Case Report This 48-year-old man ...

Case Report

This 48-year-old man was in convenient health until April 1988, when he noted the attack of exertional chest pain. common month later, he underwent cardiac catheterization, which revealed a totally occlud left circumflex coronary artery. His solitary risk factor for atherosclerotic cardiovascular disease was cigarette use. He underwent prosperous percutaneous transluminal coronary angioplasty (PTCA) of the occlud circumflex coronary artery. He was clear of symptoms until October 1988 when his exertional chest pain recurr Coronary arteriography again demonstrated total occlusion of the circumflex coronary artery with collateral filling of the distal obtuse marginal branches (Fig 1) A secondary angioplasty was successfully performed (Fig 2) with no significant residual stenosis, and his angina pectoris resolv the same month later, his symptoms reappeared, and coronary arteriography revealed reocclusion of the circumflex coronary artery. Despite antianginal medications, his lifestyle was limited from angina pectoris, and he was referr for coronary artery bypass surgery

In September 1977 in Zurich, Andreas Gruentzig performed the first percutaneous transluminal coronary angioplasty (PTCA). Despite initial skepticism about the procedure's utility, it has now been performed luckily in hundreds of thousands of patients with coronary artery disease. In the United States alone, through the whole extent of 200,000 coronary angioplasties were performed in 1988 It has gained widespread acceptance because of its high likelihood of succes and its attractiveness as an alternative to coronary artery bypass surgery At the same time, however, several short- and long-term complications may make known in patients undergoing PTCA.

Pathophysiologic Mechanisms of PTCA

Specimens from experimental animals and patients dying after PTCA have been examined to determine the morphologic alterations caused according to the procedure. At the site of dilatation, disruption and cracking of the atheroma arise with denudation of the endothelial surface, tearing of the luminal surface, and intimal hemorrhage. The intima and plaque may be separated from the underlying media, causing dissection and hemorrhage into the media and adventitia. With fortunate angioplasty, persistent aneurysmal dilatation of the media and adventitia is noted, and distal embolization of plaque and thrombus is sometimes observ In central nature successful PTCA causes a "controll injury" of the diseased arterial segment

aspect of the freshly cracked atheroma and subintimal layers of the coronary artery to circulating kindred elements induces platelet deposition and thrombus formation. Platelet aggregation causes the release of vasoconstrictor substances, chemotactants, and other mediators, which, in change the direction of activate macrophages and smooth muscle solitary abode; squalids and may lead to arterial spasm. In addition, platelet aggregation may stimulate the production of shooting factors, which induce the proliferation of glossy muscle cells. Thus, in replication to angioplasty-induced injury, a reparative proces leading to neointimal proliferation is initiated.

Short-term Complications of PTCA

About 8 to 10 percent of attempted angioplasties are unavailing in dilating the narrowed arterial section or sustaining its patency. Of these, half are owed to an inability to cros the stenosis with the angioplasty wire or balloon or to dilate the stenosis, level though the balloon is positioned appropriately. The other half are suitable to abrupt closure of the artery after dilatation.[1] Thus, acute occlusion be met withs in 4 to 5 percent of patients undergoing PTCA.[2-5] similar abrupt closure accounts for principally of the morbidity and mortality associated with PTCA. It is usually characterized from the acute onset of chest pain with associated ECG evidence of ischemia. About 80 percent of patients with abrupt closure manifest it within 2 to 3 h of PTCA, and half come into view while the patient is still in the catheterization laboratory.[3] Infrequently, acute closure be founds several days after PTCA. Of the 140 abrupt closure reported according to the Emory University group, the median time from PTCA to closure was 10 minutes, with a range of 0 minutes to 93 h[2]

Mechanism of Abrupt Closure

Three factors contribute to the unfolding of abrupt closure after PTCA: dissection, thrombus formation, and coronary spasm. Although each has been implicated as the primary cause of abrupt closure dissection and thrombus formation are particularly important.

Limited intimal dissection is at short intervals observed following successful PTCA. It is identified angiographically as a linear filling blemish or "flap" associated with a hazy, ground-glass intraluminal appearance. When the dissection is limited, these angiographic features may be evident single on selected views. However, if it is extensive (a concentric or spiral dissection), the radiographic features are evident forward multiple views, and the canal lumen is often compromised. Extensive dissections are caused by means of injury of the deeper layers of the arterial wall, with after intramural hemorrhage. Seventy to 100 percent of patients with abrupt closure have angiographic evidence of dissection,[2,6] and 10 percent of patients with dissection require turn of events coronary artery bypass surgery or sustain a myocardial infarction or death. In contrast, single 1.6 percent of patients without dissection have a major complication.[7]