Giuseppe Reale, MD. Catholic University of the Sacred Heart, Gemelli University Hospital – Rome

 “The Heart and the Mind together make a single Continent”, Emily Dickinson wrote in the late 19th Century.

Now, in the 21st, we have “Neurocardiology” dealing with the brain-heart connection, even in the field of stroke. In fact, it is quite common to observe cardiac disturbances following both hemorrhagic and ischemic stroke, such as myocardial infarction (MI), heart failure and arrhythmias1.

The key of this brain-heart connection is object of study. Many mechanisms are described, such as dysfunction of the hypothalamic-pituitary-adrenal axis, catecholamine surge and sympathetic/parasympathetic unbalance, brain blood barrier damage, stroke-related systemic inflammation and gut microbiome dysbiosis2.


Hemorrhagic stroke

Subarachnoid hemorrhage (SAH) and intracerebral hemorrhage are associated with several ECG abnormalities such as: QT elongation, “cerebral T waves”, sinus tachycardia, sinus bradycardia and premature atrial and ventricular beats. Up to 5% of SAH patients will have life-threatening arrhythmias (atrial fibrillation and flutter, ventricular tachycardias)3,4, and ECG abnormalities suggestive myocardial ischemia can be still detected after a year in 80% of SAH and intracerebral hemorrhage patients5. Cardiac Troponin T and NT-proBNP is elevated in in brain hemorrhage patients, and the high levels of circulating myocardial markers are associated with poor outcome6.

Traumatic and spontaneous intracerebral hemorrhage might determine acute cardiac dysfunction in about 7% of patients with no previous history of cardiopathy7. Takotsubo cardiomyopathy, or “stress cardiomyopathy”8, can be seen in SAH patients and is a non-ischemic cardiomyopathy with temporary impairment of the heart muscle.

As described, ECG and myocardial enzymes can give us important clues in hemorrhagic stroke management and prognosis. And do not forget that takotsubo broken heart syndrome sometimes is around the corner.


Ischemic stroke

Around 65% of ischemic stroke patients exhibit ischemic or arrhythmic ECG changes during the first 24 hours after the event9, where atrial fibrillation, QT elongation, non-specific ST segment depression, repolarization and T wave abnormalities are most frequent10. Together with ECG abnormalities, cardiac enzymes can be altered too. Although MI, cardiac arrest and heart failure seem to complicate about 6% of all ischemic stroke, you have probably encountered many ischemic stroke patients with elevated Troponin and NT-proBNP without concurrent heart diseae11,12,13. Takostubo cardiomyopathy can follow an acute ischemic stroke too and usually resolves over the following months together with the neurological functions14.

Several studies suggest an interesting link between insular stroke and cardiac dysfunction. Patients with stroke affecting this area in the brain more often experience adverse cardiac outcomes and heart wall abnormalities, than patients with non-insular stroke1,15,16.

Finally, following a stroke or TIA, you don’t only have an increased risk of new strokes, but also of myocardial infarction and death of other vascular causes17.

When we put this together, we need to consider ischemic stroke as a coronary disease risk equivalent and vice versa t, both in the acute phase and the secondary prevention18

In conclusion, in daily stroke clinical practice it is important to keep in mind the deep brain/heart connection in order not to get lost in this wide Continent.





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