The Bern Heart and Brain Interaction Study - Interaction Between Brain and Heart in Acute Ischemic Stroke

Acute ischemic stroke is caused by blockage of blood vessels in the brain. This obstruction may be due to the presence of a blood clot, which prevents the passage of blood. Because the brain is under-irrigated, nerve cells lack oxygen and nutrients and can die, which can lead to brain function disorder.

Blood vessels can be obstructed by several different mechanisms and identification of this cause is essential to minimize the risk of recurrence. For instance, it may be a blood clot that originally formed in the heart, which breaks off and is carried away by the blood flow into an artery of the brain, which it blocks. The formation of such a clot can be caused by a heart attack, as a heart attack causes reduced mobility of certain parts of the heart, which greatly increases the risk of clot formation. At the same time, a stroke can also induce cardiac changes, for example because of the production of stress hormones secreted during a stroke. These cardiac changes due to stress hormones can greatly look like cardiac changes caused by a heart attack.

As a consequence, when a stroke is caused by a heart attack, it is often very difficult to correctly diagnose the heart attack and therefore treat patients properly. Indeed, symptoms and effects of a stroke and a heart attack may be similar, although these are two completely different medical problems. In order to gain additional knowledge, the investigators aim with this study to make the diagnosis of a heart attack more precise in patients suffering from a stroke.

Hypothesis, primary and secondary objectives:

The investigators postulate that the combination of laboratory, clinical, radiological, echocardiographic and electrophysiological assessments in a predictive score can distinguish myocardial infarction (MI) and neurogenic stunned myocardium (NSM) in stroke patients (MI and NSM defined by cardiac MRI and coronary angiography).

Primary objectives: The primary objective is to assess the prevalence of MI and NSM, with or without wall motion abnormalities, in stroke patients.

Secondary objectives: Secondary objectives aim to develop a predictive score out of laboratory, clinical, radiological (brain MRI), echocardiographic and electrophysiological parameters to identify stroke patients with MI and to distinguish them from patients with NSM.

The project will add important information to the pathogenesis of NSM, the importance of MI in stroke and the clinically relevant question of the management of stroke patients with hsTnT elevations. On one hand, the project offers the chance to improve the identification of patients with relevant coronary sclerosis. The investigators postulate that most of these patients are not identified by current practice. An early identification of these patients is necessary for early treatment and prevention of cardiac events.

On the other hand, the project offers the chance to improve the identification of patients with NSM and to deliver information on clinical relevance of NSM including arrhythmias and wall motion abnormalities. Given the negative association of NSM with outcome after stroke, the identification of NSM patients is the necessary condition for a treatment trial. Beta-blockers could for instance be beneficial for stroke patients with NSM and such a project could have far-reaching consequences on the management of many acute stroke patients in the near future.

• Prevalence of sub(acute) and chronic myocardial infarction in stroke patients with and without elevated hsTnT (≥ 0.015 mg/L) [Time frame: At baseline, 24 hours, 48 hours, 3 months]
• Positive and negative predictive value of the developed predictive score to detect myocardial infarction and neurogenic stunned myocardium compared to CMR and coronary angiography [Time frame: At baseline, 24 hours, 48 hours, 72 hours, 3 months]
• Influence of neurogenic stunned myocardium on neurological outcome (as measured by modified Rankin Scale) [Time frame: At baseline, 24 hours, 3 months]
• Influence of neurogenic stunned myocardium on brain infarct size (as measured by brain MRI) [Time frame: At baseline, 24 hours, 3 months]