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Mechanisms of Late Stroke After Myocardial J Neurol Neurosurg Psychiatry: First Published As 10.1136/Jnnp.56.7.760 on 1 July 1993

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Mechanisms of Late Stroke After Myocardial J Neurol Neurosurg Psychiatry: First Published As 10.1136/Jnnp.56.7.760 on 1 July 1993 76070ournal ofNeurology, Neurosurgery, and Psychiatry 1993;56:760-764 Mechanisms of late stroke after myocardial J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.7.760 on 1 July 1993. Downloaded from infarct: the Lausanne Stroke Registry Rosario Martin, Julien Bogousslavsky, for the Lausanne Stroke Registry Group Abstract Stroke may follow acute myocardial infarc- To assess the potential mechanisms and tion in 3% of the cases,' and left ventricular patterns of late stroke after myocardial aneurysm may be a cause of delayed stroke infarct, 94 consecutive patients with first after myocardial infarction.'2 However, the ever stroke at least three months after most common cardiac abnormality after myocardial infarction (anterior 67%; myocardial infarction is not aneurysm but inferior 12%; widespread 12%) were localised wall akinesia without dilatation. As studied. Systematic investigations were the role of this abnormality in delayed stroke those of the Lausanne Stroke Registry after myocardial infarction is unclear, the aim and included brain CT, extraltranscra- of the present work was to study a group of nial Doppler ultrasound, 12-lead ECG, consecutive patients with first stroke at least three-lead continuous ECG monitoring three months after myocardial infarction to for at least 24 hours after admission, and assess the potential mechanism and patterns transthoracic two dimensional echocar- of stroke in these patients. We assessed coex- diography. All patients had an akinetic isting potential causes of stroke and com- left ventricular segment, but only 11 pared the findings with those in patients with (12%) had a visible thrombus. Eleven stroke but without akinetic left ventricular (12%) of the patients had long standing segment and in patients with another poten- hypertension and a small deep infarct so tial cardiac source of embolism. that lacunar infarction due to small artery disease was as likely to be the cause as cardioembolic stroke. There Methods was severe internal carotid artery disease Patients with stroke at least three months ( > 50% stenosis or occlusion) ipsilateral after myocardial infarction were selected from to the infarct in 20 (21%) of the patients all patients (n = 1802) consecutively included with anterior circulation stroke. A poten- in the Lausanne Stroke Registry, a hospital tial cardiac source of embolism other based computerised prospective registry of than akinetic left ventricular segment patients with first ever stroke (cerebral infarc- was found in 14 (15%) patients, atrial fib- tion or haemorrhage, neurological deficit last- rillation (12%) being the commonest. ing more than 24 hours). The characteristics Only 13 (14%) patients had no potential of this registry have been presented in detail http://jnnp.bmj.com/ cause for stroke other than akinetic left elsewhere.9 ventricular segment. The study group All patients were assessed by at least one was compared with 466 patients with first staff neurologist within six days of stroke. stroke but no akinetic left ventricular Systematic investigations included brain CT segment on two dimensional echocardio- (up to four examinations, the first within graphy, and with 94 patients with first seven days of stroke) with and without con- stroke and a potential cardiac source of trast (except when the patient was known to on September 27, 2021 by guest. Protected copyright. embolism but no akinetic left ventricular be allergic to contrast material), Doppler segment and no history of ischaemic ultrasound with frequency spectral analysis heart disease. Logistic regression analy- and B-mode echotomography (common, sis showed that older age, male sex, external, and internal carotid arteries, verte- hypercholesterolaemia, and vascular bral arteries at the retromastoid level, sub- claudication were significantly and inde- clavian arteries, ophthalmic arteries), Department of pendently associated with stroke after transcranial Doppler, 12-lead ECC, three- Neurology, Centre myocardial infarction. The findings sug- lead continuous ECC monitoring for at least Hospitalier Universitaire, gest that late stroke after myocardial 24 hours after admission, two dimensional Vaudois, Lausanne, infarction may often be a direct con- echocardiography, and standard blood and Switzerland sequence of the sequelae of myocardial urine tests. Cerebral angiography was per- R Martin infarction, but other cardiac formed in selected J Bogousslavsky potential patients. Correspondence to: causes of stroke, large artery disease, Akinetic left ventricular segment was diag- J Bogousslavsky, and lacunar stroke must also be nosed on the basis of two dimensional Department of Neurology, Centre Hospitalier considered. echocardiography. The criteria for akinetic Universitaire Vaudois, 101 1 left ventricular segment were those of the Lausanne, Switzerland. ( Neurol Neurosurg Psychiatry 1993;56:760-764) American Society of Echocardiography.10 Received 19 May 1992 and in revised form Other potential cardiac sources of embolism 17 August 1992. Myocardial wall abnormalities are a recog- included intracardiac thrombus or tumour, Accepted 13 October 1992 nised cause of embolic cerebral infarction.1-8 rheumatic mitral stenosis, prosthetic aortic Mechanisms oflate stroke after myocardial infarct: the Lausanne Stroke Registry 761 Table Number (percentage) ofpatients with risk factors 16 to 95 years)]; (2) with the patients with Previous Without previous Potential cardiac source first ever stroke who were admitted during J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.56.7.760 on 1 July 1993. Downloaded from myocardial myocardial ofembolismlno ischaemic the same period and who had another poten- infarction infarction heart disease tial cardiac source of embolism but no akinet- Total 94 466 94 ic left ventricular segment and no history of Age mean (SD) 64 (10)*t 54 (16) 48 (14) ischaemic heart disease [94 patients, 47 (50 Sex %) men and 47 (50%) women, with a mean men 84 (89)*t 268 (57) 47 (50) women 10 (11) 198 (42) 47 (50) age of 48 (14) years (range 17 to 77 years)]. Hypertension 42 (45)*t 137 (57) 13 (14) We performed statistical analysis of 2 x 2 Diabetes 17 (18)*t 37 (8) 3 (3) Smoking 36 (38) 168 (36) 34 (36) contingency tables using the x2 test (on Hypercholesterolaemia 21 (22)* 55 (12) 10 (11) Fisher's two tailed exact test when the expect- Haematocrit 25 (27) 104 (22) 14 (15) Family history 12 (13) 29 (6) 4 (4) ed number in any cell was less than 5). For Vascular claudication 12 (13)* 17 (3) 3 (3) multiple comparisons, we used the procedure Transient ischaemic attacks 24 (26) 104 (22) 26 (28) proposed by Hochberg for multiple signifi- cance testing." A logistic regression model *p < 0 05 when comparing patients with and without previous myocardial infarction. tp < 0-05 when comparing patients with previous myocardial infarction with patients with was fitted using GLIM software'2 to evaluate another potential cardiac source of embolism without ischaemic heart disease. the presence of risk factors and concomitants as coincidental factors in patients with stroke and akinetic left ventricular segment. and mitral valve, endocarditis, atrial fibrilla- tion, sick sinus syndrome, and global cardiac hypokinesia or dyskinesia. Risk factors and Results concomitants (hypertension, diabetes melli- There were 94 patients with late stroke after tus, current or former oral contraceptive use, myocardial infarction, all with akinetic left cigarette smoking, hypercholesterolaemia, ventricular segment on two dimensional venous haematocrit, history of migraine, echocardiography [84 (89A4%) men and 10 ischaemic heart disease, arrhythmia or vascu- (10.6%) women, with a mean age of 64-5 lar claudication, and family history of stroke (10-2) years (range 34 to 39 years)]. Forty or heart disease), characteristics of the stroke two (44-7%) patients had hypertension, 17 onset, clinical findings, previous transient (18%) had diabetes mellitus, 36 (38 3%) ischaemic attacks (TIAs), functional disabili- smoked cigarettes regularly, and 21 (22 3%) ty, type and cause of the stroke were defined had hypercholesterolaemia. Venous haemot- and analysed following the guidelines of the ocrit on admission was higher than 045 in 25 registry.9 (26-5%) patients, 12 (12.7%) patients had a We studied separately the subgroup of history of vascular claudication, and 12 patients with no alternative cause of stroke (12.7%) had a family history of stroke or other than myocardial infarction sequelae heart disease. When compared with the group [without coexisting large artery disease (as of patients without myocardial infarction, the detected by Doppler ultrasound and B-mode patients with old myocardial infarction were echotomography) and without evidence for significantly older, they were more frequently small artery disease (no lacunar infarct, no men, they more often had hypertension, dia- history of hypertension)], in whom the likely betes mellitus, hypercholesterolaemia, or a http://jnnp.bmj.com/ cause of stroke was cardioembolism. The history of vascular claudication (table). The patients with late stroke after myocardial figure shows the odds ratio with 95% confi- infarction were compared (1) with the dence intervals adjusted for age and sex. patients with first ever stroke who were When compared with patients with another admitted during the same period but who had potential cardiac source of embolism, the no akinetic left ventricular segment on two patients with old myocardial infarction were dimensional echocardiography
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