Heart-Brain Interactions
Shouri Lahiri
Stephan A. Mayer
INTRODUCTION
The heart-brain interaction is a vital physiologic circuit often implicated in neurologic and cardiovascular injury. Cerebral complications of cardiac procedures and stroke due to atrial arrhythmias represent important causes of neurologic disability. Recent advances and complications of cardiopulmonary support with left ventricular assist device and extracorporeal membrane oxygenation have opened the door to new neurologic diagnostic and therapeutic challenges. Conversely, severe acute brain injury is being increasingly recognized as a cause of catecholamine-mediated myocardial dysfunction, an entity that is known by many names (Table 115.1) but is most accurately described as neurogenic stunned myocardium.
Autonomic storming is similarly caused by exaggerated sympathetic effect after brain injury and is characterized by cardiovascular abnormalities including coexistent hypertension and tachycardia. Neurogenic hypotension in the absence of cardiac dysfunction usually results from abnormal vasomotor tone and is discussed in Chapter 112.
CEREBRAL COMPLICATIONS OF CARDIAC PROCEDURES
EPIDEMIOLOGY
Cerebrovascular injury is one of the most feared complications of cardiac surgery. Ischemic strokes occur in 0.8% to 5.2% of coronary artery bypass graft (CABG) surgeries, although the incidence may be decreasing with more recent publications from 2011 reporting incidence closer to 1.6%. One single-center study of more than 45,000 patients found that 40% of the strokes occurred intraoperatively with the postoperative risk for stroke peaking at 40 hours following surgery. The risk for stroke is greater for patients undergoing CABG with aortic atherosclerosis and concomitant carotid artery disease and the risk is directly proportional to the degree of stenosis. Other risk factors for perioperative stroke with CABG include atrial fibrillation, prior stroke or transient ischemic attack (TIA), and female gender. Cognitive disability in the absence of acute infarct occurs in up to 70% of patients following CABG. The reported incidences of postoperative cognitive decline are widely variable and likely reflect variability of the cardiac procedure itself to differing neuropsychiatric testing methods and control groups.
TABLE 115.1 Synonyms for Neurogenic Stunned Myocardium | |||||
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Atrial fibrillation occurs in up to 40% of patients within a few days following CABG. It occurs in up to 50% of patients after valve surgery and up to 60% of patients following valve replacement plus CABG. Eleven percent of patients develop atrial fibrillation as a late complication of CABG. In the general population, the most common causes of atrial fibrillation are hypertension, coronary heart disease, and rheumatic heart disease, with the latter being uncommon in developed countries. The risk of ischemic stroke due to atrial fibrillation may be stratified using scoring systems such as CHADS2, which incorporate additional risk factors for stroke including heart failure, advanced age, diabetes, prior stroke, female gender, etc. Refer to Chapter 44 for detailed discussion of stroke risk due to atrial fibrillation.
Left ventricular assist device (LVAD) and extracorporeal membrane oxygenation (ECMO) have dramatically changed the therapeutic landscape of severe, medically refractory cardiopulmonary failure. Neurologic complications are, however, common and occur in 8% to 25% of patients with LVADs. In a series from the University of Pittsburgh Medical Center, 61% of LVAD-related neurologic complications were due to embolic strokes and 25% were intracerebral hemorrhages. In another single center study from Columbia University, 14% of patients with LVADs developed neurologic complications of which 81% were either due to ischemic or hemorrhagic stroke. A recent review on LVAD-related bleeding and thrombosis from 2012 found that the incidence of ischemic strokes was 0.04 to 0.13 per patient-year and 0.05 to 0.8 per patient-year and for hemorrhagic strokes. Relatively, little has been reported on the neurologic complications of adult patients on ECMO. In one series, 50% of patients receiving ECMO suffered neurologic injury of which 17% were strokes defined as either ischemic stroke, hemorrhagic stroke, or subarachnoid hemorrhage. The frequency of neurologic events was likely underestimated in this study, as less than one-third of the patients underwent cerebral imaging.
PATHOBIOLOGY
The majority of strokes after cardiac surgery are ischemic, although hemorrhagic conversion of ischemic infarcts is possible. Intraoperative strokes occur due to arterial emboli arising from atherosclerosis of major vessels such as the aorta or carotid arteries or due to cerebral hypoperfusion resulting from intraoperative hypotension or diminished cardiac output. Fat and air emboli may also occur. Transcranial Doppler (TCD) ultrasonography monitoring of the middle cerebral artery has been used to quantify microemboli
during coronary bypass surgery, which in some cases exceed 60 per operation. High-risk periods for embolization include manipulation of the heart and aorta, particularly during aortic clamping and cannulation. No causal relationship has been confirmed between number of microemboli and cognitive decline, although increased burden of new ischemic lesions has been associated with postoperative cognitive decline.
during coronary bypass surgery, which in some cases exceed 60 per operation. High-risk periods for embolization include manipulation of the heart and aorta, particularly during aortic clamping and cannulation. No causal relationship has been confirmed between number of microemboli and cognitive decline, although increased burden of new ischemic lesions has been associated with postoperative cognitive decline.
Postoperative strokes are generally cardioembolic and related to postoperative arrhythmias such as atrial or ventricular fibrillation. Cerebral complications of atrial fibrillation occur due to embolization of thrombus from the left atrium or atrial appendage. Strokes due to atrial fibrillation are more likely to cause large-vessel occlusion and hemispheric injury than embolic sources arising from the carotid arteries. This was demonstrated in a study that showed that cardioembolic etiologies of stroke were 25 times likely to cause hemispheric events than retinal events. The presumed mechanism for this difference is the larger size of cardioembolic particles compared to emboli arising from the carotid arteries.
LVADs pose extraordinary challenges related to coagulopathy. Although anticoagulation is required to decrease risk of device thrombosis and thromboembolism, this comes at the cost of increased hemorrhagic complications. Furthermore, high-shear stress conditions related to LVADs are thought to induce an acquired von Willebrand syndrome by mechanical destruction of von Willebrand multimers. As a result, LVAD patients are at higher risk for both hemorrhagic and ischemic strokes. Hemorrhagic strokes in patients with mechanical circulatory devices should raise suspicion for endocarditis. The role of infections and inflammatory milieu on neurologic complications is an ongoing debate in patients both with and without mechanical circulatory devices. In one study of LVAD patients, 42% of cerebrovascular accidents occurred in patients with infections. An elevated white blood cell count was noted in patients with neurologic complications regardless of the presence or absence of infection, although it is unclear whether this represented a stress reaction from acute brain injury. The same study found thromboelastogram abnormalities in periods with infection than without infection suggesting that infection may activate platelet function and contribute to the risk of neurologic injury.
Similar to the LVAD, anticoagulation is required to decrease the risk of ECMO-related thrombosis and thromboembolism. Also analogous to the LVAD, increased platelet activation and consumption due to exposure to foreign surface area is common, further contributing to a bleeding diathesis. The net result is a significantly increased risk of bleeding in up to 40% of patients receiving ECMO. Thromboembolic complications are more common in venoarterial compared to venovenous ECMO, as blood is infused directly to the systemic circulation with the former. Greater risk of retrograde aortic blood flow and stasis of the blood due to worsening left ventricular output also increase the risk of thrombus formation.
CLINICAL FEATURES
The clinical manifestations of post-CABG strokes (or strokes due to atrial fibrillation) reflect the dysfunction of the affected neuroanatomic structures. Approximately 20% of strokes involve the posterior circulation. Symptoms attributable to the posterior circulation such as eye movement abnormalities, behavioral abnormalities, and cortical blindness should raise suspicion for a “top of the basilar” syndrome. Hemiparesis is not an invariable finding of post-CABG strokes, as isolated aphasia syndromes or cortical blindness is also encountered. When hemiparesis is present, it may be limited to hand or fine finger movements and mistaken for a compression neuropathy.
The clinical manifestations of LVAD- or ECMO-related stroke are similar to post-CABG stroke patients. Intracranial hemorrhagic complications related to these devices are more likely to have a more fulminant presentation with impairment in consciousness and rapid progression of symptoms.
DIAGNOSIS
Initial diagnosis of stroke is suggested by history and physical examination and then corroborated by cerebral imaging. The National Institute of Health Stroke Scale is a reliable 15-item scale that is validated as a measure of stroke impairment (see Chapter 15). Computed tomography (CT) of the brain is often used as an initial diagnostic test for intracranial hemorrhage because hyperacute ischemic changes may not be evident. Magnetic resonance imaging of the brain with diffusion-weighted imaging may detect ischemic abnormalities as early as within 3 minutes of symptom onset, however, may be contraindicated in patients with metallic devices such as LVADs and certain pacemakers. Blood cultures, fungal cultures, and transesophageal echocardiograms should be obtained when there is a suspicion for endocarditis and septic emboli and particularly in patients with mechanical circulatory devices. Cerebral angiography may be indicated to diagnose mycotic aneurysms.
TREATMENT
Prevention
It is critical to employ measures to prevent neurologic complications during cardiac surgery. Preoperative evaluation involves assessment of risk factors including carotid stenosis. The risk of stroke during cardiac surgery may be lowered by performing simultaneous carotid endarterectomy. Avoiding relative hypotension during cardiac surgery may improve outcomes. This was shown in a randomized trial of 248 patients where maintaining higher pressures (mean artery pressures 80 to 100 mm Hg vs. 50 to 60 mm Hg) during cardiopulmonary bypass was significantly associated with lower rates of neurologic and cardiac complications or death at 6 months [Level 1].1 Systemic hypothermia at 32°C for closed chamber and 28°C for open chamber procedures during cardiopulmonary bypass may reduce cerebral metabolic rate and prevent ischemia. Transesophageal echocardiogram reduces the risk of intraoperative strokes by enhanced detection of aortic atheroma enabling the surgeon to alter technique to reduce risk of embolization. Electroencephalography can also be used to detect cerebral ischemia during cardiac surgery, although the use of this is debated.
Acute Ischemic Stroke
Thrombolytic therapy is often contraindicated for acute ischemic stroke during the postoperative period and in patients being treated with therapeutic levels of anticoagulation. Strokes occurring due to septic emboli from infected hardware also increase the risk of hemorrhage due to thrombolysis. Alternative reperfusion techniques including endovascular therapies may be considered in the appropriate circumstances. In patients with LVADs or patients receiving ECMO, the benefits of anticoagulation for thromboembolism need to be balanced with the risks of hemorrhagic conversion of ischemic infarct for a given patient based on stroke severity and size. There are currently limited data on the optimal time frame for restarting antithrombotics; however, significant delays in restarting these medications further increase the considerable risk of thromboembolism. Other management strategies of acute ischemic stroke are discussed in Chapter 15.
Intracranial Hemorrhage
Intracranial hemorrhage is primarily a risk of LVAD and ECMO support due to the need for anticoagulation and concurrent risk of brain embolism. Initial management should involve discontinuation of all antiplatelet medications and anticoagulation. Anticoagulation reversal should be strongly considered for life-threatening hemorrhages with the understanding that these interventions may increase the risk of device thrombosis in patients with cardiopulmonary devices. Hemostatic therapy should be tailored to the specific anticoagulant exposure (see Table 38.2). For example, protamine sulfate may be used for heparin-related intracerebral hemorrhage and vitamin K with prothrombin complex concentrate/fresh frozen plasma may be used for warfarin-related intracerebral hemorrhage. Antifibrinolytics and recombinant factor VIIa may also be considered in the appropriate clinical setting. Patients undergoing treatment with LVAD or ECMO should receive platelet transfusions and DDAVP. Blood pressure should be managed as per current guidelines (see Table 38.2). Endocarditis should be treated with antibiotics and surgical evaluation (see also Chapter 63). There is currently limited data on when to restart antithrombotics after intracerebral hemorrhage. A rational approach that balances the risk of hemorrhage expansion with the considerable benefits of thromboembolic prophylaxis based on the individual clinical circumstance is appropriate until further research is available.
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