Quantification of Coronary Artery Stenosis in Very-High-Risk Patients Using Ultra-High Resolution Spectral Photon-Counting CT.

OBJECTIVE: Development of spectral photon-counting computed tomography (SPCCT) for ultra-high-resolution coronary CT angiography (CCTA) has the potential to accurately evaluate the coronary arteries of very-high-risk patients. The aim of this study was to compare the diagnostic performances of SPCCT against conventional CT for quantifying coronary stenosis in very-high-risk patients, with invasive coronary angiography (ICA) as the reference method. MATERIALS AND METHODS: In this prospective institutional review board-approved study, very-high-risk patients addressed for ICA following an acute coronary syndrome were consecutively included. CCTA was performed for each patient with both SPCCT and conventional CT before ICA within 3 days. Stenoses were assessed using the minimal diameter over proximal and distal diameters method for CCTA and the quantitative coronary angiography method for ICA. Intraclass correlation coefficients and mean errors were assessed. Sensitivity and specificity were calculated for a >50% diameter stenosis threshold. Reclassification rates for conventional CT and SPCCT were assessed according to CAD-RADS 2.0, using ICA as the gold standard. RESULTS: Twenty-six coronary stenoses were identified in 26 patients (4 women [15%]; age 64 ± 8 years) with 19 (73%) above 50% and 9 (35%) equal or above 70%. The median stenosis value was 64% (interquartile range, 48%-73%). SPCCT showed a lower mean error (6% [5%, 8%]) than conventional CT (12% [9%, 16%]). SPCCT demonstrated greater sensitivity (100%) and specificity (90%) than conventional CT (75% and 50%, respectively). Ten (38%) stenoses were reclassified with SPCCT and one (4%) with conventional CT. CONCLUSIONS: In very-high-risk patients, ultra-high-resolution SPCCT coronary angiography showed greater accuracy, sensitivity, and specificity, and led to more stenosis reclassifications than conventional CT.

Iodinated contrast media induced Kounis syndrome during coronary angiogram: a life-threatening clinical dilemma.

Kounis syndrome (KS) is a well-documented hypersensitivity vasospastic reaction induced by a variety of triggers. Clinical presentation ranges from non-specific symptoms such as dizziness and nausea to myocardial infarction. Many cases of KS were reported after the use of iodinated contrast media, mainly during radiological procedures. This report describes the case of a 46-year-old man developing coronary vasospasm and anaphylactic shock at the end of percutaneous coronary intervention. Occurrence of such pathology while performing coronary angiogram is a tricky situation for the invasive cardiologist. It requires recognising a rare syndrome and interrupting the procedure to avoid extra use of contrast media even in presence of severe coronary lesions due to vasospasm. Every interventionalist should be aware of such a presentation to recognise and react promptly when facing a potentially life-threatening clinical dilemma.

Catecholamine effects on cardiac remodelling, oxidative stress and fibrosis in experimental heart failure.

The aim of the study was to assess the relationships between oxidative stress, cardiac remodelling and fibrosis on an experimental model of heart failure with adrenergic stimulation. Large myocardial infarction (approximately 50% of the left ventricle myocardium) was obtained by ligation of the left coronary artery of normotensive male Wistar rats. Sham animals were submitted to left thoracotomy without coronary ligation. In order to perform cardiac stimulation by catecholamines, mini-osmotic pumps were implanted in animals 10 weeks after surgery to deliver noradrenalin for a 2-week period. At the end of this period, the following investigations were performed: haemodynamics, morphometry, fibrosis quantification, plasma and tissue catecholamine assay and oxidative stress status. Coronary ligation induced dilatation of left ventricle with compensatory hypertrophy of the right ventricle and of the remaining left ventricle myocardium. This remodelling process was associated in non-infarcted myocardium with increased collagen infiltration and increased oxidative stress. Ten weeks after surgery, the chronic administration of noradrenalin for 2 weeks did not increase oxidative stress. Noradrenalin, however, induced inotropic stimulation and myocardial hypertrophy, but to a lesser extent in infarcted rats compared to sham rats. Our results suggest that noradrenalin infusion to levels in excess of those seen post-infarction is associated with fibrosis and oxidative stress. Moreover, noradrenalin in infarcted animals caused additional fibrosis without further increasing oxidative stress. The mechanism of catecholamine-induced fibrosis may thus involve different processes such as ischaemia, increased mechanical stress, cytokines and neurohormones.