Platelets and von Willebrand factor in atherogenesis.

The role of platelet adhesion, activation, and aggregation in acute atherothrombotic events such as myocardial infarction and stroke is well established. There is increasing evidence that platelet-endothelial interactions also contribute to early atherosclerotic plaque initiation and growth. Through these interactions, platelet-derived factors can contribute to the proinflammatory and mitogenic status of resident mural cells. Among the many putative mechanisms for platelet-endothelial interactions, increased endothelial-associated von Willebrand factor, particularly in a multimerized form, which interacts with platelet glycoproteins and integrins, is a major factor and represents a therapeutic target in early atherogenesis.

Cardiovascular and Ventilatory Consequences of Laparoscopic Surgery.

Although laparoscopic surgery accounts for >2 million surgical procedures every year, the current preoperative risk scores and guidelines do not adequately assess the risks of laparoscopy. In general, laparoscopic procedures have a lower risk of morbidity and mortality compared with operations requiring a midline laparotomy. During laparoscopic surgery, carbon dioxide insufflation may produce significant hemodynamic and ventilatory consequences such as increased intraabdominal pressure and hypercarbia. Hemodynamic insults secondary to increased intraabdominal pressure include increased afterload and preload and decreased cardiac output, whereas ventilatory consequences include increased airway pressures, hypercarbia, and decreased pulmonary compliance. Hemodynamic effects are accentuated in patients with cardiovascular disease such as congestive heart failure, ischemic heart disease, valvular heart disease, pulmonary hypertension, and congenital heart disease. Prevention of cardiovascular complications may be accomplished through a sound understanding of the hemodynamic and physiological consequences of laparoscopic surgery as well as a defined operative plan generated by a multidisciplinary team involving the preoperative consultant, anesthesiologist, and surgeon.

Functional adaptations of the coronary microcirculation to anaemia in fetal sheep.

KEY POINTS: In fetuses, chronic anaemia stimulates cardiac growth; simultaneously, blood flow to the heart muscle itself is increased, and reserve blood flow capacity of the coronary vascular bed is preserved. Here we examined functional adaptations of the capillaries and small blood vessels responsible for delivering oxygen to the anaemic fetal heart muscle using contrast-enhanced echocardiography. We demonstrate that coronary microvascular flux rate doubled in anaemic fetuses compared to control fetuses, both at rest and during maximal flow, suggesting reduced microvascular resistance consistent with capillary widening. Cardiac fractional microvascular blood volume was not greater in anaemic fetuses, suggesting that growth of new microvascular vessels does not contribute to the increased flow per volume of myocardium. These unusual changes in microvascular function during anaemia may indicate novel adaptive strategies in the fetal heart. ABSTRACT: Fetal anaemia causes cardiac adaptations that have immediate and life-long repercussions on heart function and health. It is known that resting and maximal coronary conductance both increase during chronic fetal anaemia, but the coronary microvascular changes responsible for the adaptive response are unknown. Until recently, technical limitations have prevented quantifying functional capillary-level adaptations in the in vivo fetal heart. Our objective was to characterise functional microvascular adaptations in chronically anaemic fetal sheep. Chronically instrumented fetuses were randomized to a control group (n = 11) or were made anaemic by isovolumetric haemorrhage (n = 12) for 1 week prior to myocardial contrast echocardiography at 85% of gestation. Anaemia augmented cardiac mass by 23% without changing body weight. In anaemic fetuses, microvascular blood flow per volume of myocardium was twice that of control fetuses at rest, during vasodilatory hyperaemia, and during hyperaemia plus increased aortic pressure. The elevated blood flow was attributable almost entirely to an increase in microvascular blood flux rate whereas microvascular blood volumes were not different between groups at baseline, during hyperaemia, or with hyperaemia plus increased aortic pressure. Increased coronary microvascular flux rate in response to chronic fetal anaemia is consistent with expected reductions in capillary resistance from capillary diameter widening detected in earlier histological studies.

A Practical Approach to Mechanical Circulatory Support in Patients Undergoing Percutaneous Coronary Intervention: An Interventional Perspective.

Percutaneous mechanical circulatory support has been used to stabilize patients in cardiogenic shock and provide hemodynamic support during high-risk percutaneous coronary interventions for several decades. The goal of this paper is to provide a practical approach to percutaneous mechanical circulatory support in patients undergoing percutaneous coronary intervention with cardiogenic shock and/or high risk features to aid in decision making for interventional cardiologists.