Automated blood pressure measurement in public places.
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Biomedical subjects
Publications and source records attributed to Raymond R Townsend.
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Following a hypertension symposium held in Philadelphia, PA, on June 8, 2004, a roundtable discussion was held to discuss the treatment of hypertension in adolescents and children. The participants included Thomas D. Giles, MD, of Louisiana State College of Medicine, New Orleans, LA; Bonita Falkner, MD, of the Department of Medicine and Pediatrics, Thomas Jefferson University, Philadelphia, PA; Allan B. Schwartz, MD, of the Division of Nephrology and Hypertension, Drexel University College of Medicine, Philadelphia, PA; Raymond R. Townsend, MD, of the Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA; and Marvin Moser, MD, of the Department of Medicine/Cardiology, Yale University School of Medicine, New Haven, CT.
BACKGROUND: Calcineurin inhibitor drugs (cyclosporine and tacrolimus) given to renal transplant recipients to prevent rejection are associated with an increased incidence of hypertension. Reduced arterial compliance, which is a consequence of hypertension, is associated with an increased risk of cardiovascular disease and can be measured noninvasively using pulse wave analysis technology. The purpose of the study was to determine whether calcineurin inhibitor drugs have any effect on arterial compliance. METHODS: A total of 36 stable renal transplant recipients were evaluated using pulse wave analysis to determine large and small vessel compliance. Of the patients, 18 were receiving cyclosporine and 18 tacrolimus. Patients were matched for age and sex. RESULTS: No significant differences in systolic blood pressure, diastolic blood pressure, heart rate, or small vessel compliance were observed. There was a significant decrease in large vessel compliance in patients receiving tacrolimus versus those receiving cyclosporine, respectively (13.5 +/- 4.0 mL/mm Hg x 10 v 9.9 +/- 3.3 mL/mm Hg x 10; P =.005). CONCLUSIONS: Differences in large vessel compliance in renal transplant subjects may depend on the choice of calcineurin inhibitor. Specifically, decreased large vessel compliance in tacrolimus-treated subjects may be associated with an increased cardiovascular risk. This may be due to a difference in vascular collagen accumulation or to elastin loss in large elastic arteries.
BACKGROUND: Many patients seek complementary medicine treatments like neutraceuticals for common conditions such as hypertension. METHODS: We conducted a placebo-controlled prospective randomized crossover study in 10 hypertensive subjects to determine whether a single dose of a hydrolysate of bovine milk protein (designated C12 peptide; low and high dose), either alone or combined with alginic acid (low and high dose), reduced daytime blood pressure (BP), as determined by ambulatory BP monitoring. RESULTS: Within the five treatment regimens a significant reduction of 9.2 +/- 3.2 mm Hg in systolic BP at h 6 compared with h 2 occurred on the higher dose of alginic acid (1754 mg) combined with C12 (P = .02). The C12 peptide with the higher dose of alginic acid also showed a significant reduction of 6.0 +/- 2.0 mm Hg in diastolic BP at h 6 compared with h 2 (P = .015). CONCLUSIONS: These preliminary data are encouraging and deserve testing in a larger and longer treatment trial.
Segmental arterial mediolysis (SAM) is a rare condition caused by loss of muscular elements in the walls of medium-sized, usually visceral, arteries. This causes dissection, occlusion, aneurysm formation, and rupture. The clinical presentation is usually catastrophic as a result of vascular occlusion or rupture. Herein an unusual case of renovascular hypertension resulting from SAM is reported, which was successfully treated with balloon angioplasty.
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Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Because fructose, unlike glucose, does not stimulate insulin secretion, we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose. Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30, and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGl)] beverage. Meals were isocaloric in the two treatments. Postprandial glycemic excursions were reduced by 66 +/- 12%, and insulin responses were 65 +/- 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 +/- 7%; P < 0.005), the entire 24 h (-21 +/- 8%; P < 0.02), and the diurnal amplitude (peak - nadir) (24 +/- 6%; P < 0.0025) were reduced on the HFr day compared with the HGl day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGl meal (P < 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGl). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day (P < 0.005). Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.
Experimentally induced prolonged hyperglycemia increases insulin release in humans, and in animals has been demonstrated to increase vagal efferent activity. The objective of the present experiment was to determine whether in humans, the compensatory increase in insulin release in response to short-term mild hyperglycemia is mediated by an induction of vagal efferent activity. Lean male subjects (n = 11; body mass index, 23.6 +/- 0.8 kg/m(2)) underwent a frequently sampled iv glucose tolerance test (FSIGT) to determine B cell function and insulin sensitivity. Subjects were then tested under four conditions over 4 months. Subjects were infused for 48 h with either glucose (15% dextrose at 200 mg/m(2).min) or saline (50 ml/h). Three hours after termination of the infusion, an FSIGT was administered in the presence of either saline or atropine (0.4 mg/m(2) bolus: 0.4 mg/m(2).h). Glucose (117 +/- 14 vs. 98 +/- 5 mg/dl) and insulin (49.5 +/- 10 vs. 23 +/- 5 muU/ml) levels were significantly elevated during the 48-h glucose infusion compared with those during saline treatment. Forty-eight-hour glucose infusions increased insulin and C-peptide levels during the FSIGT. When the FSIGT was conducted in the presence of atropine after glucose infusion, C-peptide levels were significantly attenuated during the period of endogenous insulin secretion (0-20 min; 31.8 +/- 13 vs. 39.2 +/- 11.9, atropine vs. no atropine) and exogenous insulin administration [20-40 min; 18.8 +/- 10.8 vs. 31.6 +/- 12.9., atropine vs. no atropine; F(3,9) = 4.99; P < 0.026]. A significant negative correlation was found between the repression of C-peptide by muscarinic blockade and the magnitude of the C-peptide response to the glucose infusion (r = 0.60; P < 0.045). Insulin AUC was not significantly altered by the presence of muscarinic blockade. In summary, we found that prolonged mild hyperglycemia results in a compensatory increase in C-peptide secretion, which is partially mediated by an induction in vagal efferent activity.
Pheochromocytomas and paragangliomas are tumors of the autonomic nervous system; pheochromocytomas are tumors of the adrenal medulla, and paragangliomas are extra-adrenal tumors arising from either the sympathetic nervous system or parasympathetic ganglia. It has previously been estimated that approximately 10%-15% of pheochromocytomas are due to hereditary causes. However, our increased understanding of the three hereditary syndromes (neurofibromatosis 1, multiple endocrine neoplasia type 2, and von Hippel-Lindau syndrome) in which pheochromocytoma is found and the recent discovery that mutations in genes in the succinate dehydrogenase family (SDHB and SDHD) predispose to pheochromocytoma have necessitated a re-evaluation of the genetic basis of pheochromocytoma. These studies indicate that the frequency of germline mutations associated with isolated pheochromocytoma is higher than previously estimated, with both hospital-based series and a large population-based series indicating that the frequency of germline mutations in RET, VHL, SDHB, and SDHD taken together approximates 20%. In all patients with pheochromocytoma, including those with known hereditary syndrome or a positive family history, the frequency of germline mutations in these four genes together approaches 30%. Given the frequency of germline mutations, consideration should be given to genetic counseling for all patients with pheochromocytoma and is particularly important for individuals with a positive family history, multifocal disease, or a diagnosis before age 50. Identification of patients with hereditary pheochromocytoma is important because it can guide medical management in mutation-positive patients and their families. This review provides an overview of the known genetic syndromes that are commonly associated with pheochromocytoma, examines recent data on the association of germline mutations in the succinate dehydrogenase gene family with pheochromocytoma, and suggests guidelines for the genetic evaluation of pheochromocytoma patients.
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Resistance to the metabolic effects of insulin is a contender for the short list of major cardiovascular risk factors. Since the elements of the syndrome of insulin resistance were first articulated together in 1988, numerous epidemiologic investigations and treatment endeavors have established a relationship between the metabolic disarray of impaired insulin action and cardiovascular disease. Angiotensin II, the primary effector of the renin-angiotensin system, has also achieved a place in the chronicles of cardiovascular risk factors. Conspiracy mechanisms by which angiotensin II and insulin resistance interact in the pathogenesis of cardiovascular disease are reviewed, with particular attention to recent developments in this engaging area of human research.
BACKGROUND: Underenrollment and selective enrollment plague many clinical trials. Little is known about why hypertensive patients agree or refuse to participate in placebo-controlled trials (PCT) of antihypertensive drugs, whether the prospect of receiving placebo influences willingness to participate (WTP), or whether patients who participate differ from those who do not. METHODS: We described a hypothetical PCT of a new antihypertensive drug to 126 patients who would be eligible for ongoing phase III trials. We solicited patient motivations and concerns regarding trial participation by using open-ended questions, assessed the patients' stated WTP, and used logistic regression to determine patient characteristics associated with WTP. We reassessed WTP in 62 patients after revealing, in random order, that 10%, 30%, and 50% of patients would receive placebo. RESULTS: The most commonly cited motivations for participating included personal health benefits (40%), helping other patients (37%), and contributing to scientific knowledge (15%). The most common concerns were having to stop current medications (56%), inconvenience/annoyance (38%), fear of known side effects (35%), and the possibility of receiving placebo (24%). Overall, 47% of patients (95% confidence interval, 38% to 56%) were willing to participate. Younger patients (57% versus 37%; P =.01), nonsmokers (50% versus 24%; P =.04), and patients who had participated in research previously (77% versus 20%; P =.009) were all significantly more willing to participate. Fewer patients were willing to participate as the percentage who would receive placebo increased (P =.02), but randomly assigning fully half of patients to placebo still yielded maximal recruitment efficiency. CONCLUSIONS: Hypertensive patients participate in trials for altruistic and personal health reasons. Differences between patients who do or do not participate may influence trial outcomes. The proportion of patients receiving placebo influences some patients' enrollment decisions but is not a key determinant of recruitment efficiency.