Agreement of Fractional Flow Reserve Estimated by Computed Tomography With Invasively Measured Fractional Flow Reserve: A Systematic Review and Meta-Analysis.

BACKGROUND: Fractional flow reserve (FFR) is the ratio of blood pressure measured distal to a stenosis and pressure proximal to a stenosis. FFR can be estimated noninvasively using computed tomography (CT) although the usefulness of this technique remains controversial. This meta-analysis evaluated the agreement of FFR estimated by CT (FFR-CT) with invasively measured FFR. The study also evaluated the diagnostic accuracy of FFR-CT, defined as the ability of FFR-CT to classify lesions as hemodynamically significant (invasive FFR ≤0.8) or insignificant (invasive FFR >0.8). METHODS AND RESULTS: Forty-three studies reporting on 7291 blood vessels from 5236 patients were included. A moderate positive linear relationship between FFR-CT and invasively measured FFR was observed (Spearman correlation coefficient: 0.67). Agreement between the 2 measures increased as invasively measured FFR values approached 1. The overall diagnostic accuracy, sensitivity and specificity of FFR-CT were 82.2%, 80.9%, and 83.1%, respectively. Diagnostic accuracy of 90% could be demonstrated for FFR-CT values >0.90 and <0.49. The diagnostic accuracy of off-site tools was 79.4% and the diagnostic accuracy of on-site tools was 84.1%. CONCLUSIONS: The agreement between FFR-CT and invasive FFR is moderate although agreement is highest in vessels with FFR-CT >0.9. Diagnostic accuracy varies widely with FFR-CT value but is above 90% for FFR-CT values >0.90 and <0.49. Furthermore, on-site and off-site tools have similar performance. Ultimately, FFR-CT may be a useful adjunct to CT coronary angiography as a gatekeeper for invasive coronary angiogram.

First case report of myopericarditis linked to Campylobacter coli enterocolitis.

BACKGROUND: Campylobacter spp. are a common cause of mostly self-limiting enterocolitis. Although rare, pericarditis and myopericarditis have been increasingly documented as complications following campylobacteriosis. Such cases have occurred predominantly in younger males, and involved a single causative species, namely Campylobacter jejuni. We report the first case of myopericarditis following Campylobacter coli enterocolitis, with illness occurring in an immunocompetent middle-aged female. CASE PRESENTATION: A 51-yo female was admitted to a cardiology unit with a 3-days history of chest pain. The woman had no significant medical history or risk factors for cardiac disease, nor did she report any recent overseas travel. Four days prior to the commencement of chest pain the woman had reported onset of an acute gastrointestinal illness, passing 3-4 loose stools daily, a situation that persisted at the time of presentation. Physical examination showed the woman's vital signs to be essentially stable, although she was noted to be mildly tachycardic. Laboratory testing showed mildly elevated C-reactive protein and a raised troponin I in the absence of elevation of the serum creatinine kinase. Electrocardiography (ECG) demonstrated concave ST segment elevations, and PR elevation in aVR and depression in lead II. Transthoracic echocardiogram (TTE) revealed normal biventricular size and function with no significant valvular abnormalities. There were no left ventricular regional wall motion abnormalities. No pericardial effusion was present but the pericardium appeared echodense. A diagnosis of myopericarditis was made on the basis of chest pain, typical ECG changes and troponin rise. The chest pain resolved and she was discharged from hospital after 2-days of observation, but with ongoing diarrhoea. Following discharge, a faecal sample taken during the admission, cultured Campylobacter spp. Matrix assisted laser desorption ionization time-of-flight (Bruker) confirmed the cultured isolate as C. coli. CONCLUSION: We report the first case of myopericarditis with a suggested link to an antecedent Campylobacter coli enterocolitis. Although rare, myopericarditis is becoming increasingly regarded as a complication following campylobacteriosis. Our report highlights potential for pericardial disease beyond that attributed to Campylobacter jejuni. However uncertainty regarding pathogenesis, coupled with a paucity of population level data continues to restrict conclusions regarding the strength of this apparent association.