[Oral manifestations in various cardiovascular diseases].
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Prostaglandins potently regulate platelet aggregation and vascular tone. Thus they are of great importance in the blood supply of tissue. The strategy of the attempts to prevent occlusive vascular disease have been either to decrease the amount of aggregatory, vasoconstricting prostaglandins or to increase antiaggregatory, vasodilatory prostaglandins. Acetylsalicylic acid has been mostly used in attempts to inhibit platelet TxA2-synthesis without disturbing endothelial cell PGI2-synthesis. Primary prevention trials of myocardial infarction have given results of great discrepancy whereas reinfarctions are likely in part to be inhibited by acetylsalicylic acid. In the prevention of ischaemic cerebral disease, most of the trials have indicated the beneficial effect of acetylsalicylic acid, as is the case also in the prevention of venous thrombosis. It is, however, likely that the doses of acetylsalicylic acid have not been optimal in any work, and thus better results are to be awaited. The infusion of anti-aggregatory, vasodilatory prostaglandins, mainly PGI2 or PGE1, have relieved the symptoms of ischaemia of the lower extremities, coronary heart disease and Raynaud's syndrome. The technical difficulties of these infusions, however, limit their applicability to special groups of patients.
Chronic disease epidemiology emerged from a methodological necessity, namely to break the deadlock of the medical science faced with a sudden upsurge of these diseases, especially cardiovascular, after the Second World War. The author analyses the shortcomings of clinical investigation in contrast with the epidemiological approach, the qualitative and quantitative prerequisites of the latter, as well as its methodological instruments, pointing out misunderstandings and improper uses of some terms i.e., epidemiology is not one and the same thing as ecology; epidemiology precludes passive detection; the environmental agent is not identical to the risk factor; the risk factor is not diagnostic. It is worth making these distinctions in order to enhance the value of epidemiology as a first step toward prevention.
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PURPOSE: The use of different definitions of the metabolic syndrome has led to inconsistent results on the association between the metabolic syndrome and risk of cardiovascular disease. We examined the association between the metabolic syndrome and risk of cardiovascular disease. METHODS: A MEDLINE search (1966-April 2005) was conducted to identify prospective studies that examined the association between the metabolic syndrome and risk of cardiovascular disease. Information on sample size, participant characteristics, metabolic syndrome definition, follow-up duration, and endpoint assessment was abstracted. RESULTS: Data from 21 studies met the inclusion criteria and were included. Individuals with the metabolic syndrome, compared to those without, had an increased mortality from all causes (relative risk [RR] 1.35; 95% confidence interval [CI], 1.17-1.56) and cardiovascular disease (RR 1.74; 95% CI, 1.29-2.35); as well as an increased incidence of cardiovascular disease (RR 1.53; 95% CI, 1.26-1.87), coronary heart disease (RR 1.52; 95% CI, 1.37-1.69) and stroke (RR 1.76; 95% CI, 1.37-2.25). The relative risk of cardiovascular disease associated with the metabolic syndrome was higher in women compared with men and higher in studies that used the World Health Organization definition compared with studies that used the Adult Treatment Panel III definition. CONCLUSION: This analysis strongly suggests that the metabolic syndrome is an important risk factor for cardiovascular disease incidence and mortality, as well as all-cause mortality. The detection, prevention, and treatment of the underlying risk factors of the metabolic syndrome should become an important approach for the reduction of the cardiovascular disease burden in the general population.
To summarize, estrogens have powerful effects on certain biologic parameters, the alteration of which could influence cardiovascular disease risk. Estrogens have long been known to influence lipid and lipoprotein levels by decreasing LDL (the atherogenic lipoprotein) and by increasing HDL (the protective lipoprotein). THese lipid alterations could favorably influence the risk of cardiovascular disease. Estrogens also temporarily increase glucose intolerance and lower fasting glucose levels; although the former event could adversely affect cardiovascular disease risk, the clinical significance of increased glucose intolerance with low fasting levels has not been determined. There is no consistent evidence that menopausal estrogens adversely affect coagulation or blood pressure levels, although both of these parameters could be affected in selected individuals. Overall, the estrogenic effects on lipid/lipoprotein levels appear to be the most consistent and the most powerful; given this assumption, estrogens should protect against cardiovascular disease. There is another interpretation of the biologic effect of estrogens on cardiovascular risk. It is possible that estrogens may increase the risk of a thromboembolic event due to an adverse influence on coagulation parameters and, at the same time, decrease the risk of an atherogenic event (via favorably altered lipid/lipoprotein levels). This proposed dual action of estrogens may explain the apparently conflicting results of increased risks of thromboembolism and decreased risks of atherosclerosis or myocardial infarction in men treated with high doses of estrogen (36, 196, 197). In women, there is some suggestion that (low-dose) postmenopausal estrogens may increase the risk of thromboembolism (79, 204), although the majority of studies report no such increase. The difference in risk of thromboembolism between men and women using estrogens may be due to several factors. First, the dose (potency) of the estrogen used by men is usually higher than that used by postmenopausal women, and the risk of estrogen-induced thrombus formation may be dose-dependent. Second, men tend to have more atherosclerotic lesions than women and thus would have more substrate available for thrombus formation. (This hypothesis is supported by the observation that the increased risk of thromboembolism was evident in men using estrogens for the secondary prevention of cardiovascular disease.) Indirect evidence supporting the hypothesis that endogenous estrogen levels are protective against cardiovascular disease is most consistent for women.(ABSTRACT TRUNCATED AT 400 WORDS)
A case-control-study was performed to identify patients at particularly high risk of community-acquired pneumonia and nosocomial pneumonia with a special focus on cardiovascular diseases as potential risk factors. Thirty-six consecutive hospitalized patients with cardiovascular diseases and pneumonia were matched with 36 controls also suffering from cardiovascular diseases but without pneumonia. From all cardiovascular diseases only heart failure proved to be an independent risk factor for pneumonia (OR 5.69, 95 % KI 1.69 - 19.04, p = 0.0048). Both chronic (p = 0.009) and acute heart failure (p = 0.028) were associated with an increased risk of pneumonia. The risk of pneumonia was closely related to the degree of ventricular function impairment. Coronary heart disease, valvular disease, arrythmia, myocarditis, endocarditis and cardiomyopathy did not increase the risk for pneumonia unless accompanied by heart failure. Pulmonary (OR 9.24, 95 % KI 1.48 - 57.74, p = 0.00174) and renal diseases (OR 7.49, 95 % KI 1.38 - 40.76, p = 0.0197) were validated as additional independent risk factors. A history of smoking was also associated with an increased risk of pneumonia (p = 0,023). This study supports the hypothesis that heart failure resulting from cardiovascular disease and not cardiovascular disease itself mounts the risk for pneumonia.
Involuntary weight gains worsen all elements of the cardiovascular risk profile, including dyslipidemia, hypertension, insulin-resistant glucose intolerance, left-ventricular hypertrophy, hyperuricemia, and elevated fibrinogen. On the basis of data from the Framingham Heart Study and from other studies, it can be concluded that the degree of overweight is related to the rate of development of cardiovascular disease. After 26 y of follow-up in the Framingham study, each SD increment in relative weight was associated with 15% and 22% increases in cardiovascular events in men and women, respectively. Avoidance of weight gain after the age of 25 y is advisable to reduce cardiovascular mortality. There is a great potential benefit to weight loss, suggesting that weight control as a means for preventing and lessening cardiovascular disease become a national health priority. The optimal weight for avoidance of cardiovascular disease and prolonging life corresponds to a body mass index of 22.6 for men and 21.1 for women.
Rapid socioeconomic development, urbanization and improved survival have given rise to a progressive increase in the occurrence of noncommunicable diseases in the Eastern Mediterranean Region. Cardiovascular diseases have emerged as a leading cause of morbidity and mortality in many countries. The prevalence of hypertension is already high in many countries of the Region and the number of hypertensives is likely to increase further in the coming years. Although the influence of geographical, ethnic and socioeconomic factors has not been studied adequately, it seems that the epidemiological and clinical patterns of hypertension do not differ markedly from those in developed countries. The growing impact of cardiovascular disease is already understood in most countries. The human and economic costs are enormous, there is a growing demand for medical services, and the need to take action is increasingly acknowledged. Most countries have either initiated or indicated the need to establish programmes in collaboration with WHO on the prevention and control of cardiovascular disease during 1992 and 1993. In view of the scarcity of precise epidemiological information, data collection and the assessment of risk factors for coronary heart disease are expected to form the basis of preliminary activities.
Limited information exists about the consequences of hypertension during adulthood on residual life expectancy with cardiovascular disease. We aimed to analyze the life course of people with high blood pressure levels at age 50 in terms of total life expectancy and life expectancy with and without cardiovascular disease compared with normotensives. We constructed multistate life tables for cardiovascular disease, myocardial infarction, and stroke using data from 3128 participants of the Framingham Heart Study who had their 50th birthday while enrolled in the study. For the life table calculations, we used hazard ratios for 3 transitions (healthy to death, healthy to disease, and disease to death) by categories of blood pressure level and adjusted by age, sex, and confounders. Irrespective of sex, 50-year-old hypertensives compared with normotensives had a shorter life expectancy, a shorter life expectancy free of cardiovascular disease, myocardial infarction, and stroke, and a longer life expectancy lived with these diseases. Normotensive men (22% of men) survived 7.2 years (95% confidence interval, 5.6 to 9.0) longer without cardiovascular disease compared with hypertensives and spent 2.1 (0.9 to 3.4) fewer years of life with cardiovascular disease. Similar differences were observed in women. Compared with hypertensives, total life expectancy was 5.1 and 4.9 years longer for normotensive men and women, respectively. Increased blood pressure in adulthood is associated with large reductions in life expectancy and more years lived with cardiovascular disease. This effect is larger than estimated previously and affects both sexes similarly. Our findings underline the tremendous importance of preventing high blood pressure and its consequences in the population.
A small size of sample for risk factors of cardiovascular disease, such as blood pressure, plasma lipids profile, obesity, dietary status, and family history of cardiovascular disease, etc. were studied in children aged eight to eleven years. Results showed that prevalence of hypertension, systolic blood pressure > 16.0 kPa (120 mmHg) or/and diastolic blood pressure > 10.7 kPa (80 mmHg), in them was 7.2 percent, blood lipid level in 21.9 percent of the children exceeded the recommended criteria of dietary intervention, and prevalence of simple obesity was 11.7 percent. The most prominent problem in dietary status was high cholesterol intake, with a daily intake of 483.4 mg in average, and 72 percent of the children exceeded 300 mg daily, as compared with previous data, and they exposure to higher level of risk factors for cardiovascular disease. It suggests that it is necessary to strengthen surveillance for risk factors of cardiovascular disease and intervention.