Patch Rupture Research Articles

Comparison of Early Outcomes in Patients Who Underwent Common Femoral Thromboendarterectomy with Vein versus Bovine Pericardial Patches

The treatment outcomesof vein and bovine pericardial patches in thromboendarterectomy (TEA) for common femoral artery (CFA) lesions in patients with peripheral arterial disease (PAD) remain unclear. The purpose of this study was to evaluate the efficacy and safety of the bovine pericardial patch by comparing it with vein patch angioplasty. This was a multicenter retrospective study. We reviewed the data of patients who underwent TEA with patch angioplasty (vein versus bovine pericardial patch angioplasty) for PAD between January 2018 and December 2022. Indication for revascularization is PAD patients with claudication symptoms to rest pain and foot ulcers that interfere with daily life, with lesions in the CFA region. The primary endpoint was 2-year patency. The secondary endpoints were postoperative wound complications, including patch rupture, and safety of remote-phase puncture of the patch area after patch angioplasty. Within the observation period, TEA was performed on 157 limbs in 136 patients using vein patches, and on 86 limbs in 79 patients using bovine pericardial patches. The number of claudication/rest pain/tissue loss was 110/13/34 cases in the vein patch group and 57/14/15 cases in the bovine pericardial patch group, respectively. No significant differences were observed in patient characteristics. No significant between group differences were observed in operative time, blood loss, or percentage of patients who underwent concomitant revascularization during the procedure. The 2-year primary patency rates of the vein and bovine pericardial patch were 95.6% and 92.8%, respectively (P= .49). The rate of surgical site infection (SSI) in this study was 2.5% in the vein patch group and 5.8% in the bovine pericardial patch group, respectively (P=.29). Rupture of the patch occurred in 4 (2.5%) and 4 (4.7%) patients in the vein and bovine pericardial patch groups, respectively (P= .46), and the percentage of cases requiring revision of the patch site was 7 (4.5%) and 5 (5.8%) in the vein and bovine pericardial patch groups, respectively (P= .76). Postoperatively, 23 patients in the vein and 13 patients in the bovine pericardial patch groups underwent patch puncture during the remote period. The median follow-up duration from the date of the surgery to the date of the puncture was 544 days and 374 days in the vein and bovine pericardial patch groups, respectively. No patch-related complications were observed during remote stage puncture. Compared with vein patches, TEA with bovine pericardial patches had acceptable outcomes in terms of patency and postoperative complications.

Bovine pericardial patch - a good alternative in femoral angioplasty.

Bovine pericardial patch (BPP) is currently used in femoral angioplasty as an alternative for autologous vein patch (AVP), but studies comparing the results of the two methods are scarce. In this retrospective study, we aimed to discover the differences between BPP and AVP closure in long-term durability. This study consisted of all femoral endarterectomies with BPP closure performed in Helsinki University Hospital from January 1, 2014, to December 31, 2017. For comparison, the same number of consecutive patients who underwent femoral endarterectomy with AVP closure from January 1, 2014, to October 16, 2016, were reviewed. Follow-up ended December 31, 2020. The mean follow-up was 19months (range, 0-74months) in the BPP group and 22months (range, 0-79months) in the AVP group. The primary endpoint was primary patency. Secondary endpoints were restenosis at patch site detected by imaging or perioperatively, patch rupture, and deep surgical wound infection. Propensity score analysis was performed for adjustment of differences between the AVP and BPP groups. Overall primary patency was superior in the AVP group compared with the BPP group: at 1year, 96.5% vs 85.0% and at 5years, 83.0% vs 72.3% (P= .04). In propensity score-matched pairs (n= 92), no difference was found between the groups in primary patency: 95.7% and 95.7% at 1year and 92.5% and 78.6% at 5years (P= .861) or in freedom from restenosis: 100% and 100% at 1year and 89.1% and 84.0% at 5years (P= .057). Deep wound infections occurred slightly more often after BPP closure (8%) than after AVP closure (4%), but the difference was not statistically significant (P= .144). There were no patch ruptures in the BPP group, but in the AVP group, there were five ruptures (3.5%) (P= .024). BPP is compatible to AVP in femoral endarterectomy in patency and can be regarded as the safer choice considering the risk of patch rupture.

Carotid endarterectomy with saphenous vein patch angioplasty: a single-center experience.

When performing a conventional CEA it is recommended the use of patch angioplasty (PA), since previous meta-analyses have shown PA to be superior to primary closure (PRC) in terms of stroke and restenosis rates. Different materials patches can be employed although none of them has been proved to be superior. Although autologous veins are potentially more resistant to immediate thrombosis as well as infection, cons may be represented by patch rupture and late dilatation. Aim of this study is to evaluate immediate and long-term results of CEA with saphenous vein patch angioplasty (SVPA) in a single-center experience. A retrospective study was performed analyzing all patients undergoing CEA with SVPA at our institution from January 2012 to March 2020. CEA was performed in symptomatic patients with 50-99% carotid stenosis degree or asymptomatic patients with 70-99% stenosis degree. Exclusion criteria were critical limb ischemia, varicose disease, unavailability of saphenous veins, vein diameter <3.5 mm. All CEAs were performed under general anesthesia with routine shunting. Primary endpoints were perioperative stroke, death, carotid thrombosis and hematoma requiring surgery rates. Secondary endpoints included the rate of recurrent stenosis >70%, patch aneurysm/rupture/infection at follow-up. Overall, 488 interventions were performed on 461 patients. Most patients were male (77.8%) with a mean age of 71.2±8.3 years. Thirty-day mortality and stroke rates were 0.4% and 1.2% respectively. Carotid thrombosis occurred in five patients (1%). Five patients (1%) developed a surgical site hematoma requiring surgical drainage. At a mean follow-up of 34.4±25.8 months 12 restenoses (2.5%) were detected. Five-year freedom from restenosis rate was 96.7%. Restenosis at follow-up was more frequent in patients who had contralateral carotid stenosis (P=0.019). Two patients (0.4%) developed carotid patch aneurysmal degeneration at a mean follow-up of 78.7 months. No infection nor patch disruption were detected. CEA with SVPA resulted safe and effective in terms of early and late results. The perioperative complications rates we recorded were quite similar to those reported by other larger reviews and meta-analyses.

Vein Patch Closure Using Below the Knee Greater Saphenous Vein for Femoral Endarterectomy Procedures is Not Always a Safe Choice.

BackgroundThe complication of vein patch rupture is well described after carotid patch angioplasty; however, there is a paucity of data about the safety of vein patch closure in the setting of femoral endarterectomy.Methods/resultsFrom May 2012 to May 2015, 115 femoral endarterectomies with patch closure were performed. A patch rupture occurred in three cases (2.6%) with a mortality rate of 66% (2/3). In all cases the greater saphenous vein below the knee was used as patch material.Discussion/conclusionVein patches, particularly from small calibre veins, should be excluded in femoral endarterectomy procedures as they pose a substantial risk of rupture.

Electrophysiology, immunophenotype, and gene expression characterization of senescent and cryopreserved human amniotic fluid stem cells.

We characterized human amniotic fluid stem cells (AFSC) in senescent cultures (6weeks) versus cryopreserved cells using whole-cell patch-clamp, immunophenotyping, and differential gene expression profiling for senescence genes. We evidenced five ion current components (outward rectifier, A-type, inward rectifier, and big conductance Ca2+-dependent K+ currents, fast voltage-dependent Na+ currents). Senescent AFSC showed reduced expression of CD90, CD44, CD133, over 500-fold increase of interferon gamma and telomerase reverse transcriptase genes, increased cycle-dependent kinase 4 inhibitors, p53-binding protein 1, and decreased calreticulin and CD44. HLA-ABC immune expression was similar, and HLA-DR expression very low in both cell types. A subset of cryopreserved AFSC featured large inward rectifier K+ currents, voltage-dependent Na+ currents, and neural progenitor markers evidenced by immunophenotyping and RT-PCR. In all AFSC, in both culture conditions, at patch rupture the outward currents were very low, and they increased progressively over several minutes upon cytoplasm dialysis with pipette solution.

An Electrical Inspection of the Subsurface Cisternae of the Outer Hair Cell

The cylindrical outer hair cell (OHC) of Corti’s organ drives cochlear amplification by a voltage-dependent activation of the molecular motor, prestin (SLC26a5), in the cell’s lateral membrane. The voltage-dependent nature of this process leads to the troublesome observation that the membrane resistor-capacitor filter could limit high-frequency acoustic activation of the motor. Based on cable theory, the unique 30 nm width compartment (the extracisternal space, ECS) formed between the cell’s lateral membrane and adjacent subsurface cisternae (SSC) could further limit the influence of receptor currents on lateral membrane voltage. Here, we use dual perforated/whole-cell and loose patch clamp on isolated OHCs to sequentially record currents resulting from excitation at apical, middle, and basal loose patch sites before and after perforated patch rupture. We find that timing of currents is fast and uniform before whole-cell pipette washout, suggesting little voltage attenuation along the length of the lateral membrane. Prior treatment with salicylate, a disrupter of the SSC, confirms the influence of the SSC on current spread. Finally, a cable model of the OHC, which can match our data, indicates that the SSC poses a minimal barrier to current flow across it, thereby facilitating rapid delivery of voltage excitation to the prestin-embedded lateral membrane.

Upregulation of TRPM7-Like Current in Ischemia Damaged Human Atrial Cardiomyocytes

Transient receptor potential of melastatin subfamily (TRPM7) channels has been detected in the heart using molecular approaches. Recently we have identified electrophysiologically the TRPM7-like current in native human cardiomyocytes, and discovered that in ∼1/3 of patients the current was already activated at patch rupture. One of possible versions to explain this phenomenon might be related with heart pathology such as ischemic heart disease (IHD). To test this assumption we used cardiomyocytes from right atrial appendages obtained from 77 adult patients with and without IHD. With voltage-dependent and other ion channels inhibited, TRPM7-like current was recorded using the whole-cell patch-clamp technique. The TRPM7-like current studied in 136 myocytes showed a marked variation of outward (at +80 mV) and inward (at −120 mV) current densities ranging from 1.21 to 11.63 pA/pF and from −0.14 to −0.7 pA/pF, respectively. The densities of TRPM7-like current did not correlate with membrane capacitance or changes of biophysical properties. The TRPM7-like current density was homogeneous for a given sample. We established that higher TRPM7-like current values, at rupture and steady-state, were recorded in cardiomyocytes obtained from patients with IHD (in pA/pF): from 2.14±0.12 to 5.39±0.36 and from −0.39±0.02 to −0.55±0.03 for outward and inward current, respectively, versus without IHD (from 1.68±0.22 to 4.03±0.4, and from −0.29±0.04 to −0.39±0.04, respectively, at +80 mV and −120 mV). In addition, we tested influence of pH that is major component of acute myocardial ischemia. Change of extracellular pH from 7.4 to 4 markedly increased inward and outward magnitude of TRPM7-like current, which again was more pronounced in cardiomyocytes from patients with IHD. Our experiments revealed the enlarged TRPM7-like current in atrial cardiomyocytes from patients with IHD, and those cells were associated with the greatest response to the extracellular acidification.

Complexin facilitates exocytosis and synchronizes vesicle release in two secretory model systems

Complexins (Cplxs) are small, SNARE-associated proteins believed to regulate fast, calcium-triggered exocytosis. However, studies have pointed to either an inhibitory and/or facilitatory role in exocytosis, and the role of Cplxs in synchronizing exocytosis is relatively unexplored. Here, we compare the function of two types of complexin, Cplx 1 and 2, in two model systems of calcium-dependent exocytosis. In mouse neuromuscular junctions (NMJs), we find that lack of Cplx 1 significantly reduces and desynchronizes calcium-triggered synaptic transmission; furthermore, high-frequency stimulation elicits synaptic facilitation, instead of normal synaptic depression, and the degree of facilitation is highly sensitive to the amount of cytoplasmic calcium buffering. In Cplx 2-null adrenal chromaffin cells, we also find decreased and desynchronized evoked release, and identify a significant reduction in the vesicle pool close to the calcium channels (immediately releasable pool, IRP). Viral transduction with either Cplx 1 or 2 rescues both the size of the evoked response and the synchronicity of release, and it restores the IRP size. Our findings in two model systems are mutually compatible and indicate a role of Cplx 1 and 2 in facilitating vesicle priming, and also lead to the new hypothesis that Cplxs may synchronize vesicle release by promoting coupling between secretory vesicles and calcium channels.

Biochemical, single-channel, whole-cell patch clamp, and pharmacological analyses of endogenous TRPM4 channels in HEK293 cells

Human embryonic kidney cells 293 (HEK293) are widely used as cellular heterologous expression systems to study transfected ion channels. This work characterizes the endogenous expression of TRPM4 channels in HEK293 cells. TRPM4 is an intracellular Ca2+-activated non-selective cationic channel expressed in many cell types. Western blot analyses have revealed the endogenous expression of TRPM4. Single channel 22pS conductance with a linear current–voltage relationship was observed using the inside-out patch clamp configuration in the presence of intracellular Ca2+. The channels were permeable to the monovalent cations Na+ and K+, but not to Ca2+. The open probability was voltage-dependent, being higher at positive potentials. Using the whole-cell patch clamp “ruptured patch” configuration, the amplitude of the intracellular Ca2+-activated macroscopic current was dependent on time after patch rupture. Initial transient activation followed by a steady-increase reaching a plateau phase was observed. Biophysical analyses of the macroscopic current showed common properties with those from HEK293 cells stably transfected with human TRPM4b, with the exception of current time course and Ca2+ sensitivity. The endogenous macroscopic current reached the plateau faster and required 61.9±3.5μM Ca2+ to be half-maximally activated versus 84.2±1.5μM for the transfected current. The pharmacological properties, however, were similar in both conditions. One hundred μM of flufenamic acid and 9-phenanthrol strongly inhibited the endogenous current. Altogether, the data demonstrate the expression of endogenous TRMP4 channels in HEK293 cells. This observation should be taken into account when using this cell line to study TRPM4 or other types of Ca2+-activated channels.

ELIC Channels Activate Slowly in Response to Agonist Concentration Jumps

Prokaryotic members of the Cys-loop superfamily of ligand-gated channels, such as GLIC and ELIC, have given us X-ray structures of different functional states of the channel. Zimmermann & Dutzler (PLOS Biology, 9, e1001101, 2011) have recently shown that ELIC is activated by a range of primary amines, including GABA, making this channel an attractive model for investigating agonist mechanisms. As a first characterisation of ELIC channel kinetics, we have used the technique of rapid theta-tube application to elicit macroscopic agonist currents. Outside-out patches from HEK293 cells expressing ELIC were held at −100 mV and agonists were applied by concentration jumps, 400-550 ms in duration, with exchange times faster than 0.4 ms (20-80%, measured with diluted extracellular solution after patch rupture). We tested propylamine (10-50 mM), cysteamine (10-50 mM) and GABA. For propylamine and cysteamine, the speed with which the current on-relaxation developed reached a clear maximum at 50 mM. At this concentration the time constant for the current risetime was 5.4 +/- 0.75 ms (n = 6) and 7.3 +/- 0.82 ms (n = 9) for cysteamine and propylamine, respectively. Thus, the most striking property of agonist ELIC responses was their slow time course, when compared with mammalian Cys-loop channels, such as the ACh muscle nicotinic or the glycine channel. In similar experiments with glycine channels, the response risetime was effectively too fast to be characterised by this technique, as its time constant reached sub-millisecond values at 3 mM glycine.

Adenylyl cyclase/cAMP-PKA-mediated phosphorylation of basal L-type Ca 2+ channels in mouse embryonic ventricular myocytes

In fetal mammalian heart, constitutive adenylyl cyclase/cyclic AMP-dependent protein kinase A (cAMP-PKA)-mediated phosphorylation, independent of β-adrenergic receptor stimulation, could under such circumstances play an important role in sustaining the L-type calcium channel current ( I Ca,L) and regulating other PKA dependent phosphorylation targets. In this study, we investigated the regulation of L-type Ca 2+ channel (LTCC) in murine embryonic ventricles. The data indicated a higher phosphorylation state of LTCC at early developmental stage (EDS, E9.5–E11.5) than late developmental stage (LDS, E16.5–E18.5). An intrinsic adenylyl cyclase (AC) activity, PKA activity and basal cAMP concentration were obviously higher at EDS than LDS. The cAMP increase in the presence of isobutylmethylxanthine (IBMX, nonselective phosphodiesterase inhibitor) was further augmented at LDS but not at EDS by chelation of intracellular Ca 2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA)-acetoxymethyl ester (BAPTA-AM). Furthermore, I Ca,L increased with time after patch rupture in LDS cardiomyocytes dialyzed with pipette solution containing BAPTA whereas not at EDS. Thus we conclude that the high basal level of LTCC phosphorylation is due to the high intrinsic PKA activity and the high intrinsic AC activity at EDS. The latter is possibly owing to the little or no effect of Ca 2+ influx via LTCCs on AC activity, leading to the inability to inhibit AC.

Mg2+- and MgATP-inhibited and Ca2+/calmodulin-sensitive TRPM7-like current in hepatoma and hepatocytes

Although understood to be ubiquitously expressed, the functional identification and significance of Mg(2+)-inhibited, nonspecific cation currents has been established in only a few cell types. Here we identified an outwardly rectifying nonspecific cation current in quiescent rat hepatocytes and the proliferating and polarized rat hepatoma, WIF-B. Under whole cell recording conditions in which cells were bathed and dialyzed with Na-gluconate solutions, the latter Ca(2+) and Mg(2+) free, current reversed close to 0 mV, was time independent, and was greater than 10 times higher at +120 mV compared with -120 mV. Outward current at -120 mV developed slowly, from 17.7 +/- 10.3 pA/pF at patch rupture to 106.6 +/- 15.6 pA/pF at 12 min in WIF-B cells, and 4.9 +/- 2.7 to 20.6 +/- 5.6 pA/pF in rat hepatocytes. The nonspecific TRP channel inhibitor, 2-aminoethoxyphenylborate (2-APB), inhibited current (IC(50) = 72 +/- 13 microM) and caused apoptotic cell death in WIF-B cells. Rat hepatocyte survival was more resistant to 2-APB. Dialysis of WIF-B cells with physiological concentrations of Mg(2+) and Mg-ATP, but not ATP alone, inhibited current development, suggesting that Trpm7 rather than Trpm6 underlies this current. RT-PCR demonstrated that both Trpm6 and Trpm7 are expressed at similar levels in both cell types, suggesting that the functional differences noted are not transcript dependent. Intracellular Ca(2+) (IC(50) = 125 +/- 35 nM) also inhibited current development, and this could be partially relieved by the calmodulin and Ca(2+)/calmodulin-dependent kinase inhibitors W-7, staurosporine, KN-93, or calmodulin kinase II (CaMKII) inhibitory peptide. To summarize, our results show that in addition to their established Mg(2+) sensitivity, Trpm7-like channels are inhibited by cytosolic Ca(2+) in a CaMKII-dependent manner and may support hepatocellular survival during proliferation.

Is malignant pleural mesothelioma a surgical disease? A review of 83 consecutive extra-pleural pneumonectomies☆☆☆

To report on the experience with radical surgery, with emphasis on the long-term outcome, for malignant pleural mesothelioma (MPM) at a single institution. From our prospective database over a 17-year period, we reviewed 83 consecutive patients undergoing radical surgery for MPM in a multimodality programme. The long-term overall survival was analysed using the Kaplan-Meier method. A total of 83 patients (65 males, median age: 60 years) underwent an extra-pleural pneumonectomy (EPP) with a curative intent. Epitheliod MPM was the most frequent (82%) cause. A right-sided disease was present in half of the cases (n=42). The International Mesothelioma Interest Group (IMIG) stage of the disease was 2 in 36%, 3 in 45% and 4 in 9% of the cases. Preoperative chemotherapy consisting of a doublet cisplatin-pemetrexed (mean of three cycles) was offered to 10 patients (12%). Postoperative therapies, either chemotherapy or radiotherapy, were given in 25 patients (30%). The 30-day and 90-day mortality rates were 4.8% and 10.8%, respectively. Postoperative complications occurred in 39.8% and were major in 23 patients (27.7%). Re-operation was necessary in 12 cases (14.5%) for one of the following reasons: broncho-pleural fistula (n=4), bleeding (n=3), diaphragmatic patch rupture (n=3), oesophago-pleural fistula (n=1) and empyaema (n=1). The mean hospital stay was 43 days. The median survival was 14.5 months, while the overall 1-, 2- and 5-year survival rates were 62.4%, 32.2% and 14.3%, respectively. These results concur with the published data of the most experienced centre with regards to the mortality and morbidity after EPP for MPM. In line with the biggest series reported in the past, the observed 5-year survival rate of almost 15% is disappointing.

Modulation Of Hepatocellular Trpm7-like Currents By A Ca2+/calmodulin-sensitive Pathway

Non-selective cation currents play integral roles in countering cell swelling, inducing apoptotic cell shrinkage, mediating Ca2+ influx and controlling Mg2+ homeostasis. The ‘chanzymes’ TRPM6 and TRPM7 are regulated by cytosolic Mg2+, and, under specific recording conditions, Mg-ATP or cell swelling. We recently identified a Mg2+-inhibited and outwardly rectifying cation current in both rat hepatocytes and the polarized rat hepatoma x human skin fibroblast cross, WIF-B. Here we investigated the regulation of these currents by cytosolic Ca2+. Under standard whole-cell recording conditions in which cells were bathed and dialyzed with Na-gluconate solutions, the latter Ca2+- and Mg2+-free, currents reversed close to 0 mV, showed no time dependence, and were 23 times higher at +120 mV as compared with -120 mV. Current at +120 mV developed slowly over dialysis, from 17.7±10.3 pA/pF at patch rupture to 106.5±15.6 pA/pF at 12 min. Inward current at -120 mV did not change significantly. Pipette solution containing Ca2+ inhibited current development with an IC50 of 125±35 nM. 50 μM W-7 or 200 nM staurosporine relieved the inhibition by 1 μM Ca2+, implicating channel regulation by a Ca2+/calmodulin-dependent kinase (CaMK). To address the nature of the kinase involved, we dialyzed the cells with more specific inhibitors of myosin light-chain kinase (MLCK) and CaMKII. 2 μM AIP, the CaMKII inhibitor, allowed full development of current, whereas 5 μM ML-7 did not affect the Ca2+-dependent channel inhibition ¼. Inspection of the rat Trpm7 primary structure identified a specific CaMKII substrate sequence in the proximal C-terminus. Conversely neither a CaM-binding domain nor a MLCK substrate consensus sequence was identified. The combined results support the conclusion that these channels are inhibited by cytosolic concentrations of Ca2+ in a CaMKII-dependent manner. Supported by NSERC & the Jeanne Mance Foundation, Hotel Dieu Hospital.

Spontaneous Vein Graft Rupture after Infrainguinal Vascular Reconstruction: Report of Three Cases

We report three cases of spontaneous vein graft rupture within 2 weeks of infrainguinal vein bypass for limb salvage. Two of the three ruptures were in the distal vein graft and the last just beyond the proximal anastomosis. All were longitudinal slits in the vein with no proximity to branches or valves. Endovascular treatment failed in one patient. Surgical correction with graft salvage was possible in all three cases. This may be an ischemic injury analogous to carotid vein patch rupture, nonapparent trauma to the vein, or simply mechanical stress causing vein rupture with arterial flow.

Subplate Neurons Regulate Maturation of Cortical Inhibition and Outcome of Ocular Dominance Plasticity

Synaptic plasticity during critical periods of development requires intact inhibitory circuitry. We report that subplate neurons are needed both for maturation of inhibition and for the proper sign of ocular dominance (OD) plasticity. Removal of subplate neurons prevents the developmental upregulation of genes involved in mature, fast GABAergic transmission in cortical layer 4, including GABA receptor subunits and KCC2, and thus prevents the switch to a hyperpolarizing effect of GABA. To understand the implications of these changes, a realistic circuit model was formulated. Simulations predicted that without subplate neurons, monocular deprivation (MD) paradoxically favors LGN axons representing the deprived (less active) eye, exactly what was then observed experimentally. Simulations also account for published results showing that OD plasticity requires mature inhibition. Thus, subplate neurons regulate molecular machinery required to establish an adult balance of excitation and inhibition in layer 4, and thereby influence the outcome of OD plasticity.

ATP and PIP2 dependence of the magnesium-inhibited, TRPM7-like cation channel in cardiac myocytes

The Mg(2+)-inhibited cation (MIC) current (I(MIC)) in cardiac myocytes biophysically resembles currents of heterologously expressed transient receptor potential (TRP) channels, particularly TRPM6 and TRPM7, known to be important in Mg(2+) homeostasis. To understand the regulation of MIC channels in cardiac cells, we used the whole cell voltage-clamp technique to investigate the role of intracellular ATP in pig, rat, and guinea pig isolated ventricular myocytes. I(MIC), studied in the presence or absence of extracellular divalent cations, was sustained for >or=50 min after patch rupture in ATP-dialyzed cells, whereas in ATP-depleted cells I(MIC) exhibited complete rundown. Equimolar substitution of internal ATP by its nonhydrolyzable analog adenosine 5'-(beta,gamma-imido)triphosphate failed to prevent rundown. In ATP-depleted cells, inhibition of lipid phosphatases by fluoride + vanadate + pyrophosphate prevented I(MIC) rundown. In contrast, under similar conditions neither the inhibition of protein phosphatases 1, 2A, 2B or of protein tyrosine phosphatase nor the activation of protein kinase A (forskolin, 20 microM) or protein kinase C (phorbol myristate acetate, 100 nM) could prevent rundown. In ATP-loaded cells, depletion of phosphatidylinositol 4,5-bisphosphate (PIP(2)) by prevention of its resynthesis (10 microM wortmannin or 15 microM phenylarsine oxide) induced rundown of I(MIC). Finally, loading ATP-depleted cells with exogenous PIP(2) (10 microM) prevented rundown. These results suggest that PIP(2), likely generated by ATP-utilizing lipid kinases, is necessary for maintaining cardiac MIC channel activity.

Cephalic Vein for Carotid Patching

Objective To assess the effectiveness of cephalic vein patch (CVP) closure following carotid endarterectomy (CEA). Material and methods We reviewed 121 patients who underwent CEA using CVP closure. Patch-rupture, re-exploration, false aneurysm formation, re-stenosis requiring surgery, 30-day-mortality, donor site complications, stroke and TIA were noted. A small cohort of patients were reviewed at 5-years and rescanned. Results No patient suffered patch rupture or re-stenosis requiring surgery. One patient developed false aneurysm at 1 year but at the time of repair the patch was found to be intact. There were two cardiac deaths. Three patients suffered strokes of whom two made a full recovery. There were three cases of TIA. All wrist wounds healed primarily without complications. None of the 10 patients recalled for scanning at 5 years showed re-stenosis or late aneurysmal dilatation at the site of surgery. Conclusion Cephalic-vein can be harvested at the wrist without donor site complications and our experience shows it to be a convenient and safe means of closure following CEA. Compared to prosthetics it is cheaper and less susceptible to bacterial contamination. The use of CVP preserves leg veins for future cardio-vascular interventions. Long term function of CVP appears satisfactory.

Cephalic Vein for Carotid Patching

ObjectiveTo assess the effectiveness of cephalic vein patch (CVP) closure following carotid endarterectomy (CEA). Material and methodsWe reviewed 121 patients who underwent CEA using CVP closure. Patch-rupture, re-exploration, false aneurysm formation, re-stenosis requiring surgery, 30-day-mortality, donor site complications, stroke and TIA were noted. A small cohort of patients was reviewed at 5 years and rescanned. ResultsNo patient suffered patch rupture or re-stenosis requiring surgery. One patient developed false aneurysm at 1 year but at the time of repair the patch was found to be intact. There were two cardiac deaths. Three patients suffered strokes of whom two made a full recovery. There were three cases of TIA. All wrist wounds healed primarily without complications. None of the 10 patients recalled for scanning at 5 years showed re-stenosis or late aneurysmal dilatation at the site of surgery. ConclusionCephalic-vein can be harvested at the wrist without donor site complications and our experience shows it to be a convenient and safe means of closure following CEA. Compared to prosthetics it is cheaper and less susceptible to bacterial contamination. The use of CVP preserves leg veins for future cardio-vascular interventions. Long term function of CVP appears satisfactory.

Synthetic patch angioplasty proves useful in carotid endarterectomy

Patch angioplasty is performed to prevent recurrent stenosis after carotid endarterectomy (CEA). Controversy surrounds the selection of the patch material, with supporters for both autogenous tissue and synthetic patches. We reported on the efficacy of synthetic patch angioplasty. Thirty-four carotid endarterectomies with synthetic patch angioplasty, Hemashield Finesse® and Gore-Tex®, were performed on 32 patients. Twenty-eight of the thirty-four cases were classified as elective CEA and six were emergency CEA. The clinical outcome, perioperative complications, and incidence of recurrent stenosis (> or =50%), as detected by MRA and ultrasonography, were examined. Postoperatively, one severe acute stroke patient who underwent emergency CEA died from gastrointestinal bleeding. The perioperative permanent neurologic morbidity was 0% in elective CEA, and five of the six emergency CEA patients recovered. The total permanent morbidity and mortality rate in all CEA with synthetic patch angioplasty was 2.9%. No recurrent stenosis or further stroke occurred in the postoperative long-term follow-up period. Synthetic patch angioplasty in CEA is considered useful to prevent recurrent stenosis, and to avoid vein harvest site complications and patch rupture as previously described with vein patch angioplasty. Finally, there have been no thrombotic complications using synthetic patch angioplasty in emergency CEA.