Approximately 1 million patients are now treated annually in the United States with drug-eluting stents (DES). Usage of these stents is substantiated in many patient and lesion subsets by their documented relative safety and reduction in clinical restenosis in large-scale randomized clinical trials.^1,2 Such trials cannot be feasibly performed in all groups of patients. The pathology of atherosclerosis in saphenous vein grafts (SVGs) differs somewhat from that in native coronary arteries, and restenosis after bare-metal stenting (BMS) tends to occur more frequently in the former than the latter.³ Although generally considered inferior to well-designed randomized clinical trials, well-designed cohort or case-control studies have recently been found to provide similar results to randomized trials in a variety of clinical situations.^4–6 In addition, they are usually considerably less costly to perform.

More than 400,000 coronary artery bypass graft (CABG) operations are performed annually in the United States, with the saphenous vein graft (SVG) as the major type of conduit.¹ However, surgical revascularization is not definitive, and recurrent angina occurs in 5–10% of patients per year.² While progression of native coronary atherosclerosis explains some of the symptom recurrence, disease of the grafts is a major problem — over 50% of SVGs are severely diseased or occluded after 10 years.^3,4 Because re-do CABG is associated with significant morbidity and mortality, SVGs now represent 10–15% of the targets for percutaneous coronary intervention (PCI) in most institutions.⁵ However, the optimal stent type for SVG lesions remains undefined.

Conventional angiography is the gold standard in clinical practice for diagnosing atherosclerotic compromise of the coronary artery tree. However, coronary angiography has several known limitations, including a lack of correlation between the percentage of stenosis and the lesion’s physiologic importance¹ and considerable interobserver variability in classifying the lesion’s severity.^2,3

Percutaneous coronary intervention (PCI) is an established therapy for patients with symptomatic coronary artery disease including acute coronary syndromes. In patients presenting with ST-elevation myocardial infarction (STEMI), a considerable body of evidence now suggests that reperfusion with primary PCI provides better short- and long-term outcomes compared to fibrinolytic therapy.^1-3 Although widely adopted as the default strategy for patients presenting with STEMI in developed nations, there are virtually no data on the applicability, success and outcomes of primary PCI in third-world nations, particularly the Indo-Pakistan subcontinent. A few small studies from India have suggested the potential feasibility of primary PCI,^4,5 but had limited follow up and did not have the power to determine predictors of mortality.

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 of reperfusion is extended.^5,6 Therefore, it is valuable to explore some clinically feasible, applicable and effective therapeutic strategies that can address postischemic injury, particularly after long periods of reperfusion.

Current American College of Cardiology/American Heart Association guidelines for the treatment of unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI) recommend initiation of clopidogrel treatment in patients for whom percutaneous coronary intervention (PCI) is planned and who are not at high risk for bleeding.^1,2 Although the guidelines indicate that a loading dose of 300 mg to 600 mg can be used when rapid onset-of-action is required, followed by a maintenance dose of 75 mg/day, the evidence supporting the efficacy of clopidogrel in preventing cardiovascular events in patients with acute coronary syndromes (ACS), including those undergoing PCI, is largely derived from clinical trials which have evaluated the standard loading dose of 300 mg followed by 75 mg/day.

“Alle Ding’ sind Gift und nichts ohn’ Gift; allein die Dosis macht, dass ein Ding kein Gift ist”

[ All things are poison and nothing is without poison; only the dose permits something not to be poison ] – Paracelsus

Although he was born Phillip von Hohenheim, he later changed his name to Philippus Theophrastus Aureolus Bombasticus von Hohenheim, and called himself Paracelsus (literally: equal to or greater than Celsus — a Roman encyclopedist known for medical writings). No, he was not a 15th century version of the artist-formerly-known-as-Prince (glyph), but he is sometimes referred to as “the father of toxicology”, in addition to his other scientific pursuits in medicine, alchemy, astrology and occultism. He covered a lot of ground. But he was absolutely right in observing that pushing the dose of an otherwise therapeutic substance can have adverse consequences.

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 alcohol thrown in, losing even a not-too-substantial side branch could well be the turning point on the mortality curve. Sometimes the situation demands that the sacrifice be made for “a greater good”, and that’s fair enough.

Protein-losing enteropathy (PLE) is a serious, and if not treated, fatal complication of the Fontan-cavopulmonary anastomosis procedure.¹ It has been suggested that creation of a fenestration may prevent² and treat^3,4 PLE in this setup. Other therapeutic modalities have included the use of heparin,⁵ spironolactone,⁶ steroids and angiotensin-converting enzyme inhibitors with variable success.⁶ Transcatheter interventional procedures have been thought to be beneficial in the treatment of PLE, but experience in this modality is limited.⁴

We report rapid reversal of PLE following stents therapy to relieve recurrent coarctation of the aorta and left pulmonary artery stenosis in a child who underwent the Fontan procedure for hypoplastic left heart syndrome.

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 Operation)⁶ was subsequently documented. The occurrence of PLE in Fontan patients was first reported in 1980.⁷ Subsequently, a number of other authors reported PLE following the Fontan procedure.