Case of the Month

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Irum Ziauddin, PA-C; Artika Patel Loganathan, PA-C

The authors are PAs practicing in cardiology at Walter Reed Army Medical Center, Washington, DC. They have indicated no relationships to disclose relating to the content of this article.

CASE

The patient is a 61-year-old hospitalized male who experienced sudden onset of chest pressure and mild shortness of breath while lying in bed. He described the pain as substernal chest pressure or tightness with radiation to the left arm. The pain did not change with position or breathing. The patient denied nausea, vomiting, lightheadedness, or palpitations. Before the onset of symptoms, he was hemodynamically stable and asymptomatic.

History Five days previously, the patient arrived at the hospital with an acute ST segment elevation MI involving the anterior wall. He underwent emergent coronary angiography, which revealed 100% occlusion of the proximal left anterior descending artery. Two drug-eluting stents (DESs) were placed. Afterward, the patient’s ECG revealed post-MI evolutionary changes of resolving ST elevations with associated T wave inversions.

Examination The patient was afebrile. His heart rate was 95 beats per minute; BP, 99/60 mm Hg (left arm) and 95/62 mm Hg (right arm); respirations, 18 breaths per minute; and oxygen saturation, 98% on 2 L of oxygen administered by nasal cannula. The patient was an alert but anxious, thin male in mild distress, with no jugular venous distention and no carotid bruits. The cardiac examination revealed tachycardia with regular rhythm, normal S₁ and S₂, and no audible S₃ or S₄, murmurs, or rubs. The lungs were clear bilaterally; the abdomen was benign; and pulses were 2+ in all extremities without edema. The neurologic examination was nonfocal.

Cardiac enzymes measured at the time of the chest pain were creatine kinase (CK), 482 U/L; CK-MB, 26.1 ng/mL; and troponin T, 3.43 ng/mL. At admission, these were CK, 129 U/L; CK-MB, 5.3 ng/mL; and troponin T, 1.95 ng/mL. The ECG during this episode of chest pain is revealed in Figure 1. A chest film showed a normal mediastinum with no focal infiltrates, effusions, or pneumothorax.

WHAT IS YOUR DIAGNOSIS

Pulmonary embolism
In-stent restenosis
Subacute stent thrombosis
Aortic dissection

DISCUSSION

This patient had subacute stent thrombosis with classic symptoms of angina. The ECG revealed acute anterior 4- to 5-mm ST elevations, and cardiac enzymes were increased from baseline. The ST elevation in V₂ to V₅ indicates acute injury to the anterior wall.

Treatment The patient was given metoprolol (Lopressor), 5 mg IV; and unfractionated heparin, 4,000 U. A continuous eptifibatide (Integrilin) drip was started. During catheterization, the stents were found to be 100% thrombosed. Balloon angioplasty was performed, resulting in 0% residual stenosis and restoration of adequate flow. The patient remained stable after the procedure on aspirin, clopidogrel (Plavix), warfarin (Coumadin), a beta-blocker, a statin, and an ACE inhibitor. He was discharged 72 hours later without complications. At 4 weeks after discharge, the patient was doing well, with no residual complaints of chest pain.

Comment Acute stent thrombosis (AST) is generally defined as angiographic vessel occlusion occurring
within 48 hours of stent placement. If occlusion occurs up to 30 days after
the procedure, it is classified as subacute. AST typically manifests as severe
chest pain associated with ST elevations on ECG.

DESs and bare metal stents have been found to have similar incidences of stent thrombosis, although DESs have significantly reduced the occurrence of restenosis.¹ Recent studies have suggested that DESs are associated with higher incidences of late-occurring acute thrombosis (particularly due to early cessation of antiplatelet therapy).² However, newer trials suggest significant benefit to DESs with no increase in 5-year mortality rates when these devices are used with appropriate antiplatelet therapy.³ JAAPA

Erich Fogg, PA-C, MMSc, department editor

REFERENCES

	1.	Moses JW, Leon MB, Popma JJ, et al. Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery. New Engl J Med. 2003;349(14):1315-1323.
	2.	Pfisterer M, Brunner-La Rocca HP, Buser PT, et al, for the BASKET-LATE Investigators. Late clinical events after clopidogrel discontinuation may limit the benefit of drug-eluting stents: an observational study of drug-eluting versus bare-metal stents. J Am Coll Cardiol. 2006;48(12):2584-2591.
	3.	Lagerqvist B, James SK, Stenestrand U, et al. Long-term outcomes with drug-eluting stents versus bare-metal stents in Sweden. New Engl J Med. 2007;356(10):1009-1019.