Search

Objectives: The goal of this work was to evaluate the accuracy of a new heart failure (HF) sensor (HFS) (Heart Failure Sensor, CardioMEMS Inc., Atlanta, Georgia) pulmonary artery pressure (PAP) monitoring compared with Swan-Ganz (SG) (Hospira, Inc., Lake Forest, Illinois) catheterization and echocardiography (ECHO) in ambulatory HF patients., Background: There is an increasing interest in the development of ambulatory monitoring devices aiming to adjust therapy and prevent hospitalizations in HF patients., Methods: Twelve patients with HF and New York Heart Association functional class II to IV were included in this study. The HFS was deployed into the pulmonary artery under angiography, allowing wireless PAP measurement. Two independent blind operators performed 3 HFS measurements at each visit, with simultaneous ECHO at 2, 14, 30, 60, and 90 days. Swan-Ganz catheterization was performed at 0 and 60 days. Linear regression was used as a measure of agreement. Variability between methods and interobserver variability were evaluated by Bland-Altman analysis., Results: Mean age was 63 +/- 14.6 years. Systolic PAP was 64 +/- 22 mm Hg and 58 +/- 22 mm Hg for HFS and SG, respectively (p < 0.01). Both methods showed a significant correlation (r2 = 0.96 baseline, r2 = 0.90 follow-up, p < 0.01), with a mean difference of 6.2 +/- 4.5 mm Hg. Diastolic PAP was 23 +/- 14 mm Hg and 28 +/- 16 mm Hg for HFS and SG, respectively (r2 = 0.88 baseline, r2 = 0.48 follow-up, p < 0.01), with a mean difference of -1.6 +/- 6.8 mm Hg. Systolic PAP was 60 +/- 20 mm Hg and 62 +/- 12 mm Hg for HFS and ECHO, respectively (r2 = 0.75, p < 0.01), with a mean difference of -2.6 +/- 11 mm Hg. There was no significant interobserver difference., Conclusions: The HFS provides an accurate method for PAP assessment in the intermediate follow-up of HF patients.

We wished to determine whether enhanced bioavailability of bradykinin (BK) and vasodilatory prostaglandins contribute to renovascular and sodium-handling effects of angiotensin-converting enzyme (ACE) inhibition after myocardial infarction (MI). We studied rats after coronary artery ligation treated for 3 weeks with captopril or losartan (2 g/L drinking water for each agent). Hemodynamic and renal function studies were performed in conscious rats before and after sequential infusion BK inhibitor (BKI, 0.02 ng/kg/min) and indomethacin (1 mg/kg). Myocardial infarction increased filtration fraction (FF) 20% (p < .004) but did not change glomerular filtration rate (GFR), urine flow (UF), renal blood flow (RBF), renal vascular resistance (RVR), urine sodium (UNa), or fractional excretion of sodium (FENa). Captopril decreased (p < 0.001) mean arterial pressure (MAP) 25%, UF 61%, RVR 65%, and FENa 75% and increased (p < 0.05) GFR 22%, and RBF 34%. Losartan decreased (p < 0.05) MAP 27%, UF 52%, RVR 21%, and FENa 44%. In captopril-treated MI rats, BKI decreased (p < 0.05) GFR 22% and RBF 25% and increased (p < 0.05) RVR 32%, UNa 43%, and FENa 28%, whereas indomethacin decreased (p < 0.05) GFR 24% and increased (p < 0.05) UNa 86% and FENa 112%. In losartan-treated MI rats, BKI increased (p < 0.05) UNa 42% and FENa 60%, whereas indomethacin increased (p < 0.05) UNa 79% and FENa 85%. Activation of the BK and prostaglandin systems may play an important role in regulating renal function during chronic ACE inhibition, primarily by enhancing the renal vasodilatory effects of angiotensin II (AII) blockade.

The purpose of this study was to determine whether a 4-week consumption of 1.5L per day of drinking water containing monochloramine at a concentration of 2 ppm (ppm = mg/L) or 15 ppm under controlled conditions would alter parameters of lipid or thyroid metabolism in healthy men. Forty-eight men completed an 8-week protocol during which diet (600 mg cholesterol per day, 40% calories as fat) and other factors known to affect lipid metabolism were controlled. During the first 4 weeks of the protocol, all subjects consumed distilled water. During the second 4 weeks, one-third of the subjects were assigned randomly to drink 1.5 L per day of water containing 2 ppm of monochloramine, to drink 1.5 L per day of water containing 15 ppm monochloramine, or to continue drinking distilled water. Four blood samples were collected from each subject at the end of each 4-week study period. Subjects drinking monochloramine at a concentration of 2 ppm showed no significant changes in total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, apolipoproteins A1, A2, or B when compared to the distilled water group. Parameters of thyroid function also were unchanged by exposure to monochloramine at this concentration. However, subjects drinking monochloramine at a concentration of 15 ppm experienced an increase in the level of apolipoprotein B. Other parameters of lipid and thyroid metabolism did not change. We conclude that consumption of drinking water containing 2 ppm of monochloramine does not alter parameters of lipid and thyroid metabolism in healthy men. Consumption of water containing 15 ppm monochloramine may be associated with increased levels of plasma apolipoprotein B.

Animal studies and a single human epidemiological study have suggested that chlorine in drinking water may raise the level of blood cholesterol. The purpose of this study was to determine whether a 4-week exposure to drinking water chlorine (1.5 L per day) at a concentration of 20 ppm (ppm = mg/L) under controlled conditions would alter circulating parameters of lipid metabolism in healthy humans. Thirty men and thirty women each completed an 8-week protocol during which diet (600 mg cholesterol per day, 40% calories as fat) and other factors known to affect lipid metabolism were controlled. For the first 4 weeks of the protocol, all subjects consumed distilled water. For the second 4 weeks, half of the subjects were assigned randomly to drink 1.5 L per day of chlorinated water (20 ppm), while the others continued drinking distilled water. Four blood samples were collected from each subject at the end of each 4-week study period. Compared to the control group, those subjects given chlorine showed no significant changes in total plasma cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, or apolipoproteins A1, A2, or B. There was a trend toward low serum thyroxine and triiodothyronine levels in men given chlorine, though thyroid-stimulating hormone levels were unchanged. This trend, if real, was not clinically significant. Thus, short-term exposure to chlorinated drinking water at 20 ppm appears to have no significant impact on parameters of lipid or thyroid metabolism in healthy humans.

Activation of the renin-angiotensin and sympathetic nervous systems in heart failure may result in altered baroreflex control of heart rate. To determine the specific effects of treatment with captopril on baroreceptor dysfunction in heart failure, baroreflex control of heart rate was measured in conscious rats with heart failure 6 weeks after ligation of the left coronary artery. Plasma norepinephrine was measured as a reflection of sympathetic nervous system activity. After bolus injections of phenylephrine (2-50 micrograms/kg) and nitroprusside (2-50 micrograms/kg), the arterial baroreflex was analyzed by fitting percentage of mean arterial pressure changes and heart rate changes to a logistic regression function. There were no differences in baroreflex function between normal and sham-operated rats. Plasma norepinephrine was increased (P < .05) in the heart-failure rats and did not change with captopril treatment. In untreated rats, heart failure increased (P < .05) the centering point by 900%, threshold by 243% and saturation by 89%, whereas decreasing (P < .05) the operational point by 73%. There was a decrease (P < .05) in the nitroprusside-related gain and an increase (P < .05) in phenylephrine-related gain, but the overall baroreflex gain was not changed. In heart-failure rats, captopril increased (P < .05) threshold, saturation and centering point and decreased (P < .05) operational point and nitroprusside- and phenylephrine-related gain abnormalities. The increase in operational point and decreases in threshold, saturation, centering point and phenylephrine-related gain were the results of a specific interactive effect of captopril in heart failure (P = .0033, .0176, .0509, .0217 and .0567, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Study Objective: To assess the effects of ibuprofen on blood pressure control in patients being treated with antihypertensive drugs., Design: Randomized, blinded, placebo-controlled, parallel trial of ibuprofen compared with acetaminophen and with placebo in 3-week treatment periods., Setting: A general internal medicine clinic at a university hospital., Patients: Forty-five patients with essential hypertension controlled by treatment with at least two antihypertensive drugs were enrolled. Of these, 41 completed the study; treatment was discontinued in 3 of the 15 patients in the ibuprofen group due to breakage of the drug capsules, and after randomization in 1 of the 14 patients in the placebo group due to unstable angina. All 15 patients in the acetaminophen group completed the study., Interventions: All previous antihypertensive regimens were continued. During the 3-week treatment, ibuprofen, 400 mg, was administered orally every 8 hours; acetaminophen, 1 g, orally every 8 hours; or placebo, 2 capsules, orally every 8 hours., Measurements and Main Results: In the ibuprofen group, the mean increase from baseline after 3 weeks of treatment was significant in the average supine diastolic blood pressure (6.4 mm Hg; 95% confidence interval [CI], 1.05 to 11.75; p = 0.0239); supine mean arterial pressure (6.6 mm Hg; 95% CI, 1.25 to 11.95; p = 0.0205); and sitting mean arterial pressure (5.8 mm Hg; 95% CI, 1.57 to 10.04; p = 0.0123). The mean increase in blood pressure variables in the ibuprofen group was significantly different compared with the mean increase in the variables in the placebo group after 3 weeks of treatment: supine systolic blood pressure (7.1 mm Hg compared with -4.5 mm Hg; 95% CI for the difference in means, 2.5 to 20.6; p = 0.0133); supine diastolic pressure (6.4 mm Hg compared with 0.0; 95% CI for difference in means, 0.87 to 12.4; p = 0.0250); supine mean arterial pressure (6.6 mm Hg compared with -1.5; 95% CI for difference in means, 2.0 to 14.2; p = 0.0110); sitting systolic pressure (6.8 mm Hg compared with -3.7; 95% CI for difference in means, 2.0 to 19.0; p = 0.0169); sitting diastolic pressure (5.3 mm Hg compared with -1.1; 95% CI for difference in means, 0.76 to 12.1; p = 0.0273); and sitting mean arterial pressure (5.8 mm Hg compared with -2.0; 95% CI for difference in means, 1.5 to 14.1; p = 0.0169).(ABSTRACT TRUNCATED AT 400 WORDS)

The safety of sympathomimetic decongestants (SMDs) in patients with hypertension remains controversial. Little experimental evidence exists for making proper recommendations regarding their use in hypertensive subjects. In order to determine the correct role of SMDs in such patients, physicians will need criteria with which to assess new data and reevaluate the existing literature. Using standardized methodologic criteria to judge clinical trials, we critically appraised the published evidence of the effects of SMDs on blood pressure control in hypertensive patients. A search of the English literature from 1966 to 1984 revealed 12 prospective clinical studies out of 37 articles that specifically addressed the potential adverse pressor effect of SMDs. Of these, only one study evaluated hypertensive patients in a double-blind randomized fashion. Despite few threats to generalizability, the results of that investigation suggest that intranasal phenylephrine is safe in patients with controlled hypertension. The effects of phenylpropanolamine and pseudoephedrine in hypertensive patients are unclear since only small numbers of unrepresentative normotensive subjects have been studied; thus, the evidence to support the widespread belief that SMDs are unsafe in hypertensive patients is weak and circumstantial. Recommendations for treatment and methods to improve future study designs are suggested.