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There is currently no objective practical guide to intensity of drug treatment for individuals with heart failure. We hypothesised that pharmacotherapy guided by plasma concentrations of the cardiac peptide aminoterminal brain natriuretic peptide (N-BNP) would produce a superior outcome to empirical trial-based therapy dictated by clinical acumen. 69 patients with impaired systolic function (left-ventricular ejection fraction <40%) and symptomatic heart failure (New York Heart Association class II–IV) were randomised to receive treatment guided by either plasma N-BNP concentration (BNP group) or standardised clinical assessment (clinical group). During follow-up (minimum 6-months, median 9–5 months), there were fewer total cardiovascular events (death, hospital admission, or heart failure decompensation) in the BNP group than in the clinical group (19 vs 54, p=0·02). At 6 months, 27% of patients in the BNP group and 53% in the clinical group had experienced a first cardiovascular event (p=0·034). Changes in left-ventricular function, quality of life, renal function, and adverse events were similar in both groups. N-BNP-guided treatment of heart failure reduced total cardiovascular events, and delayed time to first event compared with intensive clinically guided treatment.

Our objectives were to compare the levels of circulating electrolytes, hormones, and renal function during 20 days of dehydration in camels versus the level in non-dehydrated camels and to record the effect of blocking angiotensin II AT1 receptors with losartan during dehydration. Dehydration induced significant increments in serum sodium, creatinine, urea, a substantial fall in body weight, and a doubling in plasma arginine vasopressin (AVP) levels. Plasma aldosterone, however, was unaltered compared with time-matched controls. Losartan significantly enhanced the effect of dehydration to reduce body weight and increase serum levels of creatinine and urea, whilst also impairing the rise in plasma AVP and reducing aldosterone levels. We conclude that dehydration in the camel induces substantial increments in serum sodium, creatinine, urea and AVP levels; that aldosterone levels are altered little by dehydration; that blockade of angiotensin II type 1 receptors enhances the dehydration-induced fall in body weight and increase in serum creatinine and urea levels whilst reducing aldosterone and attenuating the rise in plasma AVP.

Urotensin II has vasoconstrictive and negative inotropic effects, suggesting a possible role in circulatory regulation and pathophysiology of heart failure. We developed a sensitive specific RIA and measured plasma urotensin II in patients with heart failure and in controls. Plasma urotensin II was higher in heart failure patients (mean 3·9 pmol/L [SD 1·4]; than in controls (1·9 pmol/L [0·9]; p<0·0001). The role of urotensin II in heart failure, however, has yet to be defined.

The objectives of this study were to investigate and compare the responses of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in the circulation of hydrated, dehydrated, and dehydrated losartan - treated camels; and to document the cardiac storage form of B-type natriuretic peptide in the camel heart. Eighteen male camels were used in the study: control or hydrated camels (n = 6), dehydrated camels (n = 6) and dehydrated losartan-treated camels (n = 6) which were dehydrated and received the angiotensin II (Ang II) AT-1 receptor blocker, losartan, at a dose of 5 mg/kg body weight intravenously for 20 days. Control animals were supplied with feed and water ad-libitum while both dehydrated and dehydrated-losartan treated groups were supplied with feed ad-libitum but no water for 20 days. Compared with time-matched controls, dehydrated camels exhibited a significant decrease in plasma levels of both ANP and BNP. Losartan-treated camels also exhibited a significant decline in ANP and BNP levels across 20 days of dehydration but the changes were not different from those seen with dehydration alone. Size exclusion high performance liquid chromatography of extracts of camel heart indicated that proB-type natriuretic peptide is the storage form of the peptide. We conclude first, that dehydration in the camel induces vigorous decrements in circulating levels of ANP and BNP; second, blockade of the renin-angiotensin system has little or no modulatory effect on the ANP and BNP responses to dehydration; third, proB-type natriuretic peptide is the storage form of this hormone in the heart of the one-humped camel.

Public trust in the peer review process and the credibility of published articles depend in part on how well conflict of interest is handled during writing, peer review, and editorial decision making. Conflict of interest exists when an author (or the author's institution), reviewer, or editor has financial or personal relationships with other persons or organizations that inappropriately influence (bias) his or her actions. The potential of such relationships to create bias varies from negligible to extremely great; the existence of such relationships does not necessarily represent true conflict of interest, therefore. (Relationships that do not bias judgment are sometimes known as dual commitments, competing interests, or competing loyalties). The potential for conflict of interest can exist whether or not an individual believes that the relationship affects his or her scientific judgment. Financial relationships (such as employment, consultancies, stock ownership, honoraria, paid expert testimony) are the most easily identifiable conflicts of interest and the most likely to undermine the credibility of the journal, the authors, and of science itself. Conflicts can occur for other reasons, however, such as personal and family relationships, academic competition, and intellectual passion. All participants in the peer review and publication process must disclose all relationships that could be viewed as presenting a potential conflict of interest. Disclosure of these relationships is particularly important in connection with editorials and review articles, because bias can be more difficult to detect in those publications than in reports of original research. Editors may use information disclosed in conflict of interest and financial interest statements as a basis for editorial decisions. Editors should publish this information if they believe it will be important to readers in judging the manuscript.

Long-term effects of angiotensin-converting enzyme inhibition and metabolic control in hypertensive type 2 diabetic patients. In hypertensive type 2 diabetic patients, treatment with angiotensin-converting enzyme (ACE) inhibitors is associated with a lower incidence of cardiovascular events than those treated with calcium channel-blocking agents. However, the long-term renal effects of ACE inhibitors in these patients remain inconclusive. In 1989, we commenced a placebo-controlled, double-blind, randomized study to examine the anti-albuminuric effects of enalapril versus nifedipine (slow release) in 102 hypertensive, type 2 diabetic patients. These patients have been followed up for a mean trial duration of 5.5 ± 2.2 years. We examined the determinants, including the effect of ACE inhibition on clinical outcomes in these patients. After a six-week placebo-controlled, run-in period, 52 patients were randomized double-blind to receive nifedipine (slow release) and 50 patients to receive enalapril. After the one-year analysis, which confirmed the superior anti-albuminuric effects of enalapril (-54%) over nifedipine (+11%), all patients were continued on their previously assigned treatment with informed consent. They were subdivided into normoalbuminuric (N = 43), microalbuminuric (N = 34), and macroalbuminuric (N = 25) groups based on two of three 24-hour urinary albumin excretion (UAE) measurements during the run-in period. Renal function was shown by the 24-hour UAE, creatinine clearance (CCr), and the regression coefficient of the yearly plasma creatinine reciprocal (β-1/Cr). Clinical endpoints were defined as death, cardiovascular events, and/or renal events (need for renal replacement therapy or doubling of baseline plasma creatinine). In the whole group, patients treated with enalapril were more likely to revert to being normoalbuminuric (23.8 vs. 15.4%), and fewer of them developed macroalbuminuria (19.1 vs. 30.8%) compared with the nifedipine-treated patients (P < 0.05). In the microalbuminuric group, treatment with enalapril (N = 21) was associated with a 13.0% (P < 0.01) reduction in 24-hour UAE compared with a 17.3% increase in the nifedipine group (N = 13). In the macroalbuminuric patients, enalapril treatment (N = 11) was associated with stabilization compared with a decline in renal function in the nifedipine group, as shown by the β-1/Cr (0.65 ± 4.29 vs. -1.93 ± 2.35 1/μmol × 10-3, P < 0.05) after adjustment for baseline values. Compared with the normoalbuminuric and microalbuminuric patients, those with macroalbuminuria had the lowest mean CCr (75.5 ± 24.1 vs. 63.5 ± 21.3 vs. 41.9 ± 18.5 mL/min, P < 0.001) and the highest frequency of clinical events (4.7 vs. 5.9 vs. 52%, P < 0.001). On multivariate analysis, β-1/Cr (R2 = 0.195, P < 0.001) was independently associated with baseline HbA1c (β = -0.285, P = 0.004), whereas clinical outcomes (R2 = 0.176, P < 0.001) were independently related to the mean low-density lipoprotein cholesterol (β = 2.426, P = 0.018), high-density lipoprotein cholesterol (β = -8.797, P = 0.03), baseline UAE (β = 0.002, P = 0.04), and mean CCr during treatment (β = -0.211, P = 0.006). In this prospective cohort analysis involving 102 hypertensive, type 2 diabetic patients with varying degrees of albuminuria followed up for a mean duration of five years, we observed the importance of good metabolic and blood pressure control on the progression of albuminuria and renal function. Treatment with enalapril was associated with a greater reduction in albuminuria than with nifedipine in the entire patient group, and especially in those with microalbuminuria. In the macroalbuminuric patients, the rate of deterioration in renal function was also attenuated by treatment with enalapril.

A case report in the journal Pediatric Nephrology describes a 15-month-old girl with the syndrome of hypertension and hyponatremia (HH syndrome) due to underlying unilateral renal artery stenosis. This syndrome is typically associated with hypokalemia and severe volume depletion and sometimes proteinuria, all of which, along with hypertension and hyponatremia, are usually corrected by resolution of the underlying renal ischemia. Gross and probably sudden activation of the renin-angiotensin system in response to renal ischemia is central to the pathophysiology although the cardiac atrial and B-type natriuretic peptides probably contribute also. Initial control of the severe hypertension may, in some cases, require careful volume repletion prior to introduction of blockade of the renin-angiotensin system in order to avoid first-dose hypotension, after which correction of the underlying renal ischemia is required. Whereas the syndrome has rarely been reported in children, it is possible that, as in adults, this reflects its lack of recognition by clinicians. The HH syndrome due to unilateral renal ischemia in children may be much more common than we think.

The timeframe of benefit to health (and the economy) from an increased investment in the public healthcare system will be immediate for patients who are clinically unwell, medium-term (years) for some preventive public healthcare measures and for the teaching/training of healthcare personnel, and long-term (many years) for other preventive healthcare measures and for medical clinical research. An excellent expose on this issue can be found in the book \"The Body Economic: Why Austerity Kills\" by David Stuckler and Sanjay Basu, published in 2013.3 It is brief, readable for non-economists and clear on the disastrous human cost when governments underfund healthcare and social benefits. [...]might be the right time for the New Zealand Medical Association to join with other healthcare organisations (NZNO, specialty health colleges, etc) in making a combined, coordinated approach to our new government, making the case that adequate funding of the public healthcare system will indeed grow the economy.

Updates activities of the Canterbury Charity Hospital (CCH) and its Trust over the 3 years 2010-2012, during which the devastating Christchurch earthquakes occurred. Reviews patients' treatments, establishment of new services, expansion of the CCH, staffing, and finances. Notes in particular counselling, dental, and colonoscopy services. Highlights substantial, undocumented unmet healthcare needs in the region, which were exacerbated by the 2010/2011 earthquakes. Contends that the level of unmet healthcare in Canterbury and throughout the country should be regularly documented to inform planning of public healthcare services. Source: National Library of New Zealand Te Puna Matauranga o Aotearoa, licensed by the Department of Internal Affairs for re-use under the Creative Commons Attribution 3.0 New Zealand Licence.