Effect of Low-Dose Persistent Organic Pollutants on Mitochondrial Function: Human and in Vitro Evidence

Background@#Chronic exposure to low-dose persistent organic pollutants (POPs) can induce mitochondrial dysfunction. This study evaluated the association between serum POP concentrations and oxygen consumption rate (OCR) as a marker of mitochondrial function in humans and in vitro cells. @*Methods@#Serum concentrations of organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) were measured in 323 adults. The OCRs of platelets and peripheral blood mononuclear cells (PBMCs) were assessed in 20 mL of fresh blood using a Seahorse XF analyzer. Additionally, the in vitro effects of Arochlor-1254, β-hexachlorocyclohexane, and p,p´-dichlorodiphenyltrichloroethane at concentrations of 0.1 pM to 100 nM were evaluated in human platelets, human PBMCs, and Jurkat T-cells. @*Results@#The association between serum POP concentrations and OCR differed depending on the cell type. As serum OCP concentrations increased, basal platelet OCR levels decreased significantly; according to the OCP quintiles of summary measure, they were 8.6, 9.6, 8.2, 8.0, and 7.1 pmol/min/μg (P trend=0.005). Notably, the basal PBMC OCR levels decreased remarkably as the serum PCB concentration increased. PBMC OCR levels were 46.5, 34.3, 29.1, 16.5, and 13.1 pmol/min/μg according to the PCB quintiles of summary measure (P trend <0.001), and this inverse association was consistently observed in all subgroups stratified by age, sex, obesity, type 2 diabetes mellitus, and hypertension, respectively. In vitro experimental studies have also demonstrated that chronic exposure to low-dose POPs could decrease OCR levels. @*Conclusion@#The findings from human and in vitro studies suggest that chronic exposure to low-dose POPs can induce mitochondrial dysfunction by impairing oxidative phosphorylation.

Two Cases of High Output Heart Failure Caused by Hereditary Hemorrhagic Telangiectasia

High-output cardiac failure is a rare complication of hereditary hemorrhagic telangiectasia (HHT) usually caused by shunting of blood through atriovenous malformations (AVMs) in the liver. We describe two cases of high output heart failure due to large hepatic AVMs. Clinical suspicion of HHT based on detailed history taking and physical examination is essential for early detection and proper management of heart failure associated with HHT.

The Source of Inflammatory Response and Platelet Activation in Patients with Acute Myocardial Infarction

BACKGROUND AND OBJECTIVES: Studies on the stability of atheromatous plaques, as a determinant of the cause of complications, have been reported. Among the functional features of plaques related with vulnerability, inflammation has emerged as a leading cause of clinical presentation. The purpose of this study was to find the source of the inflammatory response in the patients with acute myocardial infarction (AMI). SUBJECTS AND METHODS: Patients with AMI, whose lesion of in either the left anterior descending artery (LAD group, n=13) or the right coronary artery (RCA group, n=11), were selected. The levels of interleukin-6 (IL-6) and P-selectin were measured in blood from the aortic root (A), great cardiac vein (G) and peripheral vein (V). The control group (n=15) included patients with either stable or variant angina. RESULTS: The levels of IL-6 were 4.77+/-6.0 (A), 11.32+/-7.8 (G) and 4.39+/-5.0 pg/mL (V) in the LAD group, and 3.64+/-2.1 (A), 6.05+/-4.9 (G) and 3.84+/-3.2 pg/mL (V) in the RCA group. Unrelated to the infarction related artery, the level of IL-6 in the great cardiac vein was significantly increased in patients with AMI. The percentages of platelet expressed P-selectin were 6.03+/-7.0 (A), 8.14+/-8.1 (G) and 8.83+/-7.9 (V) in the LAD group and 6.46+/-8.4 (A), 5.80+/-6.0 (G) and 5.91+/-6.9 (V) in the RCA group. CONCLUSION: These findings suggest that the generalized inflammatory response is activated across the coronary vascular bed in patients with AMI, regardless of the infarction related artery site. Therefore, systemic therapy, as well as local management for vulnerable plaque, would be required.

Relation of Blood Pressure Components to Left Ventricular Hypertrophy and Coronary Heart Disease with Aging

BACKGROUND AND OBJECTIVES: There is still uncertainty regarding the relative importance of systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP) in predicting the risk of cardiovascular disease. The relative importance of the BP components, as markers of left ventricular hypertrophy (LVH) and coronary artery disease (CAD), were examined in relation to age. SUBJECTS AND METHODS: In 257 subjects receiving no antihypertensive medication, LVH was determined using the M-mode echocardiography when left ventricular mass index (LVMI) was >or =129 g/m2 in men or >or =118 g/m2 in women. In a further 265 subjects, CAD was determined using the coronary angiography when stenosis of the coronary arterial diameter was >or =70%. The most important BP component was determined using a logistic regression analysis. RESULTS: With respect to LVH, in the group 0.10) for DBP, SBP and PP respectively. In the group 50 to 59 years of age, ORs were 1.65, 1.35, 1.36 (all por =60 years of age, ORs were 1.56 (p0.10), 1.07 (p>0.10), 1.21 (por =60 years of age, no BP component had a statistical significance. CONCLUSION: With increasing age, there was a gradual shift from DBP to SBP and then to PP as the marker with the greatest relation to LVH. In all age group, PP was the strongest marker of CAD.

Anomalous Origin of the Right Coronary Artery from the Diagonal Branch of the Left Anterior Descending Coronary Artery

Anomalous origin of the right coronary artery (RCA) is uncommon in patients undergoing cardiac catheterization. Most RCA anomalies are usually found incidentally. However, some anomalies may be associated with malignant courses such as myocardial ischemia, syncope or sudden cardiac death. We present a previously unreported case of a 55-year-old female who had anomalous RCA arising from the diagonal branch of LAD, a variant of L-II Lipton classification, which caused chest pain.

The Relationship between Serum Adiponectin, Essential Hypertension, LV Mass Index, and LV Diastolic Function

BACKGROUND AND OBJECTIVES: Adiponectin is known for its anti-inflammatory and anti-atherogenic effects. The purpose of this study is to characterize the relationships among serum adiponectin, essential hypertension (EH), left ventricular mass index (LVMI), and LV diastolic function. SUBJECTS AND METHODS: Serum adiponectin by RIA and body mass index were measured in 275 patients (M: F=137: 138). We calculated LVMI, E/A ratio, deceleration time (DT), and isovolumetric relaxation time (IVRT) by using echocardiograms. RESULTS: The serum adiponectin level of the hypertensive group was significantly lower than that of the non-hypertensive group (9.9+/-9.8 ug/mL vs. 12.9+/-9.5 ug/mL, p<0.05). Plasma adiponectin was negatively correlated with LVMI (r=-0.329, p<0.001), BMI (r=-0.290, p<0.001), and IVRT (r=-0.485, p<0.05), but was positively correlated with E/A (r=+0.359, p<0.001). CONCLUSION: These results suggest that a decrease in serum adiponectin is associated with an increase in blood pressure and BMI, progress of LVH, and decrease in LV diastolic function.

A Case of Anterior Papillary Muscle Rupture with Total Occlusion of Right Coronary Artery Resulting in Inferior Myocardial Infarction

The arterial supply of the posteromedial papillary muscle of the left ventricle arises from the terminal branches of the right or circumflex arteries, depending on the distribution of these arteries. The anterolateral papillary muscle of the left ventricle is supplied primarily by one or more branches from the left anterior descending coronary artery, although it may also be supplied by circumflex marginal branches. The anterolateral papillary muscle is supplied only by the branches of the left coronary artery. However, in our case, the patient demonstrated a total occlusion of the right coronary artery that resulted in acute inferior myocardial infarction with a complete anterolateral papillary muscle rupture of the left ventricule as well as acute mitral insufficiency.