Humans ; Cardiovascular Diseases/chemically induced* ; East Asian People ; Risk Factors ; Heart Disease Risk Factors ; Lipids ; Anticholesteremic Agents/adverse effects* ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Treatment Outcome

Ambient fine particulate matters (PM_2.5) refer to particulate matters with an aerodynamic diameter less than or equal to 2.5 μm. PM_2.5 enter the body through the target organ-lung, and can induce a variety of adverse health effects (such as cardiovascular diseases, diabetes, respiratory diseases, neurodegenerative diseases and adverse birth outcomes). PM_2.5 are known to have complex compositions (including water-soluble/-insoluble components and biological components), diverse sources and capacity of secondary transformation. Numerous epidemiological and toxicological studies indicated that different components of PM_2.5 may induce adverse health effects through different biological mechanisms. In adddition, co-exposure of different components and their interaction should also be considered. Thus here we have systematically reviewed studies in recent years about the toxicological effects and underlying mechanisms of different components of ambient fine particulate matters, including inflammatory response, oxidative stress, endoplasmic reticulum stress, activation of the NF-κB signaling pathway and so on. The information may give some insights into the prevention and treatment of adverse health effects caused by exposure to different components of PM_2.5.
Air Pollutants/toxicity* ; Cardiovascular Diseases/chemically induced* ; Humans ; Lung ; Oxidative Stress ; Particulate Matter/toxicity*

BACKGROUND: Particulate matter (PM), a major component of ambient air pollution, accounts for a substantial burden of diseases and fatality worldwide. Maternal exposure to PM during pregnancy is particularly harmful to children's health since this is a phase of rapid human growth and development. METHOD: In this review, we synthesize the scientific evidence on adverse health outcomes in children following prenatal exposure to the smallest toxic components, fine (PM RESULTS: Maternal exposure to fine and ultrafine PM directly and indirectly yields numerous adverse birth outcomes and impacts on children's respiratory systems, immune status, brain development, and cardiometabolic health. The biological mechanisms underlying adverse effects include direct placental translocation of ultrafine particles, placental and systemic maternal oxidative stress and inflammation elicited by both fine and ultrafine PM, epigenetic changes, and potential endocrine effects that influence long-term health. CONCLUSION Policies to reduce maternal exposure and health consequences in children should be a high priority. PM
Adult ; Air Pollutants/adverse effects* ; Air Pollution/prevention & control* ; Animals ; Cardiovascular Diseases/chemically induced* ; Child Health ; Child, Preschool ; Disease Models, Animal ; Endocrine System Diseases/chemically induced* ; Epigenomics ; Female ; Humans ; Immune System Diseases/chemically induced* ; Infant ; Infant, Newborn ; Male ; Maternal Exposure/adverse effects* ; Nervous System Diseases/chemically induced* ; Oxidative Stress ; Particle Size ; Particulate Matter/adverse effects* ; Placenta ; Pregnancy ; Pregnancy Outcome/epidemiology* ; Prenatal Exposure Delayed Effects/epidemiology* ; Respiratory Tract Diseases/chemically induced* ; Young Adult

Depression has a high incidence in patients with cardiovascular diseases (CVD) and shows adverse effects on their life quality and prognosis. With the advent of new antidepressant drugs, oral antidepressant drugs are increasingly used in CVD patients with depression, and their efficacy and safety have attracted attention. Commonly used antidepressant drugs have many adverse reactions. When applying antidepressant drugs in CVD patients, we should pay special attention to their cardiovascular adverse reactions and their interaction drugs with commonly used CVD drugs. Clinicians should comprehensively evaluate and select appropriate antidepressant drugs for patients.
Antidepressive Agents/adverse effects* ; Cardiovascular Diseases/chemically induced* ; Cardiovascular System ; Humans ; Incidence ; Patients

Heavy metal is one of pollutants existed widely in the environment, its relationship with cardiovascular disease has attracted more and more attention. In this review, the concentrations of heavy metals, including lead, cadium and asenic, in the body from several national surveillance networks and the epidemiological studies on the effects of the exposure of three heavy metals on cardiovascular system were summarized. It is suggested to strengthen nationwide surveillance for body concentrations of heavy metals in general population in order to provide baseline data for quantitative evaluation of the risk of heavy metal exposure on cardiovascular disease.
Cadmium ; Cardiovascular Diseases/chemically induced* ; Environmental Exposure/adverse effects* ; Environmental Pollutants/toxicity* ; Epidemiologic Studies ; Humans ; Lead/toxicity* ; Metals, Heavy/toxicity* ; Neoplasms ; Research/trends*

Arsenic is a unique element with distinct physical characteristics and toxicity whose importance in public health is well recognized. The toxicity of arsenic varies across its different forms. While the carcinogenicity of arsenic has been confirmed, the mechanisms behind the diseases occurring after acute or chronic exposure to arsenic are not well understood. Inorganic arsenic has been confirmed as a human carcinogen that can induce skin, lung, and bladder cancer. There are also reports of its significant association to liver, prostate, and bladder cancer. Recent studies have also suggested a relationship with diabetes, neurological effects, cardiac disorders, and reproductive organs, but further studies are required to confirm these associations. The majority of research to date has examined cancer incidence after a high exposure to high concentrations of arsenic. However, numerous studies have reported various health effects caused by chronic exposure to low concentrations of arsenic. An assessment of the health effects to arsenic exposure has never been performed in the South Korean population; thus, objective estimates of exposure levels are needed. Data should be collected on the biological exposure level for the total arsenic concentration, and individual arsenic concentration by species. In South Korea, we believe that biological exposure assessment should be the first step, followed by regular health effect assessments.
Arsenic/*toxicity/urine ; Cardiovascular Diseases/chemically induced ; *Environmental Exposure ; Environmental Pollutants/*toxicity ; Female ; Humans ; Male ; Neoplasms/chemically induced ; Reproduction/drug effects

Arsenic is a unique element with distinct physical characteristics and toxicity whose importance in public health is well recognized. The toxicity of arsenic varies across its different forms. While the carcinogenicity of arsenic has been confirmed, the mechanisms behind the diseases occurring after acute or chronic exposure to arsenic are not well understood. Inorganic arsenic has been confirmed as a human carcinogen that can induce skin, lung, and bladder cancer. There are also reports of its significant association to liver, prostate, and bladder cancer. Recent studies have also suggested a relationship with diabetes, neurological effects, cardiac disorders, and reproductive organs, but further studies are required to confirm these associations. The majority of research to date has examined cancer incidence after a high exposure to high concentrations of arsenic. However, numerous studies have reported various health effects caused by chronic exposure to low concentrations of arsenic. An assessment of the health effects to arsenic exposure has never been performed in the South Korean population; thus, objective estimates of exposure levels are needed. Data should be collected on the biological exposure level for the total arsenic concentration, and individual arsenic concentration by species. In South Korea, we believe that biological exposure assessment should be the first step, followed by regular health effect assessments.
Arsenic/*toxicity/urine ; Cardiovascular Diseases/chemically induced ; *Environmental Exposure ; Environmental Pollutants/*toxicity ; Female ; Humans ; Male ; Neoplasms/chemically induced ; Reproduction/drug effects

BACKGROUNDDyslipidemia caused by liver injury is a significant risk factor for cardiovascular complications. Previous studies have shown that hydrogen sulfide (H2S) protects against multiple cardiovascular disease states in a similar manner as nitric oxide (NO), and NO/endothelial nitric oxide synthase (eNOS) pathway is the key route of NO production. The purpose of this study was to investigate whether H2S can ameliorate the high blood pressure and plasma lipid profile in Nw-nitro-L-argininemethyl ester (L-NAME)-induced hypertensive rats by NO/eNOS pathway.

METHODSThirty-six 4-week old Sprague-Dawley (SD) male rats were randomly assigned to 6 groups (n = 6): control group, L-NAME group, control + glibenclamide group, control + NaHS group, L-NAME + NaHS group, and L-NAME + NaHS + glibenclamide group. Measurements were made of plasma triglycerides (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (CHO), glutamic-pyruvic transaminase (ALT) levels after 5 weeks. Then measurements of NO level and proteins expression of eNOS, P-eNOS, AKT, P-AKT were made in liver tissue.

RESULTSAfter 5 weeks of L-NAME treatment, the blood pressure, plasma TG ((1.22±0.12) mmol/L in L-NAME group vs. (0.68±0.09) mmol/L in control group; P < 0.05) and LDL ((0.54±0.04) mmol/L in L-NAME group vs. (0.28±0.02) mmol/L in control group; P < 0.05) concentration were significantly increased, and the plasma HDL ((0.26±0.02) mmol/L in L-NAME group vs. (0.69±0.07) mmol/L in control group; P < 0.05) concentration significantly decreased. Meanwhile the rats treated with L-NAME exhibit dysfunctional eNOS, diminished NO levels ((1.36±0.09) mmol/g protein in L-NAME group vs. (2.34±0.06) mmol/g protein in control group; P < 0.05) and pathological changes of the liver. H2S therapy can markedly decrease the blood pressure ((37.25±4.46) mmHg at the fifth week; P < 0.05), and ameliorate the plasma TG ((0.59±0.06) mmHg), LDL ((0.32±0.04) mmHg), and HDL ((0.46±0.03) mmHg) concentration in L-NAME + NaHS group (all P < 0.05). H2S therapy can also restore eNOS function and NO bioavailability and attenuate the pathological changes in the liver in L-NAME-induced hypertensive rats.

CONCLUSIONH2S protects the L-NAME-induced hypertensive rats against liver injury via NO/ eNOS pathway, therefore decreases the cardiovascular risk.

Animals ; Cardiovascular Diseases ; metabolism ; prevention & control ; Hydrogen Sulfide ; therapeutic use ; Hypertension ; chemically induced ; drug therapy ; Liver ; drug effects ; metabolism ; Male ; NG-Nitroarginine Methyl Ester ; toxicity ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase Type III ; metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; drug effects

BACKGROUND/AIMS: The increasing incidence of cardiovascular disease has led to an increase in the frequency of upper gastrointestinal (GI) hemorrhage due to the use of antiplatelet agents. This study examined the clinical characteristics of patients with upper GI hemorrhage who were administered aspirin alone or a combination treatment of antiplatelet agents. METHODS: A 656 patients who underwent drug-eluting coronary stenting at Ewha Mokdong Hospital in 2008 were divided into three groups according to the antiplatetlet agents used after the intervention; groups of aspirin alone, aspirin plus clopidogrel, and aspirin, and clopidogrel plus another antiplatelet agent, respectively. Patients admitted with GI hemorrhage in the same period without a medication history of antiplatelet or nonsteroidal anti-inflammatory drugs were used as the control hemorrhage group. The medical records were reviewed. RESULTS: Significant GI symptoms were observed in 21.1% of total patients, of whom 48.2% had ulcers. The upper GI hemorrhage rate was 3.8%. There was no significant difference in the hemorrhage rate between three groups. Compared to the control hemorrhage group, the endoscopic variables of the antiplatelet-related hemorrhage group were not significantly different. However, the Helicobacter pylori infection rate was lower, the admission period was longer, and the mortality rate was higher in the antiplatelet-related hemorrhage group (p<0.05, respectively). There was no direct association between restarting or discontinuance of antiplatelets after the hemorrhage event and mortality. CONCLUSIONS: Adding other antiplatelet agents to aspirin did not increase the hemorrhage rate. However, active diagnostic and therapeutic efforts are recommended in patients with GI symptoms during antiplatelet therapy.
Aged ; Aspirin/*adverse effects/therapeutic use ; Cardiovascular Diseases/prevention & control ; Drug Therapy, Combination ; Drug-Eluting Stents ; Endoscopy, Gastrointestinal ; Female ; Gastrointestinal Hemorrhage/*chemically induced/mortality/prevention & control ; Helicobacter Infections/complications/epidemiology ; Helicobacter pylori ; Humans ; Male ; Middle Aged ; Peptic Ulcer/complications/epidemiology ; Platelet Aggregation Inhibitors/*adverse effects/therapeutic use ; Retrospective Studies ; Risk Factors ; Ticlopidine/adverse effects/analogs & derivatives/therapeutic use

No abstract available.
Aspirin/*adverse effects/therapeutic use ; Cardiovascular Diseases/prevention & control ; Drug Therapy, Combination ; Drug-Eluting Stents ; Endoscopy, Gastrointestinal ; Gastrointestinal Hemorrhage/*chemically induced/mortality/prevention & control ; Humans ; Platelet Aggregation Inhibitors/*adverse effects/therapeutic use ; Risk Factors ; Ticlopidine/analogs & derivatives/therapeutic use