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To determine the prolonged effect of Hurricane Katrina on the incidence and timing of acute myocardial infarction (AMI) in the city of New Orleans. 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. 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). 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.

The purpose of this study was to investigate the 10-year impact of Hurricane Katrina on the incidence of acute myocardial infarction (AMI) along with contributing risk factors and any alteration in chronobiology of AMI. A single-center, retrospective, comparison study of AMI incidence was performed at Tulane University Health Sciences Center from 2 years before Hurricane Katrina to 10 years after Hurricane Katrina. A 6-year, pre-Katrina and 10-year, post-Katrina cohort were also compared according to pre-specified demographic, clinical, and chronobiological data. AMI incidence increased from 0.7% (150/21,079) to 2.8% (2,341/84,751) post-Katrina (P<0.001). The post-Katrina cohort had higher rates of coronary artery disease (36.4% vs. 47.9%, P=0.01), diabetes mellitus (31.3% vs. 39.9%, P=0.04), hyperlipidemia (45.4% vs. 59.3%, P=0.005), smoking (34.4% vs. 53.8%, P<0.001), drug abuse (10.2% vs. 15.4%, P=0.02), psychiatric illness (6.7% vs. 14.9%, P<0.001), medication non-adherence (7.3% vs. 15.3%, P<0.001), and lack of employment (7.2% vs. 16.4%, P<0.001). The post-Katrina group had increased rates of AMI during nights (29.8% vs. 47.8%, P<0.001) and weekends (16.1% vs. 29.1%, P<0.001). Even 10 years after the storm, Hurricane Katrina continues to be associated with increased incidence of AMI, higher prevalence of traditional cardiovascular and psychosocial risk factors, and an altered chronobiology of AMI toward nights and weekends. (Disaster Med Public Health Preparedness. 2019;13:217-222).

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.

Arterial restenosis after angioplasty/stenting has hindered coronary artery disease treatment, especially in diabetics. We theorized that gastrin-releasing peptide (GRP) antagonists and growth hormone-releasing hormone (GHRH) antagonists might decrease neointimal hyperplasia and restenosis in diabetic rats after common carotid arterial balloon injury. Two separate experiments were conducted to test the effects of a GRP antagonist (RC-3095) and a GHRH antagonist (MZ-4-71) on vascular smooth muscle (VSM) growth. In a preliminary in vitro experiment non-injured human aortic vascular smooth muscle (VSM) proliferation was compared between growth media and control. In a second in vivo experiment, intimal and medial area, intima/media ratio (IM) and percent stenosis were compared between injured carotid arteries in twelve Zucker type II obese rats treated with subcutaneously injected RC-3095, MZ-4-71, or control media. In the in vitro experiment, decreased VSM cell growth was observed in GRP antagonist (p < 0.05) and GHRH antagonist groups (p < 0.05) compared to the control group. In the in vivo experiment, the GRP antagonist group had a decreased IM ratio (1.63 ± 0.41, p < 0.05) and an increased area of stenosis (98.78% ± 1.48 p = NS) compared to control (2.38 ± 1.09) while the GHRH antagonist group had decreased IM ratio (1.33 ± 0.58 SD, p < 0.05) and percent area of stenosis (78.84% ± 24.97, p < 0.05) compared to control (2.38 ± 1.09). The significant decrease in both IM ratio and percent area of stenosis in the GHRH antagonist group supports the hypothesis that this peptide may reduce neointimal hyperplasia and restenosis. •Effect of GHRH and GRP antagonism on arterial intimal hyperplasia in diabetic rats.•Reduced vascular smooth muscle growth after GHRH and GRP antagonism in vitro.•GHRH antagonism reduced arterial intima to media ratio and % area stenosis in vivo.

To the Editor: Rohatgi et al. (Dec. 18 issue) 1 establish high-density lipoprotein (HDL) cholesterol efflux capacity as a relevant biomarker to predict cardiovascular events. 1 Before the measurement of cholesterol efflux capacity is widely recommended as a risk-predicting method, cholesterol efflux capacity should be compared with HDL particle concentration and other biomarkers. The assay for HDL particle concentration is less expensive and more readily available than that for cholesterol efflux capacity. It should be noted that in the present study, increasing quartiles of cholesterol efflux capacity were accompanied by a significant increase in HDL particle concentration. 1 Previous studies have shown a . . .

Epidemiologic and clinical trial associations of HF in T2DM: interpretational issues Although diabetics represent a third of patients in every large randomized clinical trial, and diabetes is present in 40% of patients hospitalized for HF, many fundamental questions remain, including precise estimates on the risk posed by diabetes in the modern era, relative contribution of HF with preserved ejection fraction (HFPEF) and HF versus reduced ejection fraction (HFREF) and clinical and biochemical predictors of HF risk in DM (Dei Cas, et al., 2015). The presence of features such as pulmonary hypertension, reduced exercise capacity, circulating markers such as NT-proBNP and cardiac magnetic resonance evidence of fibrosis/scar, may allow a priori identification of patients at risk for HHF and would allow a refined assessment of benefit/harm (Sharma & Ezekowitz, 2014).

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an infrequently diagnosed condition with a high incidence of sudden cardiac death. While the only option for cure is orthotopic cardiac transplantation, the use of an implantable cardiac defibrillator can be life saving. Accordingly, the prompt recognition of ARVC is crucial. Fortunately, a definitive diagnosis of ARVC can often be made by a combination of the clinical history and electrocardiogram alone, as illustrated by the present case. In our patient, who presented with multiple syncopal episodes and in whom ventricular tachycardia was observed shortly after her admission to the emergency department, a lengthy and expensive workup was initiated, which ultimately may have delayed implantation of an implantable cardiac defibrillator. Clinicians should be made aware of the clinical guidelines for dealing with this potentially dangerous condition so that appropriate therapy can be promptly initiated.

Abdominal paracentesis is a frequently employed diagnostic and therapeutic procedure for patients with refractory ascites, typically in patients with cirrhosis. It is generally regarded as a safe procedure with significant complications occurring in <1% of cases. Most hemorrhagic complications are due to abdominal wall trauma, during which clear evidence of active bleeding is usually visualized during the procedure. Delayed hemoperitoneum is a rare complication of large-volume paracentesis in which clinical evidence of active bleeding is typically absent until substantial blood loss has taken place (often several days to a week later), leading to an exceedingly high mortality rate. Herein we describe a case of delayed hemoperitoneum in a 55-year-old man with heart failure. This case emphasizes the importance of identifying patients who are at high risk for delayed hemoperitoneum as well as the need to closely monitor complete blood counts in the days following a large-volume paracentesis.

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.