Lp-PLA2- a novel risk factor for high-risk coronary and carotid artery disease.

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is at the crossroads of lipid metabolism and the inflammatory response. It is produced by inflammatory cells, bound to LDL and other lipoproteins, and once in the arterial wall facilitates hydrolysis of phospholipids. Elevated serum levels of Lp-PLA2 have been associated with increased cardiovascular risk in healthy populations and in patients with known vascular disease. Here, we review the role of Lp-PLA2 in the development of atherosclerosis and progression to unstable disease, the utility of Lp-PLA2 as a risk predictor for coronary and carotid events and the potential clinical benefit of pharmacologic inhibition of Lp-PLA2.

Gene delivery from a DNA controlled-release stent in porcine coronary arteries.

Expandable intra-arterial stents are widely used for treating coronary disease. We hypothesized that local gene delivery could be achieved with the controlled release of DNA from a polymer coating on an expandable stent. Our paper reports the first successful transfection in vivo using a DNA controlled-release stent. Green fluorescent protein (GFP) plasmid DNA within emulsion-coated stents was efficiently expressed in cell cultures (7.9% +/- 0.7% vs. 0.6% +/- 0.2% control, p < 0.001) of rat aortic smooth muscle cells. In a series of pig stent-angioplasty studies, GFP expression was observed in all coronary arteries (normal, nondiseased) in the DNA-treated group, but not in control arteries. GFP plasmid DNA in the arterial wall was confirmed by PCR, and GFP presence in the pig coronaries was confirmed by immunohistochemistry. Thus, DNA-eluting stents are capable of arterial transfection, and could be useful as delivery systems for candidate vectors for gene therapy of cardiovascular diseases.

Prospective study correlating fibrinopeptide A, troponin I, myoglobin, and myosin light chain levels with early and late ischemic events in consecutive patients presenting to the emergency department with chest pain.

BACKGROUND: Although thrombus formation plays a major role in acute coronary syndromes, few studies have evaluated a thrombus marker in risk stratification of patients with chest pain. Furthermore, the relation between markers that reflect myocardial injury and thrombus formation that may predict events in a heterogeneous patient population is unknown. This study correlated markers of thrombus and myocardial injury with early and late ischemic events in consecutive patients with chest pain. METHODS AND RESULTS: Serum troponin I (TnI), myoglobin, and myosin light chain levels were obtained from 247 patients and urinary fibrinopeptide A (FPA) from 178 of the 247. By multivariate analysis, patients with an elevated FPA level were 4.82 times more likely to die or have myocardial infarction, unstable angina, and coronary revascularization at 1 week (P=0.002, 95% CI 1.78, 13.03), whereas those with an elevated TnI (>0.2 ng/mL) were 9.41 times more likely (P<0.001, 95% CI 2.84, 31.17). At 6 months (excluding the index event), an elevated FPA level was an independent predictor of events, with an odds ratio of 9.57 (P<0.001, C1 3.29, 27.8), and was the only marker to predict a shorter event-free survival (P<0.001). The other markers did not independently correlate with cardiac events, although MLC incrementally increased early predictive accuracy in combination with the FPA and TnI. CONCLUSIONS: Elevated FPA and TnI correlated with cardiac events during the initial week in patients presenting to the Emergency Department with chest pain. FPA predicted adverse events and a shorter event-free survival at 6 months.

Stent-based delivery of sirolimus reduces neointimal formation in a porcine coronary model.

BACKGROUND: The purpose of this study was to determine the efficacy of stent-based delivery of sirolimus (SRL) alone or in combination with dexamethasone (DEX) to reduce in-stent neointimal hyperplasia. SRL is a potent immunosuppressive agent that inhibits SMC proliferation by blocking cell cycle progression. METHODS AND RESULTS: Stents were coated with a nonerodable polymer containing 185 microgram SRL, 350 microgram DEX, or 185 microgram SRL and 350 microgram DEX. Polymer biocompatibility studies in the porcine and canine models showed acceptable tissue response at 60 days. Forty-seven stents (metal, n=13; SRL, n=13; DEX, n=13; SRL and DEX, n=8) were implanted in the coronary arteries of 16 pigs. The tissue level of SRL was 97+/-13 ng/artery, with a stent content of 71+/-10 microgram at 3 days. At 7 days, proliferating cell nuclear antigen and retinoblastoma protein expression were reduced 60% and 50%, respectively, by the SRL stents. After 28 days, the mean neointimal area was 2.47+/-1.04 mm(2) for the SRL alone and 2.42+/-1.04 mm(2) for the combination of SRL and DEX compared with the metal (5.06+/-1.88 mm(2), P<0.0001) or DEX-coated stents (4.31+/-3.21 mm(2), P<0.001), resulting in a 50% reduction of percent in-stent stenosis. CONCLUSIONS: Stent-based delivery of SRL via a nonerodable polymer matrix is feasible and effectively reduces in-stent neointimal hyperplasia by inhibiting cellular proliferation.

Intracoronary artery thrombus formation in unstable angina: a clinical, biochemical and angiographic correlation.

OBJECTIVES: We examined the relation between the level of urinary fibrinopeptide A and the presence of angiographic intracoronary thrombus in patients with unstable angina to determine whether this marker predicts active thrombus formation. BACKGROUND: Although it is known that thrombus plays a role in acute ischemic syndromes, a noninvasive method to predict its presence in individual patients with unstable angina has not been determined. Fibrinopeptide A is a polypeptide cleaved from fibrinogen by thrombin and thus is a sensitive marker of thrombin activity and fibrin generation. METHODS: Angiographic thrombus, graded 0 to 4, and the presence of ST segment depression or T wave inversions, or both, on the electrocardiogram (ECG) were related to fibrinopeptide A levels in 24 patients with rest angina of new onset, 18 with crescendo angina, 19 with stable angina and 9 with chest pain but without coronary artery disease. All patients had chest pain within the 24 h of sample acquisition. RESULTS: The angiographic incidence of thrombus was significantly higher in patients with new onset of rest angina (67%, p < 0.001) and crescendo angina (50%, p < 0.001) as were fibrinopeptide A levels (p = 0.002). Fibrinopeptide A levels correlated significantly (p < 0.001) with the presence of a filling defect (grade 4 intracoronary thrombus) or contrast staining (grade 3). All patients with fibrinopeptide A > or = 8 ng/mg creatinine showed grade 3 to 4 thrombus and 15 of 16 patients with levels > or = 6.0 ng/mg creatinine exhibited angiographic evidence of thrombus (13 with grades 3 to 4). Patients with reversible ST changes on the ECG had significantly higher levels of fibrinopeptide A (p < 0.001), and ST changes correlated significantly with the presence of angiographic thrombus (p < 0.001). Nonetheless, a significant minority of patients with unstable angina had neither angiographic nor biochemical evidence of thrombus. CONCLUSIONS: Elevated fibrinopeptide A levels in unstable angina reflected active intracoronary thrombus formation and were present in patients with angina of new onset as well as crescendo angina. Reversible ST changes are accompanied by thrombin activity and angiographic thrombus formation. However, a sizable percentage of patients with unstable angina had no evidence of thrombus and these patients may have had transient platelet aggregation without fibrin thrombus formation.

Urinary fibrinopeptide A levels in ischemic heart disease.

Because acute coronary thrombosis can cause unstable coronary artery disease, fibrinopeptide A, a reliable marker of coagulation activity, may play a role in the evaluation of unstable ischemic syndromes. A new method of fibrinopeptide A sampling, spot urine normalized to urinary creatinine, was evaluated in patients with stable and unstable angina pectoris and acute myocardial infarction. Serial samples were obtained to characterize the changes in urinary fibrinopeptide A levels over time in patients with ischemic heart disease. Admission values (mean +/- SD) were similar in the control group (3.3 +/- 1.4 ng/mg creatinine) and the stable angina group (3.2 +/- 1.1 ng/mg creatinine) (p = NS). Values in the unstable angina group (5.7 +/- 2.6 ng/mg creatinine) were higher than those in the control (p = 0.008) and stable angina (p less than 0.001) groups. Myocardial infarction admission values (8.4 +/- 10.0 ng/mg creatinine) were higher than those in the control (p = 0.005) and stable angina (p less than 0.001) groups, but not higher than those in the unstable angina group. Peak values (the highest of multiple samples) were higher in the unstable angina group (7.6 +/- 5.9 ng/mg creatinine) than in the stable angina group (4.0 +/- 1.0 ng/mg creatinine) (p = 0.04), but not in the control group (4.5 +/- 1.9 ng/mg creatinine) (p = 0.056). The two patients with unstable angina with the highest peak values subsequently exhibited infarction. Peak values in patients with infarction (44.5 +/- 60.0 ng/mg creatinine) were significantly higher than those in patients with unstable (p = 0.03) or stable (p = 0.002) angina and control patients (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Vascular remodeling and the local delivery of cytochalasin B after coronary angioplasty in humans.

OBJECTIVES: This study sought to determine the safety, feasibility and outcome of local delivery of cytochalasin B at the site of coronary angioplasty. BACKGROUND: Previous failures in the pharmacologic prevention of restenosis may have been related to inadequate dosing at the angioplasty site as a result of systemic drug administration. Alternatively, although previous experimental protocols have typically targeted control of excess tissue growth (intimal hyperplasia), it now appears that overall arterial constriction (vascular remodeling) is the major contributor to late lumen loss. Cytochalasin B inhibits the polymerization of actin and has proved to be a potent inhibitor of vascular remodeling in animal models. METHODS: In this phase I, multicenter, randomized, controlled trial, cytochalasin B (or matching placebo) was administered to the site of a successful balloon angioplasty using a microporous local delivery infusion balloon. RESULTS: The rate of drug delivery at a constant infusion pressure varied significantly from patient to patient (range 1.7 to 20.2 ml/min), perhaps related to a variable constricting effect of the atherosclerotic plaque on the infusion balloon. The minimal stenosis diameter after the procedure was slightly better in the active drug group (1.86 +/- 0.44 vs. 1.49 +/- 0.63 mm, p < 0.03), but this difference was not seen at four to six weeks. Although the study was not powered for clinical outcomes (n = 43), the combined end point (death, nonfatal infarction or repeat revascularization) was encountered in 20% of the patients receiving cytochalasin B and in 38% of the patients receiving placebo. Clinical restenosis occurred in 18% of the treatment group and 22% of the placebo group. There were no significant differences between groups in biochemical or electrocardiographic variables. CONCLUSIONS: Cytochalasin B can be safely administered by local delivery after successful coronary angioplasty and warrants further study of its efficacy in reducing restenosis.

Local delivery of biodegradable microparticles containing colchicine or a colchicine analogue: effects on restenosis and implications for catheter-based drug delivery.

OBJECTIVES: This study sought to evaluate the delivery efficiency, intramural retention and antirestenotic efficacy of soluble colchicine or colchicine analogue delivered into the arterial wall after angioplasty as well as the efficacy of these medications after prolonged local release from biodegradable microparticles. BACKGROUND: Local delivery of pharmacologic agents is a potential treatment for restenosis. However, the delivery efficiency of the technique and the choice of agent to modulate cellular proliferation are unknown. It was hypothesized that restenosis would be unaffected by colchicine or a hydrophobic colchicine analogue with short intramural retention, whereas it would be reduced after prolonged local release. METHODS: Rabbit atherosclerotic femoral arteries underwent angioplasty followed by local delivery. Delivery efficiency and intramural retention of 3H-colchicine were evaluated. The effect of agents in soluble formulation or released from microparticles on angiographic and morphometric restenosis was evaluated at 2 weeks and compared with that in the control groups (angioplasty only and local infusion of carrier solution). RESULTS: Delivery of efficiency was 0.01% and intramural retention < 24 h. Neither soluble colchicine formulation reduced restenosis. Microparticles releasing the colchicine analogue reduced restenosis compared with control and colchicine microparticles but not angioplasty alone (p = 0.002). Delivery outside the artery was observed, and the long-term release of both colchicine resulted in toxicity to the adjacent musculature. CONCLUSIONS: Colchicine or the colchicine analogue did not reduce restenosis, although the long-term local release of the colchicine analogue reduced neointimal proliferation resulting from local delivery. Local delivery of cytotoxic agents with insufficient vascular specificity may be limited by toxicity to adjacent tissues resulting from a larger than expected delivery area and prolonged agent retention.

Methods and devices for local drug delivery in coronary and peripheral arteries.

New developments in catheter design, molecular biology, and polymer chemistry have made it possible to deliver pharmaceutical agents and genetic material directly into the arterial wall to modulate the response to injury. Several local drug delivery catheters of various designs in addition to biodegradable and coated stents are currently being evaluated as devices to facilitate local delivery of agents into the arterial wall. Approaches to locally sustained delivery include the controlled release of medications, the affinity-based delivery of medications administered systemically but accumulated locally, and gene therapy.

Transthoracic echocardiographic detection of coronary atherosclerosis.

Coronary atherosclerosis is a pathologic process that produces thickening of the walls of the coronary arteries to the point that flow through those vessels may be impaired. This study attempts to use transthoracic echocardiography to detect coronary atherosclerosis. Eighty-nine patients undergoing coronary angiography were examined with a broad-band ultrasonic transducer with a frequency between 3 and 5 MHz. A modified short axis examination was utilized to identify left main and proximal left anterior descending arteries. The examination was recorded digitally and displayed in a 32-cell, quad screen cine loop. Fifty-six of the 89 patients (63%) had obstructive coronary artery disease (CAD) (i.e, at least 1 vessel with 50% obstruction). There were 14 patients with CAD but no vessel had > or = 50% obstruction. Nineteen patients (21%) had angiographically normal arteries. The coronary echograms were judged qualitatively for brightness, uniformity, and persistence (defined as the ability to see segments of the artery walls in more frames than other segments). The length of the coronary artery visualized, the width of the left main coronary artery, and the width of the thickest segment of the coronary artery walls were quantitatively measured. More than 2 cm of the left coronary artery was seen in almost all patients. Segmental changes were noted in 52 of the 56 patients with obstructive CAD, 12 of the 14 patients with nonobstructive CAD, and 3 of the 19 patients with normal arteries. Persistence greatly enhanced the ability to judge the segmental changes. Forty-six patients with obstructive disease had wall thickness > or = 1.5 mm. Only 6 patients with nonobstructive coronary arteries had this wall thickness, and only 1 normal subject had thick walls. The ultrasonic findings were useful in predicting the presence or absence of coronary atherosclerosis to varying degrees of sensitivity and specificity based on the segmental findings and wall thickness measurements. The results of this study indicate that a transthoracic ultrasonic examination of the proximal left coronary artery could be a clinically valuable tool in the qualitative identification of coronary atherosclerosis.

Exercise echocardiography, angiography, and intracoronary ultrasound after cardiac transplantation.

Fifty-one consecutive patients underwent exercise echocardiography, angiography, and intracoronary ultrasound (ICUS) 2.5 years (range from 1 to 6) after cardiac transplantation. The average age of the donor was 29 years (range 13 to 50), and the average age of the recipient was 49 +/- 12 years. In total, 78 studies were performed, as 25 patients had >1 annual evaluation and 2 patients had 3 consecutive annual evaluations. Of the 78 angiographic studies, 40 (26 patients) had evidence of coronary artery disease, defined as a focal stenosis (>20%, n=4) or luminal irregularities (n=36). However, by ICUS all 51 patients had intimal thickening at some point, with 34 patients possessing diffuse disease and 17 focal intimal thickening only. Of the 25 serial studies, 12 progressed by at least 1 Stanford class. The sensitivity of angiography for determination of class III to IV intimal thickening was 64% and the specificity was 76%. On exercise echocardiography, 6 examinations revealed resting wall motions abnormalities, whereas 6 had inducible wall motion abnormalities with exercise. The sensitivity of exercise echocardiography to determine class III to IV intimal thickening was 15%, and the specificity was 85%. In conclusion, exercise echocardiography is an insensitive method for predicting transplant-mediated coronary artery disease, whereas luminal irregularities on angiography may predict the presence of Stanford grade III to IV intimal thickening.

Serial electrocardiographic changes in idiopathic dilated cardiomyopathy confirmed at necropsy.

Serial electrocardiographic changes in necropsy-proven idiopathic dilated cardiomyopathy are evaluated and a method of predicting heart weight using QRS amplitudes is described. In 34 patients with multiple electrocardiograms (mean 3/patient) progressive prolongation of PR interval (0.18 +/- 0.03 to 0.21 +/- 0.03, p less than 0.001) and QRS duration (0.10 +/- 0.02 to 0.13 +/- 0.03, p less than 0.0001) was noted. Progressive conduction abnormalities were common (82%). QTc interval and QRS- and T-wave axes did not change. In 50 patients with electrocardiograms within 60 days of death, total 12-lead QRS and V1 through V6 QRS amplitude correlated better with heart weight (r = 0.51, p less than 0.0001 and r = 0.55, p less than 0.0001) than the Estes-Romhilt score did. The mean total 12-lead QRS amplitude was 138 mm with a mean of 106 for V1 through V6. In 31 patients cardiac mass index was calculated and showed significant correlation with 12-lead and V1 through V6 QRS amplitudes (r = 0.68, p less than 0.0001 and r = 0.75, p less than 0.0001, respectively). The QRS amplitudes remained constant during the illness. By using total 12-lead QRS or frontal plane QRS amplitude, heart weight can be predicted as early as 2 years before death. Use of body surface area and QRS amplitude criteria increases the accuracy of heart weight prediction. Thus, progressive electrocardiographic changes are common in patients with idiopathic dilated cardiomyopathy and QRS amplitude criteria are more accurate in the prediction of left ventricular hypertrophy than standard criteria.

Predictors of clinical outcome following percutaneous intervention for in-stent restenosis.

Percutaneous intervention for the first episode of in-stent restenosis was performed in 177 patients 5.4 +/- 0.3 months after native coronary stent implantation. Medical records were reviewed and patients contacted 13.3 +/- 1.2 months after in-stent intervention to ascertain the subsequent clinical course. The effects of demographic, procedural, and angiographic variables on clinical outcomes were determined. At 2 years, Kaplan-Meier estimated survival was 93 +/- 3% and freedom from death, myocardial infarction, and a third target artery revascularization (TAR) was 67 +/- 4%. The actuarial frequency of a third TAR was 26 +/- 4% at 1 year. Stratification of outcomes according to timing of in-stent intervention revealed an approximate twofold higher frequency of adverse events among patients with early (

Extent and distribution of in-stent intimal hyperplasia and edge effect in a non-radiation stent population.

Intimal hyperplasia within the body of the stent is the primary mechanism for in-stent restenosis; however, stent edge restenosis has been described after brachytherapy. Our current understanding about the magnitude of in vivo intimal hyperplasia and edge restenosis is limited to data obtained primarily from select, symptomatic patients requiring repeat angiography. The purpose of this study was to determine the extent and distribution of intimal hyperplasia both within the stent and along the stent edge in relatively nonselect, asymptomatic patients scheduled for 6-month intravascular ultrasound (IVUS) as part of a multicenter trial: Heparin Infusion Prior to Stenting. Planar IVUS measurements 1 mm apart were obtained throughout the stent and over a length of 10 mm proximal and distal to the stent at index and follow-up. Of the 179 patients enrolled, 140 returned for repeat angiography and IVUS at 6.4 +/- 1.9 months and had IVUS images adequate for analysis. Patients had 1.2 +/- 0.6 Palmaz-Schatz stents per vessel. There was a wide individual variation of intimal hyperplasia distribution within the stent and no mean predilection for any location. At 6 months, intimal hyperplasia occupied 29.3 +/- 16.2% of the stent volume on average. Lumen loss within 2 mm of the stent edge was due primarily to intimal proliferation. Beyond 2 mm, negative remodeling contributed more to lumen loss. Gender, age, vessel location, index plaque burden, hypercholesterolemia, diabetes, and tobacco did not predict luminal narrowing at the stent edges, but diabetes, unstable angina at presentation, and lesion length were predictive of in-stent intimal hyperplasia. In a non-radiation stent population, 29% of the stent volume is filled with intimal hyperplasia at 6 months. Lumen loss at the stent edge is due primarily to intimal proliferation.

Role of vascular remodeling in the pathogenesis of early transplant coronary artery disease: a multicenter prospective intravascular ultrasound study.

BACKGROUND: Luminal narrowing in transplant coronary artery disease is thought to be primarily caused by intimal proliferation, and the role of vascular remodeling is less certain. METHODS AND RESULTS: We studied cardiac allografts from 83 prospectively recruited patients immediately and 1 year after transplant using intravascular ultrasound in a multicenter study. We measured coronary artery dimensions in 310 angiographically matched segments (175 were also fully matched by ultrasound criteria). At 1 year, lumen area changed by -1.8 +/- 3.7 mm(2) (p < 0.0001, 14% of baseline lumen area). Thirty-three percent of this luminal loss was due to intimal thickening and 67% to vessel shrinkage. Shrinkage also occurred (-0.9 +/- 3.2 mm(2), 7% of baseline total area) in segments free of detectable intimal disease at baseline and at 1 year. Using the mean baseline total vessel area (13.9 mm(2)) as the cutoff, we divided the cohort into the large and the small coronary-segment groups. The large-segment group (n = 176) shrank more (-2.6 +/- 4.4 vs. -0.03 +/- 2.8 mm(2), p < 0.0001), but intimal growth was similar in both groups (0.8 +/- 2.2 vs. 0.4 +/- 1.3 mm(2), p = not significant). Analysis of the 175 fully ultrasound matched sub-cohort showed similar results. Changes in intimal area, total vessel area, and lumen area were similar in segments with (n = 132) and segments without (n = 178) pre-existing donor disease. Despite overall shrinkage, change in total vessel area positively correlated with change in intimal area (r = 0.29, p < 0.0001). CONCLUSION: In large coronary segments, coronary artery shrinkage plays an important role in the loss of luminal diameter early after cardiac transplantation, whereas new intimal growth occurs in both large and small segments. Pre-existent donor disease does not aggravate these processes. Compensatory remodeling with increasing intimal growth retards the rate of lumen loss. As is intimal thickening, shrinkage and compensatory remodeling are important pathogenic mechanisms in transplant coronary artery disease.

Surgical management of aplasia cutis congenita.

A child born without scalp, or dura to cover the brain (aplasia cutis congenita) was successfully treated by a multidiscipline team. A coexisting rupture omphalocele forced a change in treatment from the currently recommended regimen of mandatory early scalp closure. Homograft skin was used to protect the brain during the time the omphalocele was treated and skin flaps were delayed. Fluoroscein dye was utilized to determine flap viability and predicted ischemia until after a third delaying procedure was performed. The successful outcome suggests that the present philosophy of early surgical closure being essential for survival in infants with large cranial defects can be altered and, in fact, permanent full-thickness flaps may be designed, tested for viability, and delayed while homograft skin protects the infant's brain from infection and thrombosis.

Local delivery of a hydrophobic heparin reduces neointimal hyperplasia after balloon injury in rat carotid but not pig coronary arteries.

BACKGROUND: Intimal hyperplasia following percutaneous interventional vascular procedures is a major cause of restenosis. Although heparin inhibits intimal hyperplasia, it has not proven clinically useful in part due to an inadequate duration of intramural drug residence. This study was designed to evaluate the efficacy of local delivery of hydrophobic heparin (PTIR-RS-1), exhibiting increased intramural binding, on neointimal hyperplasia after angioplasty injury. METHODS AND RESULTS: PTIR-RS-1 was delivered locally into rat carotid arteries at three doses: 0.1 mM (440 IU), 0.3 mM (1320 IU), or 1.0 mM (4400 IU). Animals were killed at 14 days. In the pig, the doses tested were the low dose in the rat and a high dose 1 log higher. Animals were killed 28 days later. Morphometric analysis was performed to evaluate the intima: media ratio in rats and the normalized neointimal area in pigs. In rats a significant reduction in neointimal to medial area ratio from 0.73 +/- 0.15 for control vs 0.80 +/- 0.27 for sodium heparin (P = NS) and 0.15 +/- 0.07 for the 0.1 mM PTIR-RS-1 dose (P < 0.008). In pigs, PTIR-RS-1 the high dose reduced the normalized neointimal area by 16%, a difference that was not statistically significant. CONCLUSIONS: Increased hydrophobicity of heparin reduced neointimal area following balloon overstretch injury in the rat carotid but not the pig coronary artery model. This study attests to the importance of performing studies evaluating the pharmacologic effect of local delivery of a medication in at least two animal models of restenosis.

Iliofemoral thrombophlebitis presenting as an acute abdomen: report and literature review.

Iliofemoral thrombophlebitis characteristically presents as acute inflammation and swelling of the affected extremity. We report a patient in whom the presenting complaints of high fever, nausea and left lower quadrant pain mimicked an acute abdomen. The diagnosis was confirmed by venogram after gallium scan and computer tomographic scan revealed abnormalities consistent with iliofemoral thrombophlebitis. This is the first report of abnormal gallium uptake in iliofemoral thrombophlebitis. Current methods of diagnosing this disorder are discussed and the literature reviewed.

Peripheral vascular complications following coronary interventional procedures.

We report the incidence, diagnosis, prevention, and treatment of peripheral vascular complications following coronary interventional procedures as reviewed in the English-language literature. Peripheral vascular complications include hematomas, pseudoaneurysms, arteriovenous fistulae, acute arterial occlusions, cholesterol emboli, and infections that occur with an overall incidence of 1.5-9%. Major predictors of such complications following coronary interventional procedures include advanced age, repeat percutaneous transluminal coronary angioplasty, female gender, and peripheral vascular disease. Minor predictors include level of anticoagulation, use of thrombolytic agents, elevated creatinine levels, low platelet counts, longer periods of anticoagulation, and use of increased sheath size. Ultrasound-guided compression repair of pseudoaneurysms and arteriovenous fistulae are discussed, as are newer methods of treatment such as hemostatic puncture closure devices. Anticipation and early recognition of possible peripheral vascular complications in conjunction with careful attention to the optimal activated clotting time for sheath removal following coronary interventional procedures may translate into fewer vascular complications as well as into shorter and less costly hospital stays.

The medical civic action program in Vietnam: success or failure?

Medical services have long been an integral part of the military and warfare. Civilians, however, are also caught up in wars. This article discusses the care of the indigenous civilians by U.S. military medical personnel during the Vietnam War. Civilian medical care is rendered both for altruistic purposes and to satisfy the policy aims of the U.S. government. Evaluation of these two aspects of the programs does not lead to the same conclusions. Doctors doubted the value of the programs, whereas the command structure was enthusiastic. For a program to be of sustained value to the people, it must persist over time and train those who will remain after U.S. forces are withdrawn. This did not occur in Vietnam. Furthermore, I doubt that medical care rendered by U.S. troops in uniform can serve to build up loyalty to another organization, such as the host government.