A 46-year-old man with atrial fibrillation, hypertension, hyperlipidemia, and diabetes is admitted with unstable angina. He undergoes coronary angiography which demonstrates a 90% stenosis of the mid left circumflex in a left dominant system. A single drug-eluting stent is deployed with an excellent angiographic result, and the patient is given aspirin and ticagrelor. The patient is admitted to the cardiac service and shortly after arriving to the floor reports new onset chest pain. A 12-lead electrocardiogram is performed:
Which of the following is the next BEST step in management?
Correct Answer: C
The 12-lead electrocardiogram demonstrates an inferoposteroapical ST segment elevation myocardial infarction (STEMI) in the context of a recently deployed stent. Stent thrombosis is an uncommon but serious complication that accounts for less than 10% of cardiac deaths following stent placement. Most cases occur within the first 30 days of placement and are independent of the stent type. The presentation is often with myocardial injury, usually with ST segment elevation (mimicking the acute coronary syndrome), or death. Treatment includes urgent coronary angiography with repeat revascularization.
Although the most common cause for stent thrombosis is P2Y12 discontinuation, other risk factors include acute coronary syndrome presentation, diabetes mellitus, side-branch stenting, greater stent length, suboptimal stent apposition. The cumulative rate of stent thrombosis is approximately 2% at 2 years and is similar for both bare metal stents and first-generation drug-eluting stents. A high index of suspicion is key for successful recognition and management.
References:
A 55-year-old male with known coronary artery disease with prior percutaneous coronary intervention of the right coronary artery 2 years prior to presentation, hyperlipidemia, and hypertension presents to the emergency department with 2 days of exertional chest pain which culminated in acute onset of “stabbing” substernal chest pain radiating to the left shoulder. Vital signs on presentation are:
Laboratory studies are notable for a cardiac troponin-T that is undetectable.
A 12-lead electrocardiogram demonstrates normal sinus rhythm, Qwaves in inferior leads, and nonspecific ST segment changes. A plain film chest radiograph is obtained (see figure below).
Which of the following is the most appropriate next step in management?
Correct Answer: B
The constellation of presenting chest pain, hypertension, widened mediastinum, and pericardial effusion must prompt a consideration of acute aortic dissection, even in the context of a presenting syndrome suspicious for unstable angina. Known risk factors for aortic dissection include male sex, history of hypertension, and advanced age, as well as connective tissue disorders. Greater than 90% of patients presenting with a type A dissection (involving the ascending aorta) report chest pain, while only 47% of patients with a type A dissection report back pain. The presenting signs for dissection include hypertension in approximately 49% of all aortic dissection presentations but only 36% of type A dissection. Plain film radiography of the chest can be suggestive but not diagnostic as only 62% of patients demonstrate a widened mediastinum.
Common complications of dissection include:
A high index of suspicion for aortic dissection is required. On examination, an upper extremity pulse deficit and/or blood pressure differential should be evaluated, and so bilateral blood pressure should be measured. Imaging modalities to confirm the diagnosis include computed tomography angiography, magnetic resonance imaging angiography, transesophageal echocardiography, and aortography. While all modalities have >95% sensitivity and specificity, contemporary computed tomography angiography is reported to have a near 100% sensitivity and 98% specificity.
A 66-year-old male with hypertension and hyperlipidemia presents with substernal chest pain. His presenting electrocardiogram demonstrates inferior ST elevations with reciprocal changes in the high lateral leads. Emergent coronary angiography is pursued with percutaneous coronary intervention undertaken on a subtotally occluded right coronary artery. Aspirin, ticagrelor, metoprolol, and atorvastatin are initiated. He is admitted to the intensive care unit for postintervention monitoring after repeat electrocardiogram shows resolution of previous ST segment elevations.
Twelve hours later, the patient develops subacute significant shortness of breath following medication administration. The patient’s oxygen saturation is 99% on room air and his physical exam is unremarkable. A repeat electrocardiogram is unchanged from postintervention. Contrasted computed tomography (CT) of the chest is negative for pulmonary embolism.
Which one of his medications is a potential culprit of his dyspnea symptoms?
Ticagrelor, a reversible and direct-acting oral antagonist of the adenosine diphosphate receptor P2Y12, is an active drug and provides more consistent P2Y12 inhibition than pro-drug clopidogrel. Ticagrelor is associated with dose-related episodes of dyspnea, via an unknown mechanism, and ventricular pauses. As many as 14% of patients initiated on ticagrelor experience dose-dependent dyspnea which is described as “sudden and unexpected air hunger” or unsatisfied inspiration. Ticagrelorrelated dyspnea typically begins within 1 week, but up to one-third may present within 24 hours. It is usually a diagnosis of exclusion after ruling out any other cardiopulmonary cause. This is especially challenging when presentation is soon after acute coronary syndrome. The symptoms resolve with cessation of ticagrelor therapy. Careful attention must be paid at the timing of cessation of ticagrelor and initiation of an alternative P2Y12 inhibitor such as clopidogrel or prasugrel.
A 65-year-old female with hypertension and hyperlipidemia develops substernal chest pressure with dyspnea. Physical exam is notable for the following:
12-lead electrocardiogram reveals the following:
What is the most likely mechanism of this patient’s dyspnea?
The patient presents with a clinical syndrome suggestive of an acute coronary syndrome (ACS). The 12-lead electrocardiogram demonstrates most notably ST segment depressions in the right precordial leads (V1-V3) with prominent R-waves. These findings could suggest a posterior myocardial infarction versus anterior subendocardial ischemia. The presence of prominent R-waves is suspicious for posterior pathologic Qwaves and makes the ST segment depressions more suggestive of infarction. Posterior leads, placed alongside the inferior border of the left scapula (at the same horizontal level as V6), could also be obtained to confirm suspicion of a transmural infarct. Portable echocardiography can be considered to clarify the diagnosis of ST elevation myocardial infarction (STEMI). Early recognition and revascularization are key to managing a posterior STEMI.
The mitral valve has two papillary muscles. The anterolateral papillary muscle receives dual blood supply from the left anterior descending artery and the left circumflex. The posteromedial papillary muscle is supplied only by the posterior descending artery which in most patients branches off the right coronary artery. In posterior myocardial infarctions, attention should be paid to the increased risk of papillary muscle ischemia leading to acute mitral regurgitation. Clinical exam may reveal a holosystolic murmur at the left sternal border with pulmonary edema that corroborates the diagnosis. A murmur, however, may not be heard in up to 50% of cases.
A 96-year-old female is admitted to the intensive care unit for closer hemodynamic monitoring following uncomplicated deployment of a drug-eluting stent to the first obtuse marginal, via the left radial artery, in the context of a presentation consistent with an ST elevation myocardial infarction (STEMI). Four hours postprocedure, the patient develops acute hypotension necessitating vasopressor support.
A 12-lead electrocardiogram is performed.
Compared to her postintervention electrocardiogram, ST segment elevations in leads II, III, aVF, V5, and V6 persist but are less prominent. Otherwise, there are no significant changes. Assessment of her left radial access site is unrevealing.
What is the best next step in management?
Complications of diagnostic coronary angiography and percutaneous coronary intervention that can cause hypotension include coronary perforation leading to cardiac tamponade, access site complications leading to bleeding, or intracoronary artery complications (dissection, stent thrombosis, stent migration) leading to left ventricular dysfunction and impaired cardiac output. In the absence of a clinical syndrome or electrocardiographic evidence of stent compromise, attention should be directed toward the access site which, particularly with radial access, can be visually inspected. In the absence of access site compromise, transthoracic echocardiography should be considered for evaluation of pericardial effusion and mechanical complications of myocardial infarction.
Coronary artery perforation is a rare complication occurring in less than 1% of treated lesions. Perforation can be caused by a wire exiting a vessel or by compromise of the vessel wall by a balloon, stent, or other intracoronary devices. Most cases of perforation are identified intraprocedurally but upward of 13% of cardiac tamponade instances can be delayed and occur within 24 hours after departure from the catheterization laboratory. Intraprocedural perforations can be managed with balloon occlusion of the perforated artery. If tamponade were to develop, emergent pericardiocentesis should be pursued. For delayed presentations, repeat angiography can be considered to identify active extravasation that may benefit from a trial of balloon occlusion or coil embolization.
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