Unstable Angina and Previous Bypass Surgery


Synopsis: Unstable angina in patients with prior coronary bypass surgery is usually due to vein graft disease or thrombus that is refractory to medical therapy.

Source: Chen L, et al. J Am Coll Cardiol 1996;28: 1493-1499.

Unstable angina in patients with previous coronary bypass surgery carries a worse prognosis than in those without prior surgery, but the reason is not known. Thus, Chen et al from the Montreal Heart Institute studied 95 consecutive patients with unstable angina (including non-Q myocardial infarction) who had previous bypass surgery (> 6 months) by coronary angiography within eight days of admission. All the patients received intravenous heparin and oral aspirin, and 46 received streptokinase intravenously in a double-blind placebo-controlled study. In the 79% in whom the culprit vessel could be determined angiographically, it was a vein graft in two-thirds and an ungrafted native coronary in almost one-quarter. Total occlusion occurred in half the vein grafts and one-quarter of the ungrafted native arteries. Thrombus was found in 37% of vein grafts and 12% of ungrafted native coronaries (P = 0.04). No clinical features separated those with culprit vein grafts from those with culprit ungrafted native arteries. Interestingly, the administration of streptokinase did not influence the findings. The age of the vein graft impacted the frequency that it was the culprit vessel vs. a native artery: 53% at less than five years; 76% at 5-10 years; and 92% at at least 10 years (P < 0.01). The investigators concluded that unstable angina in patients with prior coronary bypass surgery is usually due to vein graft disease or thrombus that is refractory to medical therapy.


Although not designed as an angiographic study, the angiographic data from this thrombolysis in patients with unstable angina and previous bypass surgery study is very interesting. Despite up to eight days of aggressive antithrombic, antiplatelet and, in half the patients, thrombolytic therapy, almost half the patients had thrombus present. This is higher than that in TIMI IIIa which performed 90-minute angiography in more than 300 patients with unstable angina. Previous bypass patients were excluded from TIMI IIIa, however. Indeed, it is the presence of the bypass grafts that explains these results. Thrombus was seen in only 12% of the ungrafted coronary arteries and in even less of the grafted arteries, but in 37% of the vein grafts. It is likely that, had these patients all been studied within the first few hours of admission, the incidence of vein graft thrombosis would have been even higher. Thus, the authors cannot be sure that their therapy did no good, only that streptokinase was not effective as studied. This result is consistent with TIMI III which used t-PA and showed no clinical benefit in unstable angina patients, even though modest reductions in coronary thrombus were demonstrated at 90 minutes.

Another interesting feature of their data was the high incidence of completely occluded culprit vessels: 50% of vein grafts and 24% of ungrafted native coronary arteries. Considering the relatively late performance of angiography, this is remarkable in an unstable angina/non-Q myocardial infarction group. These data suggest that the prior revascularization may have provided collateral flow which abrogated the development of Q-wave infarction despite complete culprit vessel occlusion. Interestingly, there were no deaths in this study, and mean left ventricular ejection fraction was greater than 60%. Thus, these patients would be considered successful post bypass patients.

The only clinical feature of predictive value was the age of the vein grafts. Patients with all arterial grafts were excluded and, in those with mixed grafts, the arterial grafts were never the culprit vessel. The older the vein grafts the more likely they were the culprit. After five years, 85% of the culprit lesions were in vein grafts. The next most common culprit source was progression in ungrafted native arteries; it was about half the cases if the operation was less than five years ago, but declined quickly after that. Progression of grafted native arteries was least frequently the culprit and often was distal to the graft site. In about one-fifth of the patients no culprit vessel was discovered.

Although short-term prognosis in this study was excellent, the authors suggested that the previously reported poor outcome of unstable angina in post-bypass patients could be explained by the high frequency of vein graft disease or thrombosis that is particularly refractory to therapy. However, their data could be interpreted differently since complete vessel occlusion was commonly found yet none of the patients had Q-wave infarction. Thus, perhaps they have a better prognosis because of revascularization-ensured collaterals or because intensive antithrombotic and antiplatelet therapy reduced thrombus size and prevented the development of Q-wave infarction. This uncertainty makes it difficult to recommend a therapeutic approach for unstable angina in post-bypass patients. Although the AHCPR guidelines recommend coronary angiography for those with unstable angina and prior revascularization, how to treat vein graft disease/thrombosis is not clear. This study suggests that medical therapy is of little benefit, yet other studies have not shown optimal angioplasty/stent results in diseased or thrombosed vein grafts. Clearly, prevention of vein graft disease is the most desirable course, and the authors suggest that this would be a good group in whom to test new prevention strategies.