Cardiac Dysfunction in Neurocritical Care: An Autonomic Perspective

Ibrahim, Mohammad S.; Samuel, Bennson; Mohamed, Wazim; Suchdev, Kushak

doi:10.1007/s12028-018-0636-3

Cited by 12 publications

(10 citation statements)

References 94 publications

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“…Nevertheless, electric isolation of the left atrial appendage has been associated with AIS occurrence [81]. Anticonvulsant agents, neuroleptics, and many other drugs commonly used in the ICU may prolong the QTc interval [82]; particular attention to this possible adverse effect must be paid in AIS patients. It is generally agreed that beta blockers are the cornerstone of medical therapy to reduce sympathetic hyperactivity and prevent cardiac remodeling after myocardial infarction [83], but the literature is inconclusive concerning their use in AIS patients.…”

Section: Other Considerationsmentioning

confidence: 99%

“…It is generally agreed that beta blockers are the cornerstone of medical therapy to reduce sympathetic hyperactivity and prevent cardiac remodeling after myocardial infarction [83], but the literature is inconclusive concerning their use in AIS patients. Beta blockers and alpha-2 antagonists demonstrated positive results for acute treatment of hypertension, while angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers are good options for chronic blood pressure control after AIS [82].…”

Section: Other Considerationsmentioning

confidence: 99%

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Brain–heart interaction after acute ischemic stroke

et al. 2020

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Early detection of cardiovascular dysfunctions directly caused by acute ischemic stroke (AIS) has become paramount. Researchers now generally agree on the existence of a bidirectional interaction between the brain and the heart. In support of this theory, AIS patients are extremely vulnerable to severe cardiac complications. Sympathetic hyperactivity, hypothalamic-pituitary-adrenal axis, the immune and inflammatory responses, and gut dysbiosis have been identified as the main pathological mechanisms involved in brain-heart axis dysregulation after AIS. Moreover, evidence has confirmed that the main causes of mortality after AIS include heart attack, congestive heart failure, hemodynamic instability, left ventricular systolic dysfunction, diastolic dysfunction, arrhythmias, electrocardiographic anomalies, and cardiac arrest, all of which are more or less associated with poor outcomes and death. Therefore, intensive care unit admission with continuous hemodynamic monitoring has been proposed as the standard of care for AIS patients at high risk for developing cardiovascular complications. Recent trials have also investigated possible therapies to prevent secondary cardiovascular accidents after AIS. Labetalol, nicardipine, and nitroprusside have been recommended for the control of hypertension during AIS, while beta blockers have been suggested both for preventing chronic remodeling and for treating arrhythmias. Additionally, electrolytic imbalances should be considered, and abnormal rhythms must be treated. Nevertheless, therapeutic targets remain challenging, and further investigations might be essential to complete this complex multi-disciplinary puzzle. This review aims to highlight the pathophysiological mechanisms implicated in the interaction between the brain and the heart and their clinical consequences in AIS patients, as well as to provide specific recommendations for cardiovascular management after AIS.

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Section: Other Considerationsmentioning

confidence: 99%

Section: Other Considerationsmentioning

confidence: 99%

Brain–heart interaction after acute ischemic stroke

et al. 2020

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“…Concurrently, abnormal sympathetic nervous system (SNS) stimulation of L-type Ca ++ channels triggers frequent after-depolarization. Ultimately, this affects myocardium rhythm and integrity, predisposing to wall motion abnormalities and formation of cardiac thrombus [ 15 , 16 ].…”

Section: Discussionmentioning

confidence: 99%

Cardio-cerebral infarction in left MCA strokes: a case series and literature review

2021

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The objective of this manuscript is to describe the challenges of Cardio-Cerebral Infarction (CCI) treatment and to highlight the variable approaches in management. CCI is a rare clinical presentation of simultaneous acute ischemic stroke (AIS) and acute myocardial infarction (AMI) and poses a therapeutic challenge for practitioners. Each disease requires timely intervention to prevent irreversible damage; however, optimal management remains unclear. We describe three cases of CCI. All three patients presented with symptomatic left MCA (M1) occlusion, with ST elevation myocardial infarction (STEMI) and left ventricular apical thrombus. Fibrinolysis and mechanical thrombectomy (MT) were discussed in all cases, but only one patient received alteplase (0.9 mg/kg) and none underwent MT. Percutaneous intervention (PCI) was done in only one case. The two patients that did not receive thrombolysis were treated with modified therapeutic heparin (no bolus), and all received antiplatelet therapy. Ultimately, all three patients passed away. CCI poses a clinical challenge for physicians including (1) optimal strategies to enable swift mechanical reperfusion to both the brain and myocardium; (2) difference in dosage of thrombolytics for AIS versus AMI; (3) risk of symptomatic intracerebral hemorrhage following administration of anticoagulation and/or antiplatelet therapy; and (4) caution with use of thrombolytics in the setting of acute STEMI due to the risk of myocardial rupture. In the absence of high quality evidence and clinical guidelines, treatment of CCI is highly individualized.

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“…Suggested haemodynamic monitoring for these patients includes ECG, continuous recording of vital signs, and echocardiography [68,70,71]. Some recent trials investigated the potential effect of specific therapies to prevent secondary cerebrovascular and cardiovascular accidents after stroke [72,73]. Amongst these, drugs such as labetalol, nicardipine, and nitroprusside have been recommended to control hypertension during the acute phase of stroke [72], when systolic blood pressure exceeds 180-200 mmHg, while angiotensin-converting-enzyme inhibitors and angiotensin II receptor blockers are advised for the management of chronic hypertension [73].…”

Section: Treatmentmentioning

confidence: 99%

“…Some recent trials investigated the potential effect of specific therapies to prevent secondary cerebrovascular and cardiovascular accidents after stroke [72,73]. Amongst these, drugs such as labetalol, nicardipine, and nitroprusside have been recommended to control hypertension during the acute phase of stroke [72], when systolic blood pressure exceeds 180-200 mmHg, while angiotensin-converting-enzyme inhibitors and angiotensin II receptor blockers are advised for the management of chronic hypertension [73]. A neuroprotective effect of propranolol has been recently demonstrated in experimental settings [11], and beta blockers have been suggested both for preventing chronic remodelling and for treatment of arrhythmias [73].…”

Section: Treatmentmentioning

confidence: 99%

Ischaemic stroke-induced distal organ damage: pathophysiology and new therapeutic strategies

Robba

Battaglini

Samary

et al. 2020

ICMx

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Acute ischaemic stroke is associated with a high risk of non-neurological complications, which include respiratory failure, cardiovascular dysfunction, kidney and liver injury, and altered immune and endocrine function. The aim of this manuscript is to provide an overview of the main forms of stroke-induced distal organ damage, providing new pathophysiological insights and recommendations for clinical management.Non-neurological complications of stroke can affect outcomes, with potential for serious short-term and long-term consequences. Many of these complications can be prevented; when prevention is not feasible, early detection and proper management can still be effective in mitigating their adverse impact. The general care of stroke survivors entails not only treatment in the acute setting but also prevention of secondary complications that might hinder functional recovery. Acute ischaemic stroke triggers a cascade of events—including local and systemic activation of the immune system—which results in a number of systemic consequences and, ultimately, may cause organ failure. Understanding the pathophysiology and clinical relevance of non-neurological complications is a crucial component in the proper treatment of patients with acute stroke.Little evidence-based data is available to guide management of these complications. There is a clear need for improved surveillance and specific interventions for the prevention, early diagnosis, and proper management of non-neurological complications during the acute phase of ischaemic stroke, which should reduce morbidity and mortality.

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Cardiac Dysfunction in Neurocritical Care: An Autonomic Perspective

Cited by 12 publications

References 94 publications

Brain–heart interaction after acute ischemic stroke

Brain–heart interaction after acute ischemic stroke

Cardio-cerebral infarction in left MCA strokes: a case series and literature review

Ischaemic stroke-induced distal organ damage: pathophysiology and new therapeutic strategies

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