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Background High-risk coronary atherosclerosis features evaluated coronary CT angiography (CCTA) were suggested to have a prognostic role. The present study aimed to evaluate the association of circulating biomarkers with high-risk plaque features assessed by CCTA. Methods A consecutive cohort of subjects who underwent CCTA because of suspected CAD was screened for inclusion in the CAPIRE study. Based on risk factors (RF) burden patients were defined as having a low clinical risk (0–1 RF with the exclusion of patients with diabetes mellitus as single RF) or an high clinical risk (≥3 RFs). In all patients, measurement of inflammatory biomarkers and CCTA analysis focused on high-risk plaque features were performed. Univariate and multivariate logistic regression analysis were used to evaluate the relationship between clinical and biological variables with CCTA advanced plaque features. Results 528 patients were enrolled in CAPIRE study. Older age and male sex appeared to be predictors of qualitative high-risk plaque features and associated with the presence of elevated total, non-calcified and low-attenuation plaque volume. Among circulating biomarkers only hs-CRP was found to be associated with qualitative high-risk plaque features (OR 2.02, p = 0.004 and 2.02, p = 0.012 for LAP and RI > 1.1, respectively) with borderline association with LAP-Vol (OR 1.52, p = 0.076); HbA1c and PTX-3 resulted to be significantly associated with quantitative high-risk plaque features (OR 1.71, p = 0.003 and 1.04, p = 0.002 for LAP-Vol, respectively). Conclusions Our results support the association between inflammatory biomarkers (hs-CRP, PTX- 3), HbA1c and high-risk atherosclerotic features detected by CCTA. Male sex and older age are significant predictors of high-risk atherosclerosis.

Objectives The authors performed a meta-analysis to evaluate the predictive value of late gadolinium enhancement (LGE) cardiac magnetic resonance for ventricular tachyarrhythmia in ischemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NICM) patients with ventricular dysfunction. Background The use of LGE to detect myocardial fibrosis and its related arrhythmic substrate is well established. Several recent studies have described the predictive value of LGE for ventricular tachyarrhythmias; however, their validity is limited by small sample size and low number of events. Methods MEDLINE and the Cochrane Library electronic databases were systematically searched to identify studies that applied LGE in ICM and NICM patients with ventricular dysfunction and reported arrhythmic clinical outcomes (sudden death, aborted sudden death, ventricular tachycardia, ventricular fibrillation, and appropriate implantable cardioverter-defibrillator [ICD] therapy, including antitachycardia pacing). A meta-analysis was performed to determine pooled odds ratios (ORs) for these arrhythmic events. Results Nineteen studies that evaluated 2,850 patients with 423 arrhythmic events over a mean/median follow-up of 2.8 years were identified. The composite arrhythmic endpoint was reached in 23.9% of patients with a positive LGE test (annualized event rate of 8.6%) versus 4.9% of patients with a negative LGE test (annualized event rate of 1.7%; p Conclusions LGE is a powerful predictor of ventricular arrhythmic risk in patients with ventricular dysfunction, irrespective of ICM and NICM etiology. The prognostic power of LGE is particularly strong in patients with severely depressed EF, which suggests its potential to improve patient selection for ICD implantation.

Background Coronary artery anomalies (CAAs) are a relatively rare condition usually diagnosed in vivo by conventional angiography. In the past few years Magnetic resonance coronary angiography (MRCA) has been used to detect CAAs and found to be highly accurate. No data is available regarding the ability of MRCA to detect previously not suspected anomalies. Methods We prospectively analyzed the origin and course of 336 patients undergoing a diagnostic Cardiovascular magnetic resonance (CMR) study. After the completion of a standard examination a navigator-echo 3D-MRCA low-quality scan was used in all the cases to rule out CAAs. The high-quality MRCA was applied only if an abnormal coronary arterial tree was seen. Results Nineteen patients with CAAs (12 men, 7 women; mean age, 53±18 years) were identified by MRCA. Six out of the 19 CAAs subjects had already been detected by other means (coronary angiography in 5, and transesophageal echocardiography in 1 case). However in none of them a complete anatomical assessment was achieved. In 13 patients CAAs were an unexpected and new finding. MRCA was able to assess the origin and proximal course of the anomalous artery in all the cases. Conclusions MRCA is able to detect the presence and anomalous course of CAAs. Besides offering precise information about already suspected CAAs, MRCA can identify anomalies previously not suspected. This study suggests a potential role for MRCA as a screening tool for CAAs in young patients with angina, ventricular arrhythmias, or unexplained syncope as well as in highly competitive athletes.

To evaluate the ability of cine magnetic resonance imaging (cine MRI) in the assessment of mitral stenosis (MS), we studied 20 patients (14 women and 6 men, mean age 60.6 +/- 8.5 years) with rheumatic mitral valve stenosis by using an 0.5 T magnet. Cine MRI showed several signs of MS. Mitral leaflet thickening, reduced diastolic opening, and abnormal valve motion toward the left ventricular outflow tract were all common features. MS was also characterized by an abnormal diastolic transmitral signal from blood. Both left atrial and left ventricular dimensions were similar to those obtained at two-dimensional echocardiography (2-DE) (r = 0.89 and r = 0.86, respectively; p less than 0.001). A significant relationship was also found between the maximum mitral leaflet separation measured by cine MRI in diastole and the mitral valve area as calculated using the pressure half-time method and continuous wave Doppler (r = 0.81; p less than 0.001). These data indicate the improved ability of MRI to detect and assess MS and also suggest that this technique may contribute to the noninvasive assessment of MS.

399 out of 474 inpatients with unstable angina were monitored for 48 h and 97 of these were found to be refractory to conventional antianginal treatments and entered a randomised double-blind study. With the initial protocol heparin infusion or bolus were compared with aspirin; with a modified protocol, heparin infusion, the best of these three treatments, was compared with alteplase. Patients were monitored for 3 days after starting treatment and then observed clinically for 4 more days. On the first days of treatment heparin infusion significantly decreased the frequency of angina (by 84-94%), episodes of silent ischaemia (by 71-77%), and the overall duration of ischaemia (by 81-86%). Heparin bolus and aspirin were not effective. Alteplase caused small (non-significant) reductions on the first day only. Only minor bleeding complications occurred.

To investigate prostaglandin biosynthesis by the heart, 21 patients undergoing cardiac catheterization and coronary angiography for congenital or acquired heart diseases other than coronary artery disease were investigated. Prostacyclin (as 6-keto-PGF1 alpha), PGE2, PGF2 alpha and TxA2 (as TxB2) were measured by specific radioimmunoassay in blood from coronary sinus, aorta, and a peripheral vein under resting conditions and following cold pressor test (CPT). PGF2 alpha was always found undetectable. In resting conditions, no significant differences in plasma 6-keto-PGF1 alpha, PGE2, or TxB2 concentrations were found among coronary sinus, aorta, and peripheral venous blood and no transcardiac gradient existed (mean: +0.4 +/- 1.2 pg/ml for 6-keto-PGF1 alpha, +0.1 +/- 0.6 pg/ml for PGE2, and -0.4 +/- 9.9 pg/ml for TxB2). CPT was able to induce a significant increase in 6-keto-PGF1 alpha and PGE2 concentration in blood from the different sampling sites and a significant transcardiac gradient was found following CPT (+11.6 +/- 7.4 pg/ml for 6-keto-PGF1 alpha (p less than 0.01) and +5.2 +/- 3.6 pg/ml for PGE2 (p less than 0.001). TxB2 levels significantly increased in peripheral venous blood (from 18.3 +/- 6.2 to 29.2 +/- 20.3 pg/ml, p less than 0.05), but they did not increase either in coronary sinus (from 21.9 +/- 9.7 to 22.9 +/- 9.8 pg/ml) or in aorta (from 22.3 +/- 4.7 to 19.1 +/- 6.5 pg/ml). Present results indicate that a cardiocoronary prostacyclin and PGE2 synthesis is inappreciable under resting conditions but it becomes remarkable following sympathetic stimulation. On the contrary, no TxA2 cardiocoronary biosynthesis seems to occur in patients free from coronary artery disease.

Thirty-seven patients affected by spontaneous angina and 15 comparable control subjects were enrolled in a 12-month prospective study to evaluate the relationship between blood clotting activation (assessed by fibrinopeptide A [FPA] plasma concentration) and the occurrence of myocardial ischemic attacks. FPA measurements and clinical examinations in patients were performed every 2 weeks. In control subjects blood sampling was performed every 4 weeks. Data from 28 patients who completed the study and from the 15 control subjects were analyzed. The clinical activity of angina was divided into three classes (asymptomatic, mildly symptomatic, and severely symptomatic) on the basis of the number and time-concentration of the ischemic attacks and ECG changes during the 15 days preceding each clinical examination. In all but one patient, a cyclic pattern of activity of coronary artery disease was observed. During follow-up studies, 624 FPA measurements were performed in patients and 173 in control subjects. Mean values were 4.68 +/- 4.53 and 1.32 +/- 0.60 ng/ml, respectively (p less than 0.001). FPA levels differed markedly in relation to the activity of angina. A relationship between FPA levels and activity of disease (r = 0.54, p less than 0.01) was found in time course. Bolus heparin administration (100 IU/kg) during the active phase of angina sharply but incompletely lowered FPA plasma levels, indicating thrombin formation both intravascularly and extravascularly. Present results indicate that a marked blood clotting activation occurs simultaneously with the outbursts of clinical activity of spontaneous angina.

Human arterial and venous segments from patients under-going operations when incubated in Tris buffer both alone and with arachidonic acid were able to produce thromboxane B 2 (assessed by radioimmunoassay). Thromoboxane B 2 (TxB 2 ) production was progressive in time (till 40 min.) and was enhanced by the addition of 1mM norepinephrien. Contamination of tissues by platelet was checked and platelets did not contribute to thromboxane formation. The investigation of the conversions of 1- 14 C arachidonic acid by vascular tissue indicated that human vascular tissues produce the metabolites of the cyclooxygenase dependent pathway and that prostacyclin is the main metabolite with a PGI 2 /TxA 2 ratio of 4:1. The arterial wall was found to posses an active lipoxygenase dependent pathway. Thromboxane production by intimal cells was neglible and the main source of thromboxane was the media. The production of thromboxane did not change in relation to age, but arterial segments from men produced significantly larger amounts of thromboxane than those from women.

Thirty-four patients with unstable angina and 14 patients with stable effort angina were investigated for cardiac prostacyclin and prostaglandin E 2 (PGE 2 ) biosynthesis, under resting conditions and after cold pressor testing. Twenty-seven patients undergoing cardiac catheterization and coronary angiography for congenital or acquired heart diseases other than coronary artery disease were studied as a control group. Prostacyclin (as 6-keto-PGF 1α ) and PGE 2 were measured by specific radioimmunoassay of blood from the coronary sinus and aorta. During resting conditions no significant differences in plasma 6-keto-PGF 1α and PGE 2 concentrations were found between coronary sinus and aortic blood, and no transcardiac gradient existed either in control subjects or in patients with stable and unstable angina, respectively. In control subjects cold pressor testing induced a significant increase in 6-keto-PGF 1α and PGE 2 levels in blood from the different sampling sites, and a significant transcardiac gradient occurred (+11.2 ± 6.4 pg/ml for 6-keto-PGF 1α and +5.1 ± 3.4 pg/ml for PGE 2 ). However, in angina patients no significant increase in 6-keto-PGF 1α and PGE 2 plasma levels was found and no transcardiac gradient was formed after cold pressor testing. These results indicate impaired cardiac prostacyclin and PGE 2 biosynthesis both in patients with stable and unstable effort angina.

Out of 34 consecutive patients with angina and treated with nifedipine, two subjects (5.8 percent) showed a significant increase of transient myocardial ischemic episodes during the period of treatment, as assessed by continuous Holter ECG monitoring. In both these patients, a large proportion of ischemic episodes happened to be asymptomatic. A relationship between nifedipine intake, heart rate increase, and number of ischemic episodes was observed. This occasional aggravation of myocardial ischemia could be related to an increase in myocardial oxygen demand medicated through a drug-induced reflex tachycardia.