The potential role of ventricular compressive therapy.

Early infarct expansion is associated with progressive ventricular dilatation and contractile dysfunction, and heralds a poor long-term prognosis. The pathophysiology of ventricular remodeling leading to CHF is hypothesized to begin with infarct expansion, which causes increased stress in the myocardium adjacent to the infarct. Increased stress in normally perfused border zone myocardium results in the production of cytokines and ROS, which in turn stimulate myocyte apoptosis, disruption of the ECM, and fibrosis. The value of ventricular compressive therapy in established CHF with the Acorn CSD is unclear. Early clinical and laboratory studies indicate that the device can be placed safely using standard surgical techniques, and that constrictive physiology is surprisingly rare. In the few patients who have received the device, however, the clinical benefit has not been dramatic. A final assessment awaits a well-designed clinical trial comparing isolated CSD placement with optimal medical management, the primary end points being death or the need for organ replacement. In contrast, the value of early ventricular compressive therapy (ie, the prophylactic prevention of infarct expansion) has been demonstrated experimentally: early ventricular restraint dramatically ameliorates remodeling. This strategy probably represents the best application of ventricular compressive therapy. Future work must ascertain the best timing for such an intervention.