Anand Irimpen

Efficacy and Safety of Automatic Remote Monitoring for Implantable Cardioverter-Defibrillator Follow-Up The Lumos-T Safely Reduces Routine Office Device Follow-Up (TRUST) Trial

Background— Monitoring implantable cardiac device function and patient condition is important. The Lumos-T Safely Reduces Routine Office Device Follow-Up (TRUST) trial tested the hypothesis that remote home monitoring with automatic daily surveillance (HM) is safe and effective for implantable cardioverter-defibrillator follow-up for 1 year and enables rapid physician evaluation of significant events. Methods and Results— In total, 1339 patients were randomized 2:1 to HM or conventional follow-up. Follow-up checks occurred at 3, 6, 9, 12, and 15 months after implantation. HM was used before office visits at 3 and 15 months in the HM group. At 6, 9, and 12 months, HM only was used but was followed by office visits if necessary. Conventional patients were evaluated with office visits only. Scheduled office visits and unscheduled evaluations, incidence of morbidity, and time elapsed from first event occurrence in each patient to physician evaluation were tracked for each group. HM and conventional patients were similar (age, 63.3±12.8 versus 64.0±12.1 years; gender, 72.0% versus 73.1% male; New York Heart Association class II, 55.9% versus 60.4%; pathology: left ventricular ejection fraction, 29.0±10.7% versus 28.5±9.8%; coronary artery disease, 64.8% versus 71.7%; primary prevention indication, 72.2% versus 73.8%; and dual-chamber implants, 57.8% versus 56.6%). HM reduced total in-hospital device evaluations by 45% without affecting morbidity. In the HM group, 85.8% of all 6-, 9-, and 12-month follow-ups were performed remotely only, indicating that HM provided sufficient assessment in the majority. Median time to evaluation was <2 days in the HM group compared with 36 days in the conventional group (P<0.001) for all arrhythmic events. Conclusions— HM is safe and allows more rapid detection of actionable events compared with conventional monitoring in patients with implantable electronic cardiac devices. Clinical Trials Registration— URL: http:/www.clinicaltrials.gov. Unique identifier: NCT00336284.

Effect of Hurricane Katrina on the incidence of acute coronary syndrome at a primary angioplasty center in New Orleans.

BACKGROUND In August 2005, New Orleans was hit by Hurricane Katrina, the costliest natural disaster in US history. Previous studies have shown an increase in acute myocardial infarction (AMI) in the immediate hours to weeks after natural disasters. The goals of our study were to detect any long-term increase in the incidence of AMI after Katrina and to investigate any pertinent contributing factors. METHODS This was a single-center retrospective cohort observational study. Patients admitted with AMI to Tulane Health Sciences Center hospital in the 2 years before Katrina and in the 2 years after the hospital reopened (5 months after Katrina) were identified from hospital records. The 2 groups (pre- and post-Katrina) were compared for prespecified demographic and clinical data. RESULTS In the post-Katrina group, there were 246 admissions for AMI, out of a total census of 11,282 patients (2.18%), as compared with 150 AMI admissions out of a total of 21,229 patients (0.71%) in the pre-Katrina group (P < 0.0001). The post-Katrina group had a significantly higher prevalence of unemployment (P = 0.0003), lack of medical insurance (P < 0.0001), medication noncompliance (P = 0.0001), smoking (P = 0.001), substance abuse (P = 0.03), first-time hospitalization (P < 0.001), local residents rather than visitors affected (P < 0.0001), and people living in temporary housing (P = 0.003). DISCUSSION The role of chronic stress in the pathogenesis of AMI is poorly understood, especially in the aftermath of natural disasters. Our data suggest that Katrina was associated with prolonged loss of employment and insurance, decreased access to preventive health services, and an increased incidence of AMI. In addition, it appears that chronic stress after a natural disaster can be associated with tobacco abuse and medication and therapeutic noncompliance. CONCLUSIONS We found a 3-fold increased incidence of AMI more than 2 years after Hurricane Katrina. Even allowing for the loss of some local hospitals after the disaster, this represents a significant change in overall health of the study population and supports the need for further study into the health effects of chronic stress.

OxLDL induces endothelial dysfunction and death via TRAF3IP2: Inhibition by HDL3 and AMPK activators

Oxidized low-density lipoprotein (oxLDL) induces endothelial cell death through the activation of NF-κB and AP-1 pathways. TRAF3IP2 is a redox-sensitive cytoplasmic adapter protein and an upstream regulator of IKK/NF-κB and JNK/AP-1. Here we show that oxLDL-induced death in human primary coronary artery endothelial cells (ECs) was markedly attenuated by the knockdown of TRAF3IP2 or the lectin-like oxLDL receptor 1 (LOX-1). Further, oxLDL induced Nox2/superoxide-dependent TRAF3IP2 expression, IKK/p65 and JNK/c-Jun activation, and LOX-1 upregulation, suggesting a reinforcing mechanism. Similarly, the lysolipids present in oxLDL (16:0-LPC and 18:0-LPC) and minimally modified LDL also upregulated TRAF3IP2 expression. Notably, whereas native HDL3 reversed oxLDL-induced TRAF3IP2 expression and cell death, 15-lipoxygenase-modified HDL3 potentiated its proapoptotic effects. The activators of the AMPK/Akt pathway, adiponectin, AICAR, and metformin, attenuated superoxide generation, TRAF3IP2 expression, and oxLDL/TRAF3IP2-mediated EC death. Further, both HDL3 and adiponectin reversed oxLDL/TRAF3IP2-dependent monocyte adhesion to endothelial cells in vitro. Importantly, TRAF3IP2 gene deletion and the AMPK activators reversed oxLDL-induced impaired vasorelaxation ex vivo. These results indicate that oxLDL-induced endothelial cell death and dysfunction are mediated via TRAF3IP2 and that native HDL3 and the AMPK activators inhibit this response. Targeting TRAF3IP2 could potentially inhibit progression of atherosclerotic vascular diseases.

Effect of Hurricane Katrina on incidence of acute myocardial infarction in New Orleans three years after the storm.

To detect a long-term increase in the incidence of acute myocardial infarction (AMI) after Hurricane Katrina and to investigate the pertinent contributing factors, we conducted a single-center retrospective cohort observational study. The patients admitted with AMI to Tulane University Hospital in the 2 years before Katrina and the 3 years after the hospital reopened were identified from the hospital medical records. The pre- and post-Katrina groups were compared for prespecified demographic and clinical data. In the 3-year post-Katrina group, 418 admissions (2.0%) for AMI occurred of a total census of 21,092 patients compared to 150 (0.7%) of a census of 21,079 in the 2-year pre-Katrina group (p <0.0001). The post-Katrina group had a greater prevalence of unemployment (p <0.0001), lack of medical insurance (p <0.001), smokers (p <0.01), medical noncompliance (p <0.0001), first-time hospitalizations (p <0.001), history of coronary artery disease (p <0.01), multiple vessel disease (p <0.05), and percutaneous coronary interventions (p <0.0001). The mean age of onset of AMI decreased from 62 years before Katrina to 59 years after Katrina (p <0.05), and a significantly greater percentage of patients were men (p <0.05). No significant differences were found between the two groups in terms of race, substance abuse, and a history of hypertension or diabetes mellitus. Our data suggest that chronic stress after natural disasters may significantly affect cardiovascular risk factors such as tobacco abuse and increase medical noncompliance. In conclusion, our data is consistent with a significant change in the overall health of the population and support the need for additional study into the health effects of chronic stress after natural disasters.

Natural Disasters and Myocardial Infarction: The Six Years After Hurricane Katrina

OBJECTIVE To determine the prolonged effect of Hurricane Katrina on the incidence and timing of acute myocardial infarction (AMI) in the city of New Orleans. PATIENTS AND METHODS Our study population consisted of 1476 patients with AMI before (August 29, 1999, to August 28, 2005) and after (February 14, 2006, to February 13, 2012) Hurricane Katrina at Tulane University Health Sciences Center to determine post-Katrina alterations in the occurrence and timing of AMI. RESULTS Compared with pre-Katrina values, there was a more than 3-fold increase in the percentage of admissions for AMI during the 6 years after Hurricane Katrina (P<.001). The percentage of admissions for AMI after Hurricane Katrina increased significantly on nights (P<.001) and weekends (P<.001) and decreased significantly on mornings (P<.001), Mondays (P<.001), and weekdays (P<.001). Patients with AMI after Hurricane Katrina also had significantly higher rates of psychiatric comorbidities (P=.01), smoking (P<.001), lack of health insurance (P<.05), and unemployment (P<.001). CONCLUSION These results indicate that the effect of natural disasters on the occurrence of AMI may persist for at least a 6-year period and may be related to various factors including population shifts, alterations in the health care system, and the effects of chronic stress and associated behaviors.

Lack of ventricular remodeling in non-Q-wave myocardial infarction.

We prospectively examined 45 patients with serial echocardiography to measure left ventricular end-diastolic volume index within 1 week and at 6 weeks after infarction. Left ventricular volume increased in patients with Q-wave infarction but not in those with non-Q or in control patients without recent infarction. Peak creatine phosphokinase levels were greater in Q-wave infarction compared with those in non-Q-wave infarction. There was a strong correlation between the change in the left ventricular end-diastolic index and the peak creatine phosphokinase level. After correcting for infarct size, there was still a difference between the two groups. Our data indicate that ventricular remodeling does not occur in non-Q-wave as opposed to Q-wave infarcts, and this may be related both to the limited amount of myocardial necrosis and to the nontransmural extent of the necrosis.

The broken heart syndrome: Takotsubo cardiomyopathy

First described in 1990, Takotsubo cardiomyopathy consists of a transient systolic dysfunction of localized segments of the left ventricle. Commonly occurring in postmenopausal women, Takotsubo is often associated with intense physical and/or emotional stress. It is traditionally identified by distinctive wall motion patterns on transthoracic echocardiogram and left ventriculography. Further understanding of the disease mechanisms and recognition of at-risk populations has potentially tremendous therapeutic benefit.

Effect of Hurricane Katrina on Chronobiology at Onset of Acute Myocardial Infarction During the Subsequent Three Years

The onset of acute myocardial infarction (AMI) has been shown to occur in a nonrandom pattern, with peaks in midmorning and on weekdays (especially Monday). The incidence of AMI has been shown to increase locally after natural disasters, but the effect of catastrophic events on AMI biorhythms is largely unknown. To assess the differences in the chronobiology of AMI in residents of New Orleans before and after Hurricane Katrina, the onset of AMI in patients at Tulane University Health Sciences Center in the 6 years before and the 3 years after Hurricane Katrina was retrospectively examined. Compared to the pre-Katrina group, the post-Katrina cohort demonstrated significant decreases in the onset of AMI during mornings (p = 0.002), Mondays (p <0.0001), and weekdays (p <0.0001) and significant increases in onset during weekends (p <0.0001) and nights (p <0.0001). These changes persisted during all 3 years after the storm. In conclusion, the normal pattern of AMI onset was altered after Hurricane Katrina, and expected morning, weekday, and Monday peaks were eliminated.

Succesful antegrade subintimal bypass restenting of in-stent chronic total occlusion.

Coronary chronic total occlusions (CTOs) are known to cause significant patient morbidity. Over the past several years, the techniques and devices for treating these CTOs have advanced tremendously. The interventional management of CTOs within previously placed coronary stents, however, remains challenging. Here, we present a case of an in‐stent restenosis of the right coronary artery CTO bypassed using a controlled subintimal dissection re‐entry technique via antegrade approach creating side‐by‐side stents.

Absence of binding of targeted analogs of somatostatin carrying cytotoxic radicals or radionuclides to growth hormone secretagogue receptors on human myocardium.

Various peripheral human tissues express receptors for growth hormone secretagogue (GHS), the highest density being in the myocardium. It was also reported that some octapeptide analogs of somatostatin (SRIH) can displace radiolabeled Tyr-Ala-hexarelin from GHS receptors on the human pituitary and heart. Thus, it is possible that radionuclide analogs of SRIH such as OctreoScan and recently developed cytotoxic SRIH analogs containing doxorubicin (DOX) intended for targeted tumor therapy, could bind to these GHS receptors, compromising the safety of compounds of this type. Therefore, we determined the binding of OctreoScan and two cytotoxic SRIH analogs consisting of octapeptide carrier RC-121 and DOX (AN-162) or 2-pyrrolino-DOX (AN-238) to human myocardium specimens. None of these compounds displayed specific binding to the human heart indicating that the clinical use of SRIH analogs linked to anthracyclines or radionuclides should not be associated with increased cardiac side effects.