Perivascular Fat: A Novel Risk Factor for Coronary Artery Disease.

Perivascular adipose tissue (PVAT) interacts with the vascular wall and secretes bioactive factors which regulate vascular wall physiology. Vice versa, vascular wall inflammation affects the adjacent PVAT via paracrine signals, which induce cachexia-type morphological changes in perivascular fat. These changes can be quantified in pericoronary adipose tissue (PCAT), as an increase in PCAT attenuation in coronary computed tomography angiography images. Fat attenuation index (FAI), a novel imaging biomarker, measures PCAT attenuation around coronary artery segments and is associated with coronary artery disease presence, progression, and plaque instability. Beyond its diagnostic capacity, PCAT attenuation can also ameliorate cardiac risk stratification, thus representing an innovative prognostic biomarker of cardiovascular disease (CVD). However, technical, biological, and anatomical factors are weakly related to PCAT attenuation and cause variation in its measurement. Thus, to integrate FAI, a research tool, into clinical practice, a medical device has been designed to provide FAI values standardized for these factors. In this review, we discuss the interplay of PVAT with the vascular wall, the diagnostic and prognostic value of PCAT attenuation, and its integration as a CVD risk marker in clinical practice.

CCTA-Guided Invasive Coronary Angiography in Patients With CABG: A Multicenter, Randomized Study.

BACKGROUND: Coronary computed tomography angiography (CCTA) in patients with post-coronary artery bypass graft (CABG) has a high diagnostic accuracy for visualization of grafts. Invasive coronary angiography (ICA) in patients with CABG is associated with increased procedural time, contrast agent administration, radiation exposure, and complications, compared with non-CABG patients. The aim of this multicenter, randomized controlled trial was to compare the strategy of CCTA-guided ICA versus classic ICA in patients with prior CABG. METHODS: Patients with prior CABG were randomly assigned (1:1 ratio) to have a CCTA before ICA (CCTA-ICA, group A) or not (ICA-only, group B). The primary end point of the study was the total volume (milliliters) of the contrast agent administered. RESULTS: A total of 251 patients were randomized, and 225 were included in analysis; 110 in group A and 115 in group B. The total contrast volume was higher in group A (184.5 [143-255] versus 154 [102-240] mL; P=0.001). The contrast volume administered during the invasive procedure was lower in group A (101.5 [60-151] versus 154 [102-240]; P<0.001). Total fluoroscopy time was decreased in group A (480 [259-873] versus 594 [360-1080] seconds; P=0.027), but total effective dose was increased (24.1 [17.7-32] versus 10.8 [5.6-18] mSv; P<0.001). The rate of contrast-induced nephropathy, periprocedural complications, and major adverse cardiac events during 3 to 5 and 30 days did not differ significantly between the 2 groups. CONCLUSIONS: A CCTA-directed ICA strategy for patients with CABG is associated with expedition of the invasive procedure, and less fluoroscopy time, at the cost of higher total contrast volume and effective radiation dose, compared with the classic ICA approach. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04631809.

Pulmonary hemorrhage in patients receiving anti-platelets- a case series and a suggested therapeutic algorithm.

Antiplatelet therapy including aspirin and thienopyridine agents (such as clopidogrel, prasugrel and ticagrelor) are often used in patients with coronary disease. Pulmonary hemorrhage due to antiplatelet therapy although very rare, when excessive, is a life-threatening event. So far, there is lack of specific guidelines for the management of these patients. We report a case series of 5 patients receiving antiplatelet therapy who were admitted to the hospital due to pulmonary hemorrhage related to antiplatelet therapy. We also propose an algorithm on the management of these patients taking into consideration the balance between thrombotic and bleeding risk and the severity of the hemorrhage.

Cell-free DNA levels as a prognostic marker in acute myocardial infarction.

Cell-free DNA that originates from cell death, circulates in peripheral blood. There are indications that the infarcted myocardium contributes to an increase of cell-free DNA levels. Our aims were to quantify levels of cell-free DNA in patients with acute myocardial infarction (AMI) and examine their correlation with myocardial markers and with postinfarction (PI) clinical course. Thirteen patients (age 57 +/- 16 year) admitted with AMI and who underwent thrombolysis with reteplase within 6 h from the onset of chest pain were studied. PB samples were collected on admission and for 5 consecutive days. Creatine kinase (CK) and troponin I (TnI) were measured on admission and every 8 h for 3 consecutive days. Clinical events were recorded throughout the hospitalization period. Cell-free DNA levels were also measured in 30 healthy controls. Log-transformed mean (+/-SE) of maximum free DNA values in patients higher than controls (6873 +/- 357 g.e./mL verses 4112 +/- 234 g.e./mL, P < 0.0001). Log-transformed maximum values of CK and TnI were correlated with log-transformed free DNA values of first (r = 0.62, P = 0.02/r = 0.68, P = 0.01) and second (r = 0.57, P = 0.04/r = 0.72, P = 0.0053) PI day. Nine patients (group A) had an uncomplicated PI clinical course and four patients (group B) had recorded events (three with angina and one death). Free DNA levels on the second PI day were higher in group B than group A (1298.0 +/- 796.0 g.e./mL verses 244.6 +/- 257.7 g.e./mL, P = 0.003). In conclusion, free DNA levels are significantly higher in patients with AMI than in controls and may play a role in the prognosis of these patients.

Marked troponin elevation after implantation of a permanent antibradycardia pacemaker.

INTRODUCTION: Transvenous insertion of endocardial leads for permanent pacing is often accompanied by minor myocardial damage, detected thanks to the high sensitivity of cardiac troponins. It is unknown whether higher troponin levels, commensurate with more severe myocardial damage, can be encountered after implantation procedures. METHODS: Over a 3-year period, 283 patients underwent an implantation of a full antibradycardia pacemaker system (pulse generator plus leads). Patients were required to have normal levels of cardiac troponin I (CTNI) on a venous blood sample taken immediately prior to elective pacemaker insertion. Post implantation CTNI levels were measured in all patients 6 hours after the procedure. Repeated samples were taken if high CTNI levels were found at 6 hours. RESULTS: Elevated CTN-I levels were found in 167 patients (59%, 95% CI: 0.53-0.64), but only 5 of them (1.8%, 95% CI=0.8 to 4.1%) had peak CTN-I levels far exceeding the range of minimal myocardial damage (i.e. CTN-I >1.5 ng/ml). Implantation of the devices was successful in all patients and we did not observe any complications. None had clinical evidence of an acute coronary event before or during the pacemaker implantation procedure and coronary angiography revealed no significant lesions in the coronary arteries. CONCLUSIONS: CTN-I elevations after pacemaker implantation may far exceed levels corresponding to minimal myocardial damage. This should be a matter of concern, especially if an early discharge is planned after pacemaker implantation.