Tracking deaths related to Hurricane Ike, Texas, 2008.

BACKGROUND: On September 13, 2008, Hurricane Ike, a category 2 storm with maximum sustained winds of 110 mph, made landfall near Galveston, Texas. Ike produced a damaging, destructive, and deadly storm surge across the upper Texas and southwestern Louisiana coasts. Thirty-four Texas counties were declared disaster areas by the Federal Emergency Management Agency; 15 counties were under mandatory evacuation orders. To describe causes of death associated with this hurricane and identify prevention strategies during the response and recovery phases, the Texas Department of State Health Services (DSHS) monitored mortality data in 44 counties throughout the state. This report summarizes Ike-related deaths reported by Texas medical examiners, justices of the peace (coroners), forensic centers, public health officials, and hospitals. METHODS: Based on the Centers for Disease Control and Prevention (CDC) disaster-related mortality surveillance form, DSHS developed a state-specific 1-page form and collected (optimally daily) data on demographic, date and place of death, and cause and circumstance of deaths. A case was defined as any death that was directly or indirectly related to Ike among evacuees, residents, nonresidents, or rescue personnel in the declared disaster counties, counties along the Texas Gulf coast or counties known to have evacuation shelters occurring September 8, 2008, through October 13, 2008. Analyzed data were shared with the state emergency operation center and the CDC on a daily basis. RESULTS: The surveillance identified 74 deaths in Texas as directly (10 [14%]), indirectly (49 [66%]), or possibly (15 [20%]) related to Ike. The majority of deaths (n=57) were reported by medical examiners. Deaths occurred in 16 counties of the 44 counties covered by the surveillance. The majority of deaths occurred in Harris and Galveston (28 [38%] and 17 [23%]), respectively. The deceased ranged in age from younger than 1 year to 85 years, with an average age of 46 years (median 50 years); 70% were male. Of the 74 deaths, 47 (64%) resulted from injuries, 23 (31%) from illnesses, and 4 (5%) were undetermined. Among the injuries, carbon monoxide poisoning (13 [18%]) and drowning (8 [11%]) were the leading causes of injury-related deaths. Cardiovascular failure (12 [16%]) was the leading cause of illness-related deaths. CONCLUSIONS: Defining the relation of death to hurricane using an active mortality surveillance system is possible. The active mortality surveillance form used in Ike provided valuable daily information to DSHS, state emergency management officials, and the CDC regarding the characteristics of deaths in the state. Most of the Ike-related deaths were caused by injury (direct and indirectly related) such as carbon monoxide poisonings and drowning and may have been preventable by educating the public.

The effect of L-arginine and creatine on vascular function and homocysteine metabolism.

Studies with L-arginine supplementation have shown inconsistent effects on endothelial function. The generation of guanidinoacetate (GAA) from L-arginine with subsequent formation of creatine and homocysteine and consumption of methionine may reduce the pool of L-arginine available for nitric oxide generation. Experimental studies suggest that creatine supplementation might block this pathway. We sought to determine the effects of L-arginine, creatine, or the combination on endothelium-dependent vasodilation and homocysteine metabolism in patients with coronary artery disease. Patients with coronary artery disease were randomized to L-arginine (9 g/day), creatine (21 g/day), L-arginine plus creatine, or placebo for 4 days (n = 26-29/group). Brachial artery flow-mediated dilation and plasma levels of L-arginine, creatine, homocysteine, methionine, and GAA were measured at baseline and follow-up. L-arginine and creatine supplementation had no effects on vascular function. L-arginine alone increased GAA (p < 0.01) and the ratio of homocysteine to methionine (p < 0.01), suggesting increased methylation demand. The combination of creatinine and L-arginine did not suppress GAA production or prevent the increase in homocysteine-to-methionine ratio. Unexpectedly, creatine supplementation (alone or in combination with L-arginine) was associated with an 11-20% increase in homocysteine concentration (p < 0.05), which was not attributable to worsened renal function, providing evidence against an effect of creatine on decreasing methylation demand. In conclusion, the present study provides no evidence that L-arginine supplementation improves endothelial function and suggests that l-arginine may increase methylation demand. Creatine supplementation failed to alter the actions of L-arginine on vascular function or suppress methylation demand. The unexpected increase in homocysteine levels following creatine supplementation could have adverse effects and merits further study, since creatine is a commonly used dietary supplement.

Relation of cumulative weight burden to vascular endothelial dysfunction in obesity.

Although excess fat mass is linked to increased cardiovascular risk, the relation between vascular phenotype and degree of obesity in high weight categories is unknown. We examined brachial artery vasomotor responses using ultrasound in 203 consecutive patients with severe obesity (mean age 44 +/- 11 years; body mass index [BMI] 46 +/- 9 kg/m(2), range 30 to 72; and body weight 128 +/- 29 kg, range 69 to 207). We studied a unique population in which 71% of subjects were characterized as morbidly obese (BMI > or =40 kg/m(2)), which included a 31% group of super-obese subjects (BMI > or =50 kg/m(2)). Brachial artery flow-mediated dilation (FMD) and nitroglycerin-mediated dilation were examined as measures of endothelium-dependent and -independent dilation, respectively, in relation to clinical, hemodynamic, and metabolic variables. Endothelial function was significantly impaired in the highest compared with the lowest tertile of body weight (FMD 6.5 +/- 4.6% vs 9.8 +/- 4.8%, p <0.001), whereas nitroglycerin-mediated dilation was similar in all groups. Univariate correlates of FMD were gender, weight, waist circumference, BMI, diastolic blood pressure, and creatinine. In multivariate analysis, weight was a strong independent significant predictor of FMD (beta = -0.23, p = 0.005) in addition to gender. Within an overweight population, cumulative weight burden remains strongly linked to progressive arterial dysfunction. In conclusion, these results suggest that cardiovascular risks intensify with higher degrees of obesity and underscore the importance of therapeutic weight loss interventions.