Preservation Of Coronary Flow Research Articles

Enhanced preservation of the rat heart after prolonged hypothermic storage with the 21-aminosteroid compound U74500A

Background. The formation of reactive oxygen species has been postulated to play a role in the initiation of tissue damage associated with ischaemia/reperfusion injury in donor hearts after hypothermic preservation. The aim of this study was to determine whether addition of U74500A to an aspartate-enriched, extracellular-based cardioplegic solution enhanced function of donor rat hearts after prolonged hypothermic storage. Methods: Excised hearts were ligated to an aortic cannula and immediately perfused retrogradely with oxygenated Krebs' solution. This preparation was then converted from Langendorff to working mode. After a 1-min stabilisation period, baseline measurements of heart rate, aortic flow, coronary flow and cardiac output were performed. Oxygenated cardioplegic solution, with or without U74500A (30 μM), was infused into the coronary circulation. Hearts were stored in the same solutions for 6 or 12 hours at 2–3°C. The hearts were reperfused and haemodynamic measurements were repeated. Water content of the hearts was determined. Results and Conclusions: Addition of lazaroid significantly improved all haemodynamic parameters measured after 12 hours storage and aortic flow at 6 hours storage compared with the untreated and vehicle control groups. The presence of the lazaroid, U74500A, was associated with significantly better preservation of coronary flow and cardiac function in the isolated rat heart after 6 or 12 hours of hypothermic storage. This suggests a novel use for this family of compounds in the transplantation context.

Intracoronary stenting compared with conventional therapy for abrupt vessel closure complicating coronary angioplasty. A matched case-control study

Objectives. A case-control analysis was performed to compare clinical outcome after intracoronary stenting with that after conventional therapy for abrupt vessel closure.Background. Previous studies have demonstrated that stenting after abrupt vessel closure results in marked angiographic improvement and preservation of coronary flow, leading to the anticipation of similar improvement in clinical outcome.Methods. Sixty-one of 92 consecutive patients treated at two clinical sites by intracoronary stenting for abrupt vessel closure were matched, according to angiographic features of closure and estimated left ventricular mass threatened by ischemia, with patients treated conventionally during the 18 months before stent availability. In 33 pairs of matched patients, vessel closure was established; in 28 pairs, it was threatened (coronary dissection or worsening stenosis with preservation of normal anterograde flow). Baseline clinical and angiographic characteristics were comparable in the two matched groups. Patients with indeterminate mechanisms of total occlusion (31%) or dissections <15 mm long (43%) predominated; patients with visible thrombus (8%) or dissections > 15 mm long (18%) were infrequently represented. Stents were successfully deployed in 60 of 61 patients at a median of 52 min (range 3 to 269) after the onset of closure.Results. When compared with conventional treatment, stenting resulted in less residual stenosis (26% vs. 49% diameter stenosis, p < 0.001), a greater likelihood of restoration of Thrombolysis in Myocardial Infarction (TIMI) grade 3 blood flow (97% vs. 72%, p < 0.001) and a reduction in the need for emergency bypass surgery (4.9% vs. 18%, p = 0.02). However, the incidence of Q wave myocardial infarction was nearly the same in the two groups (32% vs. 20%, respectively, p = NS). In the group with stenting, peak creatine kinase level and the frequency of Q wave infarction after established vessel closure increased with the time to stent placement (p = 0.001 and 0.054, respectively); the incidence of procedure-related Q wave infarction in patients who underwent stenting within 45 min of closure was very low (3.9%). In-hospital death occurred in 3.3% of patients in each treatment group. At a mean of 6.3 months of follow-up after hospital discharge, survival free from late cardiac death, myocardial infarction; bypass surgery or coronary angioplasty was 74.9% and 81.3% in the stent and the control treatment group, respectively (p = NS).Conclusions. Although early treatment of established vessel closure by intracoronary stenting was associated with a low incidence of both myocardial infarction and emergency bypass surgery, the likelihood or severity of infarction was not reduced among those in whom stents were implanted later. Patients with threatened vessel closure could not be shown to benefit from stent treatment. These data provide preliminary indications for stent placement in the acute period to be validated in larger randomized studies.

The coronary circulation in human septic shock.

Reversible myocardial depression, manifested by ventricular dilatation and decreased ejection fraction, is common in human septic shock. A proposed mechanism, based on animal studies, is myocardial ischemia resulting from inadequate coronary blood flow. Coronary flow observations have not been reported for human septic shock. To determine whether myocardial depression in human septic shock is associated with reduced coronary flow, thermodilution coronary sinus catheters were placed in seven patients with septic shock for measurements of coronary flow and myocardial metabolism. Four of the seven patients developed myocardial depression. These patients had coronary flow similar to or higher than that of control subjects and similar to that of the other three patients, who did not develop myocardial depression. None of the patients had net myocardial lactate production. In general, compared with values in control subjects, the oxygen content difference (arterial minus coronary sinus) was narrowed, and the fractional extraction of arterial oxygen was diminished. This pattern of disordered coronary autoregulation is analogous to the pattern of arteriovenous shunting in other organs in patients with septic shock. The preservation of coronary flow, the net myocardial lactate extraction, and the increased availability of oxygen to the myocardium argue against global ischemia as the cause of myocardial depression in human septic shock.