Discover some unexpected symptoms that could signal heart trouble. Often, related conditions can raise your risk. Earlier reviews reported that cardiovascular disease (CVD) prognosis .. Int J Behav Med ;–7. doi/sijbm_9. Cardiovascular disease (CVD) remains the leading cause of mortality in women in According to the American Heart Association (AHA), 13% of women in the.
Disease 13. Heart
ED is a condition where erection does not take place by either mechanism. ED can occur because of hormonal imbalance, neural disorders or lack of adequate blood supply to the penis.
The vascular endothelium has an important role in angiogenesis and vascular repair by producing regulatory substances, including NO, prostaglandin, endothelins, prostacyclin and angiotensin II. These regulatory factors regulate the blood flow to the penis by controlling smooth muscle contractility and subsequent vasoconstriction and vasodilatation. Generally, in erectile tissue, increased blood flow through the cavernosal artery increases shear stress and produces NO, which further relaxes the vascular smooth muscles and increases blood flow in the corpora cavernosa.
However, in ED, endothelial NO synthesis is reduced and there is increased endothelial cell death Figure 2. Myocardial ischaemia is caused by the reduction of coronary blood flow as a result of fixed or dynamic epicardial coronary artery stenosis, abnormal constriction or deficient relaxation of coronary microcirculation, or because of reduced oxygen-carrying capacity of the blood.
Plaque that develops in atherosclerosis can rupture causing platelet aggregation and subsequent thrombus formation, which leads to MI. The other mechanisms of myocardial ischaemia are encountered far less than atherosclerosis. Endothelial dysfunction has an important role in the progression of atherosclerosis.
Endothelial dysfunction enhances the intimal proliferation and malregulation that results in plaque destabilisation in the arteries.
This refers to estimating the risk of mortality and morbidity associated with sexual activity. The current recommendations classify patients into low-, intermediate- and high-risk, based on their New York Heart Association class. These measures are likely to reduce cardiovascular risk and improve erectile function. Patients with ED at high risk of cardiovascular events should refrain from sexual activity until they are stable from a cardiovascular point of view.
Their management should be under close supervision from a cardiologist. Guidelines recommend that phosphodiesterase type 5 PDE5 inhibitors are the first-line drug for the treatment of ED Table 1. Sildenafil citrate was the first oral drug approved for ED in the US. PDE5 inhibitors increase the number and duration of erections, as well as the percentage of successful sexual intercourse.
PDE5 inhibitors are commonly prescribed to treat ED. The second Princeton Consensus Conference reviewed their appropriate use and recent studies of placebo-controlled and post-marketing surveillance data have confirmed their safety regarding cardiovascular events.
However, sildenafil should be used carefully with nitrates because their combination can result in severe hypotension and death. In addition, there are numerous alternatives to treat angina, such as ranolazine and ivabradine, which do not interact with PDE5 inhibitors.
As a result, patients with ED wishing to take PDE5 inhibitors can safely discontinue their nitrates and replace this treatment with the other anti-anginal agents. This was a prospective, randomised crossover study that demonstrated safety of sildenafil when given 1 hour before an exercise stress test. This dose may be increased to mg or decreased to 25 mg based on side effects. The use of PDE5 inhibitors in the treatment of right heart failure and left ventricular failure associated with combined pre- and post-capillary pulmonary hypertension has been well studied.
Vacuum erection devices are an effective first-line treatment for ED, regardless of the underlying cause. They can be used in combination with PDE5 inhibitors and they have high reported satisfaction rates. They are generally well tolerated, with minor adverse effects such as bruising, pain and failure to ejaculate.
It is recommended that testosterone be measured in patients with ED because low levels are a reliable measure of hypogonadism. Hypogonadism is not only a treatable cause of ED, but can also lead to reduced or lack of response to PDE5 inhibitors. In these patients, the aim should be to keep testosterone levels in the middle range, i.
Testosterone cypionate and testosterone enanthate injections are used for replacement therapy in patients with low testosterone. Other formulations, such as gels and patches, are recommended in older patients with chronic conditions. The benefits of testosterone replacement and the potential cardiovascular risks need to be thoroughly investigated, ideally through randomised controlled trials.
Intracavernosal and intraurethral injections are second-line therapy for patients with ED. Alprostadil is the agent most commonly used for intracavernosal injections. The main adverse effects of intracavernosal injections are painful erection, priapism and development of scarring at the injection site. Another injection option is the combination of phentolamine and aviptadil. This is effective, but requires simultaneous sexual stimulation to achieve its desired effect.
Intraurethral prostaglandin E1 pellets are suppositories that are inserted into the urethra. These agents act by relaxation of cavernous smooth muscle, which elevates the intracavernosal cGMP and by blocking the local alpha-receptors, resulting in improved erectile function. Another second-line treatment is low intensity extracorporeal shockwave therapy. This can be very useful, especially in patients who failed oral therapy, but do not wish to start injections.
Penile prosthesis is recommended as third-line treatment for patients who are fit for surgery and intolerant of oral medication, injections or external device therapy.
A penile prosthesis is particularly useful in patients with severe organic ED, achieving long-term effects and high satisfaction rates without the need for further medication.
Animal studies have been conducted to evaluate the effects of gene therapy. A rat model was studied by Bivalacqua et al. This research suggested that erectile response was greater in male rats with diabetes treated with combination eNOS gene therapy and sildenafil, compared with male rats with diabetes treated with eNOS gene therapy or sildenafil alone.
Stem cell therapy is an attractive treatment modality and an appealing option for tissue regenerative therapy for ED. Stem cells are pluripotent cells that can be produced from multiple regions within the body. They have the potential to divide and differentiate into numerous kinds of human cells, such as endothelial cells and smooth muscle.
ED is a common disease affecting men with IHD. Endothelial dysfunction is the link between ED and IHD and both diseases share the same aetiology, risk factors and pathogenesis. Aggressive control of these risk factors — along with lifestyle modification — is recommended to improve symptoms of ED and reduce cardiovascular risk. However, PDE5 inhibitors can potentiate the hypotensive effect of nitrates so concomitant administration of sildenafil and nitrates is contraindicated.
Gene and stem cell therapy are being investigated as a future therapies for ED. Skip to main content. Search form Search this site. Login or register to view PDF. Atherosclerosis, endothelial dysfunction, erectile dysfunction, ischaemic heart disease, phosphodiesterase inhibitors. The authors have no conflicts of interest to declare. Limerick V94 F, Ireland. European Cardiology Review ;13 2: Other Therapies Intracavernosal and intraurethral injections are second-line therapy for patients with ED.
European Association of Urology. Guidelines on male sexual dysfunction: Eur Urol ; Erectile dysfunction and the cardiovascular patient: The link between vasculogenic erectile dysfunction, coronary artery disease, and peripheral artery disease: J Invasive Cardiol ; Heart disease risk factors predict erectile dysfunction 25 years later: The Rancho Bernardo Study.
J Am Coll Cardiol ; Crossref PubMed Giuliano F. New horizons in erectile and endothelial dysfunction research and therapies. Int J Imp Res ; Linking erectile dysfunction and coronary artery disease. J Repr Med Endocrinol ; 2: Association between erectile dysfunction and coronary artery disease and its severity.
Indian Heart J ; Common grounds for erectile dysfunction and coronary artery disease. Curr Opinion Urol ; Erectile dysfunction and risk of cardiovascular Disease.
A population-based, longitudinal study of erectile dysfunction and future coronary artery disease. Mayo Clin Proc ; Erectile dysfunction severity as a risk marker for cardiovascular disease hospitalisation and all-cause mortality: PLoS Med ; Erectile dysfunction and later cardiovascular disease in men with type 2 diabetes: Erectile dysfunction and subsequent cardiovascular disease.
Does severity of ischemic coronary disease correlate with erectile function? Int J Impot Res ; 9: Erectile dysfunction prevalence, time of onset and association with risk factors in consecutive patients with acute chest pain and angiographically documented coronary artery disease. Crossref PubMed Jackson G. Erectile dysfunction and cardiovascular disease. Arab J Urology ; Crossref PubMed Simonsen U. Interactions between drugs for erectile dysfunction and drugs for cardiovascular disease.
Int J Impot Res ; The impact of diuretic therapy on reported sexual function. Arch Intern Med ; Long-term effects on sexual function of five antihypertensive drugs and nutritional hygienic treatment in hypertensive men and women. Crossref PubMed Adverse reactions to bendrofluazide and propranolol for the treatment of mild hypertension. Effect of antihypertensive treatment with valsartan or atenolol on sexual activity and plasma testosterone in hypertensive men.
Eur J Clin Pharmacol ; Beneficial effects of switching from B-blockers to nebivolol on the erectile function of hypertensive patients. Asian J Androl , 8: Sexual activity in hypertensive men treated with valsartan or carvedilol: Am J Hypertens ; Nebivolol versus other beta blockers in patients with hypertension and erectile dysfunction. Ther Adv Urol ; 9: A randomized comparison of the effects of nebivolol and atenolol with and without chlorthalidone on the sexual function of hypertensive men.
Clin Drug Invest ; Erectile dysfunction in high-risk hypertensive patients treated with beta-blockade agents. Cardiovasc Ther ; Clin Exper Pharmacol Phys ; A review of the positive and negative effects of cardiovascular drugs on sexual function: Neth Heart J ; A prospective study of risk factors for erectile dysfunction. J Urol ; Even the high-risk charts may underestimate risk in these countries.
All remaining countries are high-risk countries. Use of the high-risk chart is recommended for all other European and Mediterranean countries. Note that several countries have undertaken national re-calibrations to allow for time trends in mortality and risk factor distributions.
Such charts are likely to better represent current risk levels. To estimate a person's year risk of CVD death, find the correct table for their gender, smoking status, and age. Within the table find the cell nearest to the person's BP and total cholesterol or cholesterol: Risk estimates will need to be adjusted upwards as the person approaches the next age category.
Low-risk persons should be offered advice to maintain their low-risk status. While no threshold is universally applicable, the intensity of advice should increase with increasing risk. The relative risk chart may be helpful in identifying and counselling in young persons, even if absolute risk levels are low. The charts may be used to give some indication of the effects of reducing risk factors, given that there will be a time lag before risk reduces and the results of RCTs in general give better estimates of benefits.
Those who stop smoking in general halve their risk. The charts can assist in risk assessment and management but must be interpreted in the light of the clinician's knowledge and experience, especially with regard to local conditions. Risk will be overestimated in countries with a falling CVD mortality, and underestimated in countries in which mortality is increasing. At any given age, risk estimates are lower for women than for men.
Inspection of the charts indicates that risk is merely deferred in women, with a year-old woman resembling a year-old man in terms of risk. Sedentary subjects and those with central obesity; these characteristics determine many of the other aspects of risk listed below.
The increased risk associated with overweight is greater in younger subjects than in older subjects. SCORE charts should be used only in those with type 1 diabetes without target organ damage. Risk rises with increasing blood sugar concentration before overt diabetes occurs. Individuals with low HDL cholesterol, increased triglycerides, fibrinogen, apolipoprotein B apoB , and lipoprotein a [Lp a ] levels, especially in combination with familial hypercholesterolaemia, and perhaps increased high-sensitivity CRP hsCRP.
In particular, a low HDL level will indicate a higher level of risk in both sexes, all age groups, and at all levels of risk. Asymptomatic individuals with preclinical evidence of atherosclerosis, for example plaque on carotid ultrasonography. The higher the risk the greater the benefit from preventive efforts, which guides the following priorities:.
Documented CVD by invasive or non-invasive testing such as coronary angiography, nuclear imaging, stress echocardiography, carotid plaque on ultrasound , previous myocardial infarction, ACS, coronary revascularization PCI, CABG , and other arterial revascularization procedures, ischaemic stroke, peripheral artery disease PAD. Many middle-aged subjects belong to this category.
This risk is further modulated by factors mentioned above. Estimation of total risk remains a crucial part of the present guidelines.
New information on diabetes is included. Information on relative as well as absolute risk is added to facilitate the counselling of younger persons whose low absolute risk may conceal a substantial and modifiable age-related risk. The priorities defined in this section are for clinical use and reflect the fact that those at highest risk of a CVD event benefit 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, but they must be interpreted in the light of both the physician's detailed knowledge of their patient and local guidance and conditions. Current systems of grading evidence give most weight to RCTs.
While this is appropriate, many lifestyle measures are less amenable to such assessment than are drug treatments, which will therefore tend to receive a higher grade. There are no recent RCTs of a total risk approach to: The young, women, older people, and ethnic minorities continue to be under-represented in clinical trials.
A systematic comparison of current international guidelines is needed to define areas of agreement and the reasons for discrepancies.
The importance of the familial prevalence of early-onset CVD is not yet sufficiently understood in clinical practice Familial prevalence of atherosclerotic disease or of major risk factors high BP, diabetes mellitus, hyperlipidaemia should be systematically sought in the first-degree relatives of any patient affected before 55 years in men and 65 years in women.
In SCORE, accounting for family history is probably very crude and is most certainly an underestimate. Family history is a variable combination of genetics and shared environment. There is evidence of strong heritability of many cardiovascular risk factors. Because of the polygenic and polyfactorial determinants of the most common CVDs, the impact of any single polymorphism remains rather modest.
Commercial testing was recently made available to predict an individual's genetic risk, including direct-to-consumer testing. The clinical benefits of commercial testing have not yet been demonstrated. In some conditions the process of genetic counselling can be optimized and extended with cascade screening, which identifies patients at risk and enables timely treatment of affected relatives, as is the case for familial hypercholesterolaemia.
The risk of CVD in women, as in men, can be reduced by not smoking, by being active, avoiding overweight, and by having a blood pressure and blood cholesterol check and intervention, if elevated Age is a good marker of duration of exposure to known and unknown CHD risk factors.
Relatively young people are at low absolute risk of a CVD event in the ensuing 10 years despite having a full complement of risk factors.
However, the relative risk chart Figure 5 indicates that his risk is already fold higher than that of a man with no risk factors. Similar considerations apply in women who are at lower absolute risk at younger ages and may have high levels of specific risk factors. In these circumstances, clinical judgement is required—risk scores guide and do not dictate treatment decisions. Investment in additional measurements such as imaging with computed tomography to obtain coronary calcium scores may be helpful, 79 but adds considerably to the cost and time involved in risk factor scoring, and its benefit remains unproven.
However, exploration of trends over time and between countries shows that the relationship varies, making this an implausible explanation. The American Heart Association AHA published an update of its guidelines for the prevention of CVD in women, 82 which emphasizes that recommendations are the same for both men and women, with few exceptions.
Clinical investigation to aid treatment decisions in younger people with high levels of risk factors requires further evaluation. Low socio-economic status, lack of social support, stress at work and in family life, depression, anxiety, hostility, and the type D personality contribute both to the risk of developing CVD and the worsening of clinical course and prognosis of CVD.
These factors act as barriers to treatment adherence and efforts to improve lifestyle, as well as to promoting health and wellbeing in patients and populations.
In addition, distinct psychobiological mechanisms have been identified, which are directly involved in the pathogenesis of CVD Recent systematic reviews confirm that people who are isolated or disconnected from others are at increased risk of dying prematurely from CVD. According to a recent review, there is moderate evidence that work-related stress e. Several systematic reviews and meta-analyses have shown that clinical depression and depressive symptoms predict incident CHD RR 1.
Large epidemiological studies indicate that panic attacks increase the risk of incident cardiovascular events HR 1. A higher mortality could only be observed in post-myocardial infarction patients with reduced systolic left ventricular function HR 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 recent meta-analysis has confirmed that anger and hostility are associated with an increased risk for cardiovascular events in both healthy and CVD populations HR 1. In most situations, psychosocial risk factors cluster in the same individuals and groups.
Mechanisms that link psychosocial factors to increased CVD risk include unhealthy lifestyle more frequent smoking, unhealthy food choice, and less physical exercise , increased healthcare utilization, and low adherence to behaviour-change recommendations or cardiac medications.
The assessment of psychosocial factors in patients and persons with CVD risk factors is crucial as a means to stratify future preventive efforts according to the individual risk profile of the patient. Standardized measurements for depression, anxiety, hostility, socio-economic status, social support, psychosocial stress, and type D personality are available in many languages and countries.
Relevance of psychosocial factors with respect to quality of life and medical outcome should be discussed with the patient, and further tailored clinical management should be considered Section 4. Routine screening for depression does not contribute to better cardiac prognosis in the absence of changes in current models of cardiovascular care.
Recent meta-analyses have shown that symptoms of anxiety and the type D personality increase risk for CVD and contribute to worse clinical outcome. There is limited evidence that routine screening for psychosocial risk factors contributes to fewer future cardiac events, as screening has not yet translated into improved healthcare models.
Although the number of potential novel risk markers is ever expanding yearly, this number scales down to a level close to unity once the possible candidates have passed through the grading of clinical evidence. Emerging biomarkers were selected from published data, if tested as alternatives or on top of classical risk factors, for their ability to predict or modify year cardiovascular morbidity or mortality.
Only circulating biomarkers assessed by standardized and validated methods and identified as risk factors worth translating into clinical practice were considered in these guidelines, in a context of cost-effectiveness for assessment of individual risk in the general population.
After removing novel biomarkers relevant to glucose metabolism, lipid metabolism, or organ-specific biomarkers, which are included in the specific sections see Section 4 , two groups of systemic biomarkers relevant to CVD risk assessment were identified:. High-sensitivity CRP has shown consistency across large prospective studies as a risk factor integrating multiple metabolic and low-grade inflammatory factors underlying the development of unstable atherosclerotic plaques, with a magnitude of effect matching that of classical major risk factors.
This marker was used in individuals showing a moderate level of risk from clinical assessment of major CVD risk factors. Higher cost of test compared with classical biological risk factors e. Similar statements are made for fibrinogen. Homocysteine has shown precision as an independent risk factor for CVD. The magnitude of effect on risk is modest, and consistency is often lacking, mainly due to nutritional, metabolic e.
LpPLA2 has recently emerged as a marker with high consistency and precision as an independent risk factor for plaque rupture and atherothrombotic events. The magnitude of effect on risk remains modest at the level of the general population; study limitations or bias are present.
Overall, emerging validated biomarkers may add value in a context of specialized practice, to assess CVD risk more precisely in specific subgroups of patients at moderate, unusual, or undefined levels of risk e.
For both biomarkers that are already well-established and novel biomarkers that arise in the future there is a need to redefine specific subgroups intermediate, undefined, or unusual CVD risk that would benefit most from the use of these biomarkers, particularly in early primary prevention.
Imaging methods can be relevant in CVD risk assessment in individuals at moderate risk The consequences of coronary atherosclerosis can be objectively assessed non-invasively using a variety of techniques such as bicycle or treadmill exercise electrocardiogram ECG testing, stress echocardiography, or radionuclide scintigraphy.
Unfortunately, sudden cardiac death is for many individuals the first manifestation of CVD. Detection of asymptomatic but diseased patients is crucial for an adequate prevention programme. At every level of risk factor exposure, there is substantial variation in the amount of atherosclerosis. This variation in disease is probably due to genetic susceptibility, combinations of different risk factors, and interactions between genetic and environmental factors.
Thus measurements of subclinical disease may be useful for improving CVD risk prediction. Non-invasive tests such as carotid artery scanning, electron-beam computed tomography, multislice computed tomography, ankle—brachial BP ratios, and magnetic resonance imaging MRI techniques offer the potential for directly or indirectly measuring and monitoring atherosclerosis in asymptomatic persons, but cost-effectiveness needs to be documented.
Magnetic resonance imaging has been evaluated as a means of assessing coronary artery stenosis. The value of this technique is still in question. Recently, coronary wall MRI detected positive remodelling in asymptomatic patients with subclinical atherosclerosis, opening up a new research field in the prevention of CVD.
Coronary calcifications indicate atherosclerosis of coronary arteries. The extent of the calcification correlates with the extent of the total coronary plaque burden. For clinical purposes, however, it is not yet known if these new variables are superior to the Agatston score.
Misunderstandings in recent years regarding coronary calcium and extrapolation to CHD are due to a mix-up of definitions: In contrast, coronary calcium scanning shows a very high negative predictive value: It is more likely in the setting of unstable angina or non-ST elevation myocardial infarction NSTEMI than in stable chest pain, and occurs more frequently in younger patients.
The Agatston score is an independent risk marker regarding the extent of CHD and prognostic impact. Although calcium scanning is widely applied today, it is especially suited for patients at moderate risk.
Recent studies have also shown that multislice computed tomography coronary angiography with decreased radiation levels is highly effective in re-stratifying patients into either a low or high post-test risk group. Population-based studies have shown a correlation 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 of plaques and their characteristics. Although the relative risk for events is slightly lower after statistical correction for the presence of traditional risk factors, the risk remains elevated at higher IMT. When IMT is used to predict the incidence of subsequent stroke, the risk is graded but non-linear, with hazards increasing more rapidly at lower IMTs than at higher IMTs.
Plaques may be characterized by their number, size, irregularity, and echodensity echolucent vs. Plaques are related to both coronary obstructive disease and the risk of cerebrovascular events. Echolucent plaques imply an increased risk of cerebrovascular events as compared with calcified plaques. Plaque characteristics as assessed by carotid ultrasound were found to be predictive of subsequent cerebral ischaemic events.
Ultrasound imaging of the carotids is a non-invasive means of assessing subclinical atherosclerosis. The extent of carotid IMT is an independent predictor of cerebral and coronary events, but seems to be more predictive in women than in men. Consequently, carotid ultrasound can add information beyond assessment of traditional risk factors that may help to make decisions about the necessity to institute medical treatment for primary prevention. Arterial stiffness has been shown to provide added value in stratification of patients.
An increase in arterial stiffness is usually related to damage in the arterial wall, as has been suggested in hypertensive patients. The ankle—brachial BP index ABI is an easy-to-perform and reproducible test to detect asymptomatic atherosclerotic disease.
The ABI also predicts further development of angina, myocardial infarction, congestive heart failure, CABG surgery, stroke, or carotid surgery. It has been shown that the extent of retinal artery atherosclerosis correlates with the extent of coronary artery atherosclerosis and with serum levels of cholesterol, triglycerides, and apoB. Vascular ultrasound screening is reasonable for risk assessment in asymptomatic individuals at moderate risk.
Measurement of coronary artery calcifications may be reasonable for cardiovascular risk assessment in asymptomatic adults at moderate risk. The role of computed tomography scanning for screening in asymptomatic patients needs further investigation. Prospective studies proving the value of coronary scanning level A evidence do not as yet exist.
Magnetic resonance imaging for detection of vascular plaque may be of interest for cardiovascular risk assessment in asymptomatic adults, but studies are still not convincing. Atherosclerosis is an inflammatory disease in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate lesions in the arterial tree.
The optimal concept of prevention in these diseases is not established, and randomized studies evaluating prognosis are not available. Management of all risk factors appears advisable even in the absence of randomized studies Influenza epidemics are associated with an increased rate of cardiovascular events. Influenza vaccination as a population-wide prevention measure was associated with a very cost-effective reduction in clinical events.
Hypertension, dyslipidaemia, and diabetes mellitus are common among patients with CKD. They are major risk factors for the development and progression of endothelial dysfunction and atherosclerosis, and contribute to the progression of renal failure—yet these patients tend to be less intensely treated than patients with normal renal function.
In a large cohort study, anaemia, decreased GFR, and microalbuminuria were independently associated with CVD and, when all were present, CVD was common and survival was reduced. There is a quantitative association between decreased GFR and cardiovascular risk: Lipid lowering appears useful in a wide range of patients with advanced CKD but with no known history of myocardial infarction or coronary revascularization: Obstructive sleep apnoea OSA is characterized by recurrent partial or complete collapse of the upper airway during sleep.
Repetitive bursts of sympathetic activity, surges of blood pressure, and oxidative stress brought on by pain and episodic hypoxaemia associated with increased levels of mediators of inflammation are thought to promote endothelial dysfunction and atherosclerosis.
It may result from psychological, neurological, hormonal, arterial, or cavernosal impairment or from a combination of these factors. ED is a marker for CVD and a predictor of future events in middle-aged and older men but not beyond that offered by the Framingham risk score.
Psoriasis appears to be an independent risk factor for myocardial infarction. The pathophysiology of psoriasis is characterized by an increase in antigen presentation, T-cell activation, and T-helper cell type 1 cytokines, resulting in thick scaly red plaques and, in some patients, arthritis. Psoriasis is also associated with markers of systemic inflammation, such as increased CRP levels. The risk of myocardial infarction associated with psoriasis is greatest in young patients with severe psoriasis, is attenuated with age, and remains increased even after controlling for traditional cardiovascular risk factors.
Patients in whom the psoriasis was classified as severe had a higher risk of myocardial infarction than patients with mild psoriasis, consistent with the hypothesis that greater immune activity in psoriasis is related to a higher risk of myocardial infarction and cardiovascular death. Patients with rheumatoid arthritis are twice as likely as the general population to suffer a myocardial infarction.
They also have a higher mortality rate after myocardial infarction, which may only partially explain their reduced life expectancy 5—10 years shorter than patients without the condition.
CVD risk is increased at an early stage of the disease, and this risk excess beyond traditional risk parameters is possibly related to systemic inflammation and a prothrombotic state.
Modification of traditional risk factors through lifestyle changes, including dietary modification, smoking cessation, and increased daily exercise, and appropriate drug prescription may be of particular importance in reducing risk in individuals with psoriasis or rheumatoid arthritis.
Non-randomized observational studies report reductions in rates of vascular events and cardiovascular death among both rheumatoid arthritis and psoriasis patients being treated with weekly methotrexate in doses ranging from 10 to 20 mg. Systemic lupus erythematosus is associated with endothelial dysfunction and an increased risk of CHD that is not fully explained by classic CHD risk factors. Chronic systemic inflammation in patients with systemic lupus erythematosus results in coronary microvascular dysfunction, with abnormalities in absolute myocardial blood flow and coronary flow reserve.
Coronary microvascular dysfunction is an early marker of accelerated coronary atherosclerosis and may contribute to the increased cardiovascular morbidity and mortality in these patients. Periodontitis is associated with endothelial dysfunction, atherosclerosis, and an increased risk of myocardial infarction and stroke.
Confounding factors, however, such as low socio-economic status and cigarette smoking probably play a significant role. Periodontitis can be considered a risk indicator for a generally decreased cardiovascular health status and its treatment is indicated as well as management of the underlying cardiovascular risk factors.
The incidence of ischaemic heart disease and stroke is increased many years after radiation exposure for treatment of lymphomas and for breast cancer, as well as for head and neck cancer. From descriptive studies, the lesions exhibit typical features of atherosclerosis, including lipid accumulation, inflammation, and thrombosis.
The use of statins may be reasonable. Cardiac allograft vasculopathy is the leading cause of late morbidity and mortality in heart transplant patients. Although it is a complex multifactorial process arising from immune and non-immune pathogenic mechanisms, the approach to cardiac allograft vasculopathy has been modification of underlying traditional risk factors and optimization of immune suppression. Important non-immune risk factors include hyperlipidaemia, hypertension, diabetes mellitus, and hyperhomocysteinaemia.
Administration of statins improves endothelial dysfunction, slows the development of cardiac allograft vasculopathy, and benefits survival. Treatment of periodontitis improves endothelial dysfunction, one of the earliest signs of atherosclerosis. Cognitive-behavioural methods are effective in supporting persons in adopting a healthy lifestyle These patterns are framed during childhood and adolescence by an interaction of environmental and genetic factors, and are maintained or even promoted by the individual's social environment as an adult.
Consequently, marked differences in health behaviour between individuals but also between social groups can be observed. In addition, these factors impede the ability to adopt a healthy lifestyle, as does complex or confusing advice from medical caregivers. Increased awareness of these factors facilitates empathy and counselling simple and explicit advice , thus facilitating behavioural change.
A friendly and positive interaction is a powerful tool to enhance an individual's ability to cope with illness and adhere to recommended lifestyle changes and medication use. Social support provided by caregivers may be of importance in helping individuals maintain healthy habits and follow medical advice.
It is of special importance to explore each individual patient's experiences, thoughts and worries, previous knowledge, and circumstances of everyday life. Individualized counselling is the basis for evoking and gaining the patient's motivation and commitment.
Decision-making should be shared between caregiver and patient also including the individual's spouse and family to the greatest extent possible, thus ensuring the active involvement of both the individual and family in lifestyle change and medication adherence. In addition, caregivers can build on cognitive-behavioural strategies to assess the individual's thoughts, attitudes, and beliefs concerning the perceived ability to change behaviour, as well as the environmental context in which attempts to change are made, and subsequently to maintain the lifestyle change.
A crucial step in changing negative into positive experiences is to help the individual to set realistic goals; goal setting combined with self-monitoring of the chosen behaviour are the main tools needed to achieve a positive outcome. Moving forward in small, consecutive steps is one of the key points in changing long-term behaviour.
As this is a specific clinical skill, communication training is important for health professionals. Combining the knowledge and skills of clinicians such as physicians, nurses, psychologists, and experts in nutrition, cardiac rehabilitation, and sports medicine into multimodal, behavioural interventions can help to optimize the preventive efforts.
Multimodal, behavioural interventions are especially recommended for individuals at very high risk and for individuals with clinically manifest CVD. These interventions include promoting a healthy lifestyle through behaviour change including nutrition, exercise training, relaxation training, weight management, and smoking cessation programmes for resistant smokers.
Evidence has confirmed cognitive-behavioural strategies to be essential components of interventions targeting lifestyle change. There is limited evidence to determine which interventions are the most effective in specific groups e.
Public health measures including smoking bans are crucial for the public's perception of smoking as an important health hazard According to estimations from SCORE, year fatal cardiovascular risk is approximately doubled in smokers. Although the rate of smoking is declining in Europe, it is still very common among individuals who have received little education; and widening education-related inequalities in smoking-cessation rates have been observed in many European countries in recent years.
The survey also found that evidence-based treatment for smoking cessation was underused. Historically, smoking was taken up mainly by men, but in recent years women have caught up or even surpassed the level of smoking among men in many regions.
Risk associated with smoking is proportionately higher in women than in men. The risk associated with smoking is primarily related to the amount of tobacco smoked daily and shows a clear dose—response relationship with no lower limit for deleterious effects.
Accumulated evidence shows that passive smoking increases the risk of CHD, with a higher relative risk than might be expected. Indeed, recently imposed public smoking bans in different geographical locations have led to a significant decrease in the incidence of myocardial infarction.
Although the exact mechanisms by which smoking increases the risk of atherosclerotic disease are not fully understood, it is clear that smoking enhances both the development of atherosclerosis and the occurrence of superimposed thrombotic phenomena. Mechanisms have been elucidated through observational cohort studies, experimental observations, and laboratory studies in humans and animals, , — and point towards the effect of smoking on endothelial function, , oxidative processes, platelet function, fibrinolysis, inflammation, — and modification of lipids and vasomotor function.
Reactive oxygen species—free radicals—present in inhaled smoke cause oxidation of plasma LDL; oxidized LDL triggers the inflammatory process in the intimae of the arteries through stimulation of monocyte adhesion to the vessel wall, resulting in increased atherosclerosis.
Plaque formation is not thought to be fully reversible and thus smokers would never be expected to reach the risk level of never-smokers concerning CVD. Most current evidence suggests that nicotine exposure from smoking has only minor effects on the atherosclerotic process, , and nicotine replacement has shown no adverse effect on outcomes in patients with cardiac disease.
The benefits of smoking cessation have been extensively reported. Studies of subjects without established CVD find risk in former smokers to be moderate between that of current and never-smokers. The risk is rapidly reduced after cessation, with significant morbidity reductions reported within the first 6 months. Smoking reduction cannot generally be recommended as an alternative to quitting smoking due to compensatory smoking to avoid nicotine abstinence symptoms, which causes harm reduction to be disproportionately smaller than assumed.
Smoking reduction has not been shown to increase probability of future smoking cessation, but some advocate nicotine-assisted smoking reduction in smokers unable or unwilling to quit. There is no age limit to the benefits of smoking cessation. Non-smokers at high risk and patients with established CVD should be advised about the effects of passive smoking and recommended to avoid exposure.
Public health measures such as smoking bans, tobacco taxation, and media campaigns are efficient aids in preventing smoking uptake and supporting smoking cessation. Quitting smoking is a complex and difficult process because the habit is strongly addictive both pharmacologically and psychologically.
The most important predictor of successful quitting is motivation, which can be increased by professional assistance. The physician's firm and explicit advice that the person should stop smoking completely is important in starting the smoking-cessation process and increases the odds of success OR 1. Smoking cessation initiated during hospital admission should continue for a prolonged period after discharge to increase success.
Smokers should be advised about expected weight gain of on average 5 kg and that the health benefits of tobacco cessation far outweigh the risks from weight gain. Most quitters quit unassisted. However, pharmacological aid consistently improves quit rates. Consequently, in addition to advice and encouragement, nicotine replacement therapy NRT and, in some cases, varenicline or bupropion should be offered to assist cessation.
NRT, varenicline, or bupropion should normally be prescribed as part of an abstinent-contingent treatment, in which the smoker makes a commitment to stop smoking on a particular date. A meta-analysis of 36 trials comparing long-term cessation rates using bupropion vs.
The partial nicotine receptor agonist varenicline has been shown to increase the chances of successful long-term smoking cessation between two- and three-fold compared with pharmacologically unassisted quit attempts, including in patients with CVD.
Current morbidity or distress may suggest use of cessation counselling and postponement of drugs other than NRT. A meta-analysis based on 14 RCTs including patients has indicated a small but significantly increased risk of cardiovascular events associated with the use of varenicline. The antidepressant nortriptyline and the antihypertensive drug clonidine aid smoking cessation, , but, owing to side effects, are second-line choices. All pharmacological smoking-cessation therapies should be used short term since long-term safety and efficacy data are lacking.
Both individual and group behavioural interventions are effective in helping smokers quit. Getting other family members who smoke to quit together with the patient is of great help. Physicians and caregivers must set an example by not smoking. There is no consistent evidence that acupuncture, acupressure, laser therapy, hypnotherapy, or electrostimulation are effective for smoking cessation.
New evidence on the health effects of passive smoking strengthens the recommendation on passive smoking. Energy intake should be limited to the amount of energy needed to maintain or obtain a healthy weight, i. In general, when following the rules for a healthy diet, no dietary supplements are needed Dietary habits are known to influence cardiovascular risk, either through an effect on risk factors such as serum cholesterol, BP, body weight, and diabetes, or through an effect independent of these risk factors.
A healthy diet also reduces the risk of other chronic diseases such as cancer. Most evidence on the relationship between nutrition and cardiovascular diseases is based on observational studies. The impact of diet can be studied on different levels. The most detailed way is looking at specific nutrients. Looking at foods or food groups is another way of evaluating diet, which is more easily translated into dietary recommendations.
Finally, there is growing interest in dietary patterns, of which the Mediterranean diet is the most studied. The dietary pattern approach can be seen as the equivalent of the shift from evaluating single risk factors to evaluating total risk profiles. The nutrients of interest with respect to CVD are fatty acids which mainly affect lipoprotein levels , minerals which mainly affect BP , vitamins, and fibre.
In the prevention of CVD through dietary changes, the fat content and fatty acid composition of the diet have been the focus of attention since the s. In prevention, the fatty acid composition of the diet is more important than the total fat content.
Our knowledge on the effects of subclasses of fatty acids saturated, monounsaturated, and polyunsaturated as well as on specific fatty acids within these subclasses e. In , Keys et al. Given the effect on serum cholesterol levels, an impact on CVD occurrence is plausible. Recently, a meta-analysis of cohort studies did not show an increase in the relative risk for CHD or CVD with higher intake of saturated fat, although there may be several methodological issues explaining this null finding.
Another important aspect is by which nutrient saturated fatty acids are replaced. Monounsaturated fatty acids have a favourable effect on HDL cholesterol levels when they replace saturated fatty acids or carbohydrates in the diet.
The polyunsaturated fatty acids can be largely divided into two subgroups: The fatty acids eicosapentaenoic acid and docosahexaenoic acid, representatives of the n -3 group, are important. They do not have an impact on serum cholesterol levels, but have been shown to reduce CHD mortality and to a lesser extent stroke mortality. A hypothesis for this differential effect is that they could prevent fatal cardiac arrhythmia.
These fatty acids are found in margarine and bakery products. The food industry has eliminated part of the trans fatty acids from their products, but there is still more to be gained from further elimination.
A small amount of trans fat in the diet will remain, coming from ruminant fat in dairy and meat products. The impact of dietary cholesterol on serum cholesterol levels is weak compared with that of the fatty acid composition of the diet.
When guidelines are followed to lower saturated fat intake, this usually also leads to a reduction in dietary cholesterol intake.
The effect of sodium intake on BP is well established. Processed foods are an important source of sodium intake. Potassium is another mineral that affects BP. The main sources of potassium are fruits and vegetables.
A higher potassium intake has been shown to reduce BP. Risk of stroke varies greatly with potassium intake: Many case—control and prospective observational studies have observed inverse associations between levels of vitamin A and E and risk of CVDs.
This protective effect was attributed to their antioxidant properties. However, intervention trials designed to confirm the causality of these relationships have failed to confirm the results from observational studies. The B-vitamins B6, B12, and folic acid have been studied for their potential to lower homocysteine levels, which has been postulated as a risk factor for CVDs.
Thus, B-vitamin supplementation to lower homocysteine levels does not lower risk. Some epidemiological studies have shown associations between vitamin D deficiency and cardiovascular disease. Conclusive evidence showing that vitamin D supplementation improves cardiovascular prognosis is however lacking, but trials are underway. Consumption of dietary fibre reduces the risk of CVD.
Although the mechanism is not elucidated completely, it is known that a high fibre intake reduces post-prandial glucose responses after carbohydrate-rich meals, and lowers total and LDL cholesterol levels. The American Institute of Medicine recommends an intake of 3. Observational studies have shown a protective effect of consumption of fruits and vegetables on CVD prevention.
Most of the evidence comes from prospective cohort studies, while RCTs are scarce. Individual studies have shown weak or non-significant effects of fruit and vegetable intake on CVD risk.
Because measurement of diet is complex, measurement error is likely to attenuate the observed relationships. Furthermore, since it is known that individuals who consume a lot of fruits and vegetables differ in many respects from those who eat few fruits and vegetables e. Nevertheless, results in different cohort studies have been quite homogeneous, and several meta-analyses have reported statistically significant effect estimates.
The protective effect of fruits and vegetables seems to be slightly stronger for the prevention of stroke compared with the prevention of CHD. One of the reasons for this can be the effect of fruits and vegetables on BP, based on the fact that they are a major source of potassium.
The DASH trial has shown that increasing fruit and vegetable intake contributed to the observed decrease in BP in the intervention arm. The recommendation is to eat at least g of fruit 2—3 servings and g of vegetables 2—3 servings per day. The protective effect of fish on CVD is attributed to the n -3 fatty acid content.
In particular, in the range of no or very low intake to moderate intake there is a strong decrease in cardiovascular risk. The public health impact of a small increase in fish consumption in the general population is therefore potentially large.
Results from epidemiological studies show a protective effect of moderate alcohol consumption on the occurrence of CVD. The relationship is J-shaped, which is not explained by special characteristics of abstainers. There seems to be a favourable effect of red wine in particular, which may be due to the effect of polyphenols especially resveratrol. With respect to the prevention of CVDs, the optimal level of intake is somewhat higher.
Sugar-sweetened soft drinks are the largest single food source of calories in the US diet and are also important in Europe. A meta-analysis has suggested that for energy consumed in the form of a liquid, compensation of caloric intake at subsequent meals could be less complete than for energy from solid food.
The cholesterol-lowering effect is additional to that obtained with a low-fat diet or use of statins. In accordance with the shift from evaluating and treating single risk factors to evaluating a person's total risk profile, more research is focusing on dietary patterns instead of on single nutrients.
Studying the impact of a total dietary pattern theoretically shows the full preventive potential of diet, because it yields a combined estimate of the impact of several favourable dietary habits. The Seven Countries Study showed a large difference in cardiovascular mortality rates between northern and southern Europe. Cumulative year coronary heart disease CHD mortality rates in different cohorts of the Seven Countries Study, according to baseline quartiles of total cholesterol level, adjusted for age, smoking, and blood pressure.
The concept of the Mediterranean diet comprises many of the nutrients and foods that have been discussed previously: A number of studies have demonstrated the protective effect of this diet, and recently a meta-analysis has been performed. Depending on the number of food items for which information was obtained, the score could range from 0 to 7—9. It is clear that dietary modifications should form the basis for CVD prevention.
Some changes in the diet will be reflected in favourable changes in measurable risk factors, such as BP and cholesterol levels.
However, it should be kept in mind that dietary habits that do not show their effect on levels of BP or blood lipids can also make an important contribution to the prevention of CVD. The requirements for a healthy diet are summarized in the key messages at the beginning of this section. The challenge for coming years is to translate nutritional guidelines into diets that are attractive to people and to find ways in which to make people change their long-standing dietary habits.
Since it is not yet clear which specific substances cause the protective effect, it is recommended to eat a varied diet, based on the above-mentioned principles. For some aspects of diet, legislation can help to change product formulation by the industry trans fatty acids and salt reduction. The industry can make an important contribution in reducing the salt content of processed foods. Accumulated new evidence supports the view that homocysteine is not a causal risk factor for CVD.
The biggest challenge in dietary prevention of CVDs is to develop more effective strategies to make people change their diet both quantitatively and qualitatively and to maintain that healthy diet and a normal weight. Regular physical activity and aerobic exercise training are related to a reduced risk of fatal and non-fatal coronary events in healthy individuals, — , subjects with coronary risk factors, and cardiac patients , over a wide age range. A sedentary lifestyle is one of the major risk factors for CVD.
Regular aerobic physical activity results in improved exercise performance, which depends on an increased ability to use oxygen to derive energy for work.
Moreover, myocardial perfusion can be improved by aerobic exercise, with an increase in the interior diameter of major coronary arteries, an augmentation of microcirculation, and an improvement of endothelial function. Physical activity also has a positive effect on many of the established risk factors for CVDs, preventing or delaying the development of hypertension in normotensive subjects and reducing BP in hypertensive patients, increasing HDL cholesterol levels, helping to control body weight, and lowering the risk of developing non-insulin-dependent diabetes mellitus.
As these conclusions are based on the results of observational studies, selection bias may be linked on the one hand to the existence of subclinical, undiagnosed diseases that may have made some individuals decrease their physical activity level before the start of the study, and on the other hand to the tendency to associate healthier habits e. However, studies controlling for these potential confounders still observed an inverse association between physical activity or cardiorespiratory fitness and all-cause and cardiovascular mortality.
Most of such a mortality-reduction effect seems to rely on a decrease in cardiovascular and CHD mortality, and the level of decreased coronary risk attributable to regular aerobic physical activity is similar to that of other lifestyle factors such as avoiding cigarette smoking.
The volume of moderate-intensity physical activity or aerobic exercise training able to provide a reduction in all-cause and cardiovascular mortality ranges from 2. Of note, similar results are obtainable by performing 1—1. Generally speaking, the exercise-related risk of major cardiovascular events in ostensibly healthy people is exceedingly low, ranging from 1 in to 1 in 2 patient-hours of exercise. Individuals who exercise only occasionally seem to have an increased risk of acute coronary events and sudden cardiac death during or after exercise.
Aerobic physical activity in patients with known CVD is usually considered as an aerobic exercise training intervention included in a cardiac rehabilitation programme.
Hence available data deal almost exclusively with cardiovascular fitness measurements and not with evaluation of habitual physical activity level. This is due to the need for a formal evaluation of both exercise capacity and exercise-associated risk in patients with established cardiac disease. In this context, the effects of physical activity alone on cardiovascular risk may not be easily discernible. More extensive use of revascularization techniques and drug treatments during recent years has progressively resulted in a relatively low-risk general population of cardiac patients, in whom significant survival improvements are less likely to occur as a result of any added intervention.
In any case, recent data confirm the existence of an inverse dose—response relationship between cardiovascular fitness evaluated by treadmill stress testing and expressed in METs and all-cause mortality in large populations of both male and female cardiovascular patients [a history of angiographically documented CHD, myocardial infarction, CABG, coronary angioplasty PCI , chronic heart failure, peripheral vascular disease, or signs or symptoms suggestive of CHD during an exercise testing].
The results were the same irrespective of use of beta-blocking agents. The effects of aerobic exercise training on the cardiac mortality rate in patients with chronic heart failure have been evaluated in a meta-analysis. Prognosis improvement was higher in patients with ischaemic aetiology, lower left ventricular ejection fraction and peak VO 2 , and higher New York Heart Association class.
In patients with CVD, available data do not allow definition of an aerobic exercise training weekly volume as precise as that indicated for healthy subjects, , and exercise prescription must be tailored to the clinical profile of the individual. Patients at low clinical risk with a previous acute myocardial infarction, CABG, PCI, or affected by stable angina pectoris or chronic heart failure can be assigned an aerobic exercise training of moderate to vigorous intensity of 3—5 sessions per week, 30 min per session, with frequency, duration, and supervision of aerobic exercise training sessions to be in any case adapted to their clinical characteristics.
Patients at moderate to high clinical risk should follow an even more strictly individualized exercise prescription, depending on the metabolic load known to evoke abnormal signs or symptoms. However, even in the more limited patients, small amounts of properly supervised physical activity are beneficial in order to enable maintenance of independent living and counteract disease-related depression.
Information is available for evidence-based aerobic exercise training prescription in specific subpopulations of cardiac patients. In patients with CVD, exercise prescription is strongly determined by exercise-related risk.
Available risk stratification algorithms help to identify patients who are at increased risk for exercise-related cardiovascular events and who may require more intensive cardiac monitoring, , and the safety of medically supervised exercise programmes that follow such indications for exercise-related risk stratification is well established.
The occurrence of major cardiovascular events during supervised aerobic exercise training in cardiac rehabilitation programmes is rare: The dose—response relationship between cardiorespiratory fitness and reduction in cardiovascular risk observed in primary prevention also holds in the secondary prevention setting.
Regular physical activity yields a long-term prognostic gain in patients with chronic heart failure. High-intensity interval training is superior to moderate-intensity continuous training in improving functional capacity and inducing favourable left ventricular remodelling in chronic heart failure patients. Psychological interventions can counteract psychosocial stress and promote healthy behaviours and lifestyle Psychological interventions aim to counteract psychosocial stress and promote health behaviours and lifestyle.
Coronary patients with clinically significant depression can be safely and effectively treated with psychotherapy 84 , 85 , — or selective serotonin re-uptake inhibitors, — although evidence for a beneficial effect on cardiac endpoints is inconclusive.
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