Unruptured ventricular septal wall dissection. A case report.

Dissection of the interventricular septum (IVS) is a rare condition, which can uncommonly complicate an acute myocardial infarction (AMI). We describe a case of unruptured IVS dissection observed 16 days after 2 close episodes of AMI. The diagnosis was made by transthoracic echocardiography. An echo-free space within the thickness of IVS, extended from the apex to the mid-portion, for a total length of about 30 mm was evident. The careful examination of the left ventricle did not reveal any discontinuity of the myocardial wall. The stable clinical condition, the absence of flow within the dissection, the demonstration of its favourable evolution during the hospitalisation and the characteristics of the underlying coronary disease (left anterior descending artery occlusion without myocardial viability) led to the decision of avoiding surgery. The predischarge contrast echocardiographic examination (Levovist) showed clearly the border of the infarcted zone and demonstrated an area reduction and echogenicity increase of the neocavitation, with partially organised thrombi. The patient recovered uneventfully and was discharged on medical therapy with a clinical and echocardiographic follow-up program. We believe that for IVS hemorrhagic dissection a nonsurgical option can be proposed; surgery should only be considered for myocardial revascularization when indicated. A close echocardiographic follow-up is mandatory.

Effects of adenosine and defibrotide adjunct to a standard crystalloid cardioplegic solution.

AIM: Adenosine has many actions potentially useful as adjunct to a cardioplegia. Defibrotide was recently shown to have protective effects during cardiac arrest. The aim of this study was to compare these 2 substances to delineate their profile of action in the setting of cardioplegic arrest. METHODS: A Langendorff model for isolated rat hearts was employed: 3 groups of 8 hearts each were used, respectively with plain St. Thomas cardioplegia as control (group C), and the same solution added with adenosine (group A) or defibrotide (group D). The hearts had a baseline perfusion for 30 minutes with Krebs-Henseleit solution at 37 degrees C, cardioplegia administration for 3 minutes, then 30 minutes of ischemia without any perfusion and finally 30 minutes of reperfusion with Krebs-Henseleit solution at 37 degrees C. RESULTS: The time to attain heart arrest was 20% shorter in group A, but this difference did not reach statistical significance (A: 13.6+/-1.5; D: 16.8+/-2.7; C: 17.3+/-2.2 s). The heart rate during reperfusion in group A was almost identical to baseline, while in both group C and D it was significantly lower (A: 101%, D: 93.4%, C: 82.4%, p<0.01).A and D decreased significantly the release of creatine phospokinase compared to group C (p=0.006). Lactate dehydrogenase release was lower in both treatment groups, although statistical significance was not reached. Peak positive dP/dT decreased more in controls during reperfusion (A: -23+/-6%, D: -17+/-5%, C: -31+/-5%, p=ns). Negative dP/dT was significantly worse in controls compared to both treatments (A: -19+/-6%, D: -12+/-5%, C: -34+/-7%, p=0.035). CONCLUSIONS: Both adenosine and defibrotide have protective effects in an isolated model of cardioplegic arrest. Adenosine is significantly more active on heart rate while defibrotide is more active on contractily. Further studies are justified in order to test the combination of these 2 drugs.