Results from epidemiological studies suggest a lowerrisk of CVD occurring with moderate one to two units per day alcoholconsumption compared with non-drinkers. This association appears not tobe explained by special characteristics of abstainers, although thepotential for residual confounding and reverse causality cannot be fullyexcluded.
Moreover, a recent Mendelian randomization study includinganalyses from 59 epidemiological studies has shed doubt on anybeneficial effect of moderate alcohol consumption, suggestingthat the lowest risks for CV outcomes were in abstainers and that anyamount of alcohol is associated with elevated BP and BMI. Sugar-sweetened soft drinks are the largest single food source ofcalories in the US diet and are important in Europe.
Regular consumption of soft drinks has been associated withoverweight, metabolic syndrome and type 2 DM. Substitution ofsugar-sweetened soft drinks with artificially sweetened drinks resultedin less weight gain in children over an month period. Regularconsumption of sugar-sweetened beverages i. The cholesterol-lowering effect is in addition to thatobtained with a low-fat diet or use of statins. Further cholesterolreduction can be obtained with higher doses of phytosterols. Studying the impact of a total dietary pattern theoretically shows the fullpreventive potential of diet since it yields a combined estimate of theimpact of several favourable dietary habits.
The Mediterranean dietcomprises many of the nutrients and foods that have been discussedpreviously: high intake of fruits, vegetables, legumes, wholegrain products,fish and unsaturated fatty acids especially olive oil ; moderateconsumption of alcohol mostly wine, preferably consumed with meals and lowconsumption of red meat, dairy products and saturated fatty acids.
The biggest challenge in dietary prevention of CVD is to develop moreeffective strategies to make people change their diet bothquantitatively and qualitatively and to maintain that healthy dietand a normal weight. Both overweight and obesity are associated with an increased risk of CVDdeath and all-cause mortality. Achieving and maintaining a healthy weight has a favourable effect onmetabolic risk factors BP, blood lipids, glucose tolerance and lowerCV risk.
There is evidence thatoptimal weight in elderly is higher than in the young andmiddle-aged. In many countries, favourable trends in major risk factors such as bloodcholesterol, BP and smoking prevalence have been observed, translating intoreduced CV mortality. However, BMI has greatly increased in all countriesover recent decades, resulting in a concomitant increase in the prevalenceof type 2 DM.
In the USA, it has been projected that if obesity trends from to continue, obesity will increasingly offset the positive effectsof declining smoking rates. Body fat stored in the abdomen intra-abdominal fat carries a higher risk than subcutaneous fat. Several measures of body fatness are available see Table D in the web addenda. Most data are available for BMI, waist:hipcircumference ratio and simple waist circumference.
The optimal level formeasurement of waist circumference is midway from the lower rib margin tothe anterior superior iliac crest, in the standing position. The WHOthresholds for waist circumference are the most widely accepted in Europe. Based on these thresholds, two action levels are recommended:. These thresholds have been calculated based on Caucasians, and it is apparentthat different cut-offs for anthropometric measurements are required indifferent races and ethnicities. Some studies argue that a specific subgroup of obeseindividuals is resistant to metabolic complications such as arterialhypertension and insulin resistance.
However, MHO individuals present ahigher all-cause mortality compared with normal weight metabolically healthyindividuals. At the population level, obesity is associated with CVD risk. However, amongthose with established CAD, the evidence is contradictory. However, this evidence should not bemisinterpreted to recommend higher target BMIs for those with establishedCVD since reverse causality may be operating. Cardiorespiratory fitnessmight influence relationships between adiposity and clinical prognosis inthe obesity paradox. Normal weight unfit individuals have a higher risk ofmortality than fit individuals, regardless of their BMI.
Overweight andobese fit individuals have mortality risks similar to normal weight fitindividuals. Although diet, exercise and behaviour modifications are the mainstaytherapies for overweight and obesity, they are often unsuccessful forlong-term treatment. A recent meta-analysis indicates that patientsundergoing bariatric surgery have a reduced risk of MI, stroke, CV eventsand mortality compared with non-surgical controls.
Knowledge and implementation of effective strategies to achieveweight loss and maintain a long-term healthy weight. Identification of the relative roles of diet, exercise and behaviourmodification in the management of overweight and obese people. Whileaccepting the simplicity of this approach and that it could beuseful in some settings, there is better scientific support for thethree targets matched to level of risk.
It should be noted that the evidence for patients withCKD is less strong. The crucial role of dyslipidaemia, especially hypercholesterolaemia, in thedevelopment of CVD is documented beyond any doubt by genetic, pathology,observational and intervention studies. In blood plasma, lipids such as cholesterol and triglycerides circulate aslipoproteins in association with various proteins apolipoproteins.
Themain carrier of cholesterol in plasma LDL-C is atherogenic. The role oftriglyceride-rich lipoproteins is currently under active investigation:chylomicrons and large very-low-density lipoproteins VLDLs appear not tobe atherogenic, but very high concentrations of these triglyceride-richlipoproteins can cause pancreatitis. Most cholesterol is normally carried in LDL-C.
Over a wide range of plasmacholesterol concentrations, there is a strong and graded positiveassociation between total as well as LDL-C and risk of CVD. The evidence that reducing plasma LDL-C reduces CVD risk is unequivocal; theresults of epidemiological studies and trials with and without statins usingangiographic or clinical endpoints confirm that the reduction of LDL-C is ofprime concern in the prevention of CVD.
Every 1. Apolipoprotein B apoB; the main apoprotein of atherogenic lipoproteins levels have also been measured in outcome studies in parallel withLDL-C. Hypertriglyceridaemia is a significant independent CVD risk factor, but theassociation is far weaker than for hypercholesterolaemia.
There are, however, no randomized trials to providesufficient evidence to derive target levels for triglycerides. This lipidpattern is also characterized by the presence of small, dense, atherogenicLDL particles. Lipoprotein a [Lp a ] is a low-density lipoprotein to which an additionalprotein called apolipoprotein a is attached. There is norandomized intervention study showing that reducing Lp a decreases CVDrisk. Apolipoprotein A1 apoA1 is the major apoprotein of high-densitylipoprotein. It is beyond doubt that the apoB:apoA1 ratio is one of thestrongest risk markers.
Since the measurement of apolipoproteins is not available toall physicians in Europe, is more costly than currently used lipid variablesand only adds moderately to the information derived from currently appliedlipid parameters, its use is not recommended. Direct methods may beless sensitive to plasma triglyceride levels. However, recent data showthat the direct methods may also be biased when triglyceride levels arehigh. Also, the values obtained with the different direct methods arenot necessarily identical, especially for low and high LDL-C values. Non-HDL-C comprises the cholesterol in low-density lipoprotein,intermediate-density lipoprotein, remnant and VLDL, thus capturing allthe information regarding pro-atherogenic lipoproteins.
Therefore, it is certainly abetter measure than calculated LDL-C for patients with increased plasmatriglyceride concentrations, but also has an additional advantage of notrequiring patients to fast before blood sampling. There is evidence fora role of non-HDL-C as a treatment target. This parameter, however, is not suggested as apredictor or main target for therapy and further population data andclinical studies are awaited. The presence of dyslipidaemias secondary to other conditions must be excludedbefore beginning treatment, as treatment of underlying disease improveshyperlipidaemia without requiring antilipidaemic therapy.
This isparticularly true for hypothyroidism. Secondary dyslipidaemias can also becaused by alcohol abuse, DM, Cushing's syndrome, diseases of the liver andkidneys and several drugs e. If possible, these patients should bereferred for specialist evaluation. In general, RCTs are the ideal evidence base for decisional thresholds andtreatment goals. For treatment goals, this requires RCTs randomly allocatingsubjects to different lipid goal levels. However, most evidence in terms oftreatment goals is derived from observational studies and from post hocanalyses of RCTs and meta-regression analyses thereof randomly allocatingdifferent treatment strategies and not treatment goals.
Hence,recommendations reflect consensus based on large-scale epidemiological dataand RCTs comparing treatment regimens, not on RCTs comparing different lipidgoal levels. In the past, an LDL-C of 2. This goal remains reasonable for most patientswho have an indication for LDL-C-lowering therapy based on calculation ofthe CV risk see section 2.
In addition, this is a secondary goal in people with elevatedtriglycerides. There are no differences in the relative reductionbetween men and women and between younger and older age or between thosewith and without DM. Possible intervention strategies as a function of totalcardiovascular risk and low-density lipoprotein cholesterollevel.
Note that risk stratification isnot applicable in familial hypercholesterolaemia, where drugtreatment is recommended, and that, in this table, drugtreatment may be considered at risks lower than the generictreatment thresholds indicated in paragraph 2. If baseline LDL-C in this category is alreadybelow the target level of 1. If patients with CKD already on ahypolipidaemic therapy enter end-stage renal disease, the therapy may bemaintained.
The currently available lipid-lowering drugs include inhibitors of3-hydroxymethylglutaryl-coenzyme A reductase statins , fibrates, bileacid sequestrants anion exchange resins , niacin nicotinic acid ,selective cholesterol absorption inhibitors e. Response to all therapy varies widely among individuals and thereforemonitoring the effect on LDL-C levels is recommended.
Data indicate that combination therapy with ezetimibe also brings a benefitthat is in line with the Cholesterol Treatment Trialists' CTT Collaboration meta-analysis supporting the notion that LDL-C reduction iskey to the achieved benefit independent of the approach used. Increased levels of liver enzymes in plasma occur occasionally during statintherapy, and in most cases are reversible.
Routine monitoring of liverenzyme values is not indicated. Because statins are prescribed on a long-termbasis, possible interactions with other drugs deserve particular andcontinuous attention, as many patients will receive pharmacological therapyfor concomitant conditions. In general, the safety profile of statins is acceptable, and earlierobservations that lipid-lowering treatment may contribute to an increase innon-CV mortality e.
For non-statin treatments, selective cholesterol absorption inhibitors e. They arerecommended as combination therapy with statins in selected patients when aspecific goal is not reached with the maximal tolerated dose of astatin. Bile acid sequestrants also decrease total cholesterol and LDL-C but arepoorly tolerated and tend to increase plasma triglyceride concentrations.
They are therefore not recommended for routine use in CVD prevention. In those rare patients with severe primaryhypertriglyceridaemia, specialist referral must be considered. Whether this approach results in thepredicted reduction in CV events is being addressed in large outcome trials;preliminary evidence suggests that this is the case. Patients with dyslipidaemia, particularly those with established CVD, DM orasymptomatic high-risk individuals, may not always reach treatment goals,even with the highest tolerated statin dose.
Therefore, combinationtreatment may be needed. It must be stressed, however, that the onlycombination that has evidence of clinical benefit one large RCT is that ofa statin combined with ezetimibe. Combinations of niacin and a statin increase HDL-C and decrease triglyceridesbetter than either of these drugs alone, but flushing is the main adverseeffect of niacin, which may affect compliance. Furthermore, there is noevidence of clinical benefit for this combination. Fibrates, particularly fenofibrate, may be useful, not only for decreasinghigh triglyceride concentrations and increasing low HDL-C, but for loweringLDL-C further when used with a statin.
There is limited evidence for thiscombination in terms of a reduction in CVD events. Other drugsmetabolized through cytochrome P should be avoided when this combinationis prescribed. Fibrates should preferably be taken in the morning andstatins in the evening to minimize peak dose concentrations and decrease therisk of myopathy.
Patients have to be instructed about warning symptoms myalgia , even though such adverse effects are very rare. Gemfibrozilshould not be added to a statin treatment, because of the high potential forinteractions. If target levels cannot be reached even on maximal doses of lipid-loweringtherapy or drug combinations, patients will still benefit from treatment tothe extent that the dyslipidaemia has been improved. In these patients,increased attention to other risk factors may help to reduce total risk. Whether functional foods and food supplements with a lipid-loweringeffect can safely reduce the risk of CVD.
Lifestyle management to aid weight control by sustainable dietary changesand increased PA levels should be central in the management of patientswith type 2 DM. Intensive management of hyperglycaemia reduces the risk of microvascularcomplications and, to a lesser extent, the risk of CVD. However, targetsshould be relaxed in the elderly, frail, those with long-duration DM andthose with existing CVD. Intensive treatment of BP in DM, with a target of mmHg systolic forthe majority, reduces the risk of macrovascular and microvascularoutcomes. A lower SBP target of mmHg further lessens the risks forstroke, retinopathy and albuminuria and should be applied to selectedpatients.
Recent evidence points to sizeable reductions in CVD mortality in DMpatients via improvements in risk factor management, although theincreasing worldwide DM prevalence will create major challenges. Moreshould be done to prevent DM. Clear reductions have occurred inCVD death rates in DM consistent with better management of risk factors,although the increasing prevalence of DM continues to create pressures on allhealth care systems. The targets, especially the glycaemic and in some cases lipids, should be lessstringently implemented in older people with DM, those with a longer duration ofDM, those with evidence of CVD and the frail.
Except for glucose management, prevention of CVD follows the same generalprinciples as for people without DM. Many treatmenttargets are more stringent for patients with DM. Typically, patients with type 2DM have multiple CVD risk factors, each requiring treatment according toexisting guidelines. The ESC and European Association for the Study of Diabetes scientificstatements advocate lifestyle management as a first measure for theprevention and management of DM.
Several dietary patterns can be adopted where thepredominance of fruits, vegetables, wholegrain cereals and low-fat proteinsources is more important than the precise proportions of total energyprovided by the major macronutrients. Salt intake should be restricted. Specific dietary recommendations include limiting saturated and trans fatsand alcohol intake, monitoring carbohydrate consumption and increasingdietary fibre.
A Mediterranean-type diet is acceptable, where fat sourcesare derived primarily from monounsaturated oils. A combination of aerobic and resistance exercise training is effective in theprevention of the progression of DM and for the control of glycaemia. Littleis known about how to promote and sustain PA; however, reinforcement byhealth care providers to patients to find sustainable ways to increase PA iscrucial. Smoking increases the risk of DM, CVD and premature death andshould be strongly discouraged see section 3a.
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This recommendationreflects greater lifetime vascular risk trajectories in these individuals. However, a proportion of DM patients at 40—50 years of age may have a low 10year risk of CVD due to normal BP and lipid levels and being non-smokers,and in such cases there remains a role for physician judgement. The UK Prospective Diabetes Study UKPDS established the importance ofintensive glucose lowering with respect to CVD risk reduction in newlydiagnosed patients with DM but not treated with modern BP- or lipid-loweringtherapies, with the best evidence to support metformin, leading to itsposition as first-line therapy.
Three trials were conducted to see if CVevents could be reduced further with more intensive glycaemia treatment andlower target HbA1c levels. The results prompted concerns about the safety of intensiveglucose lowering and the appropriateness of pursuing tight glucose control,particularly in older people with DM and in those with existing CVD.
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Moreresearch on understanding the trial results is needed. Hypertension is more common in patients with type 2 DM compared with thegeneral population. Combination treatment is commonly needed to lower BP effectively in DM. AnACE-I or an angiotensin receptor blocker ARB , where tolerated, shouldalways be included as first-line therapy because of the evidence of superiorprotective effects against initiation or progression of nephropathy.
While the most common lipid abnormality in type 2 DM is elevated triglycerideand low HDL-C, trials examining possible CVD benefits of lipid mainlytriglyceride lowering with fibrates in DM have not been positive. Patients with type 1 or type 2 DM have an increased tendency to developthrombotic phenomena. The role of aspirin in patients without CVD remains unproven. A meta-analysisof six RCTs found no statistically significant reduction in the risk ofmajor CV events or all-cause mortality when aspirin was compared withplacebo or no aspirin in people with DM and no pre-existing CVD.
In patients with DM and hypertension,microalbuminuria—even below the current threshold values—predicts CV events,and a continuous relationship between CV as well as non-CV mortality andurinary protein:creatinine ratios has been reported. Microalbuminuria can bemeasured from spot urine samples due to inaccuracy in sampling, 24 h ornight-time urine collection is discouraged by indexing the urinary albuminconcentration to the urinary creatinine concentration 2. Use more salt. Experts usually recommend limiting salt in your diet because sodium can raise blood pressure, sometimes dramatically.
For people with low blood pressure, that can be a good thing. But because excess sodium can lead to heart failure, especially in older adults, it's important to check with your doctor before increasing the salt in your diet.
Doctors often use the drug midodrine Orvaten to raise standing blood pressure levels in people with chronic orthostatic hypotension. It works by restricting the ability of your blood vessels to expand, which raises blood pressure. Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this disease. Depending on the reason for your low blood pressure, you might be able to reduce or prevent symptoms. Eat a healthy diet. Get all the nutrients you need for good health by focusing on a variety of foods, including whole grains, fruits, vegetables, and lean chicken and fish.
If your doctor suggests using more salt but you don't like a lot of salt on your food, try using natural soy sauce or adding dry soup mixes to dips and dressings. Pay attention to your body positions. Gently move from a prone or squatting to a standing position. Don't sit with your legs crossed. Before arising in the morning, breathe deeply for a few minutes and then slowly sit up before standing.
Sleeping with the head of your bed slightly elevated also can help fight the effects of gravity. If you begin to get symptoms while standing, cross your thighs in a scissors fashion and squeeze, or put one foot on a ledge or chair and lean as far forward as possible. These maneuvers encourage blood flow from your legs to your heart. Eat small, low-carb meals. To help prevent blood pressure from dropping sharply after meals, eat small portions several times a day and limit high-carbohydrate foods such as potatoes, rice, pasta and bread.
Your doctor also might recommend drinking caffeinated coffee or tea with meals to temporarily raise blood pressure. But because caffeine can cause other problems, check with your doctor before drinking more caffeinated beverages. No special preparations are necessary to have your blood pressure checked. Don't stop taking medications you think might affect your blood pressure without your doctor's advice. Mayo Clinic does not endorse companies or products. Fox Foundation www. Has connections with areas that subconsciously control movement. Spasms can often be controlled with sensory tricks to suppress the movement.
Tremors occur both at rest and during purposeful movement. Notable symptom is the loss of ability to move the eyes to look downward. We comply with the HONcode standard for trustworthy health information. This information is not intended to replace the medical advice of your health care provider.
In collaboration with premier hospitals in the Greater Cincinnati-Northern Kentucky region, we perform about deep brain stimulation surgeries a year. We encourage patients to seek treatment at a medical center that offers a team approach and the full range of treatment options, including medication, surgery, and rehabilitation.
To make an appointment call Make an Appointment. The degree to which increased CVD risk associated with several ofthe female-specific conditions occurs independent ofconventional CVD risk factors is unknown. Information on whether female-specific conditions improve riskclassification in women is unknown. CVD risk varies considerably between immigrant groups. Current risk estimation equations do not provide adequate estimationsof CVD risk in ethnic minorities. First-generation migrants usually display lower CVD mortality rates thannatives of the host country, but with time, migrants tend to approach the CVDrisk in their host country.
Immigrants from South Asia notably India and Pakistan present high CVDrates — and have a much higher prevalence ofDM, , while theprevalence of other CV risk factors is slightly lower than or comparable tonatives of the host country. Management of DM is alsosignificantly worse, while management of high BP and hypercholesterolaemiais better among South Asians than host country natives.
Immigrants from China and Vietnam present lower CVD risk than natives of thehost country, although this finding has been challenged. This seems mainly due to the higher prevalence ofsmoking, DM, dyslipidaemia, hypertension and obesity rates. Immigrants from Morocco present lower CVD rates than natives from the hostcountry. Immigrants from sub-Saharan Africa and the Caribbean present higher CVD ratesthan natives from the host country in some studies, , , but not all. Management of CVD risk factors was worsethan among natives in one study, but not in another. Based on available mortality and prospective data, the following correction factorscould be applied when assessing CVD risk using SCORE among first-generationimmigrants only.
These values reflect the best estimations from availabledata and should be interpreted with caution, but can be used to guide CVrisk management. Alternatively, ethnicity-specificCVD risk equations should be developed. Cognitive behavioural methods are effective in supporting persons inadopting a healthy lifestyle. Individual and environmental factors impedethe ability to adopt a healthy lifestyle, as does complex or confusing advicefrom 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 includingalso the individual's spouse and family.
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In addition, caregivers can build on cognitive behavioural strategies to assessthe individual's thoughts, attitudes and beliefs concerning the perceivedability to change behaviour, as well as the environmental context. Previous unsuccessful attempts often affect self-efficacy for future change.
Acrucial step is to help set realistic goals combined with self-monitoring of thechosen behaviour. Combining the knowledge and skills of caregivers such as physicians, nurses,psychologists, experts in nutrition, cardiac rehabilitation and sports medicine into multimodal behavioural interventions can optimize preventiveefforts. There is limited evidence to determine which interventions are mosteffective in specific groups e. Treatment of psychosocial risk factors can counteract psychosocialstress, depression and anxiety, thus facilitating behaviour change andimproving quality of life and prognosis.
The caregiver—patient interaction should follow the principles ofpatient-centred communication. Age- and sex-specific psychosocialaspects should be considered. Caregivers in clinical practice are in a unique position to directly supporttheir patients regarding psychosocial risk factors in individuals with high CVrisk or with established disease. Empathic, patient-centred communication helpsto establish and maintain a trustful relationship and is a powerful source ofemotional support and professional guidance in coping with psychosocialstressors, depression, anxiety, CV risk factors and CVD.
Explain essential medical facts in the patient's own language, conveyhope and relief from feelings of guilt and reinforce adaptive thoughtsand actions. In the case of severe mental symptoms, obtain treatment preferences andperform shared decision-making regarding further diagnostic andtherapeutic steps. In addition to the treatment of mood symptoms, there are several other approachesto psychosocial intervention that have proved useful. Two RCTs , have shown the favourable impact ofstress management and social support groups on the prognosis of clinical CAD.
Nurse-led interventions reveal beneficial effects on anxiety, depression andgeneral well-being in CAD patients. In hostile CAD patients, a group-based hostility-control intervention may leadnot only to decreases in behaviourally assessed hostility levels, but also todecreased levels of depression, resting heart rate HR and CV reactivity tomental stress, as well as to increased social support and satisfaction withlife.
Hence, a reduction of work stress in managers and supervisors mayhave beneficial health effects on the target individuals and may also improveperceived social support in their subordinates. Evidence that treatment of clinically significant depression and anxietyalone will prevent CVD and improve outcomes is inconclusive. Health providers should assess the PA level in any subject how many days andminutes per day are spent on average doing PA at moderate or vigorousintensity.
They should warn against inactivity and help add PA to dailylife. Subjects should be advised on appropriate types of activities and waysof progressing and should be helped to set personal goals to achieve andmaintain the benefits. For a moreeffective behaviour change, clinicians should explore practical ways toovercome barriers to exercise. For this reason, the link between primarycare and local community-based structures for activity, recreation and sportis crucial. Aerobic PA, the most studied and recommended modality, with a beneficialdose—response effect on prognosis, , , consists of movements of largemuscle mass in a rhythmic manner for a sustained period.
It includeseveryday activity, including active travel cycling or walking , heavyhousehold work, gardening, occupational activity and leisure timeactivity or exercise such as brisk walking, Nordic walking, hiking,jogging or running, cycling, cross-country skiing, aerobic dancing,skating, rowing or swimming. Similar to all other interventions, its prescription can be adjusted interms of frequency, duration and intensity.
However, practising PA belowthe lowest recommended levels should be encouraged in individuals unableto meet the minimum or in those sedentary individuals who have juststarted, with a gradual increase in activity level. Moderate or vigorous aerobic exercise should be recommended. This can beexpressed either in absolute or relative terms. By convention thiscorresponds to 3. Relative intensity is the level of effort required toperform an activity. Less fit individuals generally require a higherlevel of effort than fitter people to perform the same activity. Forindividuals on medication, it is important to consider possiblemodification of HR response and to refer to other relative intensityparameters.
Especially for older and deconditioned individuals, arelative measure of intensity is more appropriate. Classification of physical activity intensity and examples ofabsolute and relative intensity levels. Modified from Howley. PA should occur at a frequency of at least three to five sessions perweek, but preferably every day. Shorterexercise sessions i. Aerobic interval training and high-intensity interval training cannot yetbe broadly recommended until further data on safety and efficacy areavailable.
Isotonic PA stimulates bone formation and reduces bone loss; it preservesand enhances muscle mass, strength, power and functional ability, withsome evidence of benefit in lipid and BP control and insulinsensitivity, especially in combination with aerobic exercise. For older adults at risk of falls, neuromotor exercise helps to maintainand improve balance and motor skills balance, agility, coordination andgait. This includes multifaceted activities such as tai chi and yoga,and recreational activities using paddles or sport balls to challengehand—eye coordination.
The optimal volume is not known. Progressive warm-up before and cool-downafter exercise may prevent injuries and adverse cardiac events.
With the improvement in exercise tolerance, each subjectprogresses in the level of PA, but increases in any components i. Before starting more intensive leisure time activities i. Clinical evaluation, including exercise testing, may beconsidered for sedentary people with CV risk factors who intend to engage invigorous PA and sports.
The information gathered from exercise tests may beuseful in establishing a safe and effective exercise prescription. Validatedself-assessment questionnaires have been proposed for sedentary individualsentering low-intensity leisure time sports activity or startingmoderate-intensity activities see Table B in web addenda. The lower and upper limit of aerobic PA intensity, duration andfrequency to exert a beneficial effect is unknown.
The effectiveness of PA monitoring vs. There is a strong evidence base for brief interventions with advice tostop smoking, all types of nicotine replacement therapy NRT ,bupropion, varenicline and greater effectiveness of drugs incombination, except for NRT plus varenicline. The most effective arebrief interventions plus assistance with stopping using drug therapy andfollow-up support.
Electronic cigarettes e-cigarettes may help in smoking cessation butshould be covered by the same marketing restrictions as cigarettes. Smoking is a lethal addictive disorder. The year fatal CVD risk is approximately doubled insmokers. Slightly less than half of lifetime smokers will continue smoking untildeath. Although the rate of smoking is declining in Europe, it remains very commonand is increasing in women, adolescents and the sociallydisadvantaged. The survey also foundthat evidence-based treatment for smoking cessation was underused. The risks associated with smoking show a dose—response relationship with nolower limit for deleterious effects.
Tobacco smoke is more harmful when inhaled,but smokers who claim not to inhale the smoke e. Smokeless tobacco is also associated with a smallbut statistically significant increased risk of MI and stroke. Passive smoking increases the risk of CAD. Major health benefits result from reducedenvironmental tobacco smoke, with public smoking bans in various differentgeographical locations leading to significant decreases in MI rates seesection 3c.
Smoking enhances the development of both atherosclerosis and superimposedthrombotic phenomena. Smoking affects endothelial function, oxidativeprocesses, platelet function, fibrinolysis, inflammation, lipid oxidationand vasomotor function. In experimental studies, several of these effectsare fully or partly reversible within a very short time. Plaque formation isnot thought to be fully reversible and thus smokers would never be expectedto reach the risk level of never smokers concerning CVD.
Nicotinereplacement shows no adverse effect on outcomes in patients with cardiacdisease. The benefits of smoking cessation have a large evidence base. Some advantagesare almost immediate; others take more time.
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CVD risk in former smokers isin between that of current and never smokers. Significantmorbidity reductions occur within the first 6 months. Smoking reduction has not been shown to increase the probability of futuresmoking cessation, but some advocate nicotine-assisted smoking reduction insmokers unable or unwilling to quit. There is no age limit to the benefits of smokingcessation. Passive smoking should also be avoided. Professional support can increase the odds of stopping [RR 1.
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Prompting a person to try to quit, briefreiteration of CV and other health hazards and agreeing on a specific planwith a follow-up arrangement are evidence-based interventions see Figure K in web addenda. Smoking cessation programmes initiated during hospital admission shouldcontinue for a prolonged period after discharge. Smokers should be advised about expected weight gain of, on average, 5kg and that the health benefits of tobacco cessation far outweigh the risksfrom weight gain.
Following the failure of advice, encouragement and motivationalinterventions, or in addition to them, NRT, varenicline or bupropion shouldbe offered to assist cessation. The antidepressant bupropion aids long-term smoking cessation with a similarefficacy to NRT.
The partial nicotine receptor agonist varenicline at the standard doseincreases the chances of quitting more than two-fold compared with placebo 14 trials, people. Low-dose varenicline four trials, people roughly doubles the chancesof quitting and reduces the number and severity of side effects. The mainside effect of varenicline is nausea, but this is mostly mild or moderateand usually subsides over time. Clonidine has helped people to quit, but causes side effects and is thereforea second-line agent.
It is not clear whether mecamylamine used with NRThelps people to quit. Other treatments did not seem to help. So far,nicotine vaccines are not licensed for use anywhere in the world. Combining two types of NRT is as effective as using varenicline, and helpsmore people to quit than a single type of NRT. Electronic cigarettes e-cigarettes are battery-operated devices thatsimulate combustible cigarettes by heating nicotine and other chemicals intoa vapour that is inhaled.
Electronic cigarettes deliver the addictivenicotine without the vast majority of tobacco chemicals, and are probablyless harmful than tobacco. Evidence on the effectiveness of e-cigarettes is limited due to the smallnumber of trials, low event rates and wide confidence intervals. Recent evidenceindicates that e-cigarettes, as currently being used, are associated withsignificantly less quitting among smokers.
Both individual and group behavioural interventions are effective in helpingsmokers quit. Support from the individual's partner and family is important. There are no reliable data that acupuncture, acupressure, laser therapy,hypnotherapy or electrostimulation are effective for smoking cessation. Dietary habits influence CV risk, either through an effect on risk factorssuch as cholesterol, BP, body weight and DM, or through othereffects. Most evidence on the relation between nutrition and CVD is based onobservational studies; randomized clinical trials estimating the impact ofdiet on endpoints are scarce.
The nutrients of interest with respect to CVD are fatty acids which mainlyaffect lipoprotein levels , minerals which mainly affect BP , vitamins andfibre. For prevention of CVD, the types of fatty acids consumed are more importantthan the total fat content. The same has notbeen clearly shown for replacement with carbohydrates and monounsaturatedfatty acids MUFAs. The polyunsaturated fattyacids can be divided into two subgroups: omega-6 fatty acids, mainly fromplant foods, and omega-3 fatty acids, mainly from fish oils and fats.
They do not changeserum cholesterol levels and, with currently available cardioprotectivetherapies, it is debatable whether they exert a favourable effect onall-cause, CAD, and stroke mortality. The trans fatty acids, a subclass of unsaturated fatty acids, have been shownto be especially harmful due to their unfavourable impact on both totalcholesterol increase and HDL-C decrease.
These fatty acids are formedduring industrial processing hardening of fats and are present in, forexample, margarine and bakery products. The impact of dietary cholesterol on serum cholesterol levels is weakcompared with that of the fatty acid composition of the diet. Whenguidelines are followed to lower saturated fat intake, this usually alsoleads to a reduction in dietary cholesterol intake.
Although the relation between saltintake and BP remains controversial, the totality of evidence warrants saltreduction as an important way to prevent CAD and stroke. Salt reduction can be achieved by making different dietary choices fewerprocessed foods, more basic foods and the reformulation of foods loweringsalt content see Chapter 3c. Potassium has favourable effects on BP.