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.

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.

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.

Coronary angiographic significance of hyperacute ST-T changes associated with regadenoson stress.

An abnormal electrocardiographic stress test is typically characterized by ST segment depression. In rare cases, ST segment elevation is observed, which, in the absence of diagnostic Q waves, has anatomic specificity for localized myocardial ischemia. Most instances of ST elevation occurring during cardiac stress testing have been observed with exercise, with only six cases reported with pharmacologic stress. Despite different physiologic mechanisms for inducing myocardial ischemia, development of ST segment elevation during pharmacologic stress, as illustrated by the present case, may also be indicative of critical coronary stenoses, warranting urgent coronary arteriography.

Primary Streptococcus pneumoniae pericarditis.

Although commonly fatal, bacterial pericarditis is often not diagnosed antemortem due to its infrequent occurrence and fulminant course. Historically, Streptococcus pneumoniae has been the most common cause of bacterial pericarditis. Over the past 70 years, however, it has become largely eliminated and now occurs almost exclusively in immunocompromised individuals with a preceding primary site of infection. Herein, we present a case of primary S. pneumoniae pericarditis that developed over the course of 3 to 4 weeks in an immunocompetent 45-year-old man. The patient, who developed cardiac tamponade shortly after admission, experienced a rapid resolution of symptoms following pericardial drainage and initiation of antibiotics.

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.