Prevalence and risk factors for the development of abdominal aortic calcification among the US population: NHANES study.

INTRODUCTION: Abdominal aortic calcification (AAC) is an important marker of subclinical cardiovascular disease and its prognosis. Advanced age, hypertension, smoking, dyslipidemia, diabetes mellitus, and higher truncal fat are known markers of AAC in studies conducted around the world. However, literature for these risk factors and their co-occurrence is limited in the US. MATERIAL AND METHODS: We used data from dual energy X-ray absorptiometry (Hologic, v4.0) to detect the occurrence of AAC in a sample population (n = 3140) of the NHANES survey using a computer-assisted interviewing system to assess the risk factors for AAC. RESULTS: We found the national prevalence of AAC in the US to be 28.8%. After adjusting for confounders, persons with hypertension: OR = 1.66 (95% CI: 1.30-2.13) and smokers: OR = 1.63 (95% CI: 1.24-2.14) were more likely to have AAC compared to their respective counterparts. Increasing age was positively associated with AAC: OR = 1.06 (95% CI: 1.04-1.08). There was a statistically significant negative association between body mass index (BMI) and AAC, more so in smokers than in non-smokers: OR = 0.97 (95% CI: 0.94-0.97). We did not observe any statistically significant association between diabetes and AAC. CONCLUSIONS: Advanced age, smoking, and hypertension was associated with increased occurrence of AAC. Paradoxically, increasing BMI was inversely associated with AAC and there was no statistically significant association between total body and trunk fat percentages and AAC. To the best of our knowledge, this is the first study to establish the nationwide prevalence and associated factors in the US.

Outcomes of oesophageal variceal bleeding among patients with atrial fibrillation: a propensity-matched analysis of a nationwide inpatient sample.

INTRODUCTION: We aimed to determine the influence of atrial fibrillation (AF) on mortality, morbidity, length of hospital stay, and resource utilisation in patients with oesophageal variceal bleeding (OVB). MATERIAL AND METHODS: The National Inpatient Sample database (2016 and 2017) was used for data analysis using the International Classification of Diseases, Tenth Revision codes to identify patients with the principal diagnosis of OVB and AF. We assessed the all-cause in-hospital mortality, morbidity, predictors of mortality, length of hospital stay (LOS), and total costs between propensity-matched groups of OVB with AF vs. OVB alone. RESULTS: We identified 80,325 patients with OVB, of whom 4285 had OVB with AF, and 76,040 had OVB only. The in-hospital mortality was higher in OVB with AF (OR = 1.4, 95% CI: 1.09-1.83; p < 0.001). OVB with AF had higher odds of sepsis (OR = 1.4, 95% CI: 1.1-1.8; p = 0.007), acute kidney injury (OR = 1.2, 95% CI: 1.12-1.32; p < 0.001), and mechanical ventilation (OR = 1.2, 95% CI: 1.12-1.32; p < 0.001). Advanced age (OR = 1.06, 95% CI: 1.05-1.07; p < 0.001), congestive heart failure (OR = 1.7, 95% CI: 1.3-2.3; p < 0.001), coronary artery disease (OR = 1.4, 95% CI: 1.03-1.92; p = 0.02), and sepsis (OR = 1.3, 95% CI: 1.06-1.70; p = 0.01) were identified as predictors of mortality in OVB with AF. Mean LOS (7.5 ±7.4 vs. 6.0 ±7.2, p < 0.001) and mean total costs ($25,452 vs. $21,109, p < 0.001) were also higher. CONCLUSIONS: In this propensity-matched analysis, OVB with AF was associated with higher odds of in-hospital mortality, sepsis, acute kidney injury, and mechanical ventilation.

Heme Oxygenase-1 Upregulation: A Novel Approach in the Treatment of Cardiovascular Disease.

Significance: Heme oxygenase (HO) plays a pivotal role in both vascular and metabolic functions and is involved in many physiological and pathophysiological processes in vascular endothelial cells (ECs) and adipocytes. Recent Advances: From the regulation of adipogenesis in adipose tissue to the adaptive response of vascular tissue in the ECs, HO plays a critical role in the capability of the vascular system to respond and adjust to insults in homeostasis. Recent studies show that HO-1 through regulation of adipocyte and adipose tissue functions ultimately aid not only in local but also in systemic maintenance of homeostasis. Critical Issues: Recent advances have revealed the existence of a cross talk between vascular ECs and adipocytes in adipose tissue. In the pathological state of obesity, this cross talk contributes to the condition's adverse chronic effects, and we propose that specific targeting of the HO-1 gene can restore signaling pathways and improve both vascular and adipose functions. Future Directions: A complete understanding of the role of HO-1 in regulation of cardiovascular homeostasis is important to comprehend the homeostatic regulation as well as in cardiovascular disease. Efforts are required to highlight the effects and the ability to target the HO-1 gene in models of obesity with an emphasis on the role of pericardial fat on cardiovascular health.

Agonists of epoxyeicosatrienoic acids reduce infarct size and ameliorate cardiac dysfunction via activation of HO-1 and Wnt1 canonical pathway.

Myocardial infarction (MI) is complicated by ventricular fibrosis and associated diastolic and systolic failure. Emerging studies implicate Wnt1 signaling in the formation of new blood vessels. Epoxyeicosatrienoic acids (EETs)-mediated up-regulation of heme oxygenase-1 (HO-1) protects against the detrimental consequences of MI in several animal models, however, the mechanism(s) by which this occurs remains unclear. The aim of this study was to examine these mechanisms in the LAD ligation animal model of post infarcted heart failure. Specifically, we sought to clarify the mechanistic basis of the interactions of the Wnt1 canonical pathway, HO-1 and associated angiogenesis. Human microvascular endothelial cells (HMECs) were exposed to anoxia and treated with the EET agonist, NUDSA, in the presence and absence of tin mesoporphyrin (SnMP). Increased capillary density, and Wnt1 and HO-1 expression occurred in cells treated with NUDSA. Anoxic HMECs treated with NUDSA and Wnt1 siRNA, exhibited decreased in the expression of ß-catenin and the Wnt1 target gene, PPARδ (p<0.05 vs. NUDSA). Furthermore, blocking the Wnt 1 antagonist, Dickkopf 1, by siRNA increased ß-catenin and PPARδ expression, and this effect was further enhanced by the concurrent administration of NUDSA. In in vivo experiments, C57B16 mice were divided into 4 groups: sham, mice with MI via LAD ligation and mice with MI treated with NUDSA, with and without SnMP. Increased fractional area change (FAC) and myocardial angiogenesis were observed in mice treated with NUDSA (p<0.05 vs. MI). Increased expression of HO-1, Wnt1, ß-catenin, adiponectin, and phospho-endothelial nitric oxide synthetase (p-eNOS), and a decrease in the glycosylated subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, gp91(phox) expression occurred in cardiac tissue of mice treated with NUDSA (p<0.05 vs. MI). SnMP reversed these effects. This novel study demonstrates that increasing the canonical Wnt1 signaling cascade with the subsequent increase in HO-1, adiponectin and angiogenesis ameliorates fibrosis and cardiac dysfunction in a mouse model of MI and supports the hypothesis that HO-1 is an integral component of the EETs-adiponectin axis and is central for the control of resistance to fibrosis and vascular dysfunction and in part determine how they influence the cellular/vascular homeostasis and provides insight into the mechanisms involved in vascular dysfunction as well as potential targets for the treatment of CVD.

Gender differences and predictors of mortality in spontaneous coronary artery dissection: a review of reported cases.

Spontaneous coronary artery dissection (SCAD) is a rare clinical event with little available information on etiology, treatment, or outcomes. Two cases of SCAD are presented and identified cases from the literature with complete data (n = 222) are reviewed and analyzed. Female patients (71.9%) were younger (40.4 versus 46.7; p < 0.001), less likely to have coronary artery disease (3.7 versus 20.6%; p = 0.01), more likely to have left anterior descending artery (46.4 versus 25.4%; p = 0.004) and left main artery involvement (14.9 versus 3.2%; p = 0.01), and less likely to survive (50.9 versus 22.2%; p < 0.001) compared to their male counterparts. Thirty percent were in the peripartum state. Multivariate predictors of death included female sex (OR 4.27; 95% CI 1.50 to 12.2), non-treatment (OR 35.5; 95% CI 10.7 to 118.1), and earlier decade of diagnosis (OR 0.28 per increase in decade after 1980; 95% CI 0.16 to 0.49). Survival was no different by treatment type and did improve over time.