Catheterization and Cardiovascular Diagnosis 25230-234 (1992)

Delayed Resolution of Obstructing Thrombus Following Acute Closure

James Marshall, DO, John Mercuro, MD, J. David Ogilby, MD, and William J. Untereker, MD

A case of acute thrombotic closure following percutaneous coronary angioplasty dem- onstrating delayed clearance of obstructing thrombus Is reported. Although common in other clinical scenarios this has not been reported following coronary angioplasty.

Key words: angioplasty, thrombosis, thrombolysis, acute closure, collaterals

INTRODUCTION

The reported clinical experience regarding acute cor- onary occlusion following successful percutaneous trans- luminal coronary angioplasty (PTCA) has implicated three etiological processes: dissection, thrombosis, and spasm [ 11. While pathological and quantitative angio- graphic data suggest the presence of all three processes in varying degrees in the post-PTCA artery [2,3], clinical data suggest that thrombotic occlusion may be charac- terized separately as it is commonly related to clinical (unstable coronary syndrome, discontinuation of hepa- rin) and angiographic markers for thrombosis [ 1,431. Occlusive dissection, however, is probably more a func- tion of mechanical and anatomical factors [6]. As it is common to utilize intracoronary thrombolytics in con- junction with redilation when thrombosis is predomi- nant, decisions regarding emergent aortocoronary bypass for salvage will be linked to the dynamic clinical and arteriographic response to these therapies. However, be- cause of the asynchrony that may exist between satisfac- tory clinical and angiographic responses to thrombolysis and redilation, the decision to operate may occasionally be postponed or avoided. We present a case of acute occlusion that demonstrates these characteristics.

CASE REPORT

A 37-yr-old man was admitted for postinfarction an- gina. Coronary arteriography demonstrated 90% right coronary (with thrombus) and 60% anterior descending stenosis (Fig. 1) with left to right intercoronary collater- als. Adenosine thallium showed inferoposterior reperfu- sion. PTCA was performed on the RCA with an adequate result (Fig. 2), but following heparin discontinuation 24 h later, acute chest pain and ST elevation consistent with thrombotic occlusion occurred. The occluded RCA (Fig. 3) was reopened with several balloon inflations and in- tracoronary Urokinase (185.000 units bolused over 10

min) but required a lengthy procedure due to ongoing thrombosis. At no time were guide catheter damping of arterial pressure or prolonged systemic hypotension ap- parent. The activated clotting time remained greater than 320 sec throughout the procedure. The post-PTCA arte- riogram (Fig. 4) demonstrated large intracoronary thrombi, a degree of diffuse spasm, distal competitive flow, no evidence for occlusive dissection, and Grade I flow [7]. Based on the arteriogram and the time required to establish a tenuous degree of patency, the probability of reclosure was considered high. Because of the pa- tient’s clinical stability and the known presence of col- laterals, however, it was felt that surgery could be per- formed semiurgently the next day. He experienced several anginal episodes that responded rapidly to nitro- glycerin through the evening but stabilized within 24 h. Surgery was postponed and adenosine thallium 72 h later showed inferoposterior reperfusion. On full medical therapy consisting of p blocker, nitrate, calcium blocker, and aspirin preparations, he had no further symptoms and was discharged after 5 days of post-PTCA heparin (FIT greater than 60 secs) and aspirin. There was no post PTCA rise in CK enzymes. Two weeks later, the patient was readmitted with atypical angina and coronary arteriography performed (Fig. 5 ) . Repeat stress thallium was equivocal for ischemia and medical therapy contin- ued with benign follow-up thus far (4 months).

DISCUSSION

Resolution of intracoronary thrombus following thrombolysis and heparin has been previously studied in

From the Cardiac Catheterization Laboratory, Philadelphia Heart In- stitute, Presbyterian Medical Center, Philadelphia, Pennsylvania.

Received February 26. 1991; revision accepted November 4. 1991.

Address reprint requests to James Marshall, D.O., 300 Davisson Run Road, Suite 303, Clarksburgh, WV 26301.

0 1992 Wiley-Liss, Inc.

Delayed Resolution of Thrombus 231

Fig. 1. Right coronary arteriogram demonstrating s8vere stenosis and haziness.

Fig. 2. Post angioplasty result showlng minimal stenosis and small filling defect.

232 Marshall et al.

Fig. 3. Completely and acutely closed vessel postheparin discontinuation.

Fig. 4. Vessel reopened, but large filling defect and Grade I flow were apparent.

Delayed Resolution of Thrombus 233

Fig. 5. Follow-up angiogram shows complete resolution of thrombus and Grade 111 flow.

several clinical scenarios [8-lo]. While an immediate degree of patency from pharmacologic thrombolysis is adequate to accomplish salvage in acute infarction, de- layed resolution of obstructing thrombus is common [8]. Thrombosis causing unstable angina (in native or bypass conduits) may also behave similarly [ 101. Although it is unclear which processes (exogenous and endogenous thrombolysis, heparin potentiation of antithrombin 111, aspirin inhibition of platelet reactions) have the greatest influence on resolution, there is evidence that throm- bolytics and heparin play an important role in angio- graphic resolution in both acute and nonacute settings [8-lo].

Given the angiographic degree of thrombosis in this patient and its physiologic significance (persistent, well- defined collaterals), it seems likely that active thrombol- ysis continued after PTCA. The abnormal adenosine scan 72 h post-PTCA suggests continuing, though in- complete, endogenous thrombolysis (as verified by later angiography) at a time when clinical stability was appar- ent. Although this is a similar phenomenon to that re- ported after thrombolysis for infarctions, we have not seen dramatic resolution of thrombus following failed attempts at PTCA to obtain adequate angiographic pa- tency. The key elements were the limitation of myocar-

dial necrosis afforded by mechanical reperfusion and known intercoronary collaterals as well as apparent ab- sence of occlusive dissection. While collaterals protected against significant necrosis thus permitting time for res- olution of obstructing thrombus, it is possible their pres- ence may have antagonized thrombus resolution [ 1 I]. Although probably uncommon, the scenario depicted here may represent a series of events that an experienced operator may encounter. It seems both likely and inter- esting that delayed thrombolysis eventuated in a success- ful medical outcome.

ACKNOWLEDGMENTS

The authors wish to thank Ms. Debbe Green and De- nise Akers for their expert secretarial assistance.

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