduction because stroke volume increased. CONCLUSIONS: Patients with normal arterial elastance and ventricular function respond to nitroglycerin with a predominant preload reduction, whereas patients with either excessive arterial elastance or abnormal ventricular function respond with a predominant afterload reduction.

Analysis of Variance↗