If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
Some parents become rather impassioned at their children's sporting events, but for one patient, game day was extraordinarily traumatic. Shortly after arguing with another parent at her daughter's soccer match, a 34-year-old Caucasian woman began experiencing crushing and unrelenting substernal chest pressure. Two hours after the discomfort began, she sought medical attention at the emergency department. On presentation, she was dizzy and nauseous but denied diaphoresis, dyspnea, positional aggravation or alleviation of her pain, orthopnea, paroxysmal nocturnal dyspnea, or edema.
The patient had no history of smoking, heavy alcohol consumption, or illicit drug use. Her family medical history was notable for hypertension and cerebrovascular disease. A review of systems was pertinent for active menstruation at the time of presentation.
On examination, the patient was anxious but in no acute distress. She was afebrile, her heart rate was 85 beats per minute, her blood pressure was 135/58 mmHg, her respiratory rate was 21 breaths per minute, and her oxygen saturation was 98% on room air. She had no jugular venous distension, and her lungs were clear to auscultation bilaterally. Her cardiac rhythm was regular without murmurs, clicks, or gallops, and the point of maximal impulse was nondisplaced. She had no lower extremity edema.
An electrocardiogram (ECG) demonstrated normal sinus rhythm, a normal QRS axis, and anterior upsloping ST segment elevations (Figure 1A), which resolved with sublingual nitroglycerin (Figure 1B). The patient had not had a prior ECG. A chest film showed a normal cardiac silhouette with clear lung fields and no other acute pathologic process. Laboratory data were notable for the following: white blood cell count, 11.5 x 103 cells/uL; hemoglobin, 10.4 g/dL; glucose, 134 mg/dL; troponin I, 0.13 ng/mL (reference range, 0-0.04 ng/mL); and D-dimer, 152 ng/mL (reference range, 0-230 ng/mL).
After the first evaluation, it was believed that the patient's symptoms were unlikely to have been caused by coronary plaque disruption, given her sex and age. On reevaluation 3 hours after presentation, the patient continued to complain of nausea but was free of chest pain. However, her troponin I value had risen to 50 ng/mL, and a repeat ECG revealed deep T-wave inversions in the anterolateral leads (Figure 1C). A cardiology consultation was obtained.
Based on the patient's history, presentation, ECG changes, and the trajectory of cardiac biomarkers, she underwent invasive coronary angiography. Her coronary angiogram showed no significant epicardial atherosclerotic coronary artery disease, congenital coronary anomalies, or any evidence of vasospasm. However, the distal left anterior descending artery was notable for an abrupt decrement in luminal diameter and a ribbon-like appearance suggestive of coronary artery dissection (Figure 2).
Some 0.2%-1.1% of patients undergoing angiography for acute coronary syndrome are found to have spontaneous coronary artery dissection.
The first of 2 proposed mechanisms involves initiation of dissection and hemorrhage by an intimal tear and creation of a false lumen; much like classic aortic dissection. The second is rupture of the vasa vasorum, leading to intramural hemorrhage and medial dissection without intimal tearing.
Subsequent formation of an intramural hematoma could compress the true lumen, causing downstream myocardial ischemia and/or infarction.
Clinical presentation depends on the extent and severity of the dissection and the coronary artery involved. Presenting symptoms range from chest pain alone to frank acute coronary syndrome, ventricular fibrillation, and/or sudden death.
Connective tissue disorders, coronary artery spasm, strenuous exercise, emotional stress, peripartum/postpartum status, use of oral contraceptive pills, and menstruation have all been associated with spontaneous coronary artery dissection.
Recently, fibromuscular dysplasia has also been identified as an independent predictor, implying that underlying systemic vascular abnormalities predispose coronary arteries to dissection, especially in conjunction with precipitating factors such as emotional stress.
Our patient's young age, noncontributory past medical history, and the temporal relationship of chest pain to emotional distress may suggest an initial noncoronary chest pain syndrome. However, dynamic ECG changes and positive troponin levels in such patients should prompt clinicians to investigate nonatherosclerotic causes of coronary ischemia, such as coronary dissection, embolism, or vasospasm. Coronary angiography confirmed that our patient had spontaneous coronary artery dissection of the left anterior descending artery. In many other situations, spontaneous coronary artery dissection is poorly characterized by angiography, as the narrowing caused by the intramural hematoma can be misinterpreted as atherosclerotic disease.
Medical therapy alone can be implemented successfully in stable patients with middle or distal local dissection if the lumen diameter is not limited by more than 50% and coronary blood flow is adequate.
Thrombolytic drugs can cause complications in patients with spontaneous coronary artery dissection; 1 series notes that this treatment route resulted in clinical deterioration severe enough to necessitate rescue percutaneous or surgical revascularization in 60% of patients.
While percutaneous intervention is indicated in limited circumstances, particularly if a single vessel is involved, surgery is the revascularization method of choice when dissection is extensive; for example, when the left main artery, proximal left anterior descending artery, multiple vessels, or complex vessels are involved.
The technical success rate of percutaneous revascularization is only 65% in some series, with failures occurring because guide wires were passed into the false lumen, areas of dissection or hematoma were extended, or the intramural hematoma was displaced.
Retrospective studies show acceptable short- and long-term survival rates in patients who recovered from the initial event after conservative management. The hospital mortality rate in these studies was reported to be 0-4%, and 1-year and 10- year mortality rates were 1.1% and 7.7%, respectively.
For our patient, the risks of percutaneous intervention outweighed potential benefit given the distal nature of the dissection, the relatively small area of myocardial involvement, and the hemodynamic stability of the patient. She was started on aspirin and warfarin and bridged with heparin until a therapeutic international normalized ratio was achieved. Long-term anticoagulation was planned. At discharge, she was asymptomatic, and her ECG changes had resolved. Although medical management provides acceptable in-hospital, short-term, and long-term outcomes, continued close follow-up and patient education are also essential. Our patient has been event-free and continues to do well 3 years after her original presentation.
In summary, spontaneous coronary artery dissection is an important entity to consider when a young female patient with few cardiac risk factors presents with chest pain. Treatment can consist of conservative medical management or invasive—percutaneous or surgical—revascularization. Antithrombotic and antiplatelet therapy is often warranted, but the best overall duration of administration is unclear.
Clinical features, management, and prognosis of spontaneous coronary artery dissection.