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Intravascular ultrasound demonstrated a characteristic systolic compression of the bridge segments. The delayed compression release may explain the characteristic sharp early diastolic peak in coronary flow velocity found with intracoronary Doppler in vessels with myocardial bridging. Reduced coronary flow reserve may be related to this phenomenon, possibly explaining signs of ischemia detected in some of the patients, but may alternatively be a result of the presence of atherosclerosis in the segment proximal to the bridge in these patients.

Intramural hemorrhage represents a variant of aortic dissection and may be an early finding in patients who develop classic aortic dissection or rupture. Transesophageal echocardiography is an excellent method for the detection of intramural hemorrhage and for monitoring these patients.

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Background. Aortic dissection still has a poor prognosis despite progress in therapy. Therefore, this prospective follow-up study was designed to determine whether the degree of communication between true and false lumen in relation to the type of dissection, analyzed by transesophageal echocardiography, influences the risk after initiation of medical or surgical therapy.

Background —The number of infectious pathogens to which an individual has been exposed (infectious burden) may correlate with coronary artery disease (CAD). In a prospective study, we evaluated the effect of 8 pathogens and the aggregate pathogen burden on the risk for future fatal cardiac events among patients with angiographically documented CAD. Methods and Results —In 1018 patients, IgG or IgA antibodies to herpes simplex virus types 1 and 2, cytomegalovirus, Epstein-Barr virus, Haemophilus influenzae , Chlamydia pneumoniae , Mycoplasma pneumoniae , and Helicobacter pylori were determined. Moreover, highly sensitive C-reactive protein was measured. Follow-up information on cardiovascular events was obtained (mean 3.1 years, maximum 4.3 years). Seropositivities to Epstein-Barr virus ( P =0.001), H pylori ( P =0.002), and herpes simplex virus type 2 ( P =0.045) were independently associated with the future risk of cardiovascular death. An increasing number for pathogen burden was significantly predictive of the long-term prognosis ( P <0.0001). Infectious burden divided into 0 to 3, 4 or 5, and 6 to 8 seropositivities was associated with an increasing mortality of 3.7%, 7.2%, and 12.6%, respectively. Patients seropositive to >5 pathogens compared with those seropositive to <4 pathogens had a 5.1 (1.4 to 18.3) higher risk of future cardiac death. This result was mainly driven by the pathogen burden of seropositivities to Herpesviridae ( P <0.0001). The prognostic impact of total or viral pathogen burden was independent of the C-reactive protein level. Conclusions —These results support the hypothesis that the number of infectious pathogens to which an individual has been exposed independently contributes to the long-term prognosis in patients with documented CAD.

MD; for the AtheroGene InvestigatorsBackground-Recent findings suggest a causative role of infections in the pathogenesis of atherosclerosis. In hypothesizing an association between infectious agents and the development of atherosclerosis, we would expect a correlation to the extent of atherosclerosis. Moreover, this effect could be multiplied by the number of pathogens to which an individual had been exposed. Methods and Results-In 572 patients, IgG or IgA antibodies to herpes simplex virus 1 and 2, cytomegalovirus, Epstein-Barr virus, Hemophilus influenzae, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Helicobacter pylori were measured. The extent of atherosclerosis was determined by coronary angiography, carotid duplex sonography, and evaluation of the ankle-arm index. Elevated IgA antibodies against C pneumoniae (PϽ0.04) and IgG antibodies against H pylori (PϽ0.02), cytomegalovirus (PϽ0.05), and herpes simplex virus 2 (PϽ0.01) were associated with advanced atherosclerosis (Ն2 vascular regions), adjusted for age, sex, cardiovascular risk factors, and highly sensitive C-reactive protein.Infectious burden divided into 0 to 3, 4 to 5, and 6 to 8 seropositivities was significantly associated with advanced atherosclerosis, with an odds ratio (95% CI) of 1.8 (1.2 to 2.6) for 4 to 5 (PϽ0.01) and 2.5 (1.2 to 5.1) for 6 to 8 seropositivities (PϽ0.02) (adjusted). After a mean follow-up of 3.2 years, cardiovascular mortality rate was 7.0% in patients with advanced atherosclerosis and seropositive for 0 to 3 pathogens compared with 20.0% in those seropositive for 6 to 8 pathogens. Conclusions-Our results support the hypothesis that infectious agents are involved in the development of atherosclerosis.We showed a significant association between infectious burden and the extent of atherosclerosis. Moreover, the risk for future death was increased by the number of infectious pathogens, especially in patients with advanced atherosclerosis.

Background and Purpose-Recent findings suggest a causative role of infections in the pathogenesis of atherosclerosis.The extent of atherosclerosis and the prognosis of patients with atherosclerosis seem to be increased by the number of infections to which an individual has been exposed. In a prospective study, we evaluated the effect of 8 pathogens and the aggregate pathogen burden on the progression of carotid atherosclerosis. Methods-In 504 patients (74.9% men; age, 62.9Ϯ10 years), we measured intima-media thickness and prevalence of carotid artery stenosis. Follow-up measurements after a mean of 2.5 years were available in 427 patients (85%). Blood samples were taken, and IgG or IgA antibodies to Chlamydia pneumoniae, Helicobacter pylori, Haemophilus influenzae, Mycoplasma pneumoniae, cytomegalovirus, Epstein-Barr virus, and herpes simplex virus types 1 and 2 were measured. Statistical evaluation was performed with logistic regression procedures. Results-ElevatedIgA antibodies against C pneumoniae (PϽ0.04) and IgG antibodies against Epstein-Barr virus (PϽ0.01) and herpes simplex virus type 2 (PϽ0.04) were associated with progression of atherosclerosis (increase of intima-media thickness Ն0.1 mm/y or progression of carotid stenosis) after adjustment for age, sex, cardiovascular risk factors, highly sensitive C-reactive protein, and statin intake. Infectious burden, divided into 0 to 3, 4 to 5, and 6 to 8 seropositivities, was significantly associated with progression of atherosclerosis, with odds ratios of 1.8 (95% confidence interval, 1.1 to 2.9) for 4 to 5 and 3.8 (95% CI, 1.6 to 8.8) for 6 to 8 compared with 0 to 3 seropositivities after adjustment. Conclusions-Our results support the hypothesis that the number of infectious pathogens to which an individual has been exposed independently contributes to the progression of carotid atherosclerosis.