Therese Op.86 No. 1 - Score

It is also the health professional's responsibility to verify the applicable rules and regulations relating to drugs and medical devices at the time of prescription. Cardiovascular disease CVD prevention is defined as a coordinated set of actions, at the population level or targeted at an individual, that are aimed at eliminating or minimizing the impact of CVDs and their related disabilities.

Age-adjusted coronary artery disease CAD mortality has declined since the s, particularly in high-income regions. However, inequalities between countries persist and many risk factors, particularly obesity 3 and diabetes mellitus DM , 4 have been increasing substantially. If prevention was practised as instructed it would markedly reduce the prevalence of CVD.

It is thus not only prevailing risk factors that are of concern, but poor implementation of preventive measures as well. The present guidelines represent an evidence-based consensus of the 6th European Joint Task Force involving 10 professional societies. By appraising the current evidence and identifying remaining knowledge gaps in managing CVD prevention, the Task Force formulated recommendations to guide actions to prevent CVD in clinical practice. The Task Force followed the quality criteria for development of guidelines, which can be found at http: For simplification and in keeping with other European Society of Cardiology ESC guidelines, the ESC grading system based on classes of recommendation and levels of evidence has been maintained, recognising that this may be less suitable to measure the impact of prevention strategies, particularly those related to behavioural issues and population-based interventions.

This document has been developed to support healthcare professionals communicating with individuals about their cardiovascular CV risk and the benefits of a healthy lifestyle and early modification of their CV risk. In addition, the guidelines provide tools for healthcare professionals to promote population-based strategies and integrate these into national or regional prevention frameworks and to translate these in locally delivered healthcare services, in line with the recommendations of the World Health Organization WHO global status report on non-communicable diseases As in the present guidelines, the model presented in the previous document from the Fifth European Joint Task Force 11 has been structured around four core questions: Compared with the previous guidelines, greater emphasis has been placed on a population-based approach, on disease-specific interventions and on female-specific conditions, younger individuals and ethnic minorities.

Due to space restrictions for the paper version, the chapter on disease-specific intervention is on the web, together with a few tables and figures for more detail see web addenda. This implies that, apart from improving lifestyle and reducing risk factor levels in patients with established CVD and those at increased risk of developing CVD, healthy people of all ages should be encouraged to adopt a healthy lifestyle.

Healthcare professionals play an important role in achieving this in their clinical practice. There is consensus in favour of an approach combining strategies to improve CV health across the population at large from childhood onward, with specific actions to improve CV health in individuals at increased risk of CVD or with established CVD. Most studies assessing the cost-effectiveness of CVD prevention combine evidence from clinical research with simulation approaches, while cost-effectiveness data from randomized controlled trials RCTs are relatively scarce.

Hence, results obtained in one country may not be valid in another. Furthermore, changes such as the introduction of generic drugs can considerably change cost-effectiveness. CAD mortality rates could be halved by only modest risk factor reductions and it has been suggested that eight dietary priorities alone could halve CVD death.

In the last three decades, more than half of the reduction in CV mortality has been attributed to changes in risk factor levels in the population, primarily the reduction in cholesterol and blood pressure BP levels and smoking. This favourable trend is partly offset by an increase in other risk factors, mainly obesity and type 2 DM. Several population interventions have efficiently modified the lifestyle of individuals. For example, increased awareness of how healthy lifestyles prevent CVD has helped to reduce smoking and cholesterol levels. Lifestyle interventions act on several CV risk factors and should be applied prior to or in conjunction with drug therapies.

Also, legislation aimed at decreasing salt and the trans fatty acid content of foods and smoking habits is cost effective in preventing CVD. Cholesterol lowering using statins 15 , 16 and improvement in BP control are cost effective if targeted at persons with high CV risk. All current guidelines on the prevention of CVD in clinical practice recommend the assessment of total CVD risk since atherosclerosis is usually the product of a number of risk factors. A recent meta-analysis on CV risk reduction by treatment with BP-lowering drugs does, however, support the concept that absolute risk reduction is larger in those individuals at higher baseline risk.

Although clinicians often ask for decisional thresholds to trigger intervention, this is problematic since risk is a continuum and there is no exact point above which, for example, a drug is automatically indicated nor below which lifestyle advice may not usefully be offered. The risk categories presented later in this section are to assist the physician in dealing with individual people.

They acknowledge that although individuals at the highest levels of risk gain most from risk factor interventions, most deaths in a community come from those at lower levels of risk, simply because they are more numerous compared with high-risk individuals. Thus a strategy for individuals at high risk must be complemented by public health measures to encourage a healthy lifestyle and to reduce population levels of CV risk factors.

It is essential for clinicians to be able to assess CV risk rapidly and with sufficient accuracy. This realization led to the development of the risk chart used in the and Guidelines. This chart, developed from a concept pioneered by Anderson, 28 used age, sex, smoking status, blood cholesterol and systolic BP SBP to estimate the year risk of a first fatal or non-fatal CAD event. There were several problems with this chart, which are outlined in the Fourth Joint European Guidelines on prevention.

Screening is the identification of unrecognized disease or, in this case, of an unknown increased risk of CVD in individuals without symptoms. CV risk assessment or screening can be done opportunistically or systematically. Opportunistic screening means without a predefined strategy, but is done when the opportunity arises [e. Systematic screening can be done in the general population as part of a screening programme or in targeted subpopulations, such as subjects with a family history of premature CVD or familial hyperlipidaemia. While the ideal scenario would be for all adults to have their risk assessed, this is not practical in many societies.

The decision about who to screen must be made by individual countries and will be resource dependent. In a meta-analysis, GP-based health checks on cholesterol, BP, body mass index BMI and smoking were effective in improving surrogate outcomes, especially in high-risk patients. DM, hypertension concluded that risk factor improvements were modest and interventions did not reduce total or CV mortality in general populations, but reduced mortality in high-risk hypertensive and DM populations.

Perhaps application of medical treatment in addition to the lifestyle interventions that were the core component of most trials would improve efficacy. Most guidelines recommend a mixture of opportunistic and systematic screening. The costs of such screening interventions are high and these resources may be better used in people at higher CV risk or with established CVD.

In many countries, GPs have a unique role in identifying individuals at risk of but without established CVD and assessing their eligibility for intervention see section 4a. A general concern in screening, including CV risk assessment, is its potential to do harm. False positive results can cause unnecessary concern and medical treatment. Conversely, false negative results may lead to inappropriate reassurance and a lack of lifestyle changes. However, current data suggest that participating in CV screening in general does not cause worry in those who are screened.

Despite limited evidence, these guidelines recommend a systematic approach to CV risk assessment targeting populations likely to be at higher CV risk, such as those with a family history of premature CVD. Additionally, screening of specific groups with jobs that place other people at risk, e. Risk assessment is not a one-time event; it should be repeated, for example, every 5 years. Current cardiovascular disease risk estimation systems for use in apparently healthy persons, updated from 59 , All International Classification of Diseases ICD codes that could reasonably be assumed to be atherosclerotic are included, including CAD, stroke and aneurysm of the abdominal aorta.

Traditionally most systems estimated CAD risk only; however, more recently a number of risk estimation systems have changed to estimate the risk of all CVDs. The choice of CV mortality rather than total fatal plus non-fatal events was deliberate, although not universally popular. Non-fatal event rates are critically dependent upon definitions and the methods used in their ascertainment.

Critically, the use of mortality allows recalibration to allow for time trends in CV mortality. Any risk estimation system will overpredict in countries in which mortality has fallen and underpredict in those in which it has risen. Recalibration to allow for secular changes can be undertaken if good quality, up-to-date mortality and risk factor prevalence data are available.

Data quality does not permit this for non-fatal events.

Subscribers Only

For these reasons, the CV mortality charts were produced and have been recalibrated for a number of European countries. Naturally, the risk of total fatal and non-fatal events is higher, and clinicians frequently ask for this to be quantified. As noted in the introduction, thresholds to trigger certain interventions are problematic since risk is a continuum and there is no threshold at which, for example, a drug is automatically indicated. Obviously, decisions on whether treatment is initiated should also be based on patient preferences. A particular problem relates to young people with high levels of risk factors, where a low absolute risk may conceal a very high relative risk requiring intensive lifestyle advice.

Several approaches to communicating about risk to younger people are presented below refer also to section 2. The aim is to communicate that lifestyle changes can reduce the relative risk substantially as well as reduce the increase in risk that occurs with ageing. Another problem relates to older people. This could lead to excessive use of drugs in the elderly. This issue is dealt with later see section 2. It should be noted that RCT evidence to guide drug treatments in older persons is limited refer to section 2. In these charts, HDL-C is used categorically. The role of a plasma triglyceride as a predictor of CVD has been debated for many years.

Fasting triglycerides relate to risk in univariable analyses, but the effect is attenuated by adjustment for other factors, especially HDL-C. Dealing with the impact of additional risk factors such as body weight, family history and newer risk markers is difficult within the constraint of a paper chart. Examples of risk modifiers that are likely to have reclassification potential see following sections for details.

Instructions on their use follow. SCORE chart for use in high-risk European countries illustrating how the approximate risk age can be read off the chart. Thus a person in the top right-hand box, with multiple CV risk factors, has a risk that is 12 times greater than a person in the bottom left with normal risk factor levels. This may be helpful when advising a young person with a low absolute but high relative risk of the need for lifestyle change.

The risk age of a person with several CV risk factors is the age of a person of the same gender with the same level of risk but with ideal levels of risk factors. Risk age is also automatically calculated as part of the latest revision of HeartScore. Risk age has been shown to be independent of the CV endpoint used, 68 which bypasses the dilemma of whether to use a risk estimation system based on CV mortality or on total CV events. Risk age can be used in any population regardless of baseline risk and secular changes in mortality, and therefore avoids the need for recalibration.

Conventional CV risk prediction schemes estimate the 10 year risk of CV events. Lifetime CV risk prediction models identify high-risk individuals both in the short and long term. Such models account for predicted risk in the context of competing risks from other diseases over the remaining expected lifespan of an individual. Notably, 10 year risk identifies individuals who are most likely to benefit from drug therapy in the near term.

Drug treatment starts to work quite rapidly, and drug treatment can be largely informed by short-term risk, such as 10 year risk. One problem with short-term risk is that it is mostly governed by age and consequently few younger individuals, in particular women, reach treatment thresholds. It has therefore been argued that lifetime risk estimation may enhance risk communication, particularly among younger individuals and women.

Evidence for the role of lifetime risk in treatment decisions is lacking. Sufficient data for robust lifetime risk estimations, as well as meaningful risk categorization thresholds, are also lacking. Providing lifetime CV risk estimates for some groups at high risk of mortality due to competing non-CVD causes can be difficult to interpret. Importantly, evidence of the benefits of lifelong preventive therapy e. BP- or lipid-lowering drugs in younger individuals with low short-term but higher lifetime risks is lacking. For these reasons, we do not recommend that risk stratification for treatment decisions be based on lifetime risk.

However, like risk age and relative risk, it may be a useful tool in communicating about risk to individuals with high risk factor levels but who are at a low 10 year absolute risk of CV events, such as some younger people. Whatever approach is used, if absolute risk is low, a high relative risk or risk age signals the need for active lifestyle advice and awareness that drug treatment may need consideration as the person ages.

Both risk age and lifetime risk are closer to relative than absolute risk, and none provides an evidence base for drug treatment decisions. The countries considered here are those with national cardiology societies that belong to the ESC, both European and non-European. The fact that CVD mortality has declined in many European countries means that more now fall into the low-risk category.

Very-high-risk countries present levels of risk that are more than double that of low-risk countries i. Apart from the conventional major CV risk factors included in the risk charts, there are other risk factors that could be relevant for assessing total CVD risk. The Task Force recommends additional risk factor assessment if such a risk factor improves risk classification [e. In very-high-risk or very-low-risk situations, the impact of additional risk factors is unlikely to alter management decisions.

While the presence of risk modifiers may move an individual's estimated risk upward, absence of these modifiers should lead to lowering an individual's estimated risk. Several other factors that are frequently discussed in the literature, but may not have the ability to reclassify subjects, are discussed in subsequent paragraphs. Also discussed further in this section are the roles of ethnicity and of specific conditions or diseases that may be associated with a higher than calculated risk, such as CKD, autoimmune diseases, etc.

The way modifiers are related to CV risk may be very different. Family history may reflect a shared environment, genetic factors or both. Markers such as computed tomography CT calcium scoring are indicators of disease rather than risk factors for future disease. The target can be higher in frail elderly, or lower in most patients with DM see chapter 3.

While accepting the simplicity of this approach and that it could be useful in some settings, there is better scientific support for the three targets matched to level of risk. It should be noted that the evidence for patients with CKD is less strong. Estimation of total CV risk remains a crucial part of the present guidelines. The priorities risk categories defined in this section are for clinical use and reflect the fact that those at highest risk of a CVD event gain most from preventive measures.

This approach should complement public actions to reduce community risk factor levels and promote a healthy lifestyle. The principles of risk estimation and the definition of priorities reflect an attempt to make complex issues simple and accessible. Their very simplicity makes them vulnerable to criticism. Familial history of premature CVD is a crude but simple indicator of the risk of developing CVD, reflecting both the genetic trait and the environment shared among household members.

A family history of premature CVD is simple, inexpensive information that should be part of the CV risk assessment in all subjects. Family history can be a risk modifier to optimal management after the calculated risk using SCORE lies near a decisional threshold: Genetic screening and counselling is effective in some conditions, such as familial hypercholesterolaemia FH see section 3a. This paragraph will focus on genetic screening for high CV risk in the general population. Several recent genome-wide association studies have identified candidate genes associated with CVD.

Since the effect of each genetic polymorphism is small, most studies have used genetic scores to summarize the genetic component. There is a lack of consensus regarding which genes and their corresponding single nucleotide polymorphisms SNPs should be included in a genetic risk score and which method should be used to calculate the genetic score. The association of genetic scores with incident CVD has been prospectively studied, adjusting for the main CV risk factors, and most studies have found a significant association, with the relative risks varying between 1.

Therese (D Major), Op.86 No.1

The NRI is a statistical measure quantifying the usefulness of adding new variables to a risk prediction equation. Currently, many commercial tests are available, allowing an almost complete assessment of an individual's genome, and strong pressure is being applied to use this information to predict genetic risk and to make genetic testing a routine measure. Epigenetics studies the chemical changes in DNA that affect gene expression.

Methylation of genes related to CV risk factors is associated with variation in CV risk factor levels, 87 , 88 and lower DNA methylation levels are associated with an increased risk of CAD or stroke. Thus, epigenetic screening of CVD is not recommended. Low socio-economic status, defined as low educational level, low income, holding a low-status job or living in a poor residential area, confer an increased risk of CAD; the relative risk RR of CAD mortality risk is 1. People who are isolated or disconnected from others are at increased risk of developing and dying prematurely from CAD.

Acute mental stressors may act as triggers of acute coronary syndrome ACS. These stressors include exposure to natural catastrophes, as well as personal stressors e. Chronic stress at work e. The NRI improved significantly. Meta-analyses reported a 1. Hostility is a personality trait, characterized by extensive experience of mistrust, rage and anger and the tendency to engage in aggressive, maladaptive social relationships.

A meta-analysis confirmed that anger and hostility are associated with a small but significant increased risk for CV events in both healthy and CVD populations RR 1. In most situations, psychosocial risk factors cluster in individuals and groups. Mechanisms that link psychosocial factors to increased CV risk include unhealthy lifestyle [more frequent smoking, unhealthy food choices and less physical activity PA ] and low adherence to behaviour change recommendations or CV medication.

Assessment of psychosocial factors in patients and persons with CV risk factors should be considered for use as risk modifiers in CV risk prediction, especially in individuals with SCORE risks near decisional thresholds. In addition, psychosocial factors can help identify possible barriers to lifestyle changes and adherence to medication.

Standardized methods are available to assess psychosocial factors in many languages and countries. The management of psychosocial risk factors should be addressed according to Chapter 3a. In general, biomarkers can be classified into inflammatory e. However, for the purpose of overall CV risk estimation, these distinctions are generally not relevant.

Please enable Javascript in your browser's settings, and reload this page.

Also, from the perspective of risk stratification i. Among the most extensively studied and discussed biomarkers is hsCRP. This biomarker has shown consistency across large prospective studies as a risk factor integrating multiple metabolic and low-grade inflammatory factors, with RRs approaching those of classical CV risk factors. However, its contribution to the existing methods of CV risk assessment is probably small.

Meta-analyses and systematic reviews suggest that the vast majority of other circulating and urinary biomarkers have no or limited proven ability to improve risk classification. However, the extent to which they have been tested for their ability to add value to risk stratification varies considerably, , with strong evidence of reporting bias. If, despite these recommendations, biomarkers are used as risk modifiers, it is important to note that having an unfavourable biomarker profile may be associated with a somewhat higher risk, but also that a favourable profile is associated with a lower risk than calculated.

The degree to which the calculated risk is affected by biomarkers is generally unknown, but almost universally smaller than the adjusted RRs reported for these biomarkers in the literature. Although most CVD can be explained by traditional risk factors, there is substantial variation in the amount of atherosclerosis.

Thus interest has continued in the use of non-invasive imaging techniques to improve CV risk assessment. In individuals with calculated CV risks based on the major conventional risk factors near the decisional thresholds, some imaging techniques may be considered as risk modifiers to improve risk prediction and decision making. Calcifications indicate late-stage subclinical coronary atherosclerosis.

The extent of the calcification correlates with the extent of total coronary plaque burden. The quantification of CAC scoring is fairly consistent across studies. Most studies use the Agatston score. Although recent studies also showed the presence of CAC in low-risk populations, the added predictive value on CV events remains to be demonstrated.

There are concerns regarding costs and radiation exposure. Population-based studies have shown correlations between the severity of atherosclerosis in one arterial territory and the involvement of other arteries. Risk assessment using carotid ultrasound focuses on the measurement of the intima—media thickness IMT and the presence and characteristics of plaques.

The IMT-associated risk of cardiac events is also non-linear. The lack of standardization regarding the definition and measurement of IMT, its high variability and low intra-individual reproducibility have raised concerns. A recent meta-analysis failed to demonstrate any added value of IMT compared to the Framingham Risk Score in predicting future CVD, even in the intermediate risk group.

Plaques are related to both coronary and cerebrovascular events, and echolucent as opposed to calcified plaques increase ischaemic cerebrovascular events. Therefore, even though formal reclassification analyses have not been undertaken, carotid artery plaque assessment using ultrasonography may be considered to be a risk modifier in CV risk prediction in some cases.

Arterial stiffness is commonly measured using either aortic pulse wave velocity PWV or arterial augmentation index. An increase in arterial stiffness is usually related to damage in the arterial wall, as has been shown in hypertensive patients. A meta-analysis showed that arterial stiffness predicts future CVD and improves risk classification. The ankle—brachial index ABI is an easy-to-perform and reproducible test to detect asymptomatic atherosclerotic disease. The ABI is inversely related to CV risk, but there is controversy regarding its potential to reclassify patients into different risk categories.

Echocardiography is more sensitive than electrocardiography in diagnosing left ventricular hypertrophy LVH and it precisely quantifies left ventricular LV mass and geometric LVH patterns. Cardiac abnormalities detected by echocardiography have an additional predictive power. In addition, inflammatory mediators and promoters of calcification cause vascular injury and may explain why CKD is associated with CVD even after adjustment for conventional risk factors.

End-stage renal disease is associated with a very high CV risk. Influenza can trigger a CV event. Studies show an increase in rates of MI during the annual influenza season. The risk of MI or stroke was more than four times higher after a respiratory tract infection, with the highest risk in the first 3 days. Studies have linked periodontal disease to both atherosclerosis and CVD, , and serological studies have linked elevated periodontal bacteria antibody titres to atherosclerotic disease. Cardiotoxicity due to chemotherapy is related to a direct effect on the cell anthracycline-like through the generation of reactive oxygen species ROS.

Some agents fluorouracil, bevacizumab, sorafenib and sunitinib can induce a direct ischaemic effect not related to the premature development of atherosclerotic lesions. Moreover, they can increase risk factors such as hypertension and accelerate atherosclerosis, especially in older patients.

These effects can be irreversible type I agents or partially reversible type II agents and can develop many years after treatment exposure. Typically, anthracyclines are the prototype of type I agents and trastuzumab of type II agents. Cardiotoxicity due to chest radiotherapy can induce micro- and macrovascular injury. It can accelerate atherosclerosis, but this may occur many years after the initial exposure.

The first step in the identification of higher risk for cardiotoxicity consists of a careful baseline assessment of CV risk factors. Primary care, cardiology and oncology should work together to deliver optimal survivorship care that addresses CVD risk factors as well as prevalent disease. Positive health-promoting behaviour, including lifestyle factors healthy diet, smoking cessation, regular exercise, weight control should be strongly advised. Signs or symptoms of cardiac dysfunction should be monitored before and periodically during treatment for early detection of even asymptomatic abnormalities in patients receiving potentially cardiotoxic chemotherapy, and heart failure HF guideline recommendations should be followed if indicated.

In the case of a decrease in LV function during or after chemotherapy, the use of cardiotoxic agents should be avoided or delayed, if possible, until after discussion with the oncology team. This calls for adequate communication between oncology and cardiology. There is now clear evidence implicating high-grade inflammation as a pathway for accelerated vascular disease. Evidence in psoriasis is less rigorous, but a recent paper demonstrates broadly comparable CV risks in RA and in early severe psoriasis.

Hence, clinical judgment should be applied on a case-by-case basis. There is evidence from post hoc analysis of randomized trials to support a statin-associated reduction in CV risk in autoimmune conditions. OSAS is characterized by recurrent partial or complete collapse of the upper airway during sleep. Treatment options include behavioural changes, such as avoiding alcohol, caffeine or other stimulants of wakefulness before sleep, increased PA, discontinuation of sedating drugs and obesity control.

Continuous positive airway pressure is the gold-standard therapy and reduces CV mortality and events. ED and CVD share common risk factors, including age, hypercholesterolaemia, hypertension, insulin resistance and DM, smoking, obesity, metabolic syndrome, sedentary lifestyle and depression. CVD and ED also share a common pathophysiological basis of aetiology and progression. Thorough history taking, including CV symptoms and the presence of risk factors and co-morbid conditions, assessment of ED severity and physical examination are mandatory first-line elements of investigation.

Lifestyle changes are effective in improving sexual function in men: The most powerful driver of risk in all short-term 5 or 10 year CV risk algorithms is age. However, some younger individuals are at very high relative risk compared with individuals of a similar age and may have high lifetime risk: So trying to identify who may be at such risk is an important challenge. There are no data on the right age to begin collecting such information in the general population, but some guidelines advocate starting at age 40 years.

However, in the absence of a very high individual risk factor level or diagnosis of FH, their year risk will never be high enough to warrant BP- or lipid-lowering therapy. There are no data on what are the most effective methods of changing health behaviours in younger people. However, smoking cessation, healthy weight maintenance and regular aerobic activity are all important behaviours on which to provide advice and support.

Younger people with very high BP levels warranting treatment should be managed in the same way as older people with hypertension. In younger people who are judged eligible for a statin on the grounds of either FH or very high lipid levels, the management offered is the same as for older people. Very importantly, for all patients deemed to suffer with FH, the physician making the management decisions should arrange for FH screening for family members see section 3a. Age is the dominant driver of cardiovascular risk, and most individuals are already at very high risk at the age of 65 years see section 2.

Especially in the oldest old, cardiovascular risk management is controversial. Opponents argue that risk should not be treated when it is essentially age-driven. Proponents, on the other hand, point out that many preventive treatments are still effective at advanced age in terms of postponing morbidity and mortality. The Task Force has taken the position that epidemiological evidence of absolute risk reduction in clinical trials is the main driver for recommendations in this guideline.

Still, we encourage a discussion with patients regarding quality of life and life potentially gained, as well as regarding the ethical dilemmas of treating risk inherent to ageing, the total burden of drug treatment and the inevitable uncertainties of benefit. In this guideline, sections on treatment of the main risk factors contain recommendations or considerations specific to the elderly when evidence is available. Most of the elderly-specific evidence is available for BP section 3a. In general, more lenient treatment targets are advocated in the elderly.

The hypertension literature also contains increasing evidence that biological rather than calendar age is important. Evidence supporting more lenient glycaemic control targets in the elderly is also available for DM section 3a. Few areas in CVD prevention are more controversial than the mass use of statins in the elderly.

On the other hand, the cost-effectiveness of statins in these patients is offset by even small geriatric-specific adverse effects. A recent trial suggested no harm of stopping statins in the elderly with a limited life expectancy. Specific conditions that may occur in females only and may have an impact on CVD risk can be separated into obstetric and non-obstetric conditions. Studies suggest that pre-eclampsia is associated with an increase in CV risk by a factor 1. The rationale for screening these women for the occurrence of hypertension and DM is, however, quite strong.

The risk of developing DM is probably also elevated in these women, but exact estimates are not available. There are no data to suggest that recurrent pregnancy loss is associated with an increased CV risk. PCOS has been associated with an increased risk for future development of CVD, but larger studies have produced conflicting results. There are insufficient data to draw conclusions on a possible increased risk of hypertension or DM.

First-generation migrants usually display lower CVD mortality rates than natives of the host country, but with time, migrants tend to approach the CVD risk in their host country. Immigrants from South Asia notably India and Pakistan present high CVD rates — and have a much higher prevalence of DM, , while the prevalence of other CV risk factors is slightly lower than or comparable to natives of the host country. Management of DM is also significantly worse, while management of high BP and hypercholesterolaemia is better among South Asians than host country natives.

Immigrants from China and Vietnam present lower CVD risk than natives of the host country, although this finding has been challenged. This seems mainly due to the higher prevalence of smoking, DM, dyslipidaemia, hypertension and obesity rates. Immigrants from Morocco present lower CVD rates than natives from the host country.

1. Fortunes Hostage (Voice of the Wind: Shadows of Time Book 2)!
2. Macbeth (The New Cambridge Shakespeare)?
3. Energy Efficient Hardware-Software Co-Synthesis Using Reconfigurable Hardware (Chapman & Hall/CRC Computer and Information Science Series).
4. Gnomageddon!
5. Complete set?
6. No titles available;

Immigrants from sub-Saharan Africa and the Caribbean present higher CVD rates than natives from the host country in some studies, , , but not all. Management of CVD risk factors was worse than among natives in one study, but not in another. Based on available mortality and prospective data, the following correction factors could be applied when assessing CVD risk using SCORE among first-generation immigrants only.

6 Lieder, Op.86 (Brahms, Johannes)

These values reflect the best estimations from available data and should be interpreted with caution, but can be used to guide CV risk management. Individual and environmental factors impede the ability to adopt a healthy lifestyle, as does complex or confusing advice from caregivers. It is important to explore each patient's experiences, thoughts, worries, previous knowledge and circumstances of everyday life.

Individualized counselling is the basis for motivation and commitment. Decision-making should be shared between the caregiver and patient including also the individual's spouse and family. Excerpts 7 Streaming audio 7 Sound recordings 4 Vocal scores with piano 2 Art music 1 Chamber music 1 Concert television programs 1 Instrumental settings 1 Interviews 1 Live sound recordings 1 Songs 1. Coro 1 Turun kaupunginorkesteri 1. View Normal Gallery Brief. Sort by relevance relevance new to the Libraries year new to old year old to new author title.

Der Musensohn [sound recording]: Serenade [sound recording] []. Brunswick, [] Description Music recording — 1 sound disc: Selections Brahms, Johannes, Description Music recording — 1 sound disc: Summary Romanzen und Lieder, op. Lehmann, Lotte Singer Camden, N. O golden age of innocence: Victor, [] Description Music recording — 1 sound disc: Wenzig ; Abschied from the Bohemian by J. Candidus ; Willst du, dass ich geh'? Schmidt ; In den Beeren H.

The duo sonatas [sound recording]: Description Music recording — 3 sound discs: Javascript is required for this feature. These file s are part of the Werner Icking Music Collection. Editor Eusebius Mandyczewski I provide the original scanned version and the filtered, because the filter does some changes smoothening, sharpening borders and some portions of the scan get lost sometimes when they are to small e. Editor Max Friedlaender Edition Peters , No. Simrock In die Edition Peters aufgenommen , n. Edition transposed for Low Voice Scanned at dpi, cleaned with 2-point algorithm , additional manual cleaning.

Original-Ausgabe later reissue with added English text, ca.