The development and rationale of pressure-controlled intermittent coronary sinus occlusion--a new approach to protect ischemic myocardium.
The early concept of global retroperfusion and arterialisation of the coronary sinus was discarded because of unacceptable damage to the myocardium, although many authors provided evidence on the improvement of cardiac function during ischemia. Furthermore, the exact mechanism of coronary sinus retroperfusion remained poorly understood. The lack of a strong physiological basis for retroperfusion as well as the development of coronary bypass grafting lessened interest in this revascularisation technique. Renewed interest in myocardial protection via the coronary sinus emerged because of a more aggressive therapy of acute myocardial ischemia. We developed a simple retroperfusion system conceptualized as a periodical occlusion of the coronary sinus and as a redistribution of venous flow to compromised areas during acute myocardial ischemia, sweeping out toxic substances and edema during coronary venous drainage. To allow sufficient filling of the infarcted area as well as venous drainage, the occlusion versus release phase is controlled by the coronary sinus pressure. This pressure-controlled intermittent coronary sinus occlusion (P-ICSO) represents a closed loop system and therefore guarantees optimal physiologic function of the system. This report explains the proposed nature of action of enhanced washout of myocardial edema induced by P-ICSO. Moreover, beneficial effects of P-ICSO observed during canine studies are summarized. It is concluded that this new simple retroperfusion technique has the clinical potential to serve as interim support to protect deprived myocardium until definite reperfusion is available.
D001794:Blood Pressure; D006328:Cardiac Catheterization / Q000379:methods; D001026:Coronary Artery Bypass; D003327:Coronary Disease / Q000628:therapy*; D003331:Coronary Vessels; D005112:Extracorporeal Circulation; D006801:Humans; D009204:Myocardial Revascularization / Q000379:methods*; D009206:Myocardium / Q000032:analysis; D009711:Nucleotides / Q000032:analysis; D010477:Perfusion; D011312:Pressure
D009711:Nucleotides