A Case of Coronary Artery Perforation Caused by Manual Cardiopulmonary Resuscitation in the Catheterization Laboratory.

Cardiopulmonary resuscitation (CPR) is essential for the survival of cardiac arrest patients, but it can cause severe traumatic complications. In the catheterization laboratory, various physical constraints complicate the appropriate performance of CPR. However, we are not aware of reports of CPR complications in this setting. Here, we report a case of coronary artery perforation (CAP) caused by manual CPR in the catheterization laboratory. The patient, a 68-year-old woman, initially underwent successful percutaneous coronary intervention (PCI) for unstable angina. Back in the ward, the patient experienced acute stent thrombosis, which resulted in cardiac arrest, and another PCI was performed under ongoing manual CPR. Although revascularization was successful, sudden CAP occurred, leading to cardiac tamponade. Despite extensive treatment efforts, the patient died 18 hours later.Initially, the compression site of CPR was on the midline of the sternum; however, the compression site shifted to the left, to just above the left anterior descending artery, by the time that CAP was detected via angiography. This corresponded to the area where rib fractures were observed upon computed tomography, suggesting the possibility of traumatic CAP due to manual CPR. The physical constraints in the catheterization laboratory can lead to an inappropriate CPR technique and severe traumatic complications.

A method for successfully implanting an implantable cardioverter-defibrillator wrapped with an expanded polytetrafluoroethylene sheet in a patient with metal allergy.

Contact dermatitis is a severe complication of cardiac-device implantation that may be observed in patients with metal allergies. Some studies have suggested that wrapping cardiac devices with expanded polytetrafluoroethylene (ePTFE) sheets is effective in preventing contact dermatitis. Most of these studies involved pacemakers, whereas those on implantable cardioverter-defibrillators (ICDs) are rare. Herein, we report a method for the successful implantation of an ICD wrapped with an ePTFE sheet in a patient with metal allergy. The metal part of the ICD generator was tightly wrapped with an ePTFE sheet, which was sewn with ePTFE sutures approximating the edges of the generator. After the wrapping procedure, the patient entered the operating room, and the generator and an ePTFE-coated dual-coil shock lead were implanted via a standard procedure. The shock impedance in the coil-to-can vector was high immediately after the implantation, but it reduced to less than half of its initial value over a period of two weeks post-surgery. The patient did not develop any new skin problems during the 20-month follow-up. This is a method for successfully preventing contact dermatitis; however, attention to the associated high risk of infection is required. Learning objective: Wrapping an implantable cardioverter-defibrillator with an expanded polytetrafluoroethylene sheet was effective in preventing contact dermatitis after implantation. The shock impedance in the coil-to-can vector was high immediately after implantation but reduced to approximately half of its initial value with time.

Fracture of a Temporary Inferior Vena Cava Filter.

Anticoagulation is recommended for the treatment of pulmonary embolism (PE) and deep vein thrombosis (DVT). In some cases, an inferior vena cava (IVC) filter is used to prevent PE. We report the case of a 70-year-old woman who developed non-massive PE and proximal DVT, which were treated using an IVC filter; two filters were placed owing to the fracture of the filters. Few previous reports have discussed IVC fractures and the difficulty in detecting such fractures on computed tomography before retrieval. Based on our experience, we suggest that a temporary IVC filter for DVT treatment should be considered carefully.

Percutaneous Catheter Thrombus Aspiration of Right Renal Infarction Caused by Left Ventricular Thrombi due to Takotsubo Cardiomyopathy.

Takotsubo cardiomyopathy (TC) is a temporal dysfunction of the left ventricle (LV) due to psychological or physiological stress; however, it rarely causes LV thrombus. We report a case of a 49-year-old woman who developed LV thrombi due to TC despite anticoagulation therapy. The thrombi caused acute systemic infarction, with the most severe occlusion being in the right renal artery. The patient underwent percutaneous catheter aspiration thrombectomy of the right renal artery and her renal function recovered shortly after. The results of this case suggest that catheter aspiration thrombectomy is effective in the treatment of thromboembolism in TC.

IL-6 mobilizes bone marrow-derived cells to the vascular wall, resulting in neointima formation via inflammatory effects.

AIM: Among the many factors related to bone marrow cell mobilization, local inflammation induced by cytokines may drive bone marrow cells to the vascular wall, resulting in a thickened neointima. However, the relationship between inflammatory reactions and bone marrow cell invasion has not yet been fully clarified. METHODS: We inserted a large wire into the femoral artery in male balb/c(WT), interleukin (IL)-6-knockout (KO) and bone marrow-transplanted (BMT) mice that had received bone marrow cells from KO mice. Immunohistochemistry was performed to evaluate the degree of intimal hyperplasia and inflammation following vascular injury. RESULTS: Three days after the vascular injury, the number of CD34/Sca-1-positive cells in the blood was higher in the KO mice. The numbers of apoptotic cells in the neointima was lower in the KO and BMT mice at two hours after injury. The morphometric analysis performed at one and four weeks after injury showed that the intima/media ratio was significantly lower in the KO and BMT mice, while CD34-positive cells were much more frequent in the WT mice. Furthermore, re-endothelialization appeared earlier in the KO and BMT mice than in the WT mice. No differences in the levels of vascular endothelial growth factor or hepatocyte growth factor were observed in the mice sera between the WT, KO and BMT mice after injury. The in vitro culture of bone marrow cells showed more differentiated smooth muscle-like cells in the WT mice than in the KO mice. CONCLUSIONS: IL-6 is involved in neointimal formation following vascular injury, possibly acting through inflammatory effects inducing the production of bone marrow cells.

Coronary vein infusion of multipotent stromal cells from bone marrow preserves cardiac function in swine ischemic cardiomyopathy via enhanced neovascularization.

Few reports have examined the effects of adult bone marrow multipotent stromal cells (MSCs) on large animals, and no useful method has been established for MSC implantation. In this study, we investigate the effects of MSC infusion from the coronary vein in a swine model of chronic myocardial infarction (MI). MI was induced in domestic swine by placing beads in the left coronary artery. Bone marrow cells were aspirated and then cultured to isolate the MSCs. At 4 weeks after MI, MSCs labeled with dye (n=8) or vehicle (n=5) were infused retrogradely from the anterior interventricular vein without any complications. Left ventriculography (LVG) was performed just before and at 4 weeks after cell infusion. The ejection fraction (EF) assessed by LVG significantly decreased from baseline up to a follow-up at 4 weeks in the control group (P<0.05), whereas the cardiac function was preserved in the MSC group. The difference in the EF between baseline and follow-up was significantly greater in the MSC group than in the control group (P<0.05). The MSC administration significantly promoted neovascularization in the border areas compared with the controls (P<0.0005), though it had no affect on cardiac fibrosis. A few MSCs expressed von Willebrand factor in a differentiation assay, but none of them expressed troponin T. In quantitative gene expression analysis, basic fibroblast growth factor and vascular endothelial growth factor (VEGF) levels were significantly higher in the MSC-treated hearts than in the controls (P<0.05, respectively). Immunohistochemical staining revealed VEGF production in the engrafted MSCs. In vitro experiment demonstrated that MSCs significantly stimulated endothelial capillary network formation compared with the VEGF protein (P<0.0001). MSC infusion via the coronary vein prevented the progression of cardiac dysfunction in chronic MI. This favorable effect appeared to derive not from cell differentiation, but from enhanced neovascularization by angiogenic factors secreted from the MSCs.

Impact of implanted bone marrow progenitor cell composition on limb salvage after cell implantation in patients with critical limb ischemia.

OBJECTIVE: The aim of this study is to identify which factors influence limb salvage after bone marrow mononuclear cell implantation (BMI) in patients with chronic critical limb ischemia (CLI). METHODS: Thirteen no-option CLI patients treated with BMI were enrolled in the present study. Limb ischemia was assessed using the ankle-brachial index (ABI), transcutaneous oxygen tension (TcO(2)), and rest pain score. The cell populations among the implanted cells were determined by May-Giemsa staining and flow cytometry. RESULTS: Major lower extremity amputations after BMI were performed in seven patients. Before implantation, there were no significant differences between the amputation group (n=7) and the salvage group (n=6) in clinical characteristics, the ABI, the TcO(2) level, or the rest pain score. After implantation, there were no differences between the groups in the serum levels of angiogenic or inflammatory cytokines. The number of implanted BM cells was the same in the two groups, but the cells implanted in the limb salvage group were composed of significantly higher numbers of hematopoietic progenitors (erythroblasts and myeloblasts) and lymphocytes (p<0.05, respectively). The number of CD34-positive cells was somewhat greater in the salvage group than in the amputation group (p=0.09) and was positively associated with the number of erythroblasts (r(2)=0.29, p=0.06) and the number of myeloblasts (r(2)=0.59, p<0.01). CONCLUSIONS: The cellular composition of the BM cells injected may affect limb salvage after the implantation in patients with severe CLI. The favorable effects of BMI appear to reflect the impact of the progenitor cell doses.

High-dose granulocyte-colony stimulating factor promotes neointimal hyperplasia in the early phase and inhibits neointimal hyperplasia in the late phase after vascular injury.

BACKGROUND: Granulocyte-colony stimulating factor (G-CSF) affects injured arteries through early endothelialization. Some reports, however, have cautioned that the restenosis rate may increase after G-CSF injection. In the present study, high-dose G-CSF was administered to mice with vascular injury to clarify its effect. METHODS AND RESULTS: Mice were received daily subcutaneous injections of saline or a high dose (300 microg/kg) of G-CSF for 5 days after vascular injury. In the FACS analysis, CD34-/Sca-1-positive progenitor cells were more abundant in the G-CSF group (p<0.05). Neointimal hyperplasia was more evident in the G-CSF group at 1 week (p<0.05), whereas at 4 weeks it was more evident in the control group (p<0.01). TUNEL-positive cells in the arterial wall were more numerous in the G-CSF group at day 1 (p<0.01). CD34-positive cells were observed in the G-CSF group at 1 week. Re-endothelialization appeared earlier in the G-CSF group (at 4 weeks; p<0.01). An increased number of 1A4-positive smooth muscle cells were found in bone marrow cell culture treated with G-CSF. CONCLUSION: High-dose G-CSF induced neointimal proliferation through excessive inflammation and bone marrow cell mobilization in the early phase. In the late phase, however, it induced early re-endothelialization and thereby inhibited neointimal hyperplasia.

G-CSF after myocardial infarction accelerates angiogenesis and reduces fibrosis in swine.

OBJECTIVE: Recent studies have suggested that granulocyte colony-stimulating factor (G-CSF) may improve cardiac function after acute myocardial infarction (AMI) by accelerating angiogenesis or cardiomyogenesis, but negative results and side effect of G-CSF have also been reported. However, no previous studies have used large animal models of ischemia/reperfusion to investigate the effect and side effect of G-CSF after AMI. METHODS: The diagonal branch of the left anterior descending coronary artery of swine was balloon-occluded for 1 h and then reperfused. The animals of the G-CSF group were injected with G-CSF subcutaneously (5.0 microg/kg/day) for 6 days after MI and then sacrificed after 4 weeks. The control group received the same volume of saline. RESULTS: There were no differences between the groups in the rate of thrombotic obstruction or progression of stenosis lesion in coronary angiography. The ejection fraction and end-diastolic volume in the G-CSF group were not significantly improved over the control values. The fibrotic area was significantly smaller in the G-CSF group than in the controls (P<0.05), and the numbers of vessels counted in anti-von Willebrand factor and anti-alpha-smooth muscle actin-stained sections were significantly larger (P<0.005 and P<0.05, respectively). The expression of collagen III mRNA was significantly lower in the G-CSF group than in the control in the infarct (P<0.0005) and border areas (P<0.005), and TGF-beta mRNA was significantly lower in the G-CSF group in the border area (P<0.05). CONCLUSIONS: G-CSF could modify the healing process after AMI by accelerating angiogenesis in a swine ischemia/reperfusion model. At the dose administered, however, G-CSF did not seem to improve the global cardiac function.

Bone marrow cells contribute to neointimal formation after stent implantation in swine.

BACKGROUND: Recent studies suggest that neointimal cells in atherosclerotic lesions are partly derived from bone marrow (BM) cells. However, studies with large animal models have not yet clarified how BM cells contribute to neointimal formation in restenotic lesions. We examined the expression of CD34, a hematopoietic stem cell marker, in the neointima after coronary stent implantation in porcine. METHODS: Pigs underwent balloon injury in the coronary arteries followed by stent implantation. The arteries were harvested at 3, 7, and 28 days after the stenting. The samples were used for immunohistochemistry for CD34, smooth muscle embryo (SMemb), alpha-smooth muscle cell actin (alpha-SMA), macrophage, c-kit, and AC133 antibodies. In morphometric analysis, each layer of vascular wall was calculated in the sections. RESULTS: At 3 days, the expressions of CD34 and SMemb were minimal, and many macrophages were seen around the stent struts. At 7 days, co-expression of CD34 and SMemb was observed around the struts, and 11.5% of the neointimal cells were stained by CD34. In addition, c-kit positive cells and AC133 positive cells are detected in neointimal area. At 28 days, the neointima had thickened and expressed alpha-SMA rather than SMemb, and a few CD34-positive cells were detected. In morphometric analysis, luminal area/total vascular area was significantly smaller and intimal area/total vascular area was significantly bigger in 7 and 28 days than in the day of implantation. CONCLUSION: BM cells of possibly hematopoietic origin partially contributed to neointimal formation after coronary stent implantation in a large animal model.

Inhibitory effect of candesartan cilexetil on left ventricular remodeling after myocardial infarction.

Although angiotensin-converting enzyme inhibitors (ACEIs) have been shown to reduce left ventricular remodeling after acute myocardial infarction (AMI), the effects of angiotensin receptor blockers have yet to be established. This study was conducted to examine the effects of candesartan on left ventricular remodeling after AMI. Consecutive AMI patients were assigned to a candesartan group or ACEI group after successful coronary intervention. The patients in the candesartan group (n = 77, mean age, 62.8 +/- 1.3) received candesartan and the patients in the ACEI group (n = 80, mean age, 63.3 +/- 1.2) received lisinopril, enalapril, or trandolapril. Four mg was the most frequent dose in the candesartan group at 6 months. Lisinopril, enalapril, and trandolapril were administered to 52%, 27%, and 21% of the patients in the ACEI group, respectively. No significant differences in the incidences of cardiac death, nonfatal MI, or hospitalization for heart failure (P = NS) were found between the groups. The candesartan group exhibited a somewhat higher percent increase in left ventricular ejection fraction and significantly lower percent increases in left ventricular end-diastolic volume index and left ventricular end-systolic volume index compared to the ACEI group (P < 0.05, P < 0.05, respectively). Candesartan is more effective than ACEI in preventing left ventricular remodeling after AMI.

Tumor-necrosis-factor-alpha-gene-deficient mice have improved cardiac function through reduction of intercellular adhesion molecule-1 in myocardial infarction.

BACKGROUND: Tumor necrosis factor (TNF)-alpha is linked to the pathogenesis of cardiovascular diseases, but how it affects myocardial infarction (MI), so the present study examined the effects of TNF-alpha and the involvement of intercellular adhesion molecule (ICAM)-1 on MI. METHODS AND RESULTS: Left coronary arteries of C57BL/6 wild type (WT) and TNF-alpha knockout (KO) mice were ligated and the mice were killed 1, 3, and 7 days later. Fractional shortening on echocardiography of the KO mice was significantly higher than that of the WT mice from day 1 to 7 (p<0.01). The ICAM-1 mRNA in the infarcted area of the KO mice was significantly lower than that of the WT from day 1 (p<0.01) to 7. In immunohistochemistry, the expression of ICAM-1 was weaker in the KO than in the WT mice. The number of neutrophils in the KO mice peaked at day 1, but even this peak level failed to reach the levels in the infarcted (p<0.01) and peri-infarcted areas (p<0.05) in the WT. The number of macrophages in the KO mice peaked at day 7, but this peak level failed to reach the levels in the infarcted (p<0.01) and peri-infarcted areas (p<0.05) in the WT. CONCLUSION: In a permanent occlusion model of MI TNF-alpha decreased cardiac function and ameliorated myocardial remodeling through the induction of ICAM-1.