In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

Ventricular arrhythmias in cerebrovascular disease

An article from the e-journal of the ESC Council for Cardiology Practice

The cerebrovascular and the cardiovascular systems are closely related. In neurologic conditions, there is a broad spectrum of cardiac manifestations including both mechanical and electrophysiological dysfunctions. The latter range from non-specific ECG changes to various rhythm disturbances including serious, life threatening, ventricular arrhythmias.

Arrhythmias and Device Therapy

The main underlying mechanism of cardiac abnormalities in cerebrovascular (CV) disease is an abnormal autonomic nervous system function with altered sympathetic and parasympathetic output. The ECG abnormalities in CV diseases are ST elevation or depression, prolonged QT interval, T wave inversion and pathologic Q waves (1).
Hypothalamic stimulation can reproduce the ECG changes that are seen in acute CV disease (2).

The rhythm disturbances that might be seen are torsade de pointes, and other life-threatening arrhythmias, atrial fibrillation, SVT and bradycardia due to sinoatrial block, sinus arrest and AV-Block (3). Other cardiac manifestations are neurogenic pulmonary edema, myocardial damage with cardiac enzymes and troponin elevation -at autopsy, subendocardial hemorrhage and fibrosis have been described.

Subarachnoid hemorrhage

Patients with subarachnoid hemorrhage suffering from life-threatening arrhythmia (VT/VF) have high concentrations of plasma catecholamine, serum CK-MB, myosin light chain and troponin T (4). Fifty percent of patients with subarachnoid hemorrhage have hypokalemia that can lead to arrhythmias.


The control sites of the autonomic function are the insular cortex, amygdala and the lateral hypothalamus. Patients with brain stem infarctions have higher mean plasma NE levels compared to patients with hemispheric infarctions. On the other hand, patients with hemispheric lesions have a higher incidence of cardiac arrhythmias compared to patients with brain stem infarction (5).

There is a cortical asymmetry in the regulation of cardiovascular functions. Animal studies demonstrated a higher sympathetic discharge in the right hemispheric stroke compared to left-sided strokes. Strokes in the region of the insula - especially the right one - are associated with a low heart rate variability and a high incidence of sudden death (6,7).

Other manifestations of insular involvement are nocturnal increases in blood pressure, high NE levels, QT prolongations and low sympathetic and parasympathetic activities (6,7).

High risk patients who need arrhythmia monitoring in the intensive care unit are those with insular involvement, right-sided stroke, advanced age, coexisting hypertensive or coronary heart disease and those expressing intense emotional stress (3).

Mental stress

Mental stress triggers ischemia in 40 to 70% of stable coronary patients with positive exercise tests. Mental stress induced ischemia is independently associated with a higher rate of fatal and nonfatal cardiac events. It predicts events over and above exercise-induced ischemia (8).

Another entity is transient LV apical ballooning (tako-tsubo-like left ventricular dysfunction) in the absence of CAD. It occurs predominantly in women after acute emotional or physical stress. The underlying etiology is not clear, but it can be myocardial stunning due to high level of catacholamines, coronary vasospasm, plaque ruptures, and myocarditis in genetically prone patients. The treatment is mainly beta blockers and the prognosis is good (9).

Brain death

Systolic myocardial dysfunction - segmental or global - is seen in 42% of patients with brain death and it is not predicted by clinical, ECG or brain CT characteristics. Ventricular arrhythmias are more common (32% more) in patients with myocardial dysfunction (7). In spontaneous subarachnoid hemorrhages, there is a segmental myocardial dysfunction, but in head trauma there might be a segmental or global dysfunction.

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.


1) Zaroff JG, Rordorf GA, et al:Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurg 44:34-9 ,1999.

2) Poyee Tung, Alexander Kopelnik, et al. Predictors of Neurocardiogenic Injury After Subarachnoid Hemorrhage. Stroke, Feb 2004; 35: 548 - 551.

3) Cheung RT, Hachinski V. The insula and cerebrogenic sudden death.Arch Neurol. 2000 Dec; 57(12):1685-8.

4) Sato K, Masuda T, Izumi T. Subarachnoid hemorrhage and myocardial damage clinical and experimental studies. Jpn Heart J. 1999 Nov; 40(6):683-701.

5) Cechetto DF, Hachinski V. Cardiovascular consequence of experimental stroke. Baillieres Clin Neurol. 1997 Jul; 6(2):297-308.

6) Tokgozoglu SL, Batur MK, Top uoglu MA, Saribas O, Kes S, Oto A. Effects of stroke localization on cardiac autonomic balance and sudden death. Stroke. 1999 Jul; 30(7):1307-11.

7) Furio Colivicchi, Andrea Bassi, et al. Cardiac Autonomic Derangement and Arrhythmias in Right-Sided Stroke With Insular Involvement. Stroke, Sep 2004; 35: 2094 - 2098.

8) Krantz DS, Santiago HT, Kop WJ, Bairey Merz CN, Rozanski A, Gottdiener JS. Prognostic value of mental stress testing in coronary artery disease. Am J Cardiol. 1999 Dec 1; 84(11):1292-7.

9) Wittstein I. S., Thiemann D. R., et al. Neurohumoral Features of Myocardial Stunning Due to Sudden Emotional Stress. N Engl J Med 2005; 352:539-548, Feb 10, 2005.

10) Dujardin KS, McCully RB, et al. Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features. J Heart Lung Transplant. 2001 Mar; 20(3):350-7.


Vol4 N°20

Notes to editor

D. Ghanim & Y. Hasin
The BARUCH PADEH Medical Center, Poriya, Israel

*Past-chairman of the ESC Working Group on Acute Cardiac Care

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.