Automatic Defibrillator Implantation Research Articles

Short QT syndrome in pediatrics.

Short QT syndrome is a malignant cardiac disease characterized by the presence of ventricular tachyarrhythmias leading to syncope and sudden cardiac death. Currently, international guidelines establish diagnostic criteria when QTc is below 340ms. This entity is one of the main diseases responsible for sudden cardiac death in the pediatric population. In recent years, clinical, genetic and molecular advances in pathophysiological mechanisms related to short QT syndrome have improved diagnosis, risk stratification, and preventive measures. Despite these advances, automatic implantable cardiac defibrillator remains the most effective measure. Currently, six genes have been associated with short QT syndrome, which account for nearly 60% of clinically diagnosed families. Here, we review the main clinical hallmarks of the disease, focusing on the pediatric population.

Soluble ST2 and Risk of Arrhythmias, Heart Failure, or Death in Patients with Mildly Symptomatic Heart Failure: Results from MADIT-CRT.

Soluble ST2 is an established biomarker of heart failure (HF) progression. Data about its prognostic implications in patients with mildly symptomatic HF eligible to receive cardiac resynchronization therapy defibrillators (CRT-D) are limited. In a cohort of 684 patients enrolled in Multicenter Automated Defibrillator Implantation Trial (MADIT)-CRT, levels of soluble ST2 (sST2) were serially assessed at baseline and 1year (n = 410). In multivariable-adjusted models, elevated baseline sST2 was associated with an increased risk of death, death or HF, and death or ventricular arrhythmia (VA) even when adjusting for baseline brain natriuretic protein (BNP) levels. In addition, patients with lower baseline sST2 levels had greater risk reduction with CRT-D (p = 0.006). Serial assessment revealed increased risk of VA and death or VA (HR per 10% increase in sST2 1.11 (1.04-1.20), p = 0.004). Among patients with mildly symptomatic HF and eligibility for CRT-D, baseline and serial assessments sST2 may provide important information for risk stratification.

Diagnostic Accuracy of 18F-FDG PET/CT in Infective Endocarditis and Implantable Cardiac Electronic Device Infection: A Cross-Sectional Study.

A prospective study with 80 consecutive patients with suspected IE and ICED infection (65 men and 15 women with a mean age of 68 ± 13 y) between June 2013 and May 2015 was performed in our hospital. The inclusion criteria were clinically suspected IE and ICED infection at the following locations: native valve (NV) (n = 21), PV (n = 29), or ICED (n = 30) (automatic implantable defibrillator [n = 11] or pacemaker [n = 19]). Whole-body 18F-FDG PET/CT with a myocardial uptake suppression protocol with unfractionated heparin was performed in all patients. The final diagnosis of infection was established by the IE Study Group according to the clinical, echocardiographic, and microbiologic findings. A final diagnosis of infection was confirmed in 31 patients: NV (n = 6), PV (n = 12), and ICED (n = 13). Sensitivity, specificity, positive predictive value, and negative predictive value for 18F-FDG PET/CT were 82%, 96%, 94%, and 87%, respectively. 18F-FDG PET/CT was false-negative in all cases with infected NV. 18F-FDG PET/CT was able to reclassify 63 of 70 (90%) patients initially classified as possible IE by modified Duke criteria. In 18 of 70 cases, 18F-FDG PET/CT changed possible to definite IE (26%) and in 45 of 70 cases changed possible to rejected IE (64%). Additionally, 18F-FDG PET/CT identified 8 cases of septic embolism and 3 of colorectal cancer in patients with a final diagnosis of IE. 18F-FDG PET/CT proved to be a useful diagnostic tool in suspected IE and ICED infection and should be included in the diagnostic algorithm for early diagnosis. 18F-FDG PET/CT is not useful in the diagnosis of IE in NV but should be also considered in the initial assessment of this complex scenario to rule out extracardiac complications and possible neoplasms.

Abstract 19946: Airports: Out-of-hospital Chain of Survival Laboratory?

Introduction: Airports are experimentation locations in which automatic external defibrillators (AED) implementation efficacy (and efficiency) has been widely tested. Hypothesis: With a large number of passengers and a fine meshing in terms of AED availability, the aim of this study is to understand the airport cardiac arrests (ACA) in terms of care and to study their survival in such a particular location. Methods: Prospective descriptive and multicentre study based on the French national cardiac arrest registry (RéAC) data gathered between the 01/07/2011 and the 01/11/2014. Results: We analysed 78 ACA among 35667 cardiac arrests. We recorded 83.3% men. The population’s median age was 63 [52-70]. A medical aetiology was recorded in 93.6% cases and 30% had history of cardiovascular diseases. Professional first aid providers’ (generally firemen) median response time was 5 [1-10] min and mobile medical teams’ (MMT) 20 [12-30] min. Three quarter of patients were immediately cared by witnesses of which 53.8% benefited of an AED connexion ; 23.1% of them received a shock. A cardiopulmonary resuscitation (CPR) was attempted by firemen in 84.6% cases. At MMT arrival, 13.3% had a shockable rhythm and 26.7% had already sustained a return of spontaneous circulation. MMT attempted CPR in 87.2% cases and 37.2% sustained a return of spontaneous circulation (ROSC). At hospital admission, 34.6% were alive. At Day 30, 14.1% survived of which 81.9% had a good neurological outcome (CPC1-2). Among them 27.3% had a implantation of automatic defibrillator. Cardiac aetiology was proved in 28% cases and almost half of patients returned directly at home after their hospitalization. Conclusions: ACA victims are often cared very promptly by bystanders, professional first aid providers and medical teams. They also more often benefit of AED connexion and shock than cardiac arrest victims in the general population. Airports are indeed a location in which all the steps of the chain of survival are thoroughly and effectively implemented. As all these steps are patients’ survival key factors, this results in better outcome.

Mort subite et angor spastique : quelle stratégie diagnostique et thérapeutique ?

The prevalence of vasospastic angina is said to be low in Europe, but maybe because of a lack of diagnosis in the daily practice. However, coronary spasm is a common cause of cardiac arrest, especially among patients free of cardiac illness, and it should be systematically investigated after an unexplained cardiac arrest. Intracoronary spasm provocation test exposes patients to a lower risk compared to the risk of spontaneous spastic angina. Accurate modalities and diagnostic criteria have to be clarified for European population. Avoiding external causes of coronary spasm (such as cigarette smoking or more generally consuming coronary spasm inducing drugs) and prescribing antispastic medicine (first of all calcium channel blockers) are the basis of vasospastic angina treatment. However, recurrent coronary spasms have been reported despite an appropriate treatment and implantable automatic defibrillator has been implanted after case discussion when the onset of illness was cardiac arrest. We report the case of a patient recovering from cardiac arrest who had a positive spasm coronary provocation test, and was treated with calcium channel blockers and had been an automatic defibrillator implanted, with a coronary spasm provocation test performed afterward still contentious. While discussing this case, we are making a literature review of the diagnosis and treatment of spastic angina revealed by cardiac arrest.

G.P.146: Cardiac manifestations and gastro-intestinal sequelae in children with LMNA-CMD

Congenital muscular dystrophy secondary to variants in the lamin A/C gene (LMNA-CMD) typically present with hypotonia at birth, poor axial and truncal control, progressive joint contractures (sparing the elbow) and spinal rigidity. Patients with the congenital onset form can be divided into 2 severity classes: early severe (no ambulation and need for ventilator support in early childhood) and a later onset (brief period of ambulation, ventilator support in late childhood to early teenage years). We present 3 children with LMNA-CMD; all developed cardiac sequelae, diarrhea, and generalized edema. First manifestations of cardiac disease was asymptomatic atrial dysrhythmia. Cardiac disease progressed in early teenage years, in spite of appropriate rate control medication with the onset of cardiomyopathy and ventricular tachycardia. Automatic implantable cardiac defibrillators were recommended, though optimal timing of placement remains unclear. Gastro-intestinal (GI) symptoms, including diarrhea and abdominal distention may herald the onset of worsening cardiac function prior to the onset of overt cardiomyopathy. The etiology of gastrointestinal symptoms is likely multifactorial, including protein loss and gut hypo-perfusion. GI symptoms may respond to steroid therapy and a high protein diet, in spite of a negative work up for protein losing enteropathy.

Electrocardiograma de superficie en pacientes con dispositivos de estimulación cardíaca

Over the last decades, the number of patients with cardiac stimulation devices (including pacemakers, resynchronization devices and automatic implantable cardiac defibrillators) has increased exponentially, exposing an ever increasing number of health professionals from different areas of medicine to their electrocardiograms. Thorough knowledge of proper device function is crucial to understanding electrocardiographic changes induced by cardiac stimulation, identifying normal findings, and recognizing the different manifestations of device malfunction. In this article, basic concepts on device design, programming and proper function will be discussed, allowing the reader to develop an organized step wise approach to interpret the electrocardiogram of patients with cardiac stimulation devices.

Broken Hearts: The Tangled History of Cardiac Care by David S. Jones (review)

Reviewed by: Broken Hearts: The Tangled History of Cardiac Care by David S. Jones Allen B. Weisse David S. Jones. Broken Hearts: The Tangled History of Cardiac Care. Baltimore: Johns Hopkins University Press, 2013. xiv + 319 pp. $34.95 (978-1-4214-0801-9). Much of the history of cardiology as a discipline and, certainly, cardiac surgery can be encompassed by the twentieth century. Indeed, many of the principal actors in this medical saga were still alive until just a few years ago. The main events have been captured in historical works, mainly by cardiologists and cardiac surgeons. These have been supplemented by recorded interviews with major figures and often revealing memoirs. Given the magnitude of the progress made in the field, it is not surprising that some hagiographic elements have crept into some of these accounts. In Broken Hearts: The Tangled History of Cardiac Care, David S. Jones, a historian with a background in psychiatry, offers a different approach, with an expressed goal of “bringing social science perspectives to the problems of disease and therapeutics” (p. 17). He confines the scope of this work to the history of coronary heart disease and mainly the surgical approaches to its treatment. The book is divided into two essentially equal parts. In the first, Jones traces the pathological history of the essential lesions within the coronary vascular tree. Although he has omitted a few significant nineteenth-century European publications on the subject, once the primarily Anglo-American period of the twentieth century is reached, Jones demonstrates a prodigious effort in tracing the progression in our knowledge of the atherosclerotic process, finally culminating in our understanding of the vulnerable plaque, with its disruption leading to coronary thrombosis and myocardial infarction. Anyone interested in exploring this part of medical history would do well to consult his extensive bibliography. There are a few factual errors. In 1929, when Werner Forssmann performed the first human heart catheterization—on himself—he was not a cardiologist, but a surgical house officer. It was not a plastic tube he threaded up his arm vein but a ureteral catheter. And no radiopaque material was injected to assist in visualizing the tip of the catheter in his right atrium when X-ray documentation of the feat was performed. It was later on in his career that Forssmann promoted the use of such material. Fortunately, such lapses are few and far between. It is in the second part of the book that Jones comes into his own, utilizing his training both as a psychiatrist and historian. Ominously titled “Complications,” this section, in less judicious hands, might have presaged some serious physician bashing. To his credit, Jones remains evenhanded, pointing out the difficulty in making therapeutic choices. The emphasis here is on cerebral complications of embolic phenomena associated with different types of surgery and angioplasty. The problems, neurologic and psychological, inherent in the use of the heart–lung machine are also emphasized. In this context it would have been suitable to mention the role of hypothermia as it was used in open heart surgery as the sole method of brain function preservation as well as its use in association with the heart–lung machine up to the present. Even more desirable would have been Jones’s addressing the problem of sudden unexpected death from lethal arrhythimas unassociated with coronary [End Page 697] thrombosis. Many coronary patients die in this way after recovering from one or more myocardial infarctions, and it would by edifying to see what Jones would have to say about this aspect of coronary mortality and means to combat it with cardiac resuscitation efforts, automatic implantable defibrillators, and drug therapy. “Sudden death” is alluded to frequently throughout the book, but no specific focus on it is made. “Ventricular fibrillation” does not appear in the index. Perhaps the best part of the book is found in the final chapters, where Jones deals with geographic differences in practice and points out how the individual effects of race, economics, and other factors come into play with our approach to coronary disease as either patients or physicians. His message is that there is “a marked asymmetry in medical knowledge in which there is more evidence...

Brain Natriuretic Peptide and Cardiac Resynchronization Therapy in Patients With Mildly Symptomatic Heart Failure

There are limited data on the prognostic implications of brain natriuretic peptide (BNP) assessment in patients with mildly symptomatic heart failure (HF) who receive cardiac resynchronization therapy with a defibrillator (CRT-D). The effect of elevated baseline and 1-year BNP levels (dichotomized at the upper tertile BNP of 120 pg/mL) on the risk of HF or death was assessed among the cohort of 1197 patients with baseline BNP data enrolled in MADIT (Multicenter Automated Defibrillator Implantation Trial)-CRT. Elevated baseline BNP was associated with a significant 68% (P=0.007) and 58% (P=0.02) increase in the risk of HF or death among MADIT-CRT patients allocated to CRT-D and implantable cardioverter defibrillator-only therapy, respectively. At 1 year of follow-up, patients allocated to CRT-D displayed significantly greater reductions in BNP (26% reduction) levels compared with implantable cardioverter defibrillator-only patients (8% increase; P=0.005). Patients with CRT-D in whom 1-year BNP levels were reduced or remained low experienced a significantly lower risk of subsequent HF or death as compared with patients in whom 1-year BNP levels were high. Similarly, the echocardiographic response to CRT-D was highest among those who maintained low BNP levels or in whom BNP level at 1-year was reduced. Our findings suggest that assessment of baseline and follow-up BNP provides important prognostic implications in patients with mildly symptomatic HF who receive CRT.

Saving lives and reducing inappropriate device therapy: The MADIT family of implantable cardioverter-defibrillator and cardiac resynchronization therapy trials

In 1980, Mirowski et al. [1] reported the first 3 patients treated with an automatic implantable defibrillator (AID). At that time, the AID was implanted with electrodes attached to the epicardium through a surgical thoracotomy with the battery portion of the unit placed undeer the skin in the abdominal wall. The AID detected the onset of ventricular fibrillation through a unique algorithm and the device was considered a “shock box” since shock was the only therapy delivered. The U.S. Food and Drug Administration (FDA) initially provided approval for use of the AID device in high-risk cardiac patients who had been resuscitated from a prior aborted cardiac arrest. Around the same time frame, Medtronic developed a pacing approach (antitachycardia pacing [ATP]) to terminate rapid ventricular tachycardia (VT) by delivering a series of appropriately timed pacing stimuli in the interval between the QRS and T-wave complexes of the tachycardia (review article [2]). This pacing technique was effective in terminating VT in a majority of patients with ventricular tachyarrhythmias. However, this ATP approach produced acceleration of VT and even ventricular fibrillation and sudden death in a small percentage of patients, and ATP therapy was not approved by the FDA as a stand-alone therapy. The AID was initially developed by Drs. Mirowski and Mower in association with Dr. M. Stephen Heilman at the Medrad/Intec Company in Pittsburgh, Pennsylvania, and the implantable defibrillator was subsequently sold to CPI/Guidant Corporation in 1985. Although CPI/Guidant and Medtronic were competitors in the pacemaker field, both companies recognized the need for a device with tiered therapy that would include ATP and defibrillation. Through a cooperative agreement, CPI/Guidant and Medtronic jointly agreed on a device involving ATP and shock therapy, called the automatic implantable cardioverter defibrillator (AICD) for treating patients at risk for life-threatening VT and/or ventricular fibrillation.

End‐of‐Life Care in Patients with Implantable Cardioverter Defibrillators: A MADIT‐II Substudy

Implantable cardioverter defibrillator (ICD)-delivered shocks can cause substantial distress, warranting consideration of ICD deactivation at end of life. This study was designed to describe the patterns of end-of-life management in patients with ICDs. There was a retrospective chart review of 98 patients who died in the ICD arm of multicenter automated defibrillator implantation trial II (MADIT II). The pattern of ICD management and the frequency of ICD shocks delivered before death were reviewed. We identified three groups: Group 1 consisting of individuals who underwent ICD, deactivation, 15 (15%); Group 2 patients without ICD deactivation who were in hospice or with "do not resuscitate" (DNR) orders, 36 (37%); and Group 3 patients without ICD deactivation who were not in hospice care and did not have DNR orders, 47 (48%). Out of 15 deactivations, 11 (73%) occurred in the week before death. None of the patients in Group 1 received an ICD shock in the 24-hour period before death. However, one (3%) patient from Group 2 and nine (19%) patients from Group 3 had shocks during the 24hours before death (P= 0.03). In the last week before death, three (20%), two (6%), and six (13%) patients received ICD shocks in the three groups, respectively (P= 0.28). In patients with terminal conditions who are at risk for imminent death, active management of the patient's ICD, including timely discussions regarding ICD deactivation, may reduce the risk of ICD shocks during the end of life.

Cardiology for Anesthesiologists (International Anesthesiology Clinics 50, Number 2, Spring 2012).

Advances in pharmacologic and invasive techniques have vastly transformed the general practice of cardiology into one with very focused subspecialties. Anesthesiologists must adapt to these advances, as our patients present to us with treatment modalities that are ever changing. Cardiology for Anesthesiologists explores several advances and describes their corresponding anesthetic considerations.In the tradition of International Anesthesiology Clinics, Cardiology for Anesthesiologists is not a comprehensive conglomerate of all things cardiology. Rather, it is an assortment of independent topics, each written by its own group of authors. The reader should not expect to learn how to interpret an electrocardiogram or how to treat new onset atrial fibrillation. The preface explains this by describing this text as one that stays off the “beaten path” and attempts to introduce fresher topics.The book succeeds in this goal by presenting several topics that are not commonly covered in current anesthesiology texts, such as “When Cardiac Patients Need ECT” and “Inflammatory Diseases and the Heart.” “Perioperative Hypertensive Crisis: Newer Concepts” describes current literature and pharmacologic treatments and emphasizes the importance of evaluating pulse pressure rather than just suggesting a threshold for treating systolic or diastolic hypertension. In “Robotic-Assisted Cardiac Surgery,” the text leaves its strict cardiology theme. It presents a history of robotic surgery and current cardiothoracic techniques. The chapter “Congenital Heart Disease in the Adult” includes an eight-page table that briefly describes the anatomy and perioperative considerations for caring for these patients. It is a solid review, but it is not likely to be enough of a resource to help practitioners who seldom anesthetize this population formulate an anesthetic plan.A thorough discussion of modern monitoring techniques is presented in the chapter entitled “Monitoring Hemodynamic Risk in Remote Locations.” This chapter is disguised as an overview of treating ill patients outside the operating room, but is actually a review of modern invasive and noninvasive monitors, including the physics behind them. The chapter provides good descriptions of the technologies, but the devices would be better introduced in the operating room until a comfort level is achieved to allow their employment in remote locations. “Severe Heart Failure and Mechanical Circulatory Support” presents current data on the efficacy of commonly used monitors, such as pulmonary artery catheters, and describes newer treatments, including percutaneously placed ventricular assist devices.“Cardiac Electrophysiology Procedures in Clinical Practice” should not be considered to be a review of how to care for a patient with a pacemaker or automatic implantable cardiac defibrillator. The reader will not find an answer to the question, “To magnet or not to magnet?” Instead, the chapter presents an excellent review of the anatomy and physiology of arrhythmias, the electrophysiology procedures used to treat them, and suggestions for corresponding anesthetic plans.While the topic of anticoagulation therapy in the patient with a recent history of primary coronary intervention is widely available for review, there is no discussion in the text contrasting the algorithm for withholding anticoagulants perioperatively in patients with bare metal versus drug-eluding stents. When selecting a text entitled Cardiology for Anesthesiologists, the audience would likely expect a discussion of this topic. However, because these algorithms change regularly, as they have recently, they quickly become outdated and are not included here.In summary, Cardiology for Anesthesiologists is a text that will be of greatest interest to the anesthesiologist who wishes to learn about several focused topics in cardiology without having to read through well-covered themes, such as treatments for coronary artery disease and chronic hypertension. It is not written as a reference book for all cardiology topics. Instead, it introduces new topics and covers some less-discussed pathologies that are still of importance, including a great discussion of the treatment of patients with cardiac tamponade. I would highly recommend this book as an adjunct to traditional anesthesiology texts.

Ethical considerations for discontinuing pacemakers and automatic implantable cardiac defibrillators at the end-of-life

As the use of intracardiac devices has increased, the awareness of the burdens of the devices, especially the uncomfortable defibrillator shocks, has also increased. Some patients have requested device deactivation and some physicians have expressed reluctance to do so. This review will update physicians about the ethical acceptability of removal of intracardiac devices. The American Heart Rhythm Society released a consensus statement about the ethical removal of intracardiac devices. Subsequent surveys of patients and physicians demonstrate significant misunderstandings about deactivation. Physicians ought to initiate a deactivation conversation, ideally at the time of implantation. Sharing case studies about the deactivation process will enable physicians to enhance their ability to guide patients and family through thoughtful decision-making. Guidelines for deactivation should be promulgated throughout institutions that serve patients with intracardiac devices.

Posible valor pronóstico de la fibrilación y el flutter auricular en el síndrome de Brugada

To analyze the specific risk for the variables: type 1 spontaneous pattern, type 1 induced pattern, type 1 pattern with spontaneous variability, syncope, family history of sudden death, atrial fibrillation and atrial flutter with the subsequent development of malignant arrhythmic events. Forty-three Brugada patients (90% males; mean age 40.4 years), with a type 1 spontaneous pattern (74.4%) or induced by ajmaline (25.6%) were retrospectively analyzed. Of these, 58.1% presented spontaneous variability, 18.6% had family history of sudden death, 39.5% were symptomatic, and 18.6% presented atrial fibrillation or atrial flutter. The antecedents of resuscitated cardiac arrest, sudden death or appropriate shock from implantable automatic defibrillator were considered malignant arrhythmic events. During a mean follow up of 51 months, no deaths were recorded, 6.9% of the patients presented a malignant arrhythmic event, and all of them were appropriate shocks. The annual rate of events in patients with syncope was 1.7%, with a spontaneous type 1 pattern was 2.79%, and spontaneous variability was 2.87%. No malignant arrhythmic event was observed in asymptomatic patients or in those with a persistent pattern or induced type 1 pattern. The annual rate of events with positive or negative history of family sudden death was 2.94 and 1.7%, respectively. In the presence of atrial fibrillation, atrial flutter and atrial fibrillation/atrial flutter were 7.3, 15.69 and 10%, respectively. In the absence of atrial fibrillation/atrial flutter no malignant arrhythmic events were observed. Of the variables analyzed, the one that was most related to a malignant arrhythmic event was the presence of atrial fibrillation (P=.046) and atrial flutter (P=.03).

315: Cardiac iatrogenic admissions in a coronary care unit A prospective study on 7550 admissions

Iatrogenic events were defined as adverse drug reactions or complications induced by non-drug interventions, such as cardiac devices or stimulation techniques. Iatrogenic complications (IC) are associated with prolonged hospitalization and higher in-hospital mortality. In the real world IC are mainly evaluated during hospital stay. The present study focused on admission in a coronary care unit (CCU) for an adverse effect and we aimed: a) to evaluate the prevalence and the characteristics of these admissions and the types of iatrogeny; b) and to assess the in-hospital mortality. From April 2008 to May 2012, all the consecutive admissions caused IC at the CCU were prospectively studied and classified in 2 groups: 1) pharmacological adverse effect (antiarrythmics, anticoagulant, and antiplatelets), 2) non pharmacological adverse effect (pace maker, Automatic Implantable Cardiovertor Defibrillator, radiofrequency, stent, cardiac surgery). On 7550 admissions, 302 (4%) IC as admission cause were included in the study. Most patients with IC were male (58%) with a mean age at 71±15 years. The in-hospital mortality of IC group was similar to those in the general population (8% for both). The following table presents the results of the 2 groups (N (%) or mean±SD). N (%) Men Age (y) Hospital death Total 302 178(58%) 71±15 25(8%) Non pharmacological adverse effect 161 (53%) 79(49%) 75±14 13(8.1%) Pharmacological adverse effect 141 (47%) 99(70%) 67±17 12(8.5%) p p<0.001 p<0.001 p=0.891 This preliminary work shows the high frequency of iatrogenic events as a cause of CCU. Work will be necessary to better understand the causes of iatrogeny in order to limit this pathology.

Advanced hybrid coronary revascularization with robotic totally endoscopic triple bypass surgery and left main percutaneous intervention

CLINICAL SUMMARY The patient, a 57-year-old man with a history of myocardial infarction, left anterior descending coronary artery (LAD) stent, and occluded right coronary artery, automatic implantable cardiac defibrillator implantation, was seen because of ventricular tachycardia, acute non–ST segment elevation myocardial infarction, and automatic implantable cardiac defibrillator discharge. Workup identified anteroapical ischemia, complex 70% stenosis involving the distal left main coronary artery (LMCA) and all 3 major subbranch ostia, and 30% in-stent restenosis of the LAD stent. Hybrid coronary revascularization was planned, including 3-vessel, all-arterial TECAB targeting the LAD, left circumflex coronary artery, and right posterior descending coronary artery systems with staged stenting of the distal LMCA and ramus. In the operating room, left ventricular ejection fraction was 20%; however, this was considered to be reversible because outpatient left ventricular ejection fraction was 45% and implantation of a prophylactic intraaortic balloon pump resulted in significant improvement. With the da Vinci telemanipulation system (Intuitive Surgical, Sunnyvale, Calif), bilateral internal thoracic arteries (ITAs) were harvested with simultaneous harvesting of the left radial artery. An end to side right ITA–radial artery Y anastomosis was created with robotic endoscopic

When Is Deactivating an Implanted Cardiac Device Physician-Assisted Death? Appraisal of the Lethal Pathophysiology and Mode of Death

Journal of Palliative MedicineVol. 14, No. 10 Letters to the EditorWhen Is Deactivating an Implanted Cardiac Device Physician-Assisted Death? Appraisal of the Lethal Pathophysiology and Mode of DeathMohamed Y. Rady and Joseph L. VerheijdeMohamed Y. RadyDepartment of Critical Care Medicine, Mayo Clinic Hospital, Mayo Clinic, Phoenix, Arizona.Center for Biology and Society, School of Life Sciences, Arizona State University, Tempe, Arizona.Search for more papers by this author and Joseph L. VerheijdeCenter for Biology and Society, School of Life Sciences, Arizona State University, Tempe, Arizona.Department of Physical Medicine and Rehabilitation, Mayo Clinic, Phoenix, Arizona.Search for more papers by this authorPublished Online:17 Oct 2011https://doi.org/10.1089/jpm.2011.0161AboutSectionsView articleView Full TextPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View articleFiguresReferencesRelatedDetailsCited ByEthical Dilemmas at the End of Life: Islamic Perspective21 January 2016 | Journal of Religion and Health, Vol. 56, No. 2Evidence and ethics11 December 2015Ethical Challenges of Deactivation of Cardiac Devices in Advanced Heart Failure12 March 2014 | Current Heart Failure Reports, Vol. 11, No. 2Preparedness Planning Before Mechanical Circulatory Support: A “How-To” Guide for Palliative Medicine CliniciansJournal of Pain and Symptom Management, Vol. 47, No. 5Ethical Challenges With Deactivation of Durable Mechanical Circulatory Support at the End of Life6 March 2012 | Journal of Intensive Care Medicine, Vol. 29, No. 1Ethical Considerations in End-of-Life Deactivation of Durable Mechanical Circulatory Support Devices Mohamed Y. Rady and Joseph L. Verheijde10 December 2013 | Journal of Palliative Medicine, Vol. 16, No. 12Ethical considerations for discontinuing pacemakers and automatic implantable cardiac defibrillators at the end-of-lifeCurrent Opinion in Anaesthesiology, Vol. 26, No. 2Abandoning inhumane terminal withdrawal of ventilatory support and extubation in the imminently dyingCritical Care Medicine, Vol. 40, No. 6On Deactivating Cardiovascular Implanted Electronic Devices (CIEDs): Let Our People Go Brad Stuart17 October 2011 | Journal of Palliative Medicine, Vol. 14, No. 10 Volume 14Issue 10Oct 2011 InformationCopyright 2011, Mary Ann Liebert, Inc.To cite this article:Mohamed Y. Rady and Joseph L. Verheijde.When Is Deactivating an Implanted Cardiac Device Physician-Assisted Death? Appraisal of the Lethal Pathophysiology and Mode of Death.Journal of Palliative Medicine.Oct 2011.1086-1088.http://doi.org/10.1089/jpm.2011.0161Published in Volume: 14 Issue 10: October 17, 2011PDF download

Upper thoracic veins' patency in pacemaker implantation in behcet's disease: Diagnosis by echo-doppler and isotopic angiography

Recurrent vasculitis and vein thrombosis, including involvement of the superior vena cava, are serious complications of Behcet's disease, and may present an obstacle during implantation of permanent endocardial transvenous pacemaker and/or automatic defibrillator. Six male patients, known to suffer from Behcet's disease, who required pacemaker and/or defibrillator therapy were investigated. Both invasive (phlebography) and non-invasive (echo-Doppler and isotopic angiography) vascular imaging techniques were available. In one patient, total occlusion of the upper thoracic veins was demonstrated by angiography. In a second patient, following implanted defibrillator, partial left subclavian vein obstruction was demonstrated by the two noninvasive methods. In the remaining four patients, patency of the upper thoracic veins was demonstrated, prior to and following pacemaker implantation, by the two noninvasive methods, with a good correlation. As echo-Doppler or isotopic angiography are widely available, easy to perform and reproducible, it is suggested that upper thoracic vein patency in patients with Behcet's disease should be evaluated prior to and following such vascular procedure, by one of these methods, in order to prevent unnecessary attempts to cannulate obstructed or stenosed vessels.

Left ventricular epicardial admittance measurement for detection of acute LV dilation

There are two implanted heart failure warning systems incorporated into biventricular pacemakers/automatic implantable cardiac defibrillators and tested in clinical trials: right heart pressures, and lung conductance measurements. However, both warning systems postdate measures of the earliest indicator of impending heart failure: left ventricular (LV) volume. There are currently no proposed implanted technologies that can perform LV blood volume measurements in humans. We propose to solve this problem by incorporating an admittance measurement system onto currently deployed biventricular and automatic implantable cardiac defibrillator leads. This study will demonstrate that an admittance measurement system can detect LV blood conductance from the epicardial position, despite the current generating and sensing electrodes being in constant motion with the heart, and with dynamic removal of the myocardial component of the returning voltage signal. Specifically, in 11 pigs, it will be demonstrated that 1) a physiological LV blood conductance signal can be derived; 2) LV dilation in response to dose-response intravenous neosynephrine can be detected by blood conductance in a similar fashion to the standard of endocardial crystals when admittance is used, but not when only traditional conductance is used; 3) the physiological impact of acute left anterior descending coronary artery occlusion and resultant LV dilation can be detected by blood conductance, before the anticipated secondary rise in right ventricular systolic pressure; and 4) a pleural effusion simulated by placing saline outside the pericardium does not serve as a source of artifact for blood conductance measurements.

Interaction Between Enfuvirtide, an Injectable Fusion Inhibitor, and Niacin in an HIV-Infected Patient

To report a potential drug-drug interaction between enfuvirtide, an injectable HIV fusion inhibitor, and niacin in an HIV-infected man with dilated cardiomyopathy. A 47-year-old HIV-infected man with dilated cardiomyopathy and prolonged QT syndrome with an automatic implantable cardiovascular defibrillator device was prescribed subcutaneous enfuvirtide 90 mg twice daily as part of his antiretroviral regimen and oral extended-release niacin 500 mg/day for a high-density lipoprotein level of 8 mg/dL. After 1 week of concomitant therapy, the patient began experiencing extreme redness, edema, and swelling at the injection site that corresponded with the flushing sensation due to niacin. This interfered with his daily activities, leading to self-discontinuation of both agents. As the patient had tolerated enfuvirtide therapy prior to the addition of niacin, we reinitiated enfuvirtide with close follow-up, and the patient has been maintained on this agent since then without consequence. Based on the Horn Drug Interaction Probability Scale, a probable interaction occurred between enfurvirtide and niacin. We hypothesize that a drug-drug interaction occurs between enfuvirtide and niacin related to prostaglandin synthesis and mobilization of inflammatory cells, specifically Langerhans cells. A theoretical mechanism for this interaction is that the Langerhans cells in the epidermis function improperly due to the presence of HIV and the attachment of enfuvirtide. When these cells are exposed to nicotinic acid, an exaggerated immune response is produced that may lead to pain, redness, and swelling at the injection site. Prostaglandins, cytokines, and other inflammatory molecules may all have a role in this interaction. Caution should be used when coadministering enfuvirtide and niacin to HIV-infected patients.