Month: December 2018

Prevalence of hypercholesterolemia.

Since the early 1960s. the average cholesterol level among the US population has slightly decreased. But even with this reduction, 50% of American adults have cholesterol levels> 200 mg / dl, and 17% have cholesterol levels> 240 mg / dl. Low levels of HDL cholesterol and high levels of TG have a tendency to coincide and are often the result of metabolic changes leading to high levels of LDL cholesterol. Low levels of HDL cholesterol and high concentrations of TG can be observed separately or in combination with high LDL cholesterol.

Associated risk. Some cholesterol parameters have a causal relationship with an increased risk of CHD. An increase in serum LDL cholesterol by 1 mg / dL is associated with an increase in the risk of CHD by 2-3%, and at a young age, an elevated LDL cholesterol content may be associated with an even greater increase in risk. HDL has become an important independent predictor of KBS, a decrease in cholesterol cholesterol by 1 mg / dL leads to an increase in the risk of KBS by 3-4%. The ratio of total cholesterol or LDL cholesterol to cholesterol cholesterol predicts the risk of CHD better than LDL cholesterol.

Reducing this ratio by 1 unit (which can easily be achieved by prescribing statins) reduces the risk of myocardial infarction by 50%. The ratio of total cholesterol to cholesterol may be better than the ratio of apo A to apo B. The level of cholesterol also predicts risk well, since Non-HDL cholesterol correlates well with apo B, therefore costly definition of apo B is not necessary.

Inaccuracies in the determination of triglycerides (TG), intraindividual fluctuations, dependence on diet, and complex interactions between TG and other lipid parameters may disguise the contribution of TG to the development of CHD. However, the fasting TG level correlates with the risk of CHD, especially when the content of cholesterol cholesterol is taken into account. This interdependence suggests that some TG-rich lipoproteins are atherogenic. Some studies have suggested that elevated TG concentrations are an independent predictor of KBS. The clinical significance of TG, not assessed by fasting, remains unclear.

The ratio of the cost-effectiveness of quitting.

The ratio of the cost-effectiveness of quitting. The ratio of cost-effectiveness of smoking cessation is very high in both primary and secondary prevention. Intervention is usually short term and low cost. Indeed, smoking cessation is cheaper than continuing to smoke. The increase in life expectancy is large, and the earlier a person quits smoking, the greater will be the increase; for example, a 35-year-old man after smoking cessation may add to a life expectancy of 3 years.

The cost varies depending on the intensity of the intervention and the use of drugs. A Swedish study found that over a 20-year observation period, the cost of a single life saved was relatively low for bupropion compared to a nicotine patch: $ 660 for men and $ 490 for women. Some non-pharmacological approaches have also proven to be effective.

e) Guidelines and recommendations. In the U.S. clinical guidelines. The Public Health Service recognized that tobacco dependence is a chronic condition and repeated intervention is usually necessary. It is recommended that the patient be asked about smoking at each visit; U.S. also supports this strategy. Preventive Services Task Force. The U.S. manual. Preventive Services Task Force is recommended when necessary combined intervention: counseling and drug therapy. Three types of counseling and behavioral therapy are particularly effective:

(1) training;

(2) social support for treatment;

(3) social support outside treatment.

There are 6 types of first-line drug therapies that reliably increase the duration of abstinence from smoking: prolonged-release bupropion hydrochloride, nicotine tablets, chewing gums and patches, inhalers and nasal sprays.

Due to tobacco dependence and the tendency to increase in smoking over time, reducing the number of cigarettes is an unacceptable strategy. The effectiveness of interventions ranges from 6% during the year when advised by a doctor to 18% when performing self-help programs and 20-40% with pharmacological intervention using a nicotine chewing gum or patch.

It is important to reasonably explain to the patient the harm of smoking and the benefit of quitting at all stages of therapy, and the period immediately after the cardiovascular event (SSSob) is the optimal time for quitting smoking.

f) Perspective directions. In the United States, smoking cessation efforts will continue, but intensive public health efforts around the world are needed to reverse the dangerous growth trend of smoking in developing countries; for example, 60% of men in China today smoke. Of the 1.1 billion smoking population, 82% live in low- or middle-income countries. The low frequency of success of smoking cessation interventions is a challenge for clinicians, so you should focus on smoking prevention.

The effectiveness of quitting smoking in coronary heart disease

This category includes 4 primary interventions: smoking cessation, control of dyslipidemia (DLP) and blood pressure, as well as prophylactic administration of drugs by individual patients. Each intervention should be seriously discussed with patients with CVD, diabetes, as well as with patients suitable for primary prevention. This discussion should be documented.

a) prevalence. In the US, cigarette consumption in terms of 1 person. grew dramatically in the first half of the twentieth century. By 1945,> 65% of men born in 1911-1920 smoked. The annual per capita consumption of cigarettes in 1963 reached 4,286 (> 200 packs per year), but has since dropped to 1875. The prevalence of smoking among men reached a peak in 1955, when> 50% of men smoked; in women, the peak came 10 years later.

Since then, the prevalence of smoking among Americans has decreased significantly (to 21%). Currently, 23% of men and 18% of women are smokers in the population> 18 years old. The frequency of smoking among older schoolchildren increased from 30% in the mid-1980s. to 36.5% in 1997, moreover at the expense of girls, but now it is gradually decreasing. The frequency of smoking is higher among people with low socioeconomic status and educational qualifications.

b) Associated risk of smoking. Smoking increases the risk of coronary heart disease (CHD). By the middle of the XX century. The first studies that linked smoking to heart disease were published.

A 1964 Surgeon General’s report confirmed this epidemiological link, and in 1983 Surgeon General’s firmly named cigarette smoking as the main preventive cause of cardiovascular diseases (CVD). The 1989 Surgeon General’s report provided accurate data from case-control observational studies and cohort studies, mostly among men. It is established that smoking increases the frequency of CHD by 2 times and by 50% the mortality from CHD, and this risk increases with age and the number of cigarettes smoked. A similar increase in the relative risk of KBS is observed among women.

In the US, cigarette smoking is the leading modifiable cause of deaths (438 thousand deaths annually, of which 35% is cardiovascular death) and losses> 5 million years of life. Worldwide, the frequency of smoking continues to grow, with the most in developing countries; in 2000, deaths from tobacco smoking were more than 1 million compared with 1990.

c) The benefits of stopping smoking. Evidence from large-scale, randomized, risk-reduction trials of smoking cessation is limited, but observational studies have shown a clear benefit of stopping smoking. People who quit smoking reduce the excess risk of coronary events during the first 2 years by 50%, with the greatest benefit observed in the first few months. This period is followed by a gradual decrease, and after 3-5 years the risk among those who smoked earlier approaches the risk of those who have never smoked.

Coronary heart disease as a multifactorial disease

Knowledge of the biological mechanisms of atherosclerosis led to an understanding of the progression of this disease and many of its etiological factors. Coronary heart disease (CHD) develops as a result of the interaction of many RFs.

Often, people with cardiovascular diseases (CVD) simultaneously have small changes in several risk factors (RF), rather than extreme deviations in the level of one. If these risk factors (RF) are not controlled, then atherosclerosis will continue to develop. Predisposing RF, for example, genetic, interact with behavioral RF, such as diet, alcohol consumption and physical activity.

The combination of these predisposing and behavioral factors can cause metabolic changes – dyslipidemia (DLP), hypertension, obesity and diabetes, which ultimately lead to a pronounced disease. The key point in identifying susceptibility to this disease may be various diagnostic tests. Some tests that assess physical changes in the arteries, such as the thickness of the TCIM CA or the presence of calcium in the CA, can be used to assess the severity of atherosclerosis, while an exercise test helps diagnose stenosis of the ischemia.

Other tests, such as determining the level of chrish, suggest the likelihood of a cardiovascular event (SSSob), but may not clearly correlate with the severity of atherosclerosis. This latent disease can manifest as a transient ischemic attack (TIA), MI, or another Ssob. DFs useful for prediction, both modifiable and non-modifiable, can be identified at any stage of this process. For example, FRs are hereditary predispositions for heart disease and smoking. Such a metabolic factor, such as a high level of LDL, also serves as a risk factor.

Migrated IM or MI is also a strong predictor of future events. This reflects the relationship between predisposing risk factors (RF) and disease markers, which may be important for identifying people at increased risk of developing clinical complications.

Risk assessment (RF) is useful, but sometimes they are conditional, i.e. they are difficult to classify as a specific category. For example, hereditary predisposition may be in the presence of certain genes in the descendants, but also in the lifestyle of the family, which passes from one generation to another.

It is not known whether hypertension is a consequence of the influence of such features of a family lifestyle as a diet predisposing to atherosclerosis, low physical activity (NFA), or is it a manifestation of ED, thus serving as a marker of atherosclerosis.