Stroke Associated With Myocardial Infarction

8/8/2019 Stroke Associated With Myocardial Infarction

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Strokeassociated withmyocardial infarction

Stroke associated with myocardial infarction

By: David Tanne and Solomon Behar ICD Code Acute myocardial infarction:410

Other acute and subacute forms of ischemic heart disease:411Old myocardial infarction:412Intracerebral hemorrhage:431Cerebral embolism:434.1

Historical note and nomenclature

Since the early 19th century, several authors have noted theoccurrence of mural thrombi complicating acute myocardial infarction.Virchow postulated that 3 factors predispose patients to thrombosis: (1)injury of the vascular endothelial or endocardial surface, (2) circulatorystasis, and (3) a generalized hypercoagulant state (Virchow 1856). Hereported occlusion of arteries in the brain by thrombi, which seemed tohave originated in the heart, and named this phenomenon "embolism"(from the Greek word for plug).

Gordinier suggested that the sudden arterial plugging of the vesselsof the brain, viscera, or extremities indicates involvement of a branch of the left coronary, whereas signs of pulmonary infarct suggest involvementof the right coronary or its branches (Gordinier 1924). Blumer was amongthe first to extensively discuss the importance of embolism as acomplication of cardiac infarction. He stated that mural thrombi arecommon following cardiac infarction, and that fragments may detach andproduce embolic phenomena (Blumer 1937).

Clinical manifestationsStroke is a well-known, potentially disastrous complication of acutemyocardial infarction. A disorder as complex and heterogeneous as strokemay manifest in a myriad of ways, according to the part of brain involved.Clinical features are insufficiently predictive to reliably distinguish cerebralinfarction from hemorrhage, or thrombotic from embolic occlusion.Features suggestive of embolic stroke, in addition to the presence of arecent myocardial infarction or left ventricular thrombi, are abrupt onset,headache, seizures, evidence for deficits in multiple vascular territories,and embolization to other organs. Most ischemic strokes, after acutemyocardial infarction, involve the anterior circulation and are nonlacunar(Mooe et al 1999). Approximately one-third occur within 24 hours following

admission, whereas about two-thirds occur in the first week after themyocardial infarction (Behar et al 1991; Sloan et al 1997).Symptomatic intracerebral hemorrhage, the most dreaded

complication of thrombolytic therapy, usually occurs during the first 2 daysafter thrombolysis (Gore et al 1995; Gurwitz et al 1998). Patients usuallydevelop a change in the level of consciousness, headache, nausea, andvomiting, in addition to specific focal neurologic deficits, depending on thelocation of the bleeding (Sloan et al 1995). Onset can be catastrophic andrapidly fatal.



Clinical vignette

A 55-year-old, right-handed, white male with past medical history of hypertension and diabetes presented to the emergency room after 2 hoursof severe retrosternal pain radiating to the left arm and associated with

diaphoresis. The initial electrocardiogram was compatible with an acuteonset of an anteroseptal wall myocardial infarction. The patient wastreated with aspirin and intravenous streptokinase and, later,subcutaneous heparin therapy was started. Forty-eight hours aftercompletion of streptokinase therapy, he developed nonfluent aphasia andright hemiparesis (more severe in the face and upper extremity). Brain CTrevealed subtle early infarct changes in the left frontal lobe with noevidence of blood. On transthoracic echocardiography, no left ventricularthrombus was seen, but significant anterior wall motion abnormalities wereidentified. Carotid duplex demonstrated 0% to 15% stenosis in bothinternal carotid arteries. Over the next 48 hours, the neurologic deficitimproved substantially. A repeat brain CT did not reveal any secondaryhemorrhagic conversion, and the patient was discharged on oralanticoagulants for secondary prevention of an embolic stroke.

Etiology

The association between coronary artery disease and stroke can beascribed to a common pathophysiologic antecedent, atherosclerosis. In theclinical setting of acute myocardial infarction and stroke, more specificcause-and-effect relationships occur, such as the appearance of leftventricular thrombi in large anterior infarctions, or homeostatic defectsassociated with thrombolytic therapy. In addition, cardiac dysrhythmias ora decrease in stroke volume during the acute phase of myocardialinfarction can reduce cardiac output to such a degree that hemodynamiccompromise results. Strokes occurring several weeks after myocardialinfarction may be due to chronic left ventricular thrombi, an akinetic leftventricular segment, or left ventricular dysfunction. Indeed, cerebralmicroembolism was detected by transcranial Doppler more often amongpatients with acute myocardial infarction with reduced left ventricularfunction, akinetic segments, or left ventricular thrombi (Nadareishvili et al1999). For every decrease of 5% in the ejection fraction, an 18% increasein the risk of long-term stroke has been found (Loh et al 1997). Otherpotential cardiac causes of stroke, atherothrombotic large vessel diseaseand small-vessel disease, must also be considered (Martin and

Bogousslavsky 1993). It may be difficult to determine the exactmechanism of stroke in many patients, where different pathophysiologicmechanisms may be equally likely.

Left ventricular thrombi occur frequently in the course of acutemyocardial infarction and are associated with an increased embolic risk(Chiarella et al 1998). Although 2-dimensional echocardiography has somelimitations, it is a fairly accurate noninvasive method for detecting leftventricular thrombi.



Such thrombi develop in up to one-third of patients with anterior siteof myocardial infarction, but only in 0% to 5% of patients with inferiorinfarctions. The highest rate of occurrence of left ventricular thrombi isfound in patients with anterior infarcts and a low ejection fraction orcongestive heart failure (Chiarella et al 1998). Overall, the published datasuggest that cerebral embolism occurs clinically within the first 3 months

after myocardial infarction in about 10% of those withechocardiographically evident left ventricular thrombi, although it is oftendifficult to classify acute ischemic events as embolic in patients withadvanced atherosclerotic disease. Mobile thrombi, or those that protrudeinto the left ventricular cavity, appear to have the highest embolic risk.

The occurrence of intracranial hemorrhage complicating acutemyocardial infarction, still a rare event, was exceedingly rare before thethrombolytic era. Intracranial hemorrhage alone, associated withtreatment of acute myocardial infarction, is mostly coagulopathy-inducedand is associated with thrombolytic therapy, or in combination with otherantithrombotic drugs (Simoons et al 1993; Giugliano et al 2001). The maintypes of intracranial hemorrhage observed in this setting are

parenchymatous intracerebral hemorrhage, hemorrhagic transformation of cerebral infarction, or subdural hemorrhage.

Pathogenesis and pathophysiology

Most strokes complicating acute myocardial infarction in patients notreceiving thrombolysis are likely cardioembolic, as indicated by theirassociation with large anterior myocardial infarcts and left ventricularthrombi detected by echocardiography. Left ventricular thrombi usuallyoccur when the anterior wall or apex becomes akinetic or hypokinetic,enlarging the apical zone of intraventricular stasis. Inflammatory changesat the endocardial surface also enhance thrombogenicity. A systemichypercoagulable state may promote thromboembolism early after thecoronary event, whereas residual fresh thrombus may enhancecoagulation during the first 1 month to 3 months. The risk of systemicembolization from left ventricular thrombi depends on the balancebetween factors favoring thrombus formation within the ventricular cavity(endocardial injury, regional circulatory stasis, and activation of theintrinsic coagulation system) and dynamic forces of the circulation thatmay project thrombotic material into the systemic circulation, to produceclinical morbidity. Cardioembolic strokes have a propensity for secondaryhemorrhagic transformation. Hemorrhagic transformation may occur eitherbecause of distal migration of embolic fragments with reperfusion of infarcted tissue or because of collateral circulation.

Hypertensive intracerebral hemorrhages are classically located in thedistribution of perforating vessels and are associated with a number of microvascular lesions, such as Charcot-Bouchard microaneurysms. Withthrombolytic therapy, intracerebral hemorrhages are often large, lobar,and supratentorial, occasionally in multiple compartments and with fluidlevels inside the hematoma (Gebel et al 1998). Accordingly, otherunderlying conditions may contribute to the cause of bleeding, such aspreexisting vascular malformations and, probably more important in an



elderly population, cerebral amyloid angiopathy (Sloan et al 1995). Diversehemostatic derangements, depending on the thrombolytic agent used,dose, protocol of administration, and adjunctive therapy, contribute to thebleeding tendency.

EpidemiologyDevelopment of carotid atherosclerosis closely parallels coronary

atherosclerosis. Many patients with clinically apparent or silent myocardialischemia have coexistent cerebrovascular disease. Conversely, manypatients with cerebrovascular disease have various degrees of coronaryartery disease. Indeed, myocardial infarction is the leading cause of deathin patients who recover from strokes or transient ischemic attacks. Theincidence of stroke during the acute phase, following myocardial infarction,varies considerably between studies. Rates are mostly in the range of 0.8%to 3.2%. Late stroke following myocardial infarction is relatively rare,although patients are still at increased risk during the first 1 month to 2months (Tanne et al 1993). Overall, about 1 in 40 elderly patients willsuffer an ischemic stroke within 6 months of hospital discharge from theiracute myocardial infarction (Lichtman et al 2002).

Compelling evidence advances the notion that thrombolytic therapyreduces mortality from acute myocardial infarction; however, thrombolytictherapy also carries a small, but significant risk of severe bleedingcomplications, including intracranial hemorrhage. Results from placebo-controlled thrombolysis trials demonstrate a shift in type and timing of strokes including more intracranial hemorrhages and less ischemic strokes,and more strokes in the first 2 days after thrombolytic treatment andslightly less thereafter (Anonymous1988; Maggioni et al 1991). In acollaborative overview of large randomized trials, an extra 4 strokes per1000 were associated with thrombolysis versus placebo (Anonymous1994).Compared to thrombolytic therapy, primary angioplasty for acutemyocardial infarction is associated with a significantly lower rate of stroke(Cucherat et al 2001).

In the large-scale thrombolytic trials, the overall reported incidence of stroke during hospitalization for acute myocardial infarction was 0.9% to1.6%, of which intracranial hemorrhage represented 0.2% to 0.9%,depending on the type and dose of agent used (Anonymous1992; Maggioniet al 1992; Anonymous1993); however, caution must be exercised in theinterpretation of these reports, as recording and evaluation of strokes werenot standardized, and variable proportions of strokes were unclassifiable.Furthermore, thrombolytic trials often excluded high-risk individuals(above a certain age, with a history of stroke, or with uncontrolledhypertension), so reported rates may underestimate the true magnitude of this complication. Indeed, in clinical practice, a higher rate of elderlypatients with acute myocardial infarction experienced intracranialhemorrhage (Gurwitz et al 1998; Brass et al 2000). The overall risk of stroke due to thrombolytic therapy in properly selected acute myocardialinfarction patients is low, compared with the impressive reduction inmortality and, thus, is associated with a favorable benefit-risk profile.Indeed, the incidence of early cerebrovascular events among unselected



patients admitted to coronary care units in the prethrombolytic versusthrombolytic eras remained similar, although mortality from acutemyocardial infarction decreased substantially (Tanne et al 1997). Inpatients with acute coronary syndromes without persistent ST-segmentelevation, the incidence of stroke is low, but still associated withsubstantial morbidity and morality (Mahaffey et al 1999b; Cronin et al

2001). Patients undergoing early coronary artery bypass grafting surgery,but not early percutaneous coronary intervention, have a substantiallyincreased risk of stroke (Cronin et al 2001). Nevertheless, many validclinical reasons advocate performing earlier, rather than delayed, coronaryartery bypass grafting surgery.

Prevention

An optimal strategy for managing this potentially catastrophiccomplication of myocardial infarction includes identification of stroke-pronepatients and institution of preventive measures. The main predictors of stroke after acute myocardial infarction are older age, higher heart rate,diabetes, hypertension, anterior site of myocardial infarction, high cardiacenzyme levels, impaired left ventricular function, atrial arrhythmias,coronary angiography or bypass surgery, lack of aspirin use, and priorcerebrovascular disease, peripheral vascular disease, or angina (Behar etal 1991; Mooe et al 1997; Mahaffey et al 1998; Lichtman et al 2002). Thesedata are in accord, in part, with findings that left ventricular thrombi morecommonly complicate anterior infarctions, and that these thrombi,especially if protruding and mobile, are a source of embolization. A usefuland simple scoring monogram for risk assessment in the acute phase wasdeveloped based on the results of the Global Use of Strategies to OpenOccluded Coronary Arteries (GUSTO-1) trial (Mahaffey et al 1998). Thestrongest predictor identified for late stroke following myocardial infarctionis chronic atrial fibrillation (Tanne et al 1993). A risk stratification scorewas constructed from the Cooperative Cardiovascular Project for elderlypatients discharged from hospital after an acute myocardial infarction. The6-month stroke admission rate for patients with a score of 4 or higher(equaling 20% of the total sample) was equal to 4% (Lichtman et al 2002).

Anticoagulation with full-dose heparin decreases the risk of leftventricular thrombi in patients with acute anterior myocardial infarction,and may be effective in reducing the risk of embolization in those with leftventricular thrombi. Aspirin reduced the risk of early ischemic stroke byhalf in the ISIS-2 mega-trial (Anonymous 1988). Long-term oralanticoagulant treatment in survivors of myocardial infarction has beenshown to reduce the frequency of stroke by 40% to 50% over a 3-yearperiod (Azar et al 1996; Loh et al 1997). Hemorrhagic complications are anuncommon, but serious occurrence in patients treated with long-term oralanticoagulants, with rates related to the intensity of anticoagulation. Inpatients after acute myocardial infarction, anticoagulation therapy isindicated for embolic stroke prevention, and antiplatelet therapy is amatter of ongoing investigation (Fiore et al 2002; Hurlenet al 2002).Statins reduce the risk of stroke among patients at-risk foratherothrombotic disease (Heart Protection Study Collaborative Group



2002), and preliminary data suggest they may reduce of stroke the riskduring the early period after an acute coronary syndrome (Waters et al2002).

Risk factors for embolic stroke and intracranial hemorrhage followingmyocardial infarction differ. Patients at increased risk of embolic stroke,such as those with large anterior infarctions, may have the greatest

survival benefit from thrombolytic therapy. The risk of intracerebralhemorrhage was reported to increase with the following: age; a history of hypertension, cerebrovascular disease or head trauma; a high dose of thrombolytic therapy; being of the female gender; being of Africanancestry, having a low body weight; high blood pressure on presentation;and excessive prolongation of the aPTT with heparin (Gore et al 1995;Gurwitz et al 1998; Brass et al 2000). Life threatening ventriculararrhythmia and hypofibrinogenemia may play a role in some cases (Sloanet al 1995). Treatment with tissue plasminogen activator or anisoylatedplasminogen-streptokinase activator complex was associated with a higherrisk of hemorrhage than streptokinase (Anonymous1992; Maggioni et al1992; Anonymous1993). The higher than anticipated rate of intracranial

hemorrhage among patients treated with heparin or hirudin in conjunctionwith thrombolysis, in several recent trials, emphasizes the risks of morepotent anticoagulation in combination with thrombolysis. The currentlyrecommended heparin regimen is of lower-dose and is weight-adjusted(Giugliano et al 2001). An analysis, combining data from differentthrombolytic trials, identified 4 independent predictors for intracranialhemorrhage: (1) age over 65 years, (2) body weight below 70 kg, (3)hypertension on hospital admission, and (4) administration of alteplase(Simoons et al 1993). Models for individual risk assessment weredeveloped that can be used early in clinical practice (Simoons et al 1993;Brass et al 2000). Although a history of stroke increases the overall risk of intracranial hemorrhage, preliminary observational data suggest that

thrombolytic therapy may be beneficial in selected patients with acutemyocardial infarction and a history of a nonrecent stroke (Tanne et al1998). Such patients may be treated by primary coronary angioplasty, butthe option of thrombolytic therapy should not be categorically excluded.

Differential diagnosis

Most strokes can be readily recognized. A patient with an acutemyocardial infarction who develops a rapid change in neurologic statusshould be suspected of suffering a stroke. Rarely, other brain disorders (ie,seizure, tumor, subdural hematoma, or demyelination) and somemetabolic abnormalities (ie, hypoglycemia or hypoxemia) may present in asimilar fashion.

Diagnostic workup

The assessment of stroke complicating myocardial infarction should

include substantial efforts to delineate the stroke subtype. Brain imaging(CT scan or MRI) is essential for distinguishing between infarct and



hemorrhage. In trying to determine whether the etiology of a cerebralinfarction following myocardial infarction is indeed of embolic origin or of another etiology (ie, large vessel or small vessel atherosclerotic disease),neurologic features are insufficiently predictive to establish the etiology.Echocardiography and other ancillary tests, such as duplex examination of the cervical arteries and transcranial Doppler, may help define specific

vascular lesions and disease processes responsible for the stroke.A high degree of suspicion is needed when caring for patients treated

with a thrombolytic agent, so that diagnosis can be established as rapidlyas possible. The occurrence of a decreased level of alertness orappearance of a neurologic deficit, particularly during the first 24 hoursafter thrombolytic infusion, should raise suspicion of an intracranialhemorrhage until proven otherwise (Sloan et al 1995). Thrombolytic,anticoagulant, or combined therapies should be discontinued as soon assymptoms and signs are recognized. Coagulation studies should beobtained immediately to document the severity of the coagulopathy, andpreparations for reversing homeostatic abnormalities should be made,although the appropriate management is not clear (Conrad et al 1997).

Emergent CT scan of the brain is necessary to distinguish intracranialhemorrhage from cerebral infarction and other neurologic disorders. Itoccasionally may be difficult to differentiate an intracerebral hemorrhagefrom a cerebral infarction with hemorrhagic transformation.

Prognosis and complicationsStroke, complicating acute myocardial infarction, adversely affects

outcome. An estimated 3-fold in-hospital and long-term mortality wasobserved among patients with a cerebral event, in comparison with thosewithout (Behar et al 1991; Tanne et al 1997). Later strokes (in the yearfollowing hospitalization for the myocardial infarction) were associatedwith 2-fold to 3-fold increased mortality as well (Tanne et al 1993).

Although thrombolytic therapy has little effect on overall strokeoccurrence, it increases the risk of stroke death substantially (Maggioni etal 1991). In the GUSTO mega-trial, 60% of patients with primaryintracerebral hemorrhage died and 25% were disabled, versus 17% deadand 40% disabled with nonhemorrhagic infarcts. In a quality-of-life study,patients with moderate or severe residual deficits showed significantlydecreased quality of life (Gore et al 1995). Strokes were associated with a60% increase in cumulative 1-year medical costs, and follow-up costs weremore than quadrupled for stroke survivors, dominated by the cost of institutional care (Tung et al 1999).

Management

The patient with acute ischemic stroke requires appropriatesupportive care and treatment of acute complications. Following an acutecardioembolic stroke due to a left ventricular thrombi, risk for a recurrentearly embolic event is high. To decide when to start anticoagulanttreatment, one has to balance the benefit of reduction in early recurrent



embolism against the risk of potentiating secondary brain hemorrhage.Cardioembolic strokes have a propensity for secondary hemorrhagictransformation. Large embolic infarcts, as well as infarcts visible on earlyCT scans and with mass effect, are especially prone to secondaryhemorrhage. Most spontaneous hemorrhagic transformations occur within2 days to 4 days of cardioembolic stroke, but are rarely associated with

clinical deterioration. Conflicting evidence exist concerning whetheranticoagulation during this period can result in neurologic impairment and,therefore, no consensus has been reached on the optimum strategy.

In any central nervous system bleeding, early cooperation of cardiologists with neurologists, neurosurgeons, and hematologists willoptimize management decisions. Immediate treatment with protamine (if the patient received heparin), cryoprecipitate, fresh frozen plasma,platelets, and an antifibrinolytic agent should be considered for analgorithm to the management of bleeding complications (Conrad et al1997). Although onset may be catastrophic and rapidly fatal, rapidneurosurgical intervention may be beneficial in selected cases assuggested from the GUSTO I experience (Mahaffey et al 1999a), but

evidence from randomized clinical trials is lacking.

Pregnancy

No information was provided by the author.

Anesthesia

Patients suffering from both acute myocardial infarction and strokeare at an especially high anesthetic risk and, thus, are prone to highperioperative morbidity and mortality. Indeed, those who have suffered arecent myocardial infarction demonstrate high perioperative infarction anddeath. During neurosurgical procedures, the degree and potential forincrease in intracranial pressure are important considerations. The moreinformation available to predict potential intraoperative and postoperativeproblems, the better is the anesthesiologist to avoid or lessen the risk forthose events.

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Stroke Associated With Myocardial Infarction