Electrocardiographic findings of Wellens syndrome due to coronary artery-pulmonary artery fistula.

A coronary artery fistula (CAF) is an abnormal connection between a coronary artery and any of the four cardiac chambers, the large vessels, or other vascular structures. Wellens syndrome is an ST-segment elevation myocardial infarction equivalent. Although both Wellens syndrome and CAFs have been reported in the literature, they have rarely been reported in the same patient. We herein report a case clinically diagnosed as Wellens syndrome by electrocardiography (ECG) findings; coronary angiography subsequently showed a fistula originating from the left anterior descending artery and draining into the pulmonary artery. The ECG findings then returned to normal after the fistula had been closed by controlled-release coils. These events confirmed that the abnormal ECG findings of Wellens syndrome were due to the CAF.

Changes in Homocysteine Levels Affect Serum Lipid Response to Atorvastatin in Patients With Acute Coronary Syndrome: A Retrospective Observational Study.

OBJECTIVE: The present study investigated whether changes in serum homocysteine (Hcy) levels modify the effects of atorvastatin treatment on blood lipid parameters in patients with acute coronary syndrome (ACS). METHODS: A total of 159 patients with ACS who received regular, long-term treatment with 20 mg/d atorvastatin were included. Depending on the changes in Hcy parameters, they were divided into Hcy reduction (HR) and Hcy elevation (HE) groups. RESULTS: After long-term atorvastatin treatment, total cholesterol (TC), triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), apolipoprotein (Apo) B, and Hcy levels were decreased (P < .05), and the ApoAI level was increased (P < .01). Correlation and stratified analysis showed that Hcy or hyperhomocysteinemia was correlated with blood lipids. In both the HE and HR groups, the TC, LDL-C, and ApoB levels after treatment were lower than those before treatment (P < .01), and the ApoAI level was increased compared with that before treatment (P < .05). There was no difference in the reduction of TC, LDL-C, and ApoB levels or in the increase of ApoAI level (P interaction > .05) between the 2 groups. However, there was a clear opposite trend of the effect of atorvastatin on TG and high-density lipoprotein cholesterol (HDL-C) levels between the HR and HE groups (P interaction < .05). In the HR group, the HDL-C level was increased (P < .05), and TGs were decreased compared with those before treatment (P < .01). Nevertheless, in the HE group, the HDL-C level was decreased (P < .05), and TGs (P < .05) were increased compared with those before treatment. CONCLUSION: The effects of atorvastatin on TGs and HDL-C depend on changes in Hcy levels. Patients with a reduced Hcy level after atorvastatin treatment had more favorable lipid parameters.

Efficacy of implantable cardioconverter defibrillator or cardiac resynchronization therapy compared with combined therapy in survival of patients with heart failure: a meta-analysis.

The aim of this meta-analysis was to compare the efficacy of implantable cardioverter defibrillators (ICDs) and cardiac resynchronization therapy (CRT) monotherapies with CRT-ICD combined therapy. Databases were searched to identify studies that compared CRT or ICD alone with CRT-ICD combined therapy in patients with heart failure. The primary outcome was rate of death for any cause, and secondary outcomes included rate of death or hospitalization due to heart failure or any cause. Nine studies with 7679 patients were included. Combined data of ICD and CRT monotherapies found that there was a higher risk of all-cause death (odds ratio [OR] 1.348, P < 0.001) and death or hospitalization from heart failure (OR 1.368, P < 0.001) with monotherapy compared with CRT-ICD combined therapy. No significant difference was observed between mono and combined therapy groups for risk of death or hospitalization from any cause (OR 1.292, P = 0.083). Compared with ICD or CRT monotherapy, CRT-ICD therapy had favorable outcomes regarding all-cause death and the risk of hospitalization or death due to heart failure.

Sonographically guided hand kneading and compression for treatment of femoral artery pseudoaneurysms.

OBJECTIVES: The purpose of this study was to evaluate the effectiveness of sonographically guided hand kneading and compression for the treatment of femoral artery pseudoaneurysms after percutaneous intervention. METHODS: Twenty-four patients who had post-percutaneous intervention femoral artery pseudoaneurysms treated with sonographically guided compression from 2001 to 2004 and 2008 to 2009 were compared with 25 patients who had postintervention pseudoaneurysms treated with sonographically guided hand kneading and compression from 2005 to 2009. RESULTS: All 25 patients (100%) treated with 1-stage sonographically guided hand kneading and compression had pseudoaneurysm occlusion; the median treatment time was 10 minutes. Twenty-two of the 24 patients (91.7%) treated with conventional sonographically guided compression had pseudoaneurysm occlusion. One-stage compression was successful in 10 patients; 9 and 3 patients had pseudoaneurysm occlusion after 2 and 3 compression treatments, respectively. Two other patients who underwent compression treatment 3 and 4 times did not have pseudoaneurysm occlusion and required surgery. The median treatment time for sonographically guided compression was 30 minutes. The treatment time was significantly shorter for the hand-kneading and compression technique (P < .001), and significantly fewer procedures were needed (P < .001). CONCLUSIONS: Sonographically guided hand kneading and compression is as effective as sonographically guided compression alone for pseudoaneurysm occlusion after femoral artery percutaneous intervention and requires significantly less time to perform.

Stent-based delivery of tissue inhibitor of metalloproteinase-3 adenovirus inhibits neointimal formation in porcine coronary arteries.

BACKGROUND: Stent-based antiproliferative therapy appears to decrease in-stent restenosis. However, alternative approaches might produce equivalent efficacy with better long-term safety. In previous work, an adenovirus capable of expressing the tissue inhibitor of metalloproteinase-3 (RAdTIMP-3) inhibited neointima formation in cell cultures and porcine saphenous vein grafts. RAdTIMP-3 decreased smooth muscle cell migration, stabilized the extracellular matrix, and uniquely promoted apoptosis. The current study developed eluting stent technology to deliver RAdTIMP-3 during stenting of pig coronary arteries. METHODS AND RESULTS: Binding of virus to and elution from stents and transduction of pig coronary arteries were confirmed using beta-galactosidase as a reporter gene in vitro and in vivo. Deployment of RAdTIMP-3-coated stents increased apoptosis and reduced neointimal cell density, but did not increase inflammation or proliferation compared with beta-galactosidase-expressing adenovirus (RAdlacZ). Neointimal area after 28 days was significantly reduced to 1.27+/-0.19 mm2 with RAdTIMP-3 versus 2.61+/-0.31 mm2 with RAdlacZ stents (P<0.001) and 2.12+/-0.20 mm2 with bare stents (P<0.005). CONCLUSIONS: Our results demonstrate for the first time to our knowledge the feasibility of adenovirus-coated stent technology and highlight the potential of TIMP-3 to produce significant inhibition of in-stent neointima formation.

[Stent-based local delivery of therapeutic adenovirus effectively reduces neointimal proliferation in porcine coronaries].

OBJECTIVE: To find an effective means for delivering therapeutic genes of Tissue inhibitor of metalloproteinase-3 (TIMP-3) to the target sites of the dilated coronary artery for the purpose of preventing restenosis of the injured artery. METHODS: A stainless steel stent coated with a high-molecular-mass polymer phosphorylocholine, after treatment with recombinant replication-defective adenovirus designated as RAD TIMP-3, was implanted into the coronary arteries of 7 pigs (therapy group). Another 7 pigs serving as the control group received implantation of uncoated stent. In both groups, coronary artery angiography was performed before withdrawal of intubation and 28 days after the implantation. For the purpose of planimetric analysis, the stented coronary arteries were isolated and fixed followed by resin embedding. Six sections were obtained for each stent for morphological assessment. RESULTS: The lumen diameter of the therapy group was 2.32+/-0.18 mm, significantly greater than that of the control group (1.79+/-0.31 mm, P=0.014). The neointimal thickness was smaller in the therapy group (0.34+/-0.17 mm vs 0.81+/-0.32 mm, P=0.0 059). CONCLUSIONS: The stent with biosynthetic coating effectively promotes TIMP3 AdV transduction and transcription, which effectively reduces neointimal proliferation, thus confirming its role in the prevention of in-stent restenosis. This maneuver may offer an alternative to conventional drug coatings for preventing restenosis.