Protein-losing enteropathy (PLE) may be defined as excessive loss of proteins across the intestinal mucosa and is due to either a primary gastrointestinal abnormality or secondary to cardiac disease. Initial reports of PLE secondary to cardiac disease, namely, congestive heart failure,¹ constrictive pericarditis^2,3 and myocarditis⁴ were published in the early 1960s. The association of PLE with high superior vena caval pressure secondary to an obstructed Mustard baffle⁵ and superior vena cava-toright pulmonary artery anastamosis (Classical Glenn Op

Perhaps we interventionists should be more aware than we currently are of our patients’ left ventricular (LV) function or what angioplasty might do to that LV function. I am not suggesting that we don’t attach importance to this vital detail. But let’s face it, most of us don't consciously plan to preserve myocardium at all costs when we are confronted with a difficult bifurcation lesion. To the battle-ravaged ventricle that has endured the torment of hypertension, diabetes, a few previous non-ST-elevation myocardial infarctions (NSTEMIs), along with the regular pulses of

Timely reperfusion is the most effective intervention to protect the heart from myocardial infarction resulting from coronary occlusion. However, experimental studies and clinical observations have provided strong evidence in support of the existence of reperfusion-induced myocardial injury. Reperfusion injury initiates a series of adverse events that offset the benefits intended by implementing early reperfusion.^1–4 Protection elicited by pharmacological treatment applied briefly at the onset of reperfusion may be observed acutely, but may not be evident when the duration