Background: To quantify the association between effects of interventions on carotid intimamedia thickness (cIMT) progression and their effects on cardiovascular disease (CVD) risk. Methods: We systematically collated data from randomized controlled trials. cIMT was assessed as the mean value at the common-carotid-artery; if unavailable, the maximum value at the common-carotid-artery or other cIMT measures were utilized. The primary outcome was a combined CVD endpoint defined as myocardial infarction, stroke, revascularization procedures, or fatal CVD. We estimated intervention effects on cIMT progression and incident CVD for each trial, before relating the two using a Bayesian meta-regression approach. Results: We analyzed data of 119 randomized controlled trials involving 100,667 patients (mean age 62 years, 42% female). Over an average follow-up of 3.7 years, 12,038 patients developed the combined CVD endpoint. Across all interventions, each 10 μm/year reduction of cIMT progression resulted in a relative risk for CVD of 0.91 (95% credible interval 0.87-0.94), with an additional relative risk for CVD of 0.92 (0.87-0.97) being achieved independent of cIMT progression. Taken together, we estimated that interventions reducing cIMT progression by 10, 20, 30, or 40 μm/year would yield relative risks of 0.84 (0.75-0.93), 0.76 (0.67-0.85), 0.69 (0.59-0.79), or 0.63 (0.52-0.74). Results were similar when grouping trials by type of intervention, time of conduct, time to ultrasound follow-up, availability of individual-participant data, primary vs. secondary prevention trials, type of cIMT measurement, and proportion of female patients. Conclusions: The extent of intervention effects on cIMT progression predicted the degree of CVD risk reduction. This provides a missing link supporting the usefulness of cIMT progression as a surrogate marker for CVD risk in clinical trials.

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Moderate evidence for a positive association between periodontitis and CKD exists. Evidence for the opposite direction is extremely weak based on significant heterogeneity between studies.

A context-specific oral health literacy intervention was partially successful in improving oral health literacy and oral health literacy-related outcomes in this vulnerable population, but only after MI.

Observational studies and nonrandomized trials support an association between periodontal disease and atherosclerotic vascular disease. Both diseases occur frequently in Aboriginal Australians. We hypothesized that nonsurgical periodontal therapy would improve measures of arterial function and structure that are subclinical indicators of atherosclerotic vascular disease. This parallel-group, randomized, open label clinical trial enrolled 273 Aboriginal Australians aged ≥18 years with periodontitis. Intervention participants received full-mouth periodontal scaling during a single visit, whereas controls received no treatment. Prespecified primary end points measured 12-month change in carotid intima-media thickness, an indicator of arterial structure, and 3- and 12-month change in pulse wave velocity, an indicator of arterial function. ANCOVA used complete case data to evaluate treatment group differences. End points could be calculated for 169 participants with follow-up data at 3 months and 168 participants at 12 months. Intima-media thickness decreased significantly after 12 months in the intervention group (mean reduction=−0.023 [95% confidence interval {CI}, −0.038 to −0.008] mm) but not in the control group (mean increase=0.002 [95% CI, −0.017 to 0.022] mm). The difference in intima-media thickness change between treatment groups was statistically significant (−0.026 [95% CI, −0.048 to −0.003] mm; P =0.03). In contrast, there were no significant differences between treatment groups in pulse wave velocity at 3 months (mean difference, 0.06 [95% CI, −0.17 to 0.29] m/s; P =0.594) or 12 months (mean difference, 0.21 [95% CI, −0.01 to 0.43] m/s; P =0.062). Periodontal therapy reduced subclinical arterial thickness but not function in Aboriginal Australians with periodontal disease, suggesting periodontal disease and atherosclerosis are significantly associated.