కార్డియోవాస్కులర్ డిసీజెస్ & డయాగ్నోసిస్

The prevalence of congenital heart defects (CHDs) in adults has increased during the last decade such that now there are more adults with CHD than children. Advances in the diagnosis and management of CHD appear to be the reason for such a phenomenon. In this review only cyanotic CHD are addressed. The majority are likely to be those that have undergone corrective or palliative surgery, although rarely uncorrected defects may present in adulthood. Pathophysiologic effects of right to left shunt associated with cyanotic CHD are reviewed. Brief description of the anatomy of the most common cyanotic CHD, namely, tetralogy of Fallot, transposition of the great arteries, truncus arteriosus, total anomalous pulmonary venous connection and tricuspid atresia is presented followed by its management at presentation. The residual defects and their long-term effects along with management strategies for each of the above defects during adulthood are reviewed. Adults who did not have surgical correction in childhood should undergo surgical correction, but they may have a higher risk than seen in children.

Mechanical circulatory support by means of Intra-aortic Balloon Pump (IABP) is an established therapeutic means in high-risk patients undergoing coronary revascularization (e.g. due to severe left ventricular systolic dysfunction) or those with cardiogenic shock refractory to medical therapy. Despite its remarkable safety profile, complications during IABP deployment still occur, and may be life-threatening, especially because of the underlying risk of those receiving such device. Indeed, the IABP balloon may occasionally become entrapped in the transfemoral sheath during delivery. We hereby report a case in which IABP entrapment in a transfemoral sheath during initial delivery was successfully managed by means of retrograde wiring with an exchange-length 0.018” guide wire delivered through a transradial sheath. This clinical vignette provides evidence that a simple technical trick (i.e. retrograde tracking of 300 cm guide wire between the IABP shaft and the internal wall of the delivery sheath followed by guide wire externalization) may prove effective and safe in solving this potentially dangerous complication.

Unlike zebrafish and newt hearts, mammalian hearts have limited capacity to regenerate. Upon injury or disease, the adult mammalian hearts form a fibrotic scar. Recently, it was shown that neonatal mouse hearts can regenerate similarly to adult zebrafish hearts. However, this capacity quickly decreases after postnatal day 7 (P7). Understanding the molecular mechanisms underlying neonatal heart regeneration might lead to therapeutic approaches for regenerating adult mammalian hearts. In this study, we utilized an inducible transgenic mouse model to determine the effects of FGF10 growth factor over expression on neonatal mouse heart regeneration/repair. Over expression of FGF10 in myocardium enhanced the expansion of Wt1 positive epicardial cells at 21 days after heart injury through increased proliferation. However, this expansion of epicardial cells did not lead to increased epithelialto- mesenchymal transition or affect fibroblast formation or fibrosis, as seen by vimentin expression, after heart injury. Furthermore, neither continuous nor transient expression of FGF10 did not affect scar thickness or length after heart injury in neonatal hearts. Our results suggest that FGF10 can regulate epicardial cell expansion of neonatal mouse hearts after injury; however, FGF10 alone is not sufficient to cause beneficial effects on heart repair.