Anterior Ischemia Secondary to Embolization of the Posterior Descending Artery in a Patient with a Chronic Total Occlusion of th

Case Description. A 45-year-old man with a history of coronary artery disease presented to the Emergency Room of a community hospital with chest discomfort. He reported the onset of intense retrosternal chest pressure with radiation to both arms, associated with shortness of breath and diaphoresis. This discomfort was precipitated by intense manual labor, but was not relieved by rest. He experienced minimal relief from sublingual nitroglycerin administered in the ambulance. He was evaluated and treated with aspirin, heparin, and intravenous nitroglycerin. His electrocardiogram was reportedly significant for ST-segment depression in precordial leads V2-5. Reteplase (Retavase, Centocor, Inc., Malvern, Pennsylvania) was administered. He experienced partial relief of symptoms and resolution of the electrocardiographic changes. He was transferred to our institution for consideration of invasive risk stratification and possible percutaneous coronary intervention. His past medical history was significant for coronary artery disease with prior stenting (in 1996) of the left anterior descending coronary artery, hyperlipidemia, and tobacco use. His only current medication was aspirin. Physical examination was remarkable for a regular heart rate of 76 beats per minute, blood pressure of 140/85 mmHg, respiratory rate of 14 breaths per minute, height of 178 cm, weight of 86 kg, and body mass index of 27 kg/m2. The neck veins were not distended and no carotid bruits were detected. The heart sounds were normal and there were no obvious murmurs, rubs or gallops. The lungs were clear to auscultation. Abdominal and neurological examination was normal. The peripheral pulses were normal and there was no edema of the extremities. Diagnostic coronary angiography revealed critical sequential stenoses of the proximal right coronary artery (RCA) with the distal LAD filling via right-to-left collaterals from the posterior descending artery (PDA). (Figures 1 and 2). The mid left anterior descending artery (LAD) was totally occluded (Figure 3). There was mild non-obstructive disease of the left circumflex artery. Patient management. We elected to proceed with direct stenting of the proximal RCA. The ostium of the RCA was engaged with a 6 French Judkins Right 4 (JR4, Cordis Corporation, Miami Lakes, Florida) guiding catheter. The lesions were successfully crossed with a Hi-Torque Floppy guidewire (Guidant Corporation, Temecula, California) and a 4.0 x 15 mm S670 stent (Medtronic AVE, Inc., Santa Rosa, California) was deployed across the distal lesion at 16 atmospheres. A 4.0 x 9 mm S670 stent was deployed across the proximal lesion at 16 at atmospheres. At this time, the patient complained of intense retrosternal chest discomfort. Angiography revealed a good angiographic result at the site of the stent deployment, but total occlusion of the distal (PDA) (Figure 4). This was assumed to be due to embolization. A RapidTransit infusion catheter (Cordis Endovascular Systems, Inc., Miami, Florida) was placed in the PDA and intracoronary nitroglycerin, adenosine, and sodium nitroprusside were administered. Unfortunately, this did not result in recanalization of the PDA and reperfusion of the collateral vessel to the distal LAD. Similarly, attempts to cross the totally occluded PDA with the Hi-Torque Floppy guidewire and a hydrophilic guidewire (Whisper wire, Guidant Corporation) were unsuccessful. We subsequently elected to turn our attention to the total occlusion of the mid LAD in an attempt to restore flow to the distal vessel. We engaged the ostium of the left main coronary artery with a 6 French XB 3.5 cm guiding catheter (Cordis Corporation) and crossed the total occlusion with the Hi-Torque Floppy guidewire. We directly stented the mid LAD stenosis with a 3.0 x 30 mm Penta stent (Guidant Corporation). This resulted in an excellent angiographic result and relief of chest discomfort (Figure 5). The patient was started on the glycoprotein IIb/IIIa inhibitor, eptifibatide (Integrilin, Cor Therapeutics, Inc., San Francisco, California). Post-procedural medications included aspirin, clopidogrel, metoprolol, simvastatin, and nicotine patches to facilitate smoking cessation. There was no subsequent elevation of the creatine kinase MB fraction or electrocardiographic evidence of acute myocardial infarction (Q-waves). How Would You Manage This Case? James Chesebro, MD Mayo Clinic Jacksonville, Florida Although the figures were not available for coronary anatomy, the end-result of the LAD reperfusion appeared excellent with no ECG evolution or enzyme rise. The presence of collaterals suggests that there was a previous high-grade LAD stenosis. Crossing the LAD occlusion with a Floppy guidewire documents that this was a recent occlusion and shows the value of testing occlusions associated with acute symptoms for revascularization. Our serial angiographic data shows that in previously patent arteries by angiography which progress to total occlusion on a subsequent angiogram, only 17% result in myocardial infarction. Rigorous correction of all coronary risk factors is critical in this young patient with premature CAD, since all risk factors affect the Virchow triad contributing to thrombosis: rheology, substrate and blood. A baseline lipid profile should have been drawn on presentation to determine triglyceride, HDL-C, and LDL-C levels. The simvastatin dose should be a minimum of 40 mg per day. Lowering possible hypertriglyceridemia will usually raise a low HDL-C level. Progressively increased dosing to 2–3 g of niacin per day should be used to raise a low HDL-C ( 20% by adding clopidogrel to aspirin, this combined therapy should empirically be continued indefinitely. No mention is made of hyperglycemia, diabetes, homocysteine and lipoprotein (a) levels, all of which should be considered. A cardiac rehabilitation program should be started, since regular exercise reduces all cardiovascular risk factors including hyperlipidemia, diabetes, hypertension and depression. REFERENCES 1. Rauch J, Osende JI, Fuster V, Badimon JJ, Fayad Z, Chesebro JH. Thrombus formation on atherosclerotic plaques: Pathogenesis and clinical consequences. Arn Int Med 2001;134:224–238. 1. CURE Investigators. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation: The Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) trial. N Engl J Med 2001;345:494–502. 1. Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: The PCI-CURE study. Lancet 2001;358:527–533. Lloyd W. Klein, MD Rush-Presbyterian-St. Luke’s Medical Center Chicago, Illinois Although the management of this complex case is ultimately interventional, the optimal intial strategy depends on that paleocardiogenic entity, the electrocardiogram. The information provided describes only ST depressions in V2–V5; there is no note of the presence of reciprocal changes in other leads not the status of the T waves in the precordial leads. The predominant ST changes in these leads suggests that the primary event was anterior not posterior, in location. Upright T waves would suggest a posterior location whereas inverted T waves are more suggestive of an anterior location. These ECG changes disappeared with thrombolysis and partial resolution of chest pain. Non-ST segment elevation MI is best treated with glycoprotein IIb/IIIa inhibitors, and this case should have been managed as such initially, as thrombolytic therapy has been shown to have deleterious effects in this setting. The continued chest pain made acute angiography appropriate. The angiograms show a 100% mid-LAD occlusion, the morphology of which is not inconsistent with acute occlusion, and two tandem, borderline severity, eccentric right coronary stenoses, both of which have overhanging edges suggesting acutely ulcerated plaque. The onset of the episode was associated with manual labor, which is consistent with the morphology in both vessels. There are collaterals to the mid and distal LAD seen in Figures 1 and 2, traditionally interpreted as evidence that the LAD occlusion is chronic, but which is often seen with acute occlusion as well. On the basis of LAD collaterals in the absence of a definitive LAD thrombus and two ulcerated RCA lesions in association with the ECG pattern described above, the operators erroneously diagnosed posterior injury and proceeded with RCA PCI. Alternatively, they may have believed that this was an instance of “ischemia at a distance”, in which subtotal RCA closure threatened the anterior wall by decreasing collateral flow. However, the most plausible explanation, particularly in view of subsequent events, is that both LAD and RCA stenoses were active, as reported by Goldstein and colleagues (N Engl J Med, 2000). In this scenario, the initial presentation was caused by acute LAD occlusion, but the presence of collaterals prevented a full-blown ST elevation MI; the two RCA lesions were possibly active “bystanders” with acute plaque rupture but without flow limitation. Choosing the RCA as the first vessel to attempt was not prudent, regardless of whether the operator thought the LAD or the RCA was the infarct vessel. If the LAD was the infarct vessel, it should have been opened immediately. If the RCA was the infarct vessel, the LAD still should have been attempted first, as acute closure or distal embolization (as did occur) of the RCA could be catastrophic. The subsequent occurence of macroembolization to the PDA lends credence to the multiple active stenoses concept, and emphasizes the importance of glycoprotein IIb/IIIa inhibitors in the acute setting. Although no thrombus was visualized angiographically in the RCA, an ulcerated lesion in an acute coronary syndrome is almost always associated with thrombus, and this possibility should have been anticipated since angiography poorly identifies small thrombi. Multiple doses (> 5) of adenosine and nitroprusside are often required to recanalize the artery. Proceeding with LAD PCI in this circumstance was absolutely necessary, as the iatrogenic MI in progress is located anteriorly due to the loss of collaterals superimposed on the spontaneous event. The resolution of pain and absence of any enzymatic rise with the re-establishment of antegrade LAD flow proves the wisdom of this approach. William W. O’Neill, MD William Beaumont Hospital Royal Oak, Michigan This 45-year-old gentleman presents with an enormously challenging clinical and angiographic problem. Historically, it would be important to try to time the duration of LAD occlusion. Since the patient appears to have had an adequate anginal warning system, it is unlikely that the LAD coronary occlusion is more than one day old (the length of the patient’s symptoms). The patient presented to the Emergency Room with prolonged chest pain suggestive of an evolving acute myocardial infarction. His ECG, however, did not demonstrate the typical ST elevation that is usually seen with sudden total coronary occlusion. Marcus DeWood published two seminal papers in the early 1980s concerning the angiographic findings of patients presenting with ECG changes and acute MI. The first work in which he described the high prevalence of total coronary occlusion in patients with ST elevation AMI formed the scientific underpinning for repercussion therapy.1 The second paper received less attention; in it, DeWood described the findings in patients with non-Q MI.2 He described a high prevalence of subtotal coronary occlusion or total occlusion with well developed angiographic collaterals. Our patient presented with prolonged symptoms compatible with acute MI, but only ST depression in the anterior leads. He had complex disease in the RCA as well. Goldstein recently described the phenomenon of multiple culprit lesions in acute MI patients.3 He described an incidence in 30% of patients. Our patient appears to have had multiple lesions that each could have caused the acute MI he was suffering. In order to try and localize the problem, the ECG is important. In this case, the patient had ischemia/injury in his anterior ECG leads. A contrast ventriculogram would also have been helpful in confirming the location of cardiac injury. There are two anatomic bases for anterior ischemia in this case. The first and most likely is that the patient developed total occlusion of the LAD, and he had such well developed collaterals, that he did not develop ST elevation (as DeWood described twenty years ago). A second, less likely scenario is that the LAD occlusion was in fact chronic and the RCA lesions were causing “watershed” ischemia. There is no doubt that the RCA was critical as a collateral source to the LAD, and I don’t disagree with attempts to recannalize this vessel. I would have made an initial probe of the LAD first. It appears that the lesion in the LAD was very fresh, because it was easily crossed with a floppy guidewire. In the end, one can never be truly certain how fresh an occlusion is until an attempt is made to cross it with a guidewire. I think if the LAD had been tried first, it would have been obvious that it in fact was the culprit. Whether attempts at crossing the second vessel should have been undertaken at that point is debatable. In the end, these acute cases can be incredibly complex to sort out, I do think that use of ECG and contrast ventriculogram can be very helpful in localizing and treating acute coronary culprits. References 1. DeWood MA, Spores J, Notske R, et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med 1980;303:897–902. 2. DeWood MA, Stifter WF, Simpson CS, et al. Coronary arteriographic findings soon after non-Q-wave myocardial infarction. N Engl J Med 1986;315:417–423. 3. Goldstein JA, Demetriou D, Grines CL, et al. Multiple complex coronary plaques in patients with acute myocardial infarction. N Engl J Med 2000;343:915–922.