Abstract-We sought to explore the effects of salt loading in young normotensives on vascular endothelial function, echocardiographic left ventricular diastolic function, and electrocardiographic QT dispersion. Sixteen healthy normotensive male volunteers were randomized in a double-blind crossover fashion to 5-day treatment periods with either placebo or salt tablets (200 mmol/d of sodium) separated by a 2-week washout period. Throughout the study the volunteers were asked to maintain a low-salt diet. Forearm venous occlusion plethysmography and intraarterial infusions of acetylcholine (ACh), sodium nitroprusside (SNP), and N G -monomethyl-L-arginine (L-NMMA) were used to assess vascular reactivity. Baseline and postsalt loading 12-lead ECGs and echocardiograms were also obtained. Key Words: salt loading Ⅲ endothelium Ⅲ diastolic dysfunction Ⅲ QT dispersion Ⅲ blood pressure M any risk factors associated with atherosclerotic diseases have been identified over the last 5 decades. However, epidemiological data show that these conventional risk factors account for most but not all coronary artery disease burden. [1][2][3] This suggests that other factors must be causal, 1 and excess salt intake is a possible candidate. 4 There is evidence in animals that salt produces hypertension and direct target-organ damage such as myocardial hypertrophy, vascular hypertrophy, and fibrosis. 5,6 However, in man, the role of salt in cardiovascular disease continues to be contentious, 7 with most studies in man concentrating on the relationship between salt intake and blood pressure. 8,9 Salt may have blood pressure-independent adverse effect on target organs 3,9 with increasing coronary events, independently of blood pressure, 4 and left ventricular diastolic dysfunction. 10 We have previously reported that in hypertensive subjects with increased aldosterone activity, salt loading not only impairs left ventricular diastolic function, but also increases QT dispersion, a measure of cardiac electric depolarization. 11 One study has previously examined the effect of sodium loading on vascular endothelium in 7 normal subjects and found no significant effect on endothelial-dependent vasodilation. 12 However, our prior experience prompted us to repeat this with a larger study group. 11 We therefore explored whether salt loading has adverse effects on cardiovascular system in healthy volunteers. We studied the effects of salt on vascular endothelial function and on NO bioactivity, as it is accepted that endothelial dysfunction precedes frank atherosclerotic disease. 13 Secondly, we studied whether excess salt would adversely affect the left ventricular diastolic function and QT dispersion in normal individuals. These 2 effects may be interrelated because left ventricular systolic and diastolic functions are influenced in turn by the coronary endothelial function. 14 Left ventricular diastolic dysfunction in turn is also recognized to be an early sign of cardiac target-organ damage. 15 Methods Study PopulationSixteen healthy white male sub...

Background and Purpose-The purpose of this study was to investigate renal function as a long-term predictor of mortality in patients hospitalized for acute stroke. Methods-This was a cohort study done in a Scottish tertiary teaching hospital. Participants included 2042 (993 male) unselected consecutive stroke patients (mean age, 73 years) admitted to hospital within 48 hours of stroke between1988 and 1994. Follow-up was up to 7 years. Main outcome measure was all-cause mortality. Results-The total number of deaths at the end of follow-up was 1026. Most subjects (1512) had creatinine Ͻ124 mol/L.The mean calculated creatinine clearance was 54.8 mL/min (SD, 23 mL/min). Renal function indexes were analyzed by quartiles with Cox proportional-hazards model. Stroke survivors had higher calculated creatinine clearance and lower serum creatinine, urea, and ratios of urea to creatinine. Calculated creatinine clearance Ն51.27 mL/min significantly predicted better long-term survival in these stroke patients even after adjustment for confounders (age, neurological score, ischemic heart disease, hypertension, smoking, and diuretic use). Similarly, creatinine Ն119 mol/L [relative risk (RR), 1.59; 95% confidence interval (CI), 1.32 to 1.92], urea 6.8 to 8.9 mmol/L (RR, 1.34; 95% CI, 1.09 to 1.65) or Ն9 mmol/L (RR, 1.74; 95% CI, 1.42 to 2.13), and ratio of urea to creatinine Ն0.08573 mmol/mol (RR, 1.24; 95% CI, 1.03 to 1.50) remained significant predictors of mortality after adjustment for confounders. Conclusions-After acute stroke, patients with reduced admission calculated creatinine clearance, raised serum creatinine and urea concentrations (even within conventional reference intervals), and raised ratio of urea to creatinine had a higher mortality risk. This finding may be used to stratify risk and target interventions, eg, the use of angiotensin-converting enzyme inhibitors.

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Objectives:To find out what spectrum of cardiac abnormalities are found in those stroke survivors who can be deemed to be at high cardiac risk by their having long QT. Methods: 202 patients with good recovery from a cerebrovascular event occurring at least one month previously were recruited into a prospective epidemiological study. These stroke survivors underwent a battery of cardiac investigations including 12 lead ECG, echocardiography, myocardial perfusion scanning, and heart rate variability assessment. The ECGs were digitised by a single observer blinded to the blood pressure and other investigations of the patients. The maximum heart rate corrected QT interval (QTc max) in the 12 lead ECG was derived by Bazett's formula. Results: Prolonged QTc max significantly correlated with increasing blood pressure, left ventricular mass index, and depressed heart rate variability. As the number of cardiac abnormalities increased, QTc max became more prolonged. Conclusions: Long QT is significantly associated with left ventricular mass index even after adjustment for both systolic and diastolic blood pressures. Long QT was also associated with the total cardiac disease burden. These two observations may explain why stroke survivors with long QTc max were at greater risk of cardiac death.A fter surviving a stroke, more people die of cardiac causes than of a recurrent stroke. QT prolongation was recently shown to predict cardiac death in stroke survivors.1 Similar findings have been seen in many other populations. This raises the question of why QT prolongation predicts cardiac death. Two possibilities arise although they are not necessarily exclusive of each other. Firstly, QT prolongation may be a marker of treatable, hidden but potentially lethal cardiac abnormalities, such as ischaemia or left ventricular abnormalities. Secondly, QT prolongation may be a marker of arrhythmogenicity, irrespective of ischaemia or left ventricular abnormalities.The main objective of this prospective study was to test the hypothesis that maximum heart rate corrected QT interval (QTc max) prolongation is a convenient marker of treatable, hidden cardiac abnormalities in stroke survivors. If so, this may contribute strongly to its adverse prognostic significance. METHODSTwo hundred and two patients with good recovery after a recently documented stroke or transient ischaemic attack occurring at least one month previously were studied. A random sample of the stroke outpatient clinic was recruited and this comprised 70% who had been hospitalised within 72 hours after their acute cerebrovascular event plus 30% who had community strokes. Patients who had atrial fibrillation or flutter, bigeminy, paced rhythm, or bundle branch block on their ECG were excluded from QT interval analysis. (These ECG changes make the QT interval difficult to measure reliably.) Other exclusion criteria were inability to provide consent, for example, because of dementia; age greater than 90 years; and being under nursing home-type care.The study was approved by the T...

Background: We aim to assess whether social deprivation independently predicts case fatality after a stroke patient has been admitted to hospital, and to assess whether social deprivation affected duration of hospital stay. Methods: Cohort study in a tertiary teaching hospital included consecutive patients admitted to hospital within 48 h of their stroke between 1988 and 1994. Outcome measures were case fatality at 1 year and length of hospital stay. The socioeconomiccategory was derived from the postcode sectorof residence for the patients (Carstairs index). Cause of death was determined by data linkage to the Registrar General data for Scotland. Results: 2,042 stroke patients were included. A significant age difference existed between the deprivation categories (76.0 ± 10.9 years in the affluent cohort vs. 71.4 ± 10.7 years in the deprived cohort). Smoking was more common in the deprived group. ECG findings and neurological score on admission were similar between the groups. No difference existed between groups for length of hospital stay (p = 0.793), and in the proportions remaining alive at 1 year (p = 0.416). When entered into a multivariate Cox regression analysis, the deprivation categories did not predict mortality. Age, sex, Philadelphia Geriatric Center Instrumental Activities of Daily Living (IADL) Scale Score, Orgogozo neurological score on admission, and ECG abnormalities were the significant predictors. Conclusions: Stroke patients living in more socially deprived areas had their strokes at an earlier age but were not at a greater risk of dying or longer hospital stay once they had been admitted to hospital.

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Methods We used the Trust's patient level costing models from financial years 2018/19 and 2019/20 to calculate total treatment costs for the patients in the pilot prospective trial which randomised acute heart failure patients to receive inpatient vs outpatient based therapy. Patient level costing for inpatients would include hospital bed, nursing cost, consultant /ward doctor cost, non-pay costs (pharmacy including iv drugs, diagnostics e.g. pathology, radiology, ECG, echocardiography).Where patient level costs are unavailable, for example Community contacts, we have used a national average cost. . Community centre visit -HRG code of N29AF 2018/19 National average cost £71 . Home visit -HRG code of N29AF 2018/19 National average cost £71 . GP visit -National average cost of £30 [1] SD (intercept) 11.79