(Stroke. 1995;26:1697-1699.)
© 1995 American Heart Association, Inc.
Articles |
Thrombus Associated With Mitral Valve Calcification
A Possible Mechanism for Embolic Stroke
From the Section of Cardiology, Department of Medicine, Rush Medical College, Chicago, Ill.
Correspondence to Dr Jeffrey S. Soble, Section of Cardiology, Rush–Presbyterian–St Luke's Medical Center, 1653 W Congress Pkwy, Chicago, IL 60612.
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Abstract |
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 Top Abstract IntroductionCase ReportsDiscussionReferences |
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Background Several studies have demonstrated an association between mitral annular calcification and stroke; however, the pathophysiological explanation remains speculative.
Case Descriptions We describe two patients with cerebral embolism in whom mitral valve calcification was demonstrated by transthoracic echocardiography. In both patients, transesophageal echocardiography identified a mass that appeared to be thrombus on the calcified portion of the mitral apparatus. There was no evidence of a hypercoagulable state or endocarditis in either case. Repeated transesophageal echocardiography after anticoagulation demonstrated resolution of the masses in both patients.
Conclusions These cases support the hypothesis that thrombus formation may be a pathophysiological link between ischemic cerebral events and mitral annular calcification in some patients.
Key Words: cardioembolic stroke • diagnostic imaging • mitral valve • thromboembolism
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Introduction |
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TopAbstractIntroductionCase ReportsDiscussionReferences |
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Calcium deposition on the mitral valve leaflets and annulus is commonly identified by transthoracic echocardiography. MAC is detected by echocardiography in 2.8% of adults1 but in 25% of patients with cerebral embolism.2 Patients with MAC have a twofold increased risk of stroke independent of traditional risk factors3 ; however, the pathophysiological link between MAC and stroke remains speculative. Calcific emboli originating from the mitral annulus have been described but are uncommon.4 5 6 7 Thrombus has been demonstrated on a calcified mitral annulus in a single autopsy case,8 although not in a patient with thromboembolism.9
We describe two patients with cerebral embolism in whom a mass with the appearance of thrombus was identified on a calcified mitral valve using TEE. We propose that thromboembolism may be a pathophysiological link between stroke and MAC in some patients.
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Case Reports |
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TopAbstractIntroductionCase ReportsDiscussionReferences |
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Patient 1
A 74-year-old white woman presented with acute right-sided weakness and aphasia. There was no antecedent history of fever, chills, night sweats, or weight loss. There was no history of atrial fibrillation. Cardiac examination was normal. Neurological examination revealed right-sided hemiparesis involving the face, arm, and leg and a right Babinski sign. There were no clinical stigmata of endocarditis, malignancy, or collagen vascular disease. The ECG revealed normal sinus rhythm. MRI of the brain demonstrated an acute ischemic infarction in the left basal ganglia. Patchy regions of high signal intensity, consistent with infarction, were also noted in the subcortical white matter and cortex in the distribution of the left middle cerebral artery; these areas were enhanced after the administration of gadolinium. Transcranial Doppler ultrasonography demonstrated severely turbulent flow in the horizontal portion of the left middle cerebral artery. Carotid duplex ultrasonography was normal, as was a 24-hour ECG recording. Transthoracic echocardiography demonstrated moderate MAC that extended into the posterior leaflet of the valve. There was no evidence for mitral valve prolapse, myxomatous change, or rheumatic deformity. Doppler interrogation of the mitral valve did not reveal regurgitation or stenosis. Multiplane TEE (Fig 1
) demonstrated a 2-mm mobile soft
tissue density, consistent with thrombus, on the atrial surface
of the calcified posterior mitral valve annulus. This density was only
seen from the distal esophageal position in a 110° imaging plane. No
other potential intracardiac source of embolus was present. The
ascending aorta and aortic arch were free of atherosclerotic debris.
Injection of agitated saline into an antecubital vein did not reveal a
right-to-left shunt. The patient was afebrile, and multiple blood
cultures were negative. The erythrocyte sedimentation rate and
immunoglobulin levels were normal. A lupus anticoagulant was
absent.
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After the patient received 8 weeks of therapy with warfarin (prothrombin time INR, 2.0 to 3.5), multiplane TEE with the same transducer depth and rotation settings revealed complete resolution of the thrombus. She has remained free of symptoms for 10 months on warfarin therapy.
Patient 2
A 47-year-old black woman who underwent excision of a right
frontal lobe grade II astrocytoma with subsequent radiation therapy at
9 years of age experienced a 2-hour episode of aphasia and right-sided
weakness. She had experienced several brief episodes of aphasia without
motor symptoms during the previous 4 years. There was no antecedent
history of fever, chills, night sweats, arthralgia, or weight loss.
There was no history of atrial fibrillation, rheumatic fever,
endocarditis, or drug abuse. Cardiac examination revealed a grade 2/6
holosystolic murmur at the apex. Neurological examination revealed a
left-sided facial droop, slight left-sided weakness, and a left
Babinski sign that had been present since she was 9 years old.
There were no clinical stigmata of endocarditis, malignancy, or
collagen vascular disease.
MRI of the brain revealed an acute ischemic infarction in the left anterior parietal lobe. Carotid duplex ultrasonography, transcranial Doppler ultrasonography, and MR angiography of the intracranial and extracranial vessels revealed no evidence of cerebrovascular disease. A 24-hour ambulatory ECG recording was normal. A transthoracic echocardiogram revealed mild MAC, with focal thickening and calcification of the posterior mitral valve leaflet. There was no evidence of mitral valve prolapse, myxomatous change, or rheumatic deformity. Doppler examination revealed mild mitral regurgitation without stenosis.
Aspirin (325 mg/d) was prescribed; however, a recurrent episode of
aphasia prompted further evaluation. Biplane TEE (Fig 2, top
panel) revealed an 8-mm calcified nodule on the
posterior mitral valve leaflet. A 5-mm mobile soft tissue density,
which appeared to be thrombus, was adherent to the nodule. No other
potential intracardiac or aortic source of embolus was present.
Injection of agitated saline into an antecubital vein did not reveal a
right-to-left shunt. The patient was afebrile, and six sets of blood
cultures, including cultures for HACEK (Hemophilus, Actinobacillus,
Cardiobacterium, Eikinella, Kingella) organisms, failed to demonstrate
growth. The erythrocyte sedimentation rate, complement levels, and
immunoglobulin levels were normal. The antinuclear antibody titer was
mildly elevated to 1:320, in a speckled pattern. Anti-Smith,
anti-ribonucleoprotein, and anti-native DNA antibodies, lupus
anticoagulant, and rheumatoid factors were absent.
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Warfarin was prescribed, and the patient was discharged with a
prothrombin time INR of 2.1. After 8 weeks, repeated multiplane TEE
demonstrated that the diameter of the residual thrombus was reduced to
approximately 2 mm. The intensity of her anticoagulation was increased
(prothrombin time INR >3.0) for 12 additional weeks. Subsequent
multiplane TEE with the same transducer depth and rotation settings
revealed nearly complete resolution of the thrombus (Fig 2
, bottom
panel). She has remained free of symptoms for 14 months on warfarin
therapy.
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Discussion |
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TopAbstractIntroductionCase ReportsDiscussionReferences |
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Calcific changes of the mitral valve are common, especially in the elderly.1 3 4 5 Although several studies have demonstrated an association between MAC and stroke, a causal link has not been established.2 3 4 5 9 10 11 12 13 14 15 Ulceration of the mitral valve endothelium with exposure of underlying calcium has been demonstrated in autopsy studies and may provide a nidus for thrombus formation.6 8 16 In patient 1, we identified an apparent thrombus associated with MAC in a patient with cerebral embolism. In patient 2, the suspected thrombus was associated with a calcified nodule on the posterior mitral valve leaflet.
The contention that the masses identified by TEE represented residual thrombi is supported by their echocardiographic appearance, their resolution with anticoagulation, and the lack of further neurological events with anticoagulant therapy. The negative blood cultures and serological studies do not support the diagnoses of infectious or marantic endocarditis.
Although transthoracic echocardiography demonstrated mitral valve calcification in both patients, the suspected thrombus was only identified by multiplane TEE, which facilitates rapid and thorough interrogation of the mitral value. TEE also was helpful in demonstrating the need for intensification of the anticoagulant regimen in the second patient. It is noteworthy that the small residual mass on the mitral annulus of the first patient was seen only by multiplane TEE in the 110° imaging plane. It is possible that mitral valve thrombi have not been described in previous small series of TEE in patients with cryptogenic stroke17 18 19 20 because of the rigorous interrogation of the mitral valve required to visualize these masses and the lack of omniplane TEE availability at the time these studies were conducted.
These cases support the hypothesis that mitral valve calcification may serve as a nidus for thrombus formation, leading to embolic stroke. We propose that thrombus formation may be a pathophysiological link between ischemic cerebral events and MAC in some patients. Because stroke and MAC are both common, the appropriate role for TEE to detect thrombus in patients with ischemic cerebral events and MAC identified by transthoracic echocardiography requires further evaluation. Whether antiplatelet or anticoagulant therapy may prevent cerebral embolism in patients with MAC is also unknown and is worthy of further study.
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Selected Abbreviations and Acronyms |
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Received March 10, 1995; revision received May 16, 1995; accepted June 1, 1995.
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References |
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