In the 1970s potassium cardioplegia was utilized. Cardioplegia minimized the oxygen demands of the heart, thus the effects of ischemia were also minimized. Refinement of cardioplegia in the 1980s made CABG less risky (lowering perioperative mortality) and thus a more attractive option when dealing with CAD.In the late 1960s, after the work of Rene Favaloro, the operation was still performed in a few centers of excellence, but was anticipated to change the landscape of Coronary Artery Disease, a significant killer in the developed world. More and more centers began performing CABG, resulting in  114,000 procedures/year in the USA by 1979. The introduction of PCI did not lead to the abandonment of CABG; the number of both procedures continued to increase, albeit PCIs grew more rapidly. In the following decades CABG was extensively studied and compared to PCI. The absence of a clear advantage of CABG over PCI led to a small decrease in numbers of CABGs in some countries (like the USA) at the turn of the millennium, but in European countries CABG was increasingly performed (mainly in Germany). Research is still ongoing on CABG vs PCI.In the history of graft selection, again the work of Favaloro was fundamental. He established that the use of bilateral IMAs was superior to vein grafts. The following years, surgeons examined the use of other arterial grafts (splenic, gastroepiploic mesenteric, subscapular and others) but none of these matched the patency rates of IMA.
Causes
Causes of Page kidney have appeared to change over time. Initially, the phenomena were most often caused by traumatic injuries, such as contact sports or motor vehicle collisions. More recently, the majority of cases are postprocedural or secondary to mass lesions. Several factors have been implicated as contributory to this change, namely: the more liberal use of high-quality imaging and the increased utilization of invasive procedures. Documented iatrogenic causes include: intra-abdominal surgery, lithotripsy, renal biopsy, and percutaneous endopyelotomy. The biggest shift in cause comes from kidney allograft biopsy, which now accounts for the majority of Page kidney cases. Pathophysiology
Although to date there have not been any studies specific to Page kidney in humans, two studies in animals and known renal physiology provide a likely mechanism. The elevated blood pressure seen in Page kidney is thought to be caused by the activation of the renin–angiotensin–aldosterone system (RAAS). Compression of the renal parenchyma alters intrarenal blood flow, resulting in a localized decrease in blood flow to the affected nephrons. This decrease in blood flow is recognized by the juxtaglomerular (JG) cells and promotes the cleavage of prorenin into renin. Each kidney is surrounded by two layers of connective tissue, the inner renal capsule and outer renal (Gerotas) fascia. These layers thus form two potential spaces where fluid can form, the small subcapsular space and the large perinephric space. The renal capsule is fibrous and does not easily expand. Thus, even a small collection of blood in the subcapsular space can cause mass effect on the renal parenchyma.