Evolutionary associations between host traits and parasite load: insights from Lake Tanganyika cichlids.

Parasite diversity and abundance (parasite load) vary greatly among host species. However, the influence of host traits on variation in parasitism remains poorly understood. Comparative studies of parasite load have largely examined measures of parasite species richness and are predominantly based on records obtained from published data. Consequently, little is known about the relationships between host traits and other aspects of parasite load, such as parasite abundance, prevalence and aggregation. Meanwhile, understanding of parasite species richness may be clouded by limitations associated with data collation from multiple independent sources. We conducted a field study of Lake Tanganyika cichlid fishes and their helminth parasites. Using a Bayesian phylogenetic comparative framework, we tested evolutionary associations between five key host traits (body size, gut length, diet breadth, habitat complexity and number of sympatric hosts) predicted to influence parasitism, together with multiple measures of parasite load. We find that the number of host species that a particular host may encounter due to its habitat preferences emerges as a factor of general importance for parasite diversity, abundance and prevalence, but not parasite aggregation. In contrast, body size and gut size are positively related to aspects of parasite load within, but not between species. The influence of host phylogeny varies considerably among measures of parasite load, with the greatest influence exerted on parasite diversity. These results reveal that both host morphology and biotic interactions are key determinants of host-parasite associations and that consideration of multiple aspects of parasite load is required to fully understand patterns in parasitism.

The N355K atlastin 1 mutation is associated with hereditary sensory neuropathy and pyramidal tract features.

BACKGROUND AND PURPOSE: Mutations in atlastin-1 (ATL-1), a gene known to cause pure, early-onset autosomal dominant hereditary spastic paraplegia SPG3A, have been recently reported to cause hereditary sensory neuropathy I (HSN I). We describe the detailed clinical and electrophysiologic findings in the first family with ulcero-mutilating sensory neuropathy carrying the c. C1065A, p.N355K mutation in ATL-1. METHODS: Detailed clinical and electrophysiologic studies were performed in affected and at-risk family members. Motor and sensory nerve conductions studies (NCS) were carried out in upper and lower limbs. ATL-1 was screened for mutations by direct sequencing. RESULTS: Ten patients were found to carry the N355K mutation. With the exception of the two youngest patients, all had trophic skin changes in the feet consisting mainly of painless ulcers. Frequently, amputation of toes, feet, or even more proximal parts of the lower legs became necessary. A variable degree of increased muscle tone was observed in younger patients, whilst some older affected individuals only presented with hyperreflexia of patellar tendon reflexes. NCS revealed signs of an axonal motor and sensory neuropathies. CONCLUSIONS: Our family carrying the N355K ATL1 mutation, which was initially diagnosed as HSN I, enlarges the SPG3A phenotype. We therefore suggest that patients with HSN I excluded for more common causes of HSN I, and in particular, affected individuals who exhibit additional pyramidal tract features should also be screened for mutations in ATL1.

Interactions between poloxamer, PEOx-PPOy-PEOx, and non-ionic surfactant, sucrose monolaurate: A study on potential allergenic effect using model phospholipid membrane.

Sugar-based surfactants are involved in skin related allergy cases in the past decade. Skin irritation starts with the interaction of the surfactant with the skin lipids leading to lipid emulsification and eventual barrier damage. Polymers or co-surfactants can be used to mitigate the allergenic effect but the mechanism of formulation mildness on skin remains unclear. We have used the quartz crystal microbalance (QCM) together with dissipative particle dynamics (DPD) simulation, small angle x-ray scattering (SAXS) as well as cell viability tests to decipher the interactions between poloxamers and sucrose monolaurate (SML), and how these interactions could prevent the disruption of a model supported phospholipid bilayer (SLB). Poloxamer addition to the SML solution can delay or totally prevent the disruption of the SLB depending on poloxamer type and concentration. Poloxamer P407 (Pluronic® F127) delays the onset of disruption while poloxamer P188 (Pluronic® F68) does not preserve the bilayer integrity even at high concentration of up to 15% w/w. Preservation of the SLB is likely due to the differences in the aggregates formation between SML-F127 and SML-F68 mixtures with corresponding retarded motion of SML micelles through the SML-F127 polymer matrix that improved cell viability.

Abnormal expression of dysferlin in skeletal muscle and monocytes supports primary dysferlinopathy in patients with one mutated allele.

BACKGROUND: In some cases, a definitive confirmation of dysferlinopathy cannot be achieved by DNA test, because the mutation is detected in one allele only. PATIENTS AND METHODS: DYSFERLIN expression in skeletal muscle and peripheral blood monocytes (PBM) was studied by Western blot in two unrelated adult patients. The comparative C(T) method (ΔΔC(T) ) was used to calculate relative changes in dysferlin mRNA determined from real-time quantitative PCR experiments. The dysferlin gene was studied by direct sequencing of cDNA and genomic DNA and by Multiplex Ligation-dependent Probe Amplification (MLPA) analysis. RESULTS: A comparable severe reduction in dysferlin was demonstrated in both skeletal muscle and PBM. The expression of dysferlin mRNA was significantly reduced. A novel mutation in exon 47 (c.5289G>C) of the dysferlin gene in the heterozygous state, causing an amino acid change (p.Glu1763Asp), was detected in both patients. The MLPA analysis did not reveal any deletion or duplication. CONCLUSIONS: Dysferlin and/or dysferlin mRNA abnormalities are diagnostic for dysferlinopathy when mutational analysis detects a mutation in one allele only. Analysis of dysferlin mRNA can be helpful for distinguishing symptomatic heterozygotes from such patients.

Current husbandry of red pandas (Ailurus fulgens) in zoos.

The endangered red panda (Ailurus fulgens) is held in zoos worldwide. The aim of this study was to examine how red pandas are kept and managed in captivity and to compare it with the management guidelines. Sixty-nine zoos, mainly from Europe but also from North America and Australia/New Zealand, responded to our survey. The results revealed that in general zoos follow the management guidelines for most of the investigated issues. The average enclosure is almost four times larger than the minimum size recommended by the management guidelines, although seven zoos have smaller enclosures. About half the zoos do not follow the guidelines concerning visitor access and number of nest boxes. Other issues that may compromise animal welfare include proximity of neighboring carnivore species and placement of nest boxes.

Functional changes of the cortical motor system in hereditary spastic paraparesis.

BACKGROUND: Hereditary spastic paraparesis (HSP) is a heterogeneous group of disorders characterized by progressive bilateral lower limb spasticity. Functional imaging studies in patients with corticospinal tract involvement have shown reorganization of motor circuitry. Our study investigates functional changes in sensorimotor brain areas in patients with HSP. METHODS: Twelve subjects with HSP and 12 healthy subjects were studied. Functional magnetic resonance imaging (fMRI) was used to measure brain activation during right-hand finger tapping. Image analysis was performed using general linear model and regions of interest (ROI)-based approach. Weighted laterality indices (wLI) and anterior/posterior indicies (wAI and wPI) were calculated for predefined ROIs. RESULTS AND DISCUSSION: Comparing patients and controls at the same finger-tapping rate (1.8 Hz), there was increased fMRI activation in patients' bilateral posterior parietal cortex and left primary sensorimotor cortex. No differences were found when comparing patients and controls at 80% of their individual maximum tapping rates. wLI of the primary sensorimotor cortex was significantly lower in patients. Subjects with HSP also showed a relative increase in the activation of the posterior parietal and premotor areas compared with that of the primary sensorimotor cortex. Our findings demonstrate an altered pattern of cortical activation in subjects with HSP during motor task. The increased activation probably reflects reorganization of the cortical motor system.

ALS and FTLD: two faces of TDP-43 proteinopathy.

Major discoveries have been made in the recent past in the genetics, biochemistry and neuropathology of frontotemporal lobar degeneration (FTLD). TAR DNA-binding protein 43 (TDP-43), encoded by the TARDBP gene, has been identified as the major pathological protein of FTLD with ubiquitin-immunoreactive (ub-ir) inclusions (FTLD-U) with or without amyotrophic lateral sclerosis (ALS) and sporadic ALS. Recently, mutations in the TARDBP gene in familial and sporadic ALS have been reported which demonstrate that abnormal TDP-43 alone is sufficient to cause neurodegeneration. Several familial cases of FTLD-U, however, are now known to have mutations in the progranulin (GRN) gene, but granulin is not a component of the TDP-43- and ub-ir inclusions. Further, TDP-43 is found to be a component of the inclusions of an increasing number of neurodegenerative diseases. Other FTLD-U entities with TDP-43 proteinopathy include: FTLD-U with valosin-containing protein (VCP) gene mutation and FTLD with ALS linked to chromosome 9p. In contrast, chromosome 3-linked dementia, FTLD-U with chromatin modifying protein 2B (CHMP2B) mutation, has ub-ir, TDP-43-negative inclusions. In summary, recent discoveries have generated new insights into the pathogenesis of a spectrum of disorders called TDP-43 proteinopathies including: FTLD-U, FTLD-U with ALS, ALS, and a broadening spectrum of other disorders. It is anticipated that these discoveries and a revised nosology of FTLD will contribute toward an accurate diagnosis, and facilitate the development of new diagnostic tests and therapeutics.

Randomized comparison of GR-II stent and Palmaz-Schatz stent for elective treatment of coronary stenoses.

BACKGROUND: This prospective multicenter randomized clinical trial was designed to evaluate the long-term angiographic and clinical outcomes of elective treatment with the GR-II stent compared with the Palmaz-Schatz (PS) stent in patients with coronary stenoses. METHODS AND RESULTS: Seven hundred fifty-five patients with myocardial ischemia and de novo native coronary stenoses in 3- to 4-mm vessels were randomly assigned to the PS (375 patients) or the GR-II stent (380 patients). The primary end point was 12-month target lesion revascularization (TLR)-free survival. Angiography was performed at baseline and at follow-up in the first 300 consecutive patients to assess the frequency of angiographic restenosis. Procedure success was 98.5% for the GR-II stent and 99.4% for the PS stent (P:=0.19). At 30 days, patients assigned to the GR-II stent had a higher stent thrombosis rate (3.9% versus 0.3% for PS stent, P:<0.001) and TLR rate (3.9% versus 0.5% for PS stent, P:<0.001). The GR-II group had a higher follow-up restenosis frequency (47.3% versus 20.6% for the PS group, P:<0.001) and a lower 12-month TLR-free survival rate (71.7% versus 83.9% for the PS group, P:<0. 001). Multivariate logistic regression analysis identified a smaller final stent minimal lumen diameter (odds ratio [OR] 2.49, 95% CI 1. 56 to 3.98; P:<0.001), diabetes mellitus (OR 2.14, 95% CI 1.42 to 3. 22; P:<0.001), and use of the GR-II stent (OR 1.78, 95% CI 1.20 to 2. 64; P:<0.01) as independent determinants of 12-month TLR. CONCLUSIONS: On the basis of these long-term follow-up data, we conclude that use of the GR-II stent should be limited to the acute treatment of abrupt or threatened closure after failed conventional balloon angioplasty procedures.

Final results of the Can Routine Ultrasound Influence Stent Expansion (CRUISE) study.

BACKGROUND: Intravascular ultrasound (IVUS) can assess stent geometry more accurately than angiography. Several studies have demonstrated that the degree of stent expansion as measured by IVUS directly correlated to clinical outcome. However, it is unclear if routine ultrasound guidance of stent implantation improves clinical outcome as compared with angiographic guidance alone. METHODS AND RESULTS: The CRUISE (Can Routine Ultrasound Influence Stent Expansion) study, a multicenter study IVUS substudy of the Stent Anti-thrombotic Regimen Study, was designed to assess the impact of IVUS on stent deployment in the high-pressure era. Nine centers were prospectively assigned to stent deployment with the use of ultrasound guidance and 7 centers to angiographic guidance alone with documentary (blinded) IVUS at the conclusion of the procedure. A total of 525 patients were enrolled with completed quantitative coronary angiography, quantitative coronary ultrasound, and clinical events adjudicated at 9 months for 499 patients. The IVUS-guided group had a larger minimal lumen diameter (2.9+/-0.4 versus 2.7+/-0. 5 mm, P<0.001) by quantitative coronary angiography and a larger minimal stent area (7.78+/-1.72 versus 7.06+/-2.13 mm(2), P<0.001) by quantitative coronary ultrasound. Target vessel revascularization, defined as clinically driven repeat interventional or surgical therapy of the index vessel at 9 month-follow-up, occurred significantly less frequently in the IVUS-guided group (8.5% versus 15.3%, P<0.05; relative reduction of 44%). CONCLUSIONS: These data suggest that ultrasound guidance of stent implantation may result in more effective stent expansion compared with angiographic guidance alone.

Provisional stenting strategies: systematic overview and implications for clinical decision-making.

Coronary stents reduce the rates of abrupt closure, emergency coronary artery bypass graft surgery and restenosis, but do not prevent myocardial infarction or death at six months. The financial burden of increased stent use and the difficulty in managing in-stent restenosis have provided the impetus to develop provisional stenting strategies. Patients at low risk for restenosis after balloon angioplasty may not derive additional benefit from stent implantation and may be successfully managed with percutaneous transluminal coronary angioplasty (PTCA) alone. Numerous patient, lesion and procedural predictors of restenosis have been identified. Postprocedural assessment using quantitative coronary angiography, intravascular ultrasound (IVUS), coronary flow velocity reserve (CVR) or fractional flow reserve (FFR) may further enhance the ability to predict adverse outcomes after PTCA. Several studies have been performed to investigate the feasibility of provisional stenting strategies using various modalities to identify low risk patients who could be managed with PTCA alone. An optimal or "stent-like" angiographic result after PTCA is associated with favorable clinical outcomes. Preliminary results of studies using IVUS or CVR to guide provisional stenting appear promising. Angiography alone may be inadequate to identify truly low risk patients and may need to be combined with clinical factors, assessment of recoil, IVUS or physiologic indexes. Strategies that avoid unnecessary stenting in even a small proportion of patients may have large impacts on health care costs. Provisional stenting may potentially reduce costs and rates of in-stent restenosis without compromising the quality of health care delivery.

Achieving optimal results with standard balloon angioplasty: can baseline and angiographic variables predict stent-like outcomes?

OBJECTIVES: To predict which patients might not require stent implantation, we identified clinical and angiographic characteristics associated with repeat revascularization after standard balloon angioplasty. BACKGROUND: Stents reduce the risk of repeat revascularization but are costly and may lead to in-stent restenosis, which remains difficult to treat. Identification of patients at low risk for repeat revascularization may allow clinicians to reserve stents for patients most likely to benefit. METHODS: Data from five interventional trials (5,146 patients) were pooled for analysis. We identified patients with optimal angiographic results (final diameter stenosis < or =30% and no dissection) after balloon angioplasty and determined the multivariable predictors of repeat revascularization. RESULTS: Optimal angiographic results were achieved in 18% of patients after angioplasty. The repeat revascularization rate at six months was lower for patients with optimal results (20% vs. 26%, p < 0.001) but still higher than observed in stent trials. Independent predictors of repeat revascularization were female gender (odds ratio [OR] 1.67, p = 0.01), lesion length > or =10 mm (OR 1.62, p = 0.03) and proximal left anterior descending coronary artery lesions (OR 1.62, p = 0.03). For the 8% of patients with optimal angiographic results and none of these risk factors, the repeat revascularization and target vessel revascularization rates were 14% and 8% respectively, similar to rates after stent implantation. Cost analysis estimated that $78 million per year might be saved in the U.S. with a provisional stenting strategy using these criteria compared with elective stenting. CONCLUSIONS: A combination of baseline characteristics and angiographic results can be used to identify a small group of patients at very low risk for repeat revascularization after balloon angioplasty. Provisional stenting for these low risk patients could substantially reduce costs without compromising clinical outcomes.

Acute and long-term cost implications of coronary stenting.

OBJECTIVES: We compared the acute and one year medical costs and outcomes of coronary stenting with those for balloon angioplasty (percutaneous transluminal coronary angioplasty) in contemporary clinical practice. BACKGROUND: While coronary stent implantation reduces the need for repeat revascularization, it has been associated with significantly higher acute costs compared with coronary angioplasty. METHODS: We studied patients treated at Duke University between September 1995 and June 1996 who received either coronary stent (n = 384) or coronary angioplasty (n = 159) and met eligibility criteria. Detailed cost data were collected initially and up to one year following the procedure. Our primary analyses compared six and 12 month cumulative costs for coronary angioplasty- and stent-treated cohorts. We also compared treatment costs after excluding nontarget vessel interventions; after limiting analysis to those without prior revascularization; and after risk-adjusting cumulative cost estimates. RESULTS: Baseline clinical characteristics were generally similar between the two treatment groups. The mean in-hospital cost for stent patients was $3,268 higher than for those receiving coronary angioplasty ($14,802 vs. $11,534, p < 0.001). However, stent patients were less likely to be rehospitalized (22% vs. 34%, p = 0.002) or to undergo repeat revascularization (9% vs. 26%, p = 0.001) than coronary angioplasty patients within six months of the procedure. As such, mean cumulative costs at 6 months ($19,598 vs. $19,820, p = 0.18) and one year ($22,140 vs. $22,571, p = 0.26) were similar for the two treatments. Adjusting for baseline predictors of cost and selectively examining target vessel revascularization, or those without prior coronary intervention yielded similar conclusions. CONCLUSIONS: In contemporary practice, coronary stenting provides equivalent or better one-year patient outcomes without increasing cumulative health care costs.

A randomized, placebo-controlled trial of enoxaparin after high-risk coronary stenting: the ATLAST trial.

OBJECTIVES: We performed a multicenter, double-blind placebo-controlled trial to examine the efficacy and safety of enoxaparin in patients at high risk for stent thrombosis (ST). BACKGROUND: The optimal antithrombotic regimen for such patients is unknown. METHODS: We randomized 1,102 patients with clinical, angiographic or ultrasonographic features associated with an increased risk of ST to receive either twice-daily injections of weight-adjusted enoxaparin or placebo for 14 days after stenting. All patients received aspirin and ticlopidine. The primary end point was a 30-day composite end point of death, myocardial infarction (MI) or urgent revascularization. RESULTS: The target enrollment for the study was 2,000 patients. However, the trial was terminated prematurely at 1,102 patients after interim analysis revealed an unexpectedly low event rate. The primary outcome occurred in 1.8% enoxaparin-treated patients versus 2.7% treated with placebo (odds ratio [OR] 0.66; 95% confidence interval [CI] 0.29 to 1.5, p = 0.30); for death or MI the rates were 0.9% vs. 2.2%, respectively (OR 0.41, 95% CI 0.14 to 1.2, p =0.13); and for MI, 0.4% vs. 1.6%, respectively (OR 0.22, 95% CI 0.05 to 0.99, p = 0.04). The groups had comparable rates of major bleeding (3.3% for enoxaparin, 1.6% for placebo, p =0.08), but minor nuisance bleeding was increased with enoxaparin (25% vs. 5.1%, p < 0.001). CONCLUSIONS: The clinical outcomes of patients at increased risk of ST are more favorable than previously reported, rendering routine oral antiplatelet therapy adequate for most. However, given its relative safety and potential to reduce the risk of subsequent infarction, a 14-day course of enoxaparin may be considered for carefully selected patients.

Hereditary motor and sensory neuropathy associated with auditory neuropathy in a Gypsy family.

In a Slovene Gypsy family of 19 subjects from four generations three patients with clinical characteristics compatible with hereditary motor and sensory neuropathy -Lom (HMSNL), were found. They had severe distal and milder proximal muscle atrophy and weakness with areflexia of myotatic jerks. Two had facial weakness at the time when already wheelchair bound. All sensory modalities were affected distally in the limbs. Sluggish pupillary responses to light and convergence were found. They had skeletal abnormalities. One patient had polydactily on the hand. Nerve conduction studies were compatible with demyelinative polyneuropathy. Nerve biopsy showed mainly axonal loss without hypertrophic changes. Auditory neuropathy was diagnosed in all of them. None of the patients had duplication of 17pl.2-12 or point mutations in the Protein zero, Peripheral myelin protein and Connexin32 genes. Similar disorder that mapped to 8q24 was previously described in some Bulgarian and Italian Gypsy families. Members of our family may suffer from the same hereditary disease and may carry the same ancestor mutation, which was in the past spread in European Gypsy populations.

Relation of CTG expansion and clinical variables to electrocardiogram conduction abnormalities and sudden death in patients with myotonic dystrophy.

We prospectively followed 63 patients with myotonic dystrophy (DM) after establishing diagnosis of DM for an average 8 years in an attempt to detect conduction disturbances (by electrocardiography and/or Holter monitoring) and sudden cardiac events (sudden death, cardiac syncope) and correlate them to potential predicting factors (CTG repeat expansion in the myotonin protein kinase gene and several clinical variables: clinical type and duration of DM, age and sex). Twenty-six patients developed conduction disturbances, five patients died suddenly, and two patients experienced cardiac syncope necessitating urgent implantation of pacemaker. Analysis showed no significant correlation between conduction disturbances and/or cardiac events and CTG expansion. Furthermore, no correlation was found with type of DM, whereas conduction disturbances and sudden cardiac events correlated with patients' age, duration of disease and male sex. Results on our cohort of DM patients show that CTG expansion has no role in predicting neither conduction abnormalities nor sudden death. It seems that risk of sudden death increases with duration of disease and age, and that risk is higher in male patients.

Low-molecular-weight heparins in coronary stenting (the ENTICES trial). ENoxaparin and TIClopidine after Elective Stenting.

The role of low-molecular-weight heparins (LMWHs) in the management of stent thrombosis, although expected to produce fewer hemorrhagic complications than warfarin anticoagulation regimens, is poorly defined. The ENoxaparin and TIClopidine after Elective Stenting (ENTICES) trial was designed to compare a combination of a LMWH (enoxaparin), ticlopidine, and aspirin with the conventional warfarin anticoagulant treatment in patients who received coronary stents, in an effort to decrease stent thrombosis and ischemic clinical events. The results show that the enoxaparin regimen produced significantly fewer clinical events and vascular complications than the conventional warfarin anticoagulant regimen.

Outcome after prolonged balloon inflations of greater than 20 minutes for initially unsuccessful percutaneous transluminal coronary angioplasty.

Prolonged balloon inflation with or without autoperfusion techniques is a common initial approach to major dissection or abrupt occlusion after percutaneous transluminal coronary angioplasty (PTCA). To assess such a strategy in the setting of unsuccessful angioplasty, 40 patients who underwent prolonged balloon inflations of greater than 20 minutes between January and July of 1991 after initially unsuccessful angioplasty were studied. These patients (median age 59 years) underwent PTCA for progressive or unstable angina (16[40%]), symptomatic or asymptomatic residual stenosis after myocardial infarction (10[25%]), acute myocardial infarction (3[8%]), stable angina (3[8%]), reinfarction (2[5%]), and other indications (6[15%]). The significant stenoses were primarily in the proximal and midportions of the right coronary (53%), left anterior descending (30%) and left circumflex (17%) coronary arteries. Before prolonged balloon inflation, the longest single inflation was 11 +/- 6 minutes and the total time of all inflations was 17 +/- 8 minutes (mean +/- standard deviation). Stenosis was reduced from 91 +/- 9 to 68 +/- 16% before prolonged inflation. After prolonged balloon inflation of 30 +/- 9 minutes, the residual stenosis was 47 +/- 21% (p = 0.0001 vs value before prolonged inflation). Furthermore, improvements in the appearance of filling defects or dissections, or both, occurred in 19 patients (48%). Procedural success was obtained in 32 of 40 patients (80%). Coronary bypass grafting was performed in 8 patients (20%): 4 after unsuccessful PTCA (3 emergently) and 4 electively after initially successful PTCA. Although 5 patients had creatine kinase-MB elevations greater than 20 IU/liter after the procedure, only 1 sustained a Q-wave myocardial infarction. There were no deaths in the hospital.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosing coronary arterial stent thrombosis and arterial closure.

This single-center review of a consecutive series of patients requiring reexamination by angiography within 1 week of a coronary stent placement due to chest pain reveals that patients treated with a poststent anticoagulation regimen of warfarin and aspirin, and those with lower poststent deployment dilation pressures, have an increased risk of subacute stent thrombosis. Repeat cardiac catheterization within the first week after coronary artery stent implantation should be reserved for patients with significant electrocardiographic changes.

Treatment of long coronary artery narrowings with long angioplasty balloon catheters.

Balloon angioplasty of long coronary artery narrowings has been associated with a lower rate of acute success, and a higher rate of acute complications and restenosis than that observed for short narrowings. Angioplasty catheters with longer length balloons (30 and 40 mm) are now available, and the objective of this study was to determine the acute and long-term success for patients with long coronary artery narrowings treated with these longer balloons. All patients with long narrowings (> or = 10 mm) treated with long balloons at 1 institution over a 1-year period were identified (93 narrowings in 89 patients), and acute and long-term outcomes were carefully documented. Procedural success (residual stenosis < or = 50%) was 97%. Abrupt closure occurred in 6% and major dissection in 11% of narrowings. Clinical success (procedural success without in-hospital death, bypass surgery or myocardial infarction) was achieved in 90% of patients. Repeat catheterization was performed in 61 patients (76% of those eligible), and restenosis was found in 50 to 55%, depending on the definition used. The treatment of long coronary artery narrowings using angioplasty catheters with longer balloons leads to high rates of acute success. However, there is a high rate of restenosis. New interventional devices for long lesions should be compared with long balloons in a randomized controlled trial.

Outcomes following interventions in small coronary arteries with the use of hand-crimped Palmaz-Schatz stents.

Although coronary stenting has been shown to be effective, retrospective studies have suggested that stents do not provide better results than angioplasty in small coronary arteries. We sought to examine procedural, in-hospital, and long-term outcomes of patients undergoing small-vessel stenting with Palmaz-Schatz stents hand-crimped on a balloon catheter <3 mm in diameter. We retrospectively analyzed the outcomes of 117 patients who underwent this type of coronary stent implantation at Duke University Medical Center between January 1, 1997 and May 30, 1998. The clinical indications for percutaneous revascularization included unstable angina in 67.5% of patients, acute myocardial infarction in 4.3%, postinfarct angina in 3.4%, silent ischemia in 3.4%, and stable angina in 1% of patients. Quantitative angiographic analysis was performed immediately before angioplasty and after stent implantation. Stents were used for elective indications in 24%, for suboptimal angiographic result in 61.5%, and for abrupt and/or threatened closure in 14.5% of patients. Reference vessel diameter was similar before and after the procedure. Minimum luminal diameter increased from 0.63 to 2.35 mm, an acute gain of 1.72+/-0.43 mm. Percent stenosis decreased from 74.2% to 4.7%. The clinical composite of death (n = 1, 1%), nonfatal myocardial infarction (n = 6, 5.1%), and revascularization (n = 1, 1%) occurred in-hospital in only 8 patients (6.8%), resulting in clinical procedure success in 109 patients (93%). Our data suggest that stents designed for vessels >3.0 mm can be deployed in small vessels, with a low in-hospital event rate. However, target lesion revascularization in small vessels remains high. Development of antiproliferative strategies could improve long-term outcomes for small-vessel interventions.