Objectives: To examine the putative physiologic role of epicardial fat to buffer the coronary arteries and to review the data on deformation and vibration in coronary arteries. Methods: OvidSP Medline, Embase, and PubMed were systematically searched. Eligible articles on vibration in arteries and deformation of coronary arteries were assessed. Results: Coronary arteries are unique because they undergo substantial deformations with twisting, bending, and stretching that are due to cardiac contraction and the tethering of the large coronary arteries to the epicardial surface of the heart. In addition, phasic coronary artery pressure and blood flow are not synchronous producing a high negative stress phase angle between circumferential strain and wall shear. Fluid flow–induced vibrations, a universal finding in conduits transporting fluid with pulsatile flow, have been documented in arteries. Arterial vibration can damage the structure of arterial wall, especially elastin and endothelial cells, leading to alterations in the arterial function. Support for a beneficial mechanical role for epicardial fat is based on the data that wrapping material to the outside of conduits not only reduces the vibration but also decreases their movement. The overall impact of an external wrap is a reduction in the probability of conduit fatigue and failure. Characteristics of the artery, such as shear modulus, are a function of the properties of each layer of the artery. The application of epicardial fat to the adventitia of arteries alters the biophysical characteristics of the artery which is the sum of each layer including the epicardial fat. Vibration, resonance, and deformation energy are lost when they hit the surface of an absorbing material. Conclusions: The integration of the biophysics of coronary arteries with knowledge of material damping principles supports a physiologic role for epicardial fat to buffer deformation and vibration in coronary arteries.
During a routine cervicothoracic dissection, an anomalous carotid vascular system was discovered. Anomalies of the carotid vascular system are clinically significant due to their principal role in supplying blood to the neck, head, and brain. Our findings reveal a severe morphological variation of the carotid vascular system, which significantly increases the risk of developing central nervous system ischemia. Variations in morphology, including kinking and tortuosity, of the carotid arterial system described in this study should be considered when evaluating the symptoms consistent with central nervous system ischemia. The individual studied suffered from dementia as well as a past medical history of cardiovascular accident (CVA), Hypertension (HTN), and depression, which can be clinically related to the morphological variations seen in the carotid arterial system.
The primary purpose of this article is to provide a broad overview of the research on the long-term effects of childhood risk factors on cardiovascular diseases (CVDs) during adulthood and to outline recommendations for prevention of CVDs based on evidence-based interventions (EBIs). CVDs are the leading cause of death and a major cause of disability in the United States and globally. Risk factors for CVDs are already identifiable in children and youth, and include both modifiable factors (e.g., unhealthy diet, physical inactivity, tobacco smoking), and factors that cannot be changed (e.g., age, heredity, sex). A fundamental issue has been the severity of the long-term effects of childhood risk factors (i.e., behavioral and intermediate risk factors) on subsequent cardiovascular health. It is clear from the empirical evidence that risk factors for CVDs can develop during childhood and adolescence. These risk factors in childhood have been linked to adverse health outcomes, including CVDs, during adulthood. The findings thus far suggest that, in order to be effective and reduce the risk of adulthood CVDs, intervention strategies should begin during childhood. The findings also underscore the importance of adopting a healthy lifestyle as early in life as possible.
Sirolimus was isolated in 1975 and was initially approved for the treatment of renal transplant rejection. The main mechanism of action is mTOR inhibition, which prevents cell cycle progression. The first-in-human study of the sirolimus-eluting stent (SES) was initiated in 1999 in Sao Paulo Brazil and Rotterdam. The study demonstrated a reduction in restenosis after SES implantation when compared with bare-metal stents. The first approved drug-eluting stent was the SES Cypher®. Several modifications in stent platform and polymer coating have been made, in an effort to improve deliverability and to reduce inflammatory response secondary to nonbiocompatible polymers. Bioabsorbable polymer and polymer-free technologies are the main characteristic of the second- and third-generation SES. Larger studies with longer follow-up are needed to prove the efficacy of those stents when compared with previous platforms.
The use of oral anticoagulation to reduce stroke risk from thromboembolism has become the cornerstone of management of atrial fibrillation. Dabigatran is a direct thrombin inhibitor, which in contrast to warfarin, does not require regular blood draws for monitoring effect. Randomized controlled studies suggest that dabigatran may be more effective than warfarin at higher doses without an increased bleeding risk, and equally effective at lower doses, with lower bleeding risk. With these apparent advantages comes a higher cost, and limited use in patients with underlying renal or liver disease. In addition, the inability to measure anticoagulant effect, as with warfarin, presents a double-edged sword for clinical use of dabigatran. In this review, we discuss the mechanisms of action, clinical effect, and place in therapy of dabigatran as a possible replacement for warfarin.
