Periodontal and coronary heart disease in patients undergoing coronary angiography

Periodontal inflammation has been implicated in atherosclerosis and coronary heart disease (CHD). Coronary angiography (CA) is used in the assessment of CHD; only a few studies have evaluated periodontal disease (PD) and angiographic measures of coronary atherosclerosis. The aim of this study was to investigate the association between CHD and PD. In this prospective epidemiologic study, 466 patients underwent CA and were assessed for PD. All patients underwent physical, laboratory, cardiac, and dental examination including dental x-rays. Periodontal disease and coronary angiograms were evaluated blindly by a dentist and 2 cardiologists, respectively. A coronary stenosis greater than 50% was ruled as CHD. Periodontal disease was defined and measured with the Community Periodontal Index of Treatment Needs (CPITN); and if at least 2 sextants (segments dividing mandible and maxilla into 6) were recorded as having CPITN of at least 3 (signifying that sextant had periodontal pocket depth ≥3.5 mm), the patient was coded as having PD. Three-hundred forty-nine patients (74.9%) had CHD assessed by CA The CHD patients had PD in 55.6% vs 41.9% in the non-CHD patients (P < .01). The CPITN scores were significantly higher in patients with vs without CHD, 2.43 vs 2.16, respectively (P = .023). After adjusting for age, sex, and risk factors for atherosclerosis with additional inclusion of C-reactive protein and erythrocyte sedimentation rate, PD remained significantly related to CHD (odds ratio = 1.9; 95% confidence interval, 1.2-3.1). Other predictors for CHD were male sex, age, high-density lipoprotein cholesterol, and diabetes. Our results demonstrate an increased odds ratio for angiographically determined CHD in patients with PD and that CHD and PD may cluster in particular groups of a population. Our data indicate that PD represents a potentially modifiable risk factor that is both preventable and treatable with predictable treatments that pose negligible risk.     

Influence of total cholesterol levels on long-term mortality in coronary heart disease: a reappraisal

To examine the prognostic significance of total cholesterol levels at baseline in subjects with stable coronary heart disease, 605 patients with stable coronary heart disease were enrolled; 45 of these did not meet inclusion criteria, 41 were lost to follow-up and 40 opted for coronary bypass surgery. Data of the remaining 479 (389 males, 90 females) were analysed. There were 102 males in group I (cholesterol < 200 mg/dL), 187 in group II (cholesterol 200-239 mg/dL), and 100 in group III (cholesterol > or = 240 mg/dL) and 49 females in group I and 41 in group II. The groups were evenly matched for age and numbers with stable angina or survivors of myocardial infarction. Proportion of smokers, hypertensives, diabetics or obese was also similar (p > 0.05). Mean follow-up in years in men was 6.82 +/- 3.15 in group I, 6.37 +/- 3.11 in group II and 6.81 +/- 2.84 in group III while in women it was 6.95 +/- 2.84 in group I and 7.03 +/- 2.58 years in group II and was not different in various groups (p > 0.05). The overall cardiovascular mortality in various groups in men was 20.6 percent in group I, 28.9 percent in group II and 23.0 percent in group III and in women it was 14.3 percent in group I and 22.0 percent in group II. The crude mortality rate was 2.51 percent per year in males and 1.77 percent per year in females. Actuarial survival at end of seven years in males was 0.76 +/- 0.05 in group I, 0.67 +/- 0.04 in group II, and 0.67 +/- 0.05 in group III and in females it was 0.85 +/- 0.05 in group I and 0.73 +/- 0.09 in group II. The cumulative hazard rates per 1000 person- year follow-up in group I, II and III in males were, at age less than 50 years: 5.4 +/- 5, 19.8 +/- 7, 17.4 +/- 8; at 50-59 years: 23.8 +/- 11, 38.5 +/- 9, 39.8 +/- 13; and at 60 years and over: 76.9 +/- 20, 112.6 +/- 20, 108.2 +/- 28, respectively (p < 0.001 on comparison of group I with groups II and III). In females the trends were not significant. Total cholesterol levels at baseline predict long-term cardiovascular mortality in men with stable coronary heart disease.     

Alcohol and coronary heart disease: a meta-analysis

Objective. To estimate parameters of the function relating alcohol consumption with the risk of coronary heart disease and to identify the sources of heterogeneity in the parameter estimates. Methods. A search of the epidemiological literature from 1966 to 1998 was performed using several bibliographic databases. Meta-regression models were fitted to evaluate non-linear effects of alcohol intake on the relative risk. The effects of some characteristics of the studies, including an index of their quality, were considered as putative sources of heterogeneity of the estimates. Publication bias was also investigated. Findings. Among the 196 initially reviewed articles, 51 were selected. Since qualitative characteristics of the studies were significant sources of heterogeneity, the pooled dose-response functions were based on the 28 cohort studies with higher quality. Risk decreased from 0 to 20 g/day (RR = 0.80; 95% CI: 0.78, 0.83); there was evidence of a protective effect up to 72 g/day (RR = 0.96; 95% CI: 0.92, 1.00) and increased risk above ≥ 89 g/day (RR = 1.05; 95% CI: 1.00, 1.11). Lower protective effects and harmful effects were found in women, in men living in countries outside the Mediterranean area and in studies where fatal events were used as the outcome. Evidence of publication bias for moderate intakes and of heterogeneity of the estimates across studies for higher intakes were found. Conclusions. The degree of protection from moderate doses of alcohol should be reconsidered. Further research investigating the effect of drinking patterns on the risk of coronary heart disease should be performed. Caution in making general recommendations is needed.     

Diabetes and the heart: coronary heart disease.

1. Diabetics have a greater risk of experiencing and of dying from a CHD event than age matched non-diabetics. 2. The excess risk is particularly notable in insulin dependent female diabetics who seem to lose the usual 'protection' accorded to women. 3. The cause or causes of the excess risk are not known. There are a variety of 'risk factors' observed in diabetics which, in sum, may contribute. 4. At least in insulin-dependent diabetics some cardiac morbidity and mortality may also be due, not to coronary heart disease, but to a cardiomyopathy secondary to intramural obstructive vascular disease and/or disordered myocardial metabolism. 5. No therapy has yet been convincingly proved to reduce (or to increase) the risk of cardiac morbidity or mortality. Nevertheless, in treating diabetics there is an a priori case for using diets designed to lower plasma lipid levels as well as the blood sugar, for early treatment of hypertension and for discouraging cigarette smoking.     

Chronic rheumatic heart disease in India: a reappraisal of pathologic changes.

Rheumatic heart disease contributes to significant cardiac morbidity and mortality in India. The disease predominantly affects the valvular endocardium culminating in crippling valvular deformities, preferentially involving the mitral valve which may be severely affected in children and young adults. This appears to be unique to India and has been termed juvenile mitral stenosis. It is characterized by cardiomegaly, refractory congestive heart failure, and marked by elevated pulmonary vascular pressures and a progressive, fulminant clinical course. Autopsies of patients dying of rheumatic heart disease revealed that the mitral valve was most commonly afflicted either alone or in combination with the aortic and tricuspid valves in 31.6% and 52.8%, respectively. Organic involvement of the tricuspid valve was documented in 38.4% of cases. The extent and severity of the disease process was most marked in the mitral valve, followed by the aortic and tricuspid valves. Mitral valves showed various degrees of calcification, moderate or severe calcification being observed in 36.4%. Chronic inflammatory cell infiltration was observed in both calcified and non-calcified valves. The phenotypic profile of the inflammatory cells by immunohistochemical staining revealed a significant number to be T-helper/inducer lymphocytes. Lungs from cases of mitral stenosis exhibited prominent vascular and parenchymal changes. Pulmonary vessels revealed moderate to marked medial hypertrophy of the medium sized branches of the pulmonary artery. Dilatation lesions were also seen in a few cases. The most striking parenchymal change was the prominent smooth muscle in the bronchoalveolar walls. The extent and severity of the vascular and parenchymal changes were more marked in juvenile patients. The presence of inflammatory cells in cases of chronic heart disease reflects a possible ongoing insult/injury to some persistent antigenic stimulus by beta hemolytic streptococcal antigens that have primed the various target tissues. Further study of surface characteristics of various mesenchymal cells may help in understanding the nature and pathogenesis of this serious cardiac problem.     

Periodontal infections and coronary heart disease: role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease (CORODONT) study

BACKGROUND: Chronic inflammation from any source is associated with increased cardiovascular risk. Periodontitis is a possible trigger of chronic inflammation. We investigated the possible association between periodontitis and coronary heart disease (CHD), focusing on microbiological aspects. METHODS: A total of 789 subjects (263 patients with angiographically confirmed, stable CHD and 526 population-based, age- and sex-matched controls without a history of CHD) were included in the Coronary Event and Periodontal Disease (CORODONT) study. Subgingival biofilm samples were analyzed for periodontal pathogens Actinobacillus actinomycetemcomitans, Tannerella forsythensis, Porphyromonas gingivalis, Prevotella intermedia, and Treponema denticola using DNA-DNA hybridization. The need for periodontal treatment in each subject was assessed using the Community Periodontal Index of Treatment Needs (CPITN). The main outcome measures included total periodontal pathogen burden, number of the various periodontal pathogens in the subgingival biofilm, and periodontal treatment needs (according to the CPITN). RESULTS: In multivariable analyses, we found a statistically significant association between the periodontal pathogen burden (log10 of the sum of all pathogens) (odds ratio [OR], 1.92; 95% confidence interval [CI], 1.34-2.74; P<.001) or the number of A actinomycetemcomitans in periodontal pockets (log10) (OR, 2.70; 95% CI, 1.79-4.07; P<.001) and the presence of CHD. In addition, a statistically significant association between an increase in mean CPITN score by 1 and the presence of CHD (OR, 1.67; 95% CI, 1.08-2.58; P = .02) was observed. CONCLUSIONS: Our findings suggest an association between periodontitis and presence of CHD. Periodontal pathogen burden, and particularly infection with A actinomycetemcomitans, may be of special importance.     

Subclinical hypothyroidism and the risk of coronary heart disease: a meta-analysis

Purpose

Subclinical hypothyroidism has been associated with elevated cholesterol and increased risk for atherosclerosis, but data on the risk of coronary heart disease (CHD) are conflicting. We performed a systematic review to determine whether subclinical hypothyroidism is associated with CHD in adults.

Methods

We searched MEDLINE from 1966 to April 2005, and the bibliographies of key articles to identify studies that provided risk estimates for CHD or cardiovascular mortality associated with subclinical hypothyroidism. Two authors independently reviewed each potential study for eligibility, assessed methodologic quality, and extracted the data.

Results

We identified 14 observational studies that met eligibility criteria. Subclinical hypothyroidism increased the risk of CHD (summary odds ratio [OR]: 1.65, 95% confidence interval [CI], 1.28-2.12). The summary OR for CHD was 1.81 (CI, 1.38-2.39) in 9 studies adjusted or matched for demographic characteristics, and 2.38 (CI, 1.53-3.69) after pooling the studies that adjusted for most cardiovascular risk factors. Sensitivity analyses including only population-based studies and those with formal outcome adjudication procedures yielded similar results. Subgroup analyses by type of study design showed a similar trend, but lower risk, in the 5 prospective cohort studies (OR 1.42, CI, 0.91-2.21), compared with the case-control and cross-sectional studies (OR 1.72, CI, 1.25-2.38).

Conclusion

Our systematic review indicates that subclinical hypothyroidism is associated with an increased risk of CHD. Clinical trials are needed to assess whether thyroxine replacement reduces the risk of CHD in subjects with subclinical hypothyroidism.     

Blood pressure and coronary heart disease: a review of the evidence

Overviews of randomized controlled trials and prospective observational studies provide the most reliable data on the association between blood pressure and coronary heart disease (CHD). The totality of evidence indicates a strong association between blood pressure and CHD, which is continuous down to levels of at least 115 mm Hg systolic. Overall, for those 60 to 69 years of age, a 10 mm Hg lower systolic blood pressure is associated with about one-fifth lower risk of a CHD event. The size and shape of this association is consistent across regions, for males and females, and for fatal events as well as nonfatal myocardial infarction. Trials comparing active treatment to placebo or no treatment have demonstrated that the benefits of blood pressure lowering with different classes of drugs (e.g., diuretics, beta-blockers, ACE inhibitors, calcium antagonists) are broadly similar, with approximately one-fifth reduction in CHD. ACE inhibitors achieve this with relatively modest blood pressure reductions, but the size of the reduction for calcium antagonists remains uncertain and appears somewhat less than expected from the blood pressure reduction. Trials confirm the expectation from cohort studies of benefits increasing with the amount of blood pressure lowering, and benefit accruing among those with average or even below average blood pressure. Observational data suggest that the proportional association is attenuated with age, but attenuation is less evident in trial data. However, in both cohort studies and clinical trials, CHD risk differences associated with a given blood pressure difference increase with age. The important points to emerge from this review are, first, that the relative benefits of blood pressure lowering for CHD prevention are likely to be consistent across a range of different populations. Second, there is likely to be considerable benefit with blood pressure lowering below "traditional" hypertension thresholds, especially in those with high absolute risk. Third, initiating and maintaining the maximum tolerated blood pressure reduction is a more important issue than choice of initial agent. Finally, and most importantly, the large majority of people have suboptimal blood pressure (e.g., systolic > 115 mm Hg) and so initiatives to lower blood pressure population-wide are an essential adjunct to targeted treatment programs.     

Understanding the heart: CT and MRI for coronary heart disease

Methods of noninvasive evaluation of coronary artery disease-including multidetector row computed tomography, electron beam computed tomography, magnetic resonance imaging, and nuclear studies (single photon emission computed tomography, positron emission tomography)-are reviewed.     

C-reactive protein and coronary heart disease: a critical review

Modestly elevated baseline concentrations of C-reactive protein (CRP), the classical acute phase protein, are associated with the long-term risk of coronary heart disease in general populations, whilst the major acute phase response of CRP following myocardial infarction is associated with death and cardiac complications. The pathogenic and clinical significance of these associations is controversial. Here we critically review the evidence and describe large-scale epidemiological studies, novel experiments and possible specific therapies which will rigorously inform the debate. We distinguish between the potential pathogenicity of high acute phase circulating CRP concentrations in individuals with substantial tissue damage and modest but persistent increases in baseline values in generally healthy subjects.     

Smoking and acute coronary heart disease: a comparative study

Nine hundred and seventy eight patients with a first documented myocardial infarction were studied to detect smoking related differences in clinical profile and in-hospital outcome. The distribution of infarct sites differed significantly between smokers and non-smokers. Smokers had higher peak cardiac enzyme concentrations. In spite of this, smokers had a better prognosis than non-smokers. There are important differences between smokers and non-smokers, both in clinical profile and in-hospital outcome, which may reflect a difference in the nature of the underlying coronary disease.     

Family coronary heart disease: a call to action

A family history of coronary heart disease (CHD) is an accepted risk factor for cardiovascular events and is independent of common CHD risk factors. Advances in the understanding of genetic influences on CHD risk provide the opportunity to apply this knowledge and improve patient care. Utility of inherited cardiovascular risk testing exists by utilizing both phenotypes and genotypes and includes improved CHD risk prediction, selection of the most appropriate treatment, prediction of outcome, and family counseling. The major impediment to widespread clinical adoption of this concept involves un-reimbursed staff time, educational needs, access to a standardized and efficient assessment mechanism, and privacy issues. The link between CHD and inheritance is indisputable and the evidence strong and consistent. For clinicians, the question is how to utilize this information, in an efficient manner, in order to improve patient care and detection of high-risk family members.