Stromal cell-derived factor-1alpha improves infarcted heart function through angiogenesis in mice.

Background: Local delivery of stromal cell-derived factor-1alpha (SDF-1) has been demonstrated to improve hind limb ischemia through enhanced neovascularization in animals. It was hypothesized that local administration of SDF-1 also contributes to neovascularization of ischemic heart.

Method: Acute myocardial infarction was created by left coronary artery ligation in C57BL/6J mice.

Remodeling of gap junctions in ischemic and nonischemic forms of heart disease.

Electrical activation of the myocardium to produce effective pumping of blood depends on the orderly coordinated spatial and temporal transfer of current from one cell to another via gap junctions. Normal ventricular myocytes are extensively coupled by gap junctions and have the capacity to rapidly increase the amount of connexin within gap junction plaques to meet physiological demands for enhanced cell-cell communication. However, myocytes can also rapidly uncouple in response to injury or disease.

Map-guided surgery for atrial fibrillation.

Background: Although current surgical procedures result in a high success rate for atrial fibrillation, they are not guided by electrophysiologic findings in individual patients and thus might include unnecessary incisions in some patients or be inappropriate for other patients. We sought to determine whether intraoperative mapping is beneficial for the surgical treatment of atrial fibrillation.

Methods: A 256-channel 3-dimensional dynamic mapping system with custom-made epicardial patch electrodes was used to examine the atrial activation during atrial fibrillation and to determine the optimal procedure in 37 patients with continuous and 9 patients with intermittent atrial fibrillation intraoperatively.

Spontaneous and inducible ventricular arrhythmias after myocardial infarction in mice.

Introduction: Remodeling of gap junctions has been implicated in development of ventricular arrhythmias following myocardial infarction (MI) but the specific contribution of reduced electrical coupling is not known. We addressed this question using hearts from mice heterozygous for a connexin43 null allele (Cx43(+/-)).

Methods: To determine whether Cx43-deficient mice exhibit increased spontaneous ventricular arrhythmias in the setting of chronic ischemic heart disease, radiofrequency transmitters were implanted in wild-type and Cx43(+/-) mice 2 days or 9 weeks after left anterior descending coronary artery ligation or sham operations.

Coronary artery bypass grafting without cardiopulmonary bypass: a five-year experience.

The current drive to practice less invasive surgery is changing surgical practice towards safer and simpler procedures. The practice of coronary artery bypass grafting (CABG) on a beating heart without cardiopulmonary bypass (CPB), off-pump CABG or OPCAB, has been gaining great attention as an alternative approach to conventional CABG. Since the first adoption of OPCAB in 1997 at our department, 181 patients have undergone OPCAB.

Connexin43 as a determinant of myocardial infarct size following coronary occlusion in mice.

Objectives: The purpose of this study was to define the role of cell-cell coupling as an independent determinant of infarct size following coronary occlusion.

Background: Electrical uncoupling induced by acute ischemia enhances arrhythmogenesis, but it may also protect the heart by limiting intercellular spread of chemical mediators of injury.

Methods: The left anterior descending coronary artery was ligated in wild-type (Cx43(+/+)) mice and Cx43-deficient (Cx43(+/-)) mice that are heterozygous for a null allele in the gene encoding the major gap junction channel protein, connexin43 (Cx43).

Echocardiographic evaluation of ventricular remodeling in a mouse model of myocardial infarction.

Gene-targeting in mice is a powerful tool to define molecular mechanisms of ischemic heart disease that determine infarct size, postinfarct left ventricular (LV) remodeling, and arrhythmogenesis. Coronary ligation in mice is becoming a widely used model of myocardial infarction (MI), but the pathophysiologic consequences of MI in mice and its relevance to human MI have not been fully elucidated. To characterize structural and functional changes during evolving MI, we analyzed 2-dimensional-based reconstruction of the left ventricle by noninvasive echocardiography obtained 1 day and 1 week after surgical ligation of the left anterior descending coronary artery in mice.