A 58-year-old woman is brought to the emergency department because of sudden-onset difficulty speaking and weakness of her right arm that began 45 minutes ago. Her husband reports that she was in her usual state of health until symptoms abruptly developed during breakfast. Her medical history is significant for rheumatic fever during childhood and progressive exertional dyspnea over the past several years. She takes no medications. Temperature is 36.8°C (98.2°F), blood pressure is 142/86 mm Hg, pulse is 118/min and irregularly irregular, respiratory rate is 18/min, and oxygen saturation is 97% on room air. Neurologic examination demonstrates expressive aphasia and right facial and upper-extremity weakness. Cardiac examination reveals a low-pitched diastolic rumble best heard at the cardiac apex with the patient in the left lateral decubitus position. An opening snap is present after S2. ECG demonstrates atrial fibrillation with a ventricular rate of 120/min. Noncontrast CT of the head demonstrates no evidence of intracranial hemorrhage. Transthoracic echocardiography reveals severe mitral stenosis with marked left atrial enlargement.
Which of the following is the most likely mechanism responsible for this patient’s neurologic deficits?
The correct answer is:
B) Cardioembolism originating from the left atrium
This patient has an acute ischemic stroke caused by a cardioembolus arising from the left atrium. Several clues point toward this diagnosis: rheumatic mitral stenosis, marked left atrial enlargement, atrial fibrillation, and abrupt onset of focal neurologic deficits.
Mitral stenosis causes chronically elevated left atrial pressure, leading to progressive atrial dilation. The enlarged atrium provides a substrate for atrial fibrillation, which further promotes blood stasis, particularly within the left atrial appendage. Stagnant blood flow predisposes to thrombus formation, and embolization of these thrombi can cause ischemic stroke, acute limb ischemia, mesenteric ischemia, or other systemic embolic events.
A high-yield Step 2 principle is that rheumatic mitral stenosis and atrial fibrillation represent a particularly high-risk combination for thromboembolic complications. The presence of severe left atrial enlargement further increases this risk.
The murmur described, a low-pitched diastolic rumble with an opening snap, is classic for mitral stenosis and helps identify the underlying cardiac lesion responsible for the embolic event.
Answer choice A: Atherosclerotic plaque rupture within the carotid artery, is incorrect.
Carotid atherosclerosis is a common cause of ischemic stroke, but this vignette provides a much more compelling embolic source. Severe mitral stenosis, marked left atrial enlargement, and atrial fibrillation strongly suggest a cardioembolic mechanism.
Answer choice C: Hypertensive intracerebral hemorrhage, is incorrect.
Intracerebral hemorrhage typically presents with evidence of bleeding on head CT. This patient’s CT is negative for hemorrhage. Furthermore, the clinical scenario strongly supports embolic ischemic stroke.
Answer choice D: Lacunar infarction due to small vessel lipohyalinosis, is incorrect.
Lacunar infarcts are usually associated with chronic hypertension and diabetes mellitus and produce characteristic subcortical syndromes. They are not typically associated with atrial fibrillation or severe valvular heart disease.
Answer choice E: Septic embolization from infective endocarditis, is incorrect.
Septic emboli usually occur in the setting of infective endocarditis and are often accompanied by fever, bacteremia, or valvular vegetations. No evidence of infection is present in this case.
Key Learning Point
Rheumatic mitral stenosis causes left atrial enlargement and predisposes to atrial fibrillation. Thrombus formation within the left atrium can lead to systemic cardioembolism, making ischemic stroke one of the most important complications of advanced mitral stenosis.
