Increased arterial expression of a glycosylated haptoglobin isoform after balloon dilation

OBJECTIVE: Haptoglobin is a novel cell migration factor that is expressed in arteries after sustained flow changes and involved in arterial restructuring. Arterial restructuring is the major determinant of arterial shrinkage after balloon dilation. Although the function of extrahepatic haptoglobin expression is not yet understood, local haptoglobin expression may provide the tissue with functionally different haptoglobin due to post-translational modifications. We hypothesized that haptoglobin expression is increased during arterial restructuring after balloon dilation and compared glycosylation patterns between arterial and liver haptoglobin. METHODS: Arterial haptoglobin expression was studied in rabbits at 0, 2, 7, 14 and 28 days after balloon dilation (n=36) using real-time polymerase chain reaction, Western blotting and in situ hybridization. Two-dimensional gel electrophoresis and lectin affinity blotting were used to identify liver and arterial haptoglobin glycoforms. RESULTS: Arterial haptoglobin mRNA (5.7-fold, P=0.01) and protein levels (1.4-fold, P=0.01) were increased after balloon dilation whereas liver haptoglobin expression remained constant. Haptoglobin was expressed in the adventitia of balloon dilated rabbit arteries, which was confirmed in human atherosclerotic arteries. Comparison between liver and arterial haptoglobin demonstrated the expression of artery-specific haptoglobin glycoforms. CONCLUSIONS: This study demonstrates that arterial haptoglobin expression is increased early after balloon dilation whereas liver haptoglobin expression does not change. Furthermore, arterial haptoglobin consists of an unique set of glycoforms compared to haptoglobin produced in the liver.     

Balloon mitral valvuloplasty via retrograde left atrial catheterization

A technique for performing retrograde catheterization of the left atrium followed by double balloon mitral valvuloplasty without transseptal catheterization is described. Three patients have undergone double balloon mitral valvuloplasty by means of this technique, all with marked improvement in postdilatation mitral valve areas. The technique avoids iatrogenic atrial septal defects and is less difficult to perform than transseptal catheterization.     

Balloon embolisation of a coronary arterial fistula

Coronary arterial fistulas traditionally are treated surgically. We describe a case in which a fistula between the right coronary artery and right ventricle was treated by balloon embolisation. Coronary arteriography 13 months later showed that the fistula remained occluded, and that the coronary artery had returned to a normal size. In suitable cases, embolisation of coronary arterial fistulas is an effective alternative to surgery, and can restore normal coronary arterial anatomy.     

Immediate arterial hemostasis after cardiac catheterization: Initial experience with a new puncture closure device

A novel device for obtaining arterial hemostasis after invasive procedures was tested in 30 patients undergoing diagnostic catheterization (26 patients) or coronary angioplasty (4 patients). The device is deployed through an arterial sheath and forms a positive mechanical seal both inside and outside the defect in the arterial wall. The components are all bioabsorbable. Thirteen patients received a heparin bolus during the catheterization procedure. The activated clotting time recorded in 15 patients just prior to device deployment averaged 264 sec. 29 of 32 attempted device deployments were successful (91%); and the remaining 3 devices pulled completely out as called for by design in the event of incomplete deployment. Twenty-nine patients ultimately achieved successful hemostasis using the device, with the other patient receiving manual hemostasis. Of these 29, hemostasis was immediate and complete in 19 patients. Light digital pressure was required in another 8 patients for less than 5 min. There was minor delayed bleeding requiring supplemental light pressure in several cases. A total of 11 patients required supplemental pressure in addition to the hemostasis device. The use of bolus heparin was significantly (P = 0.05, Fisher's exact test) related to the requirement for supplemental pressure. Three patients developed hematomas, one of which was present prior to device deployment. The other two patients had received bolus heparin. No patient required transfusion or surgical repair. There was no change in the ankle/brachial systolic blood pressure index after device deployment or at late (30–60 day) follow-up. Ultrasound studies revealed no significant pathology relative to the device. There was no residual evidence of the device at 2 month follow-up ultrasound study. Thus the Kensey Nash Hemostatic Puncture Closure Device can safely, reliably, and rapidly provide arterial hemostasis after cardiac catheterization procedures. Its use warrants further study in comparison to standard manual hemostasis.     

Pediatric arterial catheterization using a 3.2 french catheter

Retrograde arterial catheterization was performed in 105 infants and small children (median age 6 mo) using a 3.2 French pigtail catheter made of ultrathin walled white Teflon. Three catheter lengths were used, (40, 50, and 65 cm). Pressure recordings and ease of sampling were judged excellent in all. All 118 angiograms (60 ventricular) were performed without complication except for two episodes of external catheter rupture. Angiographic quality was rated excellent in 41 %, good in 39%, fair in 18%, and poor in only 2%. Among the 81 patients in whom only this catheter was used percutaneously, pedal pulses were lost in 5%. Postcatheterization testing identified ranges of volume and flow-rate characteristics which included 8 ml at 15 ml/sec (40 cm length), at 11 ml/sec (50 cm length), and at 9 ml/sec (65 cm catheter). We conclude that this small catheter is relatively safe and satisfactory for retrograde catheterization of infants and small children.     

Delayed, distant arterial injury after brachial artery catheterization

The occurrence of iatrogenic arterial injury secondary to catheterization for angiographic studies has been well documented in the literature for over a decade. It has been well established that patients should be carefully evaluated post-catheterization and if absence of the pulse distal to the arteriotomy site is discovered, most should undergo exploration for identification and correction of the problem. Between 0.3 and 24% of patients undergoing brachial artery catheterization have been found to have a diminished or absent radial pulse after the procedure. In the vast majority of cases the problem has been solved by local exploration of the arteriotomy site. However, in a small but definite number of cases late thrombotic complications have become manifest, and in two cases reported in 1981 and in the case report to follow, thrombotic complications have become manifest months later, secondary to injury well proximal to the arteriotomy site.     

Smooth muscle--specific expression of CYP4A1 induces endothelial sprouting in renal arterial microvessels

Cytochrome P450 (CYP) 4A1 has been characterized as the most efficient arachidonic acid omega-hydroxylase catalyzing the formation of 20-hydroxyeicosatetraenoic acid (20-HETE), a potent constrictor of the renal and cerebral microcirculation and a mitogen for smooth muscle cells. We constructed adenoviruses expressing the CYP4A1 cDNA or LacZ under the control of the smooth muscle cell-specific promoter SM22alpha (Ad-SM22-4A1 and Ad-SM22-nLacZ, respectively). Beta-galactosidase expression was detected in Ad-SM22-nLacZ-transduced vascular smooth muscle A7r5 and PAC1 cells, but not in Ad-SM22-nLacZ-transduced 3T3 fibroblasts or vascular endothelial cells. Likewise, CYP4A1 mRNA and protein were detected in Ad-SM22-4A1-transduced A7r5 and PAC1 cells. Ad-SM22-4A1-transduced A7r5 cells metabolized lauric acid to 12-hydroxy-lauric acid at a rate 5 times greater than that of cells transduced with Ad-SM22-nLacZ (4.79+/-1.77 versus 0.97+/-0.57 nmol 12-hydroxy lauric acid/10(6) cells per h). Smooth muscle-specific LacZ expression was also detected in microdissected renal interlobar arteries transduced with Ad-SM22-nLacZ. Arteries transduced with Ad-SM22-4A1 produced higher levels of 20-HETE (4.04+/-0.29 and 13.43+/-2.84 ng/mg protein in Ad-SM22-nLacZ-transduced and Ad-SM22-4A1-transduced arteries, respectively) and demonstrated a marked angiogenic activity measured as the total length of sprouting neovessels (12.63+/-3.66 mm in Ad-SM22-4A1-transduced vessels versus 1.79+/-0.89 mm in Ad-SM22-nLacZ-transduced vessels). This angiogenic activity represented endothelial cell sprouting and was fully blocked by treatment with HET0016, a selective inhibitor of CYP4A-catalyzed reactions. The inhibitory effect of HET0016 was reversed by addition of a 20-HETE agonist. We conclude that Ad-SM22-4A1 drives a smooth muscle-specific functional expression of CYP4A1 and demonstrates increased angiogenesis, presumably via increased production of 20-HETE.     

Innominate aterial arteriovenous fistula complicating retrograde brachial arterial catheterization.

Arteriovenous fistula of the innominate artery occurred in a patient 3 weeks after retrograde brachial arterial catheterization was performed 1 day before aortocoronary bypass surgery. Intramural dissection was noted at catheterization, and a mediastinal hematoma at operation. Exploration of the hematoma in the course of catheterization might have prevented the arteriovenous fistula, which necessitated a second operation 3 weeks after the first. To our knowlege this complication of retrograde brachial catheterization has not previously been described. We recommend that known injuries to cervical or thoracic arteries occurring just before operations requiring extracorporeal circulation be explored to prevent late complications. Recent injuries to the cervical and thoracic arteries that are not acessible to external compression should be exposed and treated during sternotomy to prevent late complications if heparinization is contemplated.     

Titin isoform expression in normal and hypertensive myocardium

OBJECTIVE: Titin isoform expression patterns were examined to explain previously observed genetic differences in rat cardiac passive tension. METHODS: Rat ventricles from male spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats (normotensive) were used to analyze the titin isoform patterns. The hypertensive status was verified by blood pressure measurements and heart weight to body weight ratios. Gel electrophoresis and scanning densitometry were performed to determine ratios of myosin heavy chain and titin isoforms expressed. In situ hybridization using a cRNA probe specific for N2BA titin and a positive control in the N2B unique region was used to demonstrate tissue location of the titin message. RESULTS: Regression analysis of titin isoform ratios, myosin heavy chain isoform ratios, and heart weight to body weight ratios all suggest a smaller proportion of N2BA titin (longer isoform) was expressed in rat left ventricles with increased hypertrophy. In situ hybridization showed that the N2BA and N2B isoforms were co-expressed within most of the cardiomyocytes. Agarose gel electrophoresis demonstrated two different N2BA titin isoforms in all rat ventricles. CONCLUSIONS: Expression of less N2BA and more N2B titin in response to pressure overload will result in higher passive tension upon stretch at a given sarcomere length and thus affect cardiac performance.