Nailed It: Conservative Management of Penetrating Injury and Potential Infection of a Cardiovascular Implantable Electronic Device.

A 47-year-old man with a history of ischemic cardiomyopathy and chronic systolic heart failure presented after he inadvertently shot himself in the left upper chest with a pneumatic nail gun, penetrating his implantable cardioverter defibrillator (ICD) generator. The device was noninterrogable, consistent with device failure. A new ICD was attached to the existing right ventricular lead, which showed no evidence of traumatic damage and normal lead parameters on interrogation. Aggressive debridement and antibiotic irrigation of the ICD pocket was performed and an antibacterial envelope was used. Bacterial culture of the ICD pocket grew Bacillus species. The patient completed a course of at least 14 days of oral clindamycin. At follow-up, there were no signs or symptoms of systemic or local wound infection.

A completely fractured zotarolimus-eluting stent in an aortocoronary saphenous vein bypass graft.

Drug-eluting stents (DES) have significantly improved the rate of target vessel revascularization in comparison with bare metal stents. DES fracture was not reported in multicenter randomized clinical trials, but several case reports of DES fracture have been published, mostly with sirolimus-eluting stents. DES fracture is associated with stent restenosis and thrombosis. We report a zotarolimus-eluting stent fracture in an aortocoronary saphenous vein graft (SVG) bypass. The patient presented with chest pain and a non-ST-elevation myocardial infarction. He underwent cardiac catheterization that showed a complete fracture of a zotarolimus-eluting stent in the ostium of a sequential SVG to the diagonal and obtuse coronary arteries. His management included coronary angioplasty and retrieval of the proximal fractured segment. We discuss the potential causes for this stent fracture and suggest caution when using a DES in an ostial location of a SVG bypass, especially in a highly mobile vessel.

A perioperative management algorithm for cardiac rhythm management devices: the PACED-OP protocol.

BACKGROUND: Limited data are available regarding the perioperative management of cardiac rhythm management devices (CRMDs) exposed to intraoperative electromagnetic interference. We postulated that implementation of a simple, standardized approach to CRMD management using our own institution's Pacing And Cardioverting Electronic Devices peri-Operative Protocol (the PACED-OP protocol) would be associated with a reduction in the amount of device reprogramming without an increase in CRMD-related complications. METHODS: Records of patients with CRMDs undergoing 497 consecutive surgical procedures were analyzed retrospectively. Roughly half (51%, n = 254) of these procedures occurred before implementation of the PACED-OP protocol, when patients were generally treated according to the American Society of Anesthesiologists' 2005 guidelines. These cases were compared to the remaining surgeries that occurred after implementation of the PACED-OP protocol. Records were screened for evidence of intraoperative CRMD malfunction that was directly associated with the use of electrocautery. Postoperative complications that could be indirectly or possibly linked to electrocautery-mediated CRMD malfunction were also identified. RESULTS: Implementation of the PACED-OP protocol was associated with a significant reduction in the odds of device reprogramming (adjusted odds ratio [aOR] 0.19, P < 0.001). There was no direct evidence of CRMD malfunction in either cohort. The rate of postoperative complications that could be indirectly or possibly linked with electrocautery-mediated CRMD damage did not differ significantly between cohorts (aOR = 1.37, 95% confidence interval 0.56-3.3, P = 0.49). CONCLUSION: The PACED-OP protocol implementation was associated with a significant reduction in the odds of device reprogramming without a significant difference in the odds of CRMD-related complications.

A comparison of VerifyNowR with PlateletMappingR--detected aspirin resistance and correlation with urinary thromboxane.

BACKGROUND: Aspirin-resistant platelet activation in whole blood is attributable to a transcellular pathway not detected by isolated platelet aggregometry. Aspirin resistance as defined by urinary thromboxane levels is associated with increased risk for myocardial infarction or cardiac death. Whole blood point-of-care assays may also detect aspirin resistance. METHODS: We compared PlateletMapping® with VerifyNow® for detecting aspirin resistance in 200 patients undergoing invasive cardiac procedures. This included 10 patients not receiving aspirin therapy for comparison. The assay results were correlated with urinary 11-dehydro-thromboxane B2 collected 2 to 8 hours after the procedure. RESULTS: PlateletMapping detected aspirin resistance in 32% of patients. VerifyNow detected aspirin resistance in 6% of patients. A patient's compliance with aspirin therapy was confirmed by a <20% aggregation response to arachidonic acid by light transmission aggregometry. Aspirin-resistant patients as determined by PlateletMapping had significantly (P<0.001) higher urinary 11-dehydro-thromboxane B2 levels than aspirin-sensitive patients but significantly (P=0.001) lower levels than patients not receiving aspirin therapy. There was no significant difference in urinary 11-dehydro-thromboxane B2 for aspirin-resistant compared with aspirin-sensitive patients as determined by VerifyNow, but the confidence intervals were wide. There was no significant correlation of resistance as defined by PlateletMapping with aspirin dose. However, there was significant increased aspirin sensitivity with clopidogrel (0.0006) or statin (0.004) cotherapies. There also was a significant correlation of smoking with aspirin resistance. CONCLUSIONS: These results indicate that PlateletMapping could be a useful point-of-care assay to identify aspirin-resistant patients for better perioperative risk stratification and management.

Aorto-right atrial fistula following transseptal catheterization and catheter ablation for atrial fibrillation.

Aorto-cameral fistula, either congenital or acquired, is an abnormal connection between the ascending aortic root and one of the cardiac chambers. We report a case of a 61-year-old male with history of atrial fibrillation and 2 radiofrequency ablation procedures, referred to us for surgical Cox Maze procedure. Preoperative cardiac computerized tomography revealed a fistulous connection between the aortic root and the right atrium. Later, the patient underwent successful surgical closure of the fistula during the Cox Maze procedure. In this paper, we also discuss the clinical presentation, natural history, anatomy of the interatrial septum, and management of aorto-cameral fistula.

Measurement of patients' bivalirudin plasma levels by a thrombelastograph ecarin clotting time assay: a comparison to a standard activated clotting time.

Standard activated clotting time (ACT) tests have a poor correlation to bivalirudin levels, leading to uncertainty regarding adequate anticoagulation in percutaneous coronary intervention patients. We tested a Thrombelastograph (TEG) ecarin clotting time (ECT) assay for sensitivity to bivalirudin using blood from 80 patients undergoing interventional cardiology procedures with bivalirudin anticoagulation. This was compared to a standard Hemochron ACT assay using diatomaceous earth. With the TEG assay, the direct thrombin activator, ecarin, was used to initiate coagulation and measured as the reaction time. Plasma samples were evaluated for bivalirudin by a chromogenic assay at an independent hematological laboratory. Linear regression of the standard ACT versus bivalirudin level gave an r = 0.306 whereas the TEG ECT gave a much higher r2 = 0.746 (both P < 0.0001). The TEG ECT should prove more useful than the standard ACT for monitoring bivalirudin anticoagulation across the clinically therapeutic range.

Frequency of nonresponse antiplatelet activity of clopidogrel during pretreatment for cardiac catheterization.

Platelet function was evaluated before and after clopidogrel therapy in 50 cardiology candidates scheduled for intervention; results were averaged from optical platelet aggregation with 2 significantly correlated point-of-care instruments, Thrombelastograph and Ichor PlateletWorks. Although this was a limited study with few complications, the failure of clopidogrel therapy (30% nonresponders with <10% average platelet inhibition) was not correlated with clinical pretreatment variables, including atorvastatin therapy, postintervention bleeding complications, or major adverse coronary events.

Rectus sheath hematoma with low molecular weight heparin administration: a case series.

BACKGROUND: Rectus sheath hematoma is an uncommon but potentially serious bleeding complication that can occur spontaneously or as a result of anticoagulation administration. CASE PRESENTATION: Case number one: A 62 year old chronically ill Caucasian female develops a rectus sheath hematoma seven days after hospital discharge. The previous hospitalization included low molecular weight heparin administration for deep vein thrombosis prophylaxis. The patient ultimately chooses comfort care and expires due to sepsis and respiratory failure. Case number two: A 79 year old Caucasian male develops a rectus sheath hematoma during hospital admission where LMWH is used for deep vein thrombosis prophylaxis. He is managed conservatively; however, his hematocrit drops from 46 to 25.8%. Case number three: A 44 year old chronically ill Caucasian female is treated with therapeutic low molecular weight heparin for recent deep vein thrombosis during a hospital admission. She develops a large rectus sheath hematoma requiring embolization as well as blood transfusion. CONCLUSION: We believe this reflects an underreported significant cause of morbidity and mortality with low molecular weight heparin administration. We review the pathophysiology of rectus sheath hematoma as well as its presentation, diagnosis, and treatment. We identify at-risk populations and proposed contributing factors. We also discuss factors leading to underreporting as well as preventive strategies implemented at our institution.

Giant coronary artery aneurysms: review and update.

Giant coronary artery aneurysms are rare, with a reported prevalence of 0.02% to 0.2%. Causative factors include atherosclerosis, Takayasu arteritis, congenital disorders, Kawasaki disease, and percutaneous coronary intervention. Most giant coronary artery aneurysms are asymptomatic, but some patients present with angina pectoris, sudden death, fistula formation, pericardial tamponade, compression of surrounding structures, or congestive heart failure. Clinical sequelae include thrombus formation, embolization, fistula formation, and rupture. Surgical correction is generally accepted as the preferred treatment for giant coronary artery aneurysms. We present an illustrative case of a giant 70 × 40-mm coronary artery aneurysm in a 56-year-old man who declined surgery and died one month later. In addition, we provide a review of the medical literature on giant coronary artery aneurysms.

Cor triatriatum sinister in a 43-year-old man with syncope.

Cor triatriatum sinister, a congenital cardiac anomaly involving a fibromuscular membrane that partitions the left atrium into 2 chambers, has been reported in only 0.1% to 0.4% of patients with congenital heart disease. The posterosuperior chamber receives blood from the pulmonary veins, and the anteroinferior chamber contains the left atrial appendage and mitral valve orifice. Most patients are diagnosed with the condition in infancy or childhood; adult cases are rare. We describe a case of cor triatriatum sinister in a 43-year-old man whose only presenting symptom was recurrent syncope. He underwent corrective resection of the membrane and was asymptomatic thereafter. In addition to discussing the patient's case, we review the relevant medical literature.

Use of a novel access technology for femoral artery catheterization: results of the RECITAL trial.

OBJECTIVE: To present results of a registry of a novel vascular access device. BACKGROUND: Arterial access has been largely unchanged for 60 years. The Arstasis device creates a novel shallow-angle arterial access designed to facilitate hemostasis without use of a vascular closure device (VCD) or implantation of a foreign body for closure. This is the first publication to report the outcomes of Arstasis access. METHODS: Patients (n = 346) underwent routine diagnostic cardiac catheterization (Dx) at 8 sites in the United States. Patients were assessed for device success, time to hemostasis (TTH), early sit up, time to ambulation (TTA), time-to-discharge-eligibility (TTDe) as well as safety; 249 patients had Dx only, 97 crossed over to PCI. RESULTS: Device deployment was successful in 97%; the other 3% converted to routine access. Mean TTH and TTA for Dx were 4.0 ± 2.5 minutes and 1.5 ± 1.2 hours, respectively; for PCI it was 6.9 ± 5.1 minutes and 3.2 ± 3.3 hours. A subset of 245 patients (72.9%) sat up within 30 minutes after hemostasis; early sit-up was successful in all but 1 (99.6%). TTDe for Dx was 2.7 ± 1.6 hours. There were no major access-site related complications; minor complications were primarily subclinical hematomas in 1.2%. CONCLUSIONS: Arstasis access is associated with short TTH and TTA, early sit up after sheath pull, and accelerated TTDe, achieved without use of VCDs or implantation of a foreign body, with high success and minimal complication rates.

Matrix of regularity for improving the quality of ECGs.

The 12-lead electrocardiography (ECG) is the gold standard for diagnosis of abnormalities of the heart. However, the ECG is susceptible to artifacts, which may lead to wrong diagnosis and thus mistreatment. It is a clinical challenge of great significance differentiating ECG artifacts from patterns of diseases. We propose a computational framework, called the matrix of regularity, to evaluate the quality of ECGs. The matrix of regularity is a novel mechanism to fuse results from multiple tests of signal quality. Moreover, this method can produce a continuous grade, which can more accurately represent the quality of an ECG. When tested on a dataset from the Computing in Cardiology/PhysioNet Challenge 2011, the algorithm achieves up to 95% accuracy. The area under the receiver operating characteristic curve is 0.97. The developed framework and computer program have the potential to improve the quality of ECGs collected using conventional and portable devices.

Lipid-lowering efficacy of red yeast rice in a population intolerant to statins.

Chinese red yeast rice is a dietary supplement containing monacolins, unsaturated fatty acids, and phytosterols capable of lowering low-density lipoprotein (LDL) cholesterol. Few studies have reported on its use in clinical practice or in statin-intolerant patients. We reviewed approximately 1,400 clinical charts and identified 25 patients treated with red yeast rice for > or =4 weeks. The patients were included if they had pre- and post-treatment lipid levels without simultaneous changes in other lipid-lowering medications. These patients had experienced myalgias (68%), gastrointestinal intolerance (16%), and/or elevated alanine aminotransferase levels (8%) with previous use of other lipid-lowering agents. The total cholesterol decreased 15% (-37 +/- 26 mg/dl, p <0.001) and LDL cholesterol decreased 21% (-35 +/- 25 mg/dl, p <0.001) during 74 +/- 39 days of treatment. Most (92%) patients tolerated the treatment, and many (56%) achieved their LDL cholesterol goal. In patients unable to tolerate daily statin use, the total cholesterol level decreased 13% (-33 +/- 10 mg/dl, p <0.001) and LDL cholesterol decreased 19% (-31 +/- 4 mg/dl, p <0.001). In conclusion, red yeast rice modestly decreased total and LDL cholesterol, was well-tolerated, and was an acceptable alternative in patients intolerant of other lipid-lowering medications.

Post interventional cardiology urinary thromboxane correlates with PlateletMapping detected aspirin resistance.

INTRODUCTION: We have previously defined aspirin resistance detected by TEG PlateletMapping using arachidonic acid (AA). This aspirin resistance is observed as platelet activation (>20%) by AA in whole blood, even though the isolated platelets are inhibited by aspirin. This platelet activation in whole blood is due to a transcellular pathway mediated by platelets and leukocytes. METHODS: To determine if this PlateletMapping assay of aspirin resistance on pre-procedure blood samples correlated with an in vivo response we assayed the first voided urine samples collected 2-8 hours post interventional cardiology procedures for 11-dehydro thromboxane B2. RESULTS AND CONCLUSIONS: We detected 27 aspirin resistant patients out of a total of 81 (33%), in agreement with our previous study. All of these patients were on aspirin therapy, confirmed by a <20% aggregation response to AA by light transmission platelet aggregometry using isolated platelet rich plasma. Aspirin resistant patients urine samples (14 out of a total of 60 patients analyzed) contained significantly (P=0.008) higher 11-dehydro thromboxane B2 levels than the other 46 aspirin sensitive patients urine samples. Since our previous study implicated 12- and 15-lipoxygenases in this pathway, we also assayed for polymorphisms to determine any correlation with aspirin resistance. A correlation was found in a polymorphism affecting the lipoxygenase domain of platelet 12-lipoxygenase. This result indicates that aspirin resistance detected in whole blood by the TEG PlateletMapping assay correlates with a physiological consequence in terms of thromboxane formation. This is the first report of such a correlation.

Influence of channel blockers on cardiac alternans.

Sudden cardiac arrest (SCA) due to fatal cardiac arrhythmias such as ventricular fibrillation is the leading cause of death in the United States, killing 350,000 Americans each year. Thus, it is of great importance to investigate the mechanisms that can suppress abnormal heart rhythms. In this work, we study the effects of drugs such as channel blockers through mathematical modeling of cardiac electrophysiological phenomena. In particular, we carry out multi-level simulations to study how channel blockers affect arrhythmias at cellular, fiber, and tissue levels. Numerical simulations show that the drugs have different effects at different scales (cellular versus fiber or tissue). Moreover, the drugs may appear to be arrhythmic in one model but antiarrhythmic in another. These observations indicate that analysis and simulation based on multiple scales and multiple models are crucial to fully understand the properties of drugs in treating arrhythmias.

A novel modification of the Thrombelastograph assay, isolating platelet function, correlates with optical platelet aggregation.

Flow cytometry, singlet platelet counting, and optical aggregation have been used to monitor clopidogrel and glycoprotein IIb/IIIa (GPIIb/IIIa) platelet antagonists. Optical aggregation is considered the gold standard, but neither it nor flow cytometry is convenient in larger-scale clinical studies or point-of-care systems. Singlet platelet counting, a point-of-care assay correlated with optical platelet aggregation, only provides a measurement of platelet function at a single point in time. The Thrombelastograph is used to assay whole blood for thrombin-generated maximal clot-shear elasticity, referred to as the maximal amplitude (MA). Although platelet dysfunction, thrombocytopenia, and the in vitro effect of strong inhibitors such as IIb/IIIa antagonists can be observed, with thrombin generation milder platelet inhibitors cannot be assessed. We modified the Thromboelastograph assay, using reptilase and factor XIIIa, to form a clot, without thrombin generation, in heparinized whole blood. The resulting clot MA is dependent on added platelet agonists such as ADP or arachidonic acid, is sensitive to platelet antagonists, and provides a continuous measure of platelet function more analogous and better correlated with optical aggregation. This novel modification of the Thromboelastograph assay should prove to be a useful point-of-care whole-blood assay with which to monitor the effects of GPIIb/IIIa, ADP, and thromboxane A(2)-receptor-inhibiting drugs in patients.