Pathophysiology,Diagnosis, and Management of Coronary No-Reflow Phenomenon

Coronary no-reflow phenomenon is a lethal mechanism of ongoing myocardial injury, following successful revascularization of an infarct-related coronary artery. Incidence of this phenomenon is high following percutaneous intervention, and is associated with adverse in-hospital and long-term outcomes. Several mechanisms such as ischemia-reperfusion injury and distal microthromboembolism in genetically susceptible patients and those with preexisting endothelial dysfunction have been implicated. However, the exact mechanism in humans is still poorly understood. Several investigative and treatment strategies within and outside the cardiac catheterization laboratory have been proposed, but have not uniformly shown success in reducing mortality or in preventing adverse left ventricular remodeling resulting from this condition. The aim of this article is to provide a brief and concise review of the current understanding of the pathophysiology, clinical predictors, and investigations and management of coronary no-reflow phenomenon.     

Aortic Delamination—A Possible Precursor of Impending Catastrophe

Aortic diameter is a powerful predictor of adverse aortic events, such as aortic rupture or dissection, forming the basis of prophylactic surgical repair criteria. Limited evidence is available regarding the association of aortic wall thickness (AWT) with these adverse aortic events. We present the case and surgical video of a 73-year-old man with chest pain and an increased AWT, who underwent ascending aortic repair and deep hemiarch placement under deep hypothermic circulatory arrest. Surgical pathology demonstrated evidence of aortic delamination and medial separation, indicative of an impending dissection. The patient recovered uneventfully, and his chest pain ultimately resolved after open repair. In this patient, increased AWT was felt to be the precursor to a potential aortic catastrophe.     

Simian virus (SV) 40 like sequences in cell lines and tumour biopsies from Australian malignant mesotheliomas

Background : Simian virus (SV) 40 sequences have been found in some, but not all studies of mesotheliomas. This virus is known to cause tumours in rodents but its role in human oncogenesis remains controversial.
Aims : The aim of this study therefore was to determine whether SV40 is associated with the development of mesotheliomas in Australia. The absence of the virus or its gene products in tissue derived from mesotheliomas would detract from this possibility.
Methods : We used polymerase chain reaction from three pairs of primers to amplify different regions of the large T antigen from DNA from cell lines and cDNA from both cell lines and an independent set of tumour biopsies from patients with mesothelioma.
Results : We examined five human mesothelioma cell lines that were established in our laboratories. In addition, we examined several tumour biopsies from seven different patients. SV40 like sequences were present in all the cell lines and in at least one sample from each of the patients examined.
Conclusions : The large T antigen of SV40 or an SV40 like virus is expressed in Australian mesotheliomas and therefore could be aetiologically-associated with tumourigenesis. Alternatively, these sequences could be expressed subsequent to the development of the disease.     

The effect of parity on placental weight and birth weight: Interaction with placental alkaline phosphatase polymorphism

The effect of parity on placental weight and birth weight is examined through a series of birth records from an Indian population in Calcutta. Placental weight and birth weight increase with parity, the maximum increment occurring between parities 1 and 2. This is compatible with a hypothesis of sensitization of the mother to foetal, paternally derived, antigens.

The three common placental alkaline phosphatase enzymic genotypes have no effect on determining foetal development.