Exposure to household air pollution from biomass-burning cookstoves and HbA1c and diabetic status among Honduran women.

Household air pollution from biomass cookstoves is estimated to be responsible for more than two and a half million premature deaths annually, primarily in low and middle-income countries where cardiometabolic disorders, such as Type II Diabetes, are increasing. Growing evidence supports a link between ambient air pollution and diabetes, but evidence for household air pollution is limited. This cross-sectional study of 142 women (72 with traditional stoves and 70 with cleaner-burning Justa stoves) in rural Honduras evaluated the association of exposure to household air pollution (stove type, 24-hour average kitchen and personal fine particulate matter [PM2.5 ] mass and black carbon) with glycated hemoglobin (HbA1c) levels and diabetic status based on HbA1c levels. The prevalence ratio (PR) per interquartile range increase in pollution concentration indicated higher prevalence of prediabetes/diabetes (vs normal HbA1c) for all pollutant measures (eg, PR per 84 µg/m3 increase in personal PM2.5 , 1.49; 95% confidence interval [CI], 1.11-2.01). Results for HbA1c as a continuous variable were generally in the hypothesized direction. These results provide some evidence linking household air pollution with the prevalence of prediabetes/diabetes, and, if confirmed, suggest that the global public health impact of household air pollution may be broader than currently estimated.

A critical review of the evidence supporting aldosterone in the etiology and its blockade in the treatment of obesity-associated hypertension.

Obesity is epidemic and is associated with increased blood pressure, which often manifests as treatment-resistant hypertension. Mineralocorticoids have been hypothesized to have a pathogenic role in human obesity-associated hypertension. In this review, we critically appraise the existing data regarding aldosterone in the pathophysiology and treatment of obesity-associated hypertension. We begin by reviewing the mechanisms by which obesity may increase mineralocorticoid activity. We then discuss human studies of plasma and urine aldosterone in obesity and with weight loss. From these studies, we conclude that aldosterone is often, but not always, mildly increased in obesity. Further study is needed to define circumstances in which aldosterone is increased in obesity. We discuss clinical studies in which measures of body size or weight were evaluated as potential predictors of response to mineralocorticoid receptor antagonists. In addition, we review three randomized, controlled clinical trials that exemplify a rigorous approach to determining the role of mineralocorticoid activity in a human disease. We propose that a similar clinical trial is warranted in order to definitively clarify the role of inappropriate mineralocorticoid activity in the etiology of human obesity-associated hypertension. Finally, we conclude that additional research is needed into the possible role of non-aldosterone mineralocorticoids in human obesity-associated hypertension.

Usefulness of visceral obesity (waist/hip ratio) in predicting vascular endothelial function in healthy overweight adults.

Vascular endothelial dysfunction (VED) is associated with obesity; however, its etiology remains controversial. By determining the predictors of fasting and postprandial endothelial function in overweight adults without other cardiovascular risk factors, we were able to investigate novel mechanisms directly linking obesity to VED. Thirty-two healthy adults (body mass index [BMI] > or =27 kg/m(2)) underwent determination of fasting low-density lipoprotein (LDL) particle size, high sensitivity C-reactive protein levels, anthropometric measurements, and endothelial function by flow-mediated dilation (FMD) of the brachial artery. Postprandial lipemia and FMD were measured 4 hours after ingestion of a high-fat meal. Blood pressures and fasting levels of lipoproteins, glucose, insulin, and fatty acids were within normal limits in all subjects. An abdominal fat pattern, as determined by an increased waist/hip ratio (WHR), was the sole significant predictor of FMD (r = -0.58, p = 0.001), despite no significant correlation between whole body obesity (BMI) and FMD. At comparable levels of BMI, obese subjects with a WHR > or =0.85 had a significantly blunted FMD compared with those with a WHR <0.85 (3.93 +/- 2.85% vs 8.34 +/- 5.47%, p = 0.016). Traditional coronary risk factors, C-reactive protein, postprandial lipemia, and LDL particle size did not predict FMD. We found no appreciable alteration in the postprandial state from fasting FMD (6.31 +/- 4.62% vs 6.25 +/- 5.47%, p = 0.95). The same results were found when women were analyzed alone. Increased abdominal adiposity determined by a simple WHR is a strong independent predictor of VED even in healthy overweight adults; this is a finding unexplained by alterations in conventional risk factors, systemic inflammation, or the atherogenic lipoprotein pattern.

Mechanism of differential effects of antihypertensive agents on serum lipids.

Essential hypertension is frequently associated with the metabolic abnormalities of insulin resistance and dyslipidemia. This prevalent clustering of multiple cardiovascular risk factors may help explain the less-than-expected improvement in coronary heart disease mortality provided by simple blood pressure reduction alone. Many antihypertensive medications effectively reduce blood pressure while providing no benefit or even causing a detrimental effect on the associated metabolic abnormalities. beta-Blockers and diuretics tend to negatively affect both glucose tolerance and plasma lipids. Calcium channel blockers, angiotensin converting enzyme inhibitors, and angiotensin II receptor blockers are most often found to be metabolically neutral. alpha-Blockers provide the most favorable metabolic effects of antihypertensive agents by improving both insulin sensitivity and dyslipidemia. The multiple physiologic mechanisms by which blood pressure medications alter plasma lipids are discussed in detail. The effects of antihypertensive medications on postprandial lipid metabolism and the associated postprandial lipemia-induced endothelial dysfunction deserve special attention.

Autonomic imbalance, hypertension, and cardiovascular risk.

Essential hypertension conveys an increased risk of cardiovascular morbidity and mortality. The common finding of an autonomic imbalance in these patients contributes not only to the etiology of hypertension itself, but also to the cardiac risk and resulting adverse sequelae. A high sympathetic tone in particular is responsible for many of the metabolic, hemodynamic, trophic, and rheologic abnormalities that cluster in patients with high blood pressure. Methods to clarify the respective importance of prereceptor versus receptor abnormalities for the etiology of insulin resistance are warranted. Results of large hypertension clinical trials examining the degree of cardioprotection offered by newer medications that are neutral or beneficial to the vast array of underlying abnormalities are a few years away. In the meantime, utilization of antihypertensive drugs that reduce sympathetic overactivity and are metabolically beneficial is a reasonable clinical alternative in hypertensive patients with the metabolic syndrome or with signs of autonomic imbalance.

Home blood pressure: accuracy is independent of monitoring schedules.

Long-term morbidity and mortality from hypertension are more closely related to home than to casual office blood pressure levels. There is no generally accepted recommendation on how to best schedule home blood pressure (HBP) recordings, perhaps because the effect of varying the home monitoring schedule on the HBP average is not well studied. The goals of this analysis are to describe the effects of HBP monitoring schedules on the accuracy of resultant HBP averages and to determine which monitoring schedule parameters correlate with HBP accuracy. Twelve published studies, each including home, office, and awake ambulatory blood pressure means were identified. Accuracy of office and HBP averages were determined by their agreement with corresponding awake ambulatory averages. Variations in HBP monitoring schedule parameters did not significantly affect the accuracy of the resultant HBP averages among the studies. In univariate analyses, no individual parameter correlated significantly with the final HBP average accuracy. As the total number of HBP readings obtained increased, or as other monitoring schedule parameters intensified, the superior accuracy of HBP levels as compared to that of casual office values also failed to significantly improve. No HBP accuracy differences were found among groups characterized by different HBP schedule parameter ranges. In conclusion, the accuracy of HBP measurements, as determined by their agreement with an awake ambulatory mean, is maintained regardless of substantial variations in HBP monitoring schedules. Therefore, the majority of the benefits derived from HBP monitoring will likely be achieved by obtaining only a few HBP measurements using a minimally complex monitoring schedule.

Measurement variation among 12 electronic home blood pressure monitors.

Although there are AAMI and BHS standards for accuracy of electronic home electronic blood pressure monitors (HBPM), patient composition differences and differences in manufacturer's algorithm for calculation of the systolic and diastolic measurement may result in measurement differences between monitors. The aim of this study was the measurement of differences among HBPM. Paired comparisons were performed between the Omron 712c electronic home monitor and each of 12 other HBPM (Sunbeam 7654, Sunbeam 7623, Omron 711, Omron 432c, A&D-UA767, Lumiscope 1085M, Omron 725CIC, Assure A30, Lumiscope 1083N, Omron 815, Omron 605, and Assure BD-W20), in addition to comparison to the auscultatory method by trained observers. Measurements were made in normotensive subjects in an ambulatory setting. The main outcome measures were systolic and diastolic blood pressure measurements. All of the HBPM, except for the Sunbeam 7654 and the Assure A30/ BD-W20 (wrist) models, demonstrated small differences of <4/4 mm Hg for systolic/diastolic measurements with pulse measurement differences of <3 beats/min. These differences were less than the differences previously reported for office BP auscultation of 6/5-10 mm Hg for systolic/diastolic measurements. The Omron 712c, passing previous AAMI and BHS standards, measured the systolic reading within 2 mm Hg of auscultatory mercury or aneroid measurement and under-measured the diastolic by 6-9 mm Hg. Differences in the patient composition studied could account for the difference. The wrist and finger manometers performed clinically similar to the Omron 712c, except for the Assure BD-W20, which overmeasured the diastolic by 7 mm Hg. It is concluded that the small differences among the various HBPM, which are less than those in clinical office auscultation, should encourage greater use of electronic manometers in the office and at home.

Role of secondary prevention in congestive heart failure due to coronary artery disease.

Preventing the progression of established heart failure can be difficult, as multiple factors contribute to the continual decline of cardiac function. Blunting the activated neurohormonal response to a decreased systolic function is a proven means of slowing progression of CHF. Preventing further CAD and cardiac ischemia may also prove to be an effective mechanism. Two trials with HMGCoA reductase inhibitors lend support to this hypothesis. Studies using ACE inhibitors may also support this notion. Since a major portion of heart failure in the USA is caused by CAD, preventing CHF progression may be related to the prevention of CAD. Using ACE inhibitors and lipid-lowering agents, in addition to standard measures of CAD risk factor modification, may prove useful in future trials to retard the progression of heart failure. Further research and clinical trials involving this method of CHF prevention are warranted.