Antithrombotic Therapy for Cerebrovascular Disorders: Echocardtographic Finding

Antithrombotic Therapy for Cerebrovascular Disorders: Echocardtographic FindingThe yield of echocardiography in identifying potential cardioembolic causes of ischemic stroke/TIA varies widely in the recent literature depending on the patient population and criteria for a cardioembolic source. For example, many authors include mitral valve prolapse (MVP) as a cardioembolic source, while others do not. Using a restricted criteria, about 10% (range 4-16%) of patients with ischemic stroke will have a potential embolic source by echocardiography (Table 1). Of these patients will have other clinical manifestations of heart disease; the yield of echocardiography for embolic sources in ischemic stroke/TIA patients is only 1-2% (range, 06%) (Table 1). In younger stroke patients without cerebrovascular disease, the yield is higher. Prolonged ECG monitoring (via telemetry or ambulatory Holter monitoring) in acute ischemic stroke/TIA patients detects unsuspected, potentially embologenic arrhythmias (AF, sick sinus syndrome) in about 2% (range, 0-4%) of patients in recent reports. there

Controversy continues to surround the issue of which ischemic stroke/TIA patients should be evaluated with echocardiography, as the yield for definite cardioembolic sources is low (1-2%) in the subset of 40% without other clinical evidence of heart disease. Vigorous efforts to define stroke/TIA mechanisms are warranted, as stroke is a seriously disabling and sometimes lethal disorder, and preventive strategies are critical. Further, management of cerebral ischemia cannot be undertaken in isolation, ignoring concomitant heart disease that usually limits life. Evaluation and optimal management of coexistent cardiac disease is important in all patients with brain ischemia, cardioembolic or due to other mechanism. We recommend that echocardiography be performed liberally in patients with threatened stroke in whom cerebrovascular mechanisms are deemed unlikely. Prolonged ECG monitoring may be limited to high-risk patients (eg, palpitations, suspicious standard ECG) and/or those without definition of stroke mechanism after a thorough evaluation who have clinical features compatible with cardioembolic stroke.

Table 1—Echocardtographic Finding,i in Stroke FaHents: Recent Series

Authors Av. %(+)t % Cardiac Thrombus % Mitral Stenosis % LV Aneurysm % Other (+) %MVP %MAC %N1
Pop* Age No.
Bogousslavskyetal TIA 63 215 4 2 0.5 2 1 3 4 56
( + )HD 75 11 35
(-)hd 140 0.7 67
Rem et al Stroke/TIA 64 127 6 5 ? 2 2 7 5 44
Fogelholm et al Stroke/ITA 60 97 12 1 1 0 0 9 40
(+) HD 63 16 25
(-)HD 34 6 6 68
Come et al* Echo lab 66 280 16 1 4 7 7 2 65
( + ) HD 173 25 53
( —) HD 107 2 1 1 86
Robbins et al Echo lab 60 116 11 4 2 3 3 5
(+) HD 80 16
(-)hd 36 0
Todnemetal Echo lab 51 194 4 0.5 1 2 1.5 2
Nishideetal Stroke/TIA 66 350 15 8 11 ? 2 3 8 63
Gagliardietal Stroke/TIA 43 88 5-11 0 0 ? 2 24 41
(+) CD 27 ? 41
(-)CD 61 7 0 0 3 3 34 41
Good et al Stroke/ITA (”) CD 63 65 2-12 2 0 0 10 2 8 49