[Perioperative factors affecting the length of hospital stay after cesarean section of pregnant women with heart disease].

Objective: To explore the related factors influencing the length of hospital stay(LOS) of pregnant women with heart disease (PWHD) after cesarean section. Methods: A total of 306 patients with PWHD who underwent cesarean section from January 2012 to March 2019 were collected. Among them, 203 patients had not undergone heart surgery (uncorrected group) and 103 patients who had undergone heart surgery (corrected group) during the same period. Demographic, perioperative and postoperative data were recorded. Predictors associated with postoperative LOS were determined using univariate and multivariate linear regression analysis models. Results: (1) The median LOS after cesarean section in the uncorrected group was 6 days (5-8 days). The results of univariate linear regression analysis showed that 38 parameters had significant impact on LOS (P<0.05). The results of multivariate linear regression analysis showed that 5 parameters were independent risk factors for prolonged LOS in the uncorrected group; among them, the median LOS in uncorrected group with hypertensive disorders of pregnancy was 3 days longer than that in patients with PWHD alone [7 days (5-8 days) vs 4 days (4-5 days), ß=0.195, P=0.001]; the median LOS in uncorrected group with high serum creatinine was 3 days longer than normal patients [7 days (5-13 days) vs 4 days (4-5 days), ß=0.145, P=0.015]; the LOS of patients who chose general anesthesia was 2 days longer than that of patients who chose spinal anesthesia [6 days (4-8 days) vs 4 days (4-5 days), ß=0.154, P=0.007]; the LOS of patients with postoperative pulmonary infection was 4 days longer than that of patients without pulmonary infection [8 days (5-15 days) vs 4 days (4-5 days), ß=0.269, P<0.01]; the LOS of patients who admitted to ICU after surgery was 2 days longer than that not admitted patients [6 days (5-8 days) vs 4 days (4-5 days), ß=0.268, P<0.01]. (2) The median LOS after cesarean section in corrected group was 4 days (4-5 days). The results of univariate linear regression analysis showed that 8 parameters had significant impact on the LOS (all P<0.05). The results of multivariate linear regression analysis showed that 2 parameters, which were American Society of Anesthesiologists (ASA) grade (ß=0.198, P=0.028) and intraoperative blood loss (ß=0.285, P=0.003), were the independent risk factors for prolonged LOS in corrected group. Conclusion: Preoperative with hypertensive disorders of pregnancy, preoperative creatinine increase, intraoperative general anesthesia, postoperative pulmonary infection, and postoperative admission to ICU are independent predictors of prolonged LOS in uncorrected patients with PWHD; ASA classification and intraoperative bleeding are independent predictor of prolonged postoperative LOS in patients with corrected PWHD.

Dietary Sodium 'Controversy'-Issues and Potential Solutions.

PURPOSE OF REVIEW: High dietary sodium is estimated to be the leading dietary risk for death attributed to 1.8 million deaths in 2019. There are uniform recommendations to reduce sodium consumption based on evidence that increased dietary sodium is responsible for approximately a third of the prevalence of hypertension, and meta-analyses of randomized controlled trials show that sodium reduction lowers blood pressure, cardiovascular disease, and total mortality. Nevertheless, there is a perception that the beneficial effect of reducing dietary sodium is controversial. We provide experiential evidence relating to some sources of the controversy and propose potential solutions. RECENT FINDINGS: Inappropriate research methodology, lack of rigor in research, conflicts of interest and commercial bias, questions of professional conduct, and lack of policies to protect public interests are likely to contribute to the controversy about reducing dietary sodium. There is a failure to protect policies to reduce dietary sodium from nonscientific threats. Significant efforts need to be made to ensure the integrity of nutritional research and maintain public trust.

Salt reduction in the United Kingdom: a successful experiment in public health.

The United Kingdom has successfully implemented a salt reduction programme. We carried out a comprehensive analysis of the programme with an aim of providing a step-by-step guide of developing and implementing a national salt reduction strategy, which other countries could follow. The key components include (1) setting up an action group with strong leadership and scientific credibility; (2) determining salt intake by measuring 24-h urinary sodium, identifying the sources of salt by dietary record; (3) setting a target for population salt intake and developing a salt reduction strategy; (4) setting progressively lower salt targets for different categories of food, with a clear time frame for the industry to achieve; (5) working with the industry to reformulate food with less salt; (6) engaging and recruiting of ministerial support and potential threat of regulation by the Department of Health (DH); (7) clear nutritional labelling; (8) consumer awareness campaign; and (9) monitoring progress by (a) frequent surveys and media publicity of salt content in food, including naming and shaming, (b) repeated 24-h urinary sodium at 3-5 year intervals. Since the salt reduction programme started in 2003/2004, significant progress has been made as demonstrated by the reductions in salt content in many processed food and a 15% reduction in 24-h urinary sodium over 7 years (from 9.5 to 8.1 g per day, P<0.05). The UK salt reduction programme reduced the population's salt intake by gradual reformulation on a voluntary basis. Several countries are following the United Kingdom's lead. The challenge now is to engage other countries with appropriate local modifications. A reduction in salt intake worldwide will result in major public health improvements and cost savings.

Plasma sodium and blood pressure in individuals on haemodialysis.

To study the relationship between pre-dialysis plasma sodium and blood pressure (BP), we performed an audit of patients who were on stable haemodialysis at St Bartholomew's and The Royal London Hospital from 1 June 2009 to 15 June 2010. There were 651 patients with 7445 dialysis sessions where both plasma biochemistry and BP were measured before haemodialysis. We found a significant association between plasma sodium and both systolic and diastolic BP. A 1 mmol l(-1) increase in plasma sodium was related to 0.65/0.36 mm Hg increase in BP (P<0.001 for both systolic and diastolic BP) after adjusting for potential confounding factors, including weight gain between dialyses and plasma albumin, both of which are crude indices of extracellular fluid volume. A separate analysis excluding individuals who were on BP treatment showed a similar relationship, with a 1-mmol l(-1) increase in plasma sodium associated with 0.82/0.56 mm Hg increase in BP (P<0.001 for both, N=177). These results provide further support for the accumulating evidence that plasma sodium has an important role in regulating BP, which may be independent of extracellular volume. Our findings in conjunction with other evidence suggest that small changes in plasma sodium could be an important mechanism for the beneficial effects of lower dialysate sodium and lower salt intake on BP in haemodialysis patients.

A comprehensive review on salt and health and current experience of worldwide salt reduction programmes.

Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. Raised blood pressure (BP), cholesterol and smoking, are the major risk factors. Among these, raised BP is the most important cause, accounting for 62% of strokes and 49% of coronary heart disease. Importantly, the risk is throughout the range of BP, starting at systolic 115 mm Hg. There is strong evidence that our current consumption of salt is the major factor increasing BP and thereby CVD. Furthermore, a high salt diet may have direct harmful effects independent of its effect on BP, for example, increasing the risk of stroke, left ventricular hypertrophy and renal disease. Increasing evidence also suggests that salt intake is related to obesity through soft drink consumption, associated with renal stones and osteoporosis and is probably a major cause of stomach cancer. In most developed countries, a reduction in salt intake can be achieved by a gradual and sustained reduction in the amount of salt added to food by the food industry. In other countries where most of the salt consumed comes from salt added during cooking or from sauces, a public health campaign is needed to encourage consumers to use less salt. Several countries have already reduced salt intake, for example, Japan (1960-1970), Finland (1975 onwards) and now the United Kingdom. The challenge is to spread this out to all other countries. A modest reduction in population salt intake worldwide will result in a major improvement in public health.

Salt and blood pressure in children and adolescents.

To study the relationship between salt intake and blood pressure in children and adolescents, we analysed the data of a large cross-sectional study (the National Diet and Nutrition Survey for young people), which was carried out in Great Britain in 1997 in a nationally representative sample of children aged between 4 and 18 years. A total of 1658 participants had both salt intake and blood pressure recorded. Salt intake was assessed by a 7-day dietary record. The average salt intake, which did not include salt added in cooking or at the table, was 4.7+/-0.2 g/day at the age of 4 years. With increasing age, there was an increase in salt intake, and by the age of 18 years, salt intake was 6.8+/-0.2 g/day. There was a significant association of salt intake with systolic blood pressure as well as with pulse pressure after adjusting for age, sex, body mass index and dietary potassium intake. An increase of 1 g/day in salt intake was related to an increase of 0.4 mm Hg in systolic and 0.6 mm Hg in pulse pressure. The magnitude of the association with systolic blood pressure is very similar to that observed in a recent meta-analysis of controlled trials where salt intake was reduced. The consistent finding of our present analysis of a random sample of free-living individuals with that from controlled salt reduction trials provides further support for a reduction in salt intake in children and adolescents.

Increased consumption of fruit and vegetables is related to a reduced risk of coronary heart disease: meta-analysis of cohort studies.

Increased consumption of fruit and vegetables has been shown to be associated with a reduced risk of coronary heart disease (CHD) in many epidemiological studies, however, the extent of the association is uncertain. We quantitatively assessed the relation between fruit and vegetable intake and incidence of CHD by carrying out a meta-analysis of cohort studies. Studies were included if they reported relative risks (RRs) and corresponding 95% confidence interval (CI) of CHD with respect to frequency of fruit and vegetable intake. Twelve studies, consisting of 13 independent cohorts, met the inclusion criteria. There were 278,459 individuals (9143 CHD events) with a median follow-up of 11 years. Compared with individuals who had less than 3 servings/day of fruit and vegetables, the pooled RR of CHD was 0.93 (95% CI: 0.86-1.00, P=0.06) for those with 3-5 servings/day and 0.83 (0.77-0.89, P<0.0001) for those with more than 5 servings/day. Subgroup analyses showed that both fruits and vegetables had a significant protective effect on CHD. Our meta-analysis of prospective cohort studies demonstrates that increased consumption of fruit and vegetables from less than 3 to more than 5 servings/day is related to a 17% reduction in CHD risk, whereas increased intake to 3-5 servings/day is associated with a smaller and borderline significant reduction in CHD risk. These results provide strong support for the recommendations to consume more than 5 servings/day of fruit and vegetables.

Importance of controlling blood pressure.

Cardiovascular disease is the leading cause of death and disability world-wide. Blood pressure, throughout the range seen in developed countries, is the most important risk factor for cardiovascular disease. Lowering blood pressure within the whole population by lifestyle interventions, such as reducing dietary salt intake and increasing the consumption of fruit and vegetables, will be of great benefit. Blood pressure-lowering trials also demonstrate immense benefits in preventing strokes, heart failure and coronary heart disease. There are no differences in outcome between the different methods used to lower blood pressure and the benefit is proportional to the degree of blood pressure-lowering. Thiazide diuretics are effective in lowering blood pressure and have been the most widely prescribed blood pressure-lowering drugs. They work by causing both sodium and water loss, but also cause potassium loss and a fall in plasma potassium levels. The latter may mitigate the beneficial effects from blood pressure-lowering. Some diuretics, such as spironolactone, affect the distal tubule and do not cause a fall in plasma potassium levels. However, spironolactone has endocrine side-effects associated with the fact that it is not specific for the mineralocorticoid receptor. The development of a more selective aldosterone antagonist without endocrine side-effects could be a major advance as it would be able to oppose the effects of aldosterone, both on sodium retention and potassium loss and the other vascular effects.

Effect of longer-term modest salt reduction on blood pressure.

BACKGROUND: Many randomised trials assessing the effect of salt reduction on blood pressure show reduction in blood pressure in individuals with high blood pressure. However, there is controversy about the magnitude and the clinical significance of the fall in blood pressure in individuals with normal blood pressure. Several meta-analyses of randomised salt reduction trials have been published in the last few years. However, most of these included trials of very short duration (e.g. 5 days) and included trials with salt loading followed by salt deprivation (e.g. from 20 to 1 g/day) over only a few days. These short-term experiments are not appropriate to inform public health policy which is for a modest reduction in salt intake over a prolonged period of time. A meta-analysis by Hooper et al is an important attempt to look at whether advice to achieve a long-term salt reduction (i.e. more than 6 months) in randomised trials causes a fall in blood pressure. However, most trials included in this meta-analysis achieved a small reduction in salt intake; on average, salt intake was reduced by 2 g/day. It is, therefore, not surprising that this analysis showed a small fall in blood pressure, and that a dose-response to salt reduction was not demonstrable. OBJECTIVES: To assess the effect of the currently recommended modest reduction in salt intake (WHO 2003; SACN 2003; Whelton 2002), on blood pressure in individuals with normal and elevated blood pressure. To assess whether the magnitude of the reduction in blood pressure is dependent on the magnitude of the reduction in salt intake. SEARCH STRATEGY: We searched MEDLINE, EMBASE, Cochrane library, CINAHL, and reference list of original and review articles. SELECTION CRITERIA: We included randomised trials with a modest reduction in salt intake and a duration of 4 or more weeks. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two persons. Mean effect sizes were calculated using both fixed and random effect models using Review Manager 4.2.1 software. Weighted linear regression was used to examine the relationship between the change in urinary sodium and the change in blood pressure. We used funnel plots to detect publication and other biases in the meta-analysis. MAIN RESULTS: Seventeen trials in individuals with elevated blood pressure (n=734) and 11 trials in individuals with normal blood pressure (n=2220) were included. In individuals with elevated blood pressure the median reduction in 24-h urinary sodium excretion was 78 mmol (4.6 g/day of salt), the mean reduction in systolic blood pressure was -4.97 mmHg (95%CI:-5.76 to -4.18), and the mean reduction in diastolic blood pressure was -2.74 mmHg (95% CI:-3.22 to -2.26). In individuals with normal blood pressure the median reduction in 24-h urinary sodium excretion was 74 mmol (4.4 g/day of salt), the mean reduction in systolic blood pressure was -2.03 mmHg (95% CI: -2.56 to -1.50) mmHg, and the mean reduction in diastolic blood pressure was -0.99 mmHg (-1.40 to -0.57). Weighted linear regression analyses showed a correlation between the reduction in urinary sodium and the reduction in blood pressure. REVIEWERS' CONCLUSIONS: Our meta-analysis demonstrates that a modest reduction in salt intake for a duration of 4 or more weeks has a significant and, from a population viewpoint, important effect on blood pressure in both individuals with normal and elevated blood pressure. These results support other evidence suggesting that a modest and long-term reduction in population salt intake could reduce strokes, heart attacks, and heart failure. Furthermore, our meta-analysis demonstrates a correlation between the magnitude of salt reduction and the magnitude of blood pressure reduction. Within the daily intake range of 3 to 12 g/day, the lower the salt intake achieved, the lower the blood pressure.

Cost of poor blood pressure control in the UK: 62,000 unnecessary deaths per year.

High blood pressure is the most important risk factor for cardiovascular disease. With the information on systolic blood pressure from the recently published meta-analysis of prospective studies, we calculated the reductions in stroke and ischaemic heart disease with control of all hypertensives to a systolic blood pressure of 140 mmHg. For adults there would be a reduction of 28-44% in stroke and 20-35% in ischaemic heart disease depending on age. In the UK, this would prevent approximately 21,400 stroke deaths and 41,400 ischaemic heart disease deaths each year. Around half of those who suffer a stroke or ischaemic heart disease survive, there would be a proportionate decrease in these people as well. These amount to approximately 42,800 strokes and 82,800 ischaemic heart diseases saved, making a total of 125,600 events saved a year in the UK. This would result in a reduction in disability and major cost savings both to individuals, their families and the Health Service. The blood pressure levels and control of blood pressure in many countries are similar to those in the UK, so the reductions in stroke and ischaemic heart disease worldwide, if the same control of high blood pressure could be obtained, would be immense.

Potassium: more beneficial effects.

Over 70 years ago, potassium was found to have a natriuretic effect and was used in patients with heart failure. However, it took many years for its role in the control of blood pressure to be recognized. Recently, epidemiological and clinical studies in man and experimental studies in animals have shown that increasing potassium intake towers blood pressure and that communities with a high potassium intake tend to have lower population blood pressures. Several studies have shown an interaction between salt intake and potassium intake. However, the recent DASH-Sodium (Dietary Approaches to Stop Hypertension) study demonstrates an additive effect of a low salt and high potassium diet on blood pressure. Increasing potassium intake may have other beneficial effects, for example, reducing the risk of stroke and preventing the development of renal disease independent of its effect on blood pressure. A high potassium intake reduces calcium excretion and could play an important role in the management of hypercalciuria and kidney stone formation, as well as bone demineralization. Potassium intake may also play an important role in carbohydrate intolerance. A reduced serum potassium increases the risk of lethal ventricular arrhythmias in those at risk, i.e. patients with ischemic heart disease, heart failure or left ventricular hypertrophy, and increasing potassium intake may prevent this. In this article, we address the evidence for the important role of potassium intake in regulating blood pressure and other beneficial effects of potassium which may be independent of and additional to its effect on blood pressure.

Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public health.

Two recent meta-analyses of randomised salt reduction trials have concluded that there is little purpose in reducing salt intake in the general population. However, the authors, as with other previous meta-analyses, included trials of very short duration (eg 1 week or less) and trials of acute salt loading followed by abrupt reductions to very low salt intake (eg from 20 to less than 1 g of salt/day). These acute salt loading and salt depletion experiments are known to increase sympathetic tone, and with salt depletion cause a rise in renin release and, thereby, plasma angiotensin II. These trials are not appropriate, therefore, for helping to inform public health policy, which is for a more modest reduction in salt intake, ie, from a usual intake of approximately 10 to approximately 5 g of salt per day over a more prolonged period of time. We carried out a meta-analysis to assess the effect of a modest salt reduction on blood pressure. Our data sources were MEDLINE, EMBASE, Cochrane library, CINAHL, and the reference lists of original and review articles. We included randomised trials with a modest reduction in salt intake and a duration of 4 or more weeks. Meta-analysis, meta-regression, and funnel plots were performed. A total of 17 trials in hypertensives (n=734) and 11 trials in normotensives (n=2220) were included in our study. The median reduction in 24-h urinary sodium excretion was 78 mmol (equivalent to 4.6 g of salt/day) in hypertensives and 74 mmol in normotensives. The pooled estimates of blood pressure fall were 4.96/2.73+/-0.40/0.24 mmHg in hypertensives (P<0.001 for both systolic and diastolic) and 2.03/0.97+/-0.27/0.21 mmHg in normotensives (P<0.001 for both systolic and diastolic). Weighted linear regression analyses showed a dose response between the change in urinary sodium and blood pressure. A reduction of 100 mmol/day (6 g of salt) in salt intake predicted a fall in blood pressure of 7.11/3.88 mmHg (P<0.001 for both systolic and diastolic) in hypertensives and 3.57/1.66 mmHg in normotensive individuals (systolic: P<0.001; diastolic: P<0.05). Our results demonstrate that a modest reduction in salt intake for a duration of 4 or more weeks does have a significant and, from a population viewpoint, important effect on blood pressure in both hypertensive and normotensive individuals. This meta-analysis strongly supports other evidence for a modest and long-term reduction in population salt intake, and would be predicted to reduce stroke deaths immediately by approximately 14% and coronary deaths by approximately 9% in hypertensives, and reduce stroke and coronary deaths by approximately 6 and approximately 4%, in normotensives, respectively.

Effect of salt intake on renal excretion of water in humans.

Two studies were performed to determine the quantitative relationship between salt intake and urinary volume (U(v)) in humans. In study 1, 104 untreated hypertensives were studied on the fifth day of a high- and a low-salt diet. The 24-hour U(v) was 2.2 L (urinary sodium [U(Na)] 277 mmol) on the high-salt diet and decreased to 1.3 L (P<0.001) (U(Na) 20.8 mmol) on the low-salt diet. The reduction in 24-hour U(v) was significantly related to the decrease in 24-hour U(Na) (P<0.001) and predicts that a 100-mmol/d reduction in salt intake would decrease 24-hour U(v) by 367 mL. In study 2, 634 untreated hypertensives were studied on their usual diet. There was a significant relationship between 24-hour U(v) and U(Na) (P<0.001). This predicts that a 100-mmol/d reduction in salt intake would decrease 24-hour U(v) by 454 mL. The International Study of Salt and Blood Pressure (INTERSALT) of 1731 hypertensives and 8343 normotensives on their usual diet showed that 24-hour U(v) was significantly related to U(Na) (P<0.001) and predicted that a 100-mmol/d reduction in salt intake would decrease 24-hour U(v) by 379 and 399 mL in hypertensives and normotensives, respectively. These findings document the important effect that salt intake has on U(v). The recommended reduction in salt intake in the general population is from 10 to 5 g/d. This would reduce fluid intake in the population by approximately 350 mL/d per person. This would have a large impact on the sales of soft drinks, mineral water, and beer.

Importance of the renin system for determining blood pressure fall with acute salt restriction in hypertensive and normotensive whites.

Hypertensive (n=93) and normotensive (n=39) white individuals were given a high sodium intake of approximately 350 mmol/d for 5 days followed by a low sodium intake of 10 to 20 mmol/d for 5 days. With this acute and large reduction in salt intake, no significant change was seen in blood pressure in the normotensive individuals, but blood pressure decreased in the hypertensive individuals. Compared with normotensive subjects, hypertensive patients had a 7/7-mm Hg greater fall in blood pressure (P<0.05 for systolic and P<0.01 for diastolic, adjusted for age), with similar changes in urinary sodium excretion. From the high-salt to low-salt diet, plasma renin activity rose from 0.90 to 5.99 ng. mL(-1). h(-1) in normotensives, whereas in hypertensives it rose from 0.73 to only 3.14 ng. mL(-1). h(-1) (P<0.05 between hypertensives and normotensives). Plasma aldosterone rose by 1396 pmol/L in normotensive subjects and by 511 pmol/L in hypertensive patients (P<0.05). Significant inverse correlations were obtained for all subjects between the fall in blood pressure from the high-salt to low-salt diet and the rise in plasma renin activity and aldosterone that occurred in addition to the absolute level on the low-salt diet. These results demonstrate that the larger fall in blood pressure with an acute reduction in salt intake in hypertensives compared with normotensives is, at least in part, due to a less-responsive renin-angiotensin-aldosterone system in the hypertensive patients.