ECG manifestations of acute stroke, do you have a mastery?

Cerebral heart syndrome refers to the general term
for ECG abnormalities (acute myocardial infarction, myocardial ischemia, arrhythmia), subendocardial hemorrhage, or heart failure caused by acute encephalopathy, subarachnoid hemorrhage, large-scale cerebral infarction, and acute head injury involving the hypothalamus and autonomic nerve centers.

ECG manifestations of acute stroke

Of the causes of death in stroke patients, stroke itself is the first, while cardiac events are second
.

Data accumulated in the past 50 years show that acute stroke can damage the heart, even a normal heart
.

As early as 1954, Bureh et al.

ECG changes after acute stroke usually occur within the l week, and a series of Holter ECG shows that ECG changes after stroke are temporary
.

1 Types of ECG manifestations in acute stroke

Arrhythmias occur in 20% to 40% of patients with acute ischemic stroke and cerebral hemorrhage, while arachnoid hemorrhage occurs in almost 100% of patients
.

In addition, bradycardia, atrial flutter, ventricular presbycusis, polymorphic ventricular tachycardia, torsades de pointe, and ventricular fibrillation
can occur.

Acute stroke can directly damage the cerebral center that regulates the heart, and the right cerebral hemisphere is more likely to cause severe arrhythmias than the left cerebral hemisphere, and therefore more likely to cause death
due to cardiac arrest.

In patients with acute stroke ECG abnormalities, most are manifested by multi-lead broad and deep inverted T waves, and the two branches of the inverted T wave are asymmetrical
.

The incidence of atrial fibrillation was 47% higher in patients with cerebral thrombosis, 71% higher in patients with subarachnoid hemorrhage, and 18%
of sinus arrhythmias.

1.

ECG findings of central muscle ischemia in acute stroke are common
.

Patients with acute ischemic stroke with increased TnT concentrations have a worse prognosis than those with normal TnT, and the mechanism may be increased levels of catecholamines circulating in the blood, particularly in patients with cerebral hemorrhage, but there is no evidence of
clinical myocardial infarction.

In some patients, an increase in troponin can reflect a link
between coronary artery disease and acute stroke.

However, myocardial injury seen in acute stroke is due to focal myocardial injury (myocytolysis) due to activation of the sympathetic adrenal system, which is associated
with insula injury.

2.

(1) Atrial fibrillation / atrial flutter: atrial fibrillation in the center of arrhythmia in acute stroke accounts for 25% to 47%.

Among them, the proportion of atrial fibrillation in patients with cerebral infarction is greater than that of cerebral hemorrhage
.

(2) Ventricular arrhythmias: 14% of patients with subarachnoid hemorrhage develop ventricular arrhythmias
.

(3) QT interval prolongation: In patients with acute stroke, the dispersion of the QT interval increases within the first 24 hours
.

The incidence of QT interval prolongation is high
in patients with subarachnoid hemorrhage.
Increased QTc discretization is an important prognostic factor
in patients with cerebral hemorrhage.
In the ECG manifestations of acute cerebral infarction, QT interval prolongation and QT
interval dispersion are also common.

(4) Others: sinus bradycardia, bundle branch block, atrioventricular block, etc
.

2 ECG manifestations of acute cerebral hemorrhage

ECG manifestations of acute cerebral hemorrhage include myocardial ischemia, non-ST-segment elevation myocardial infarction, and arrhythmias, including tachycardia, bradycardia, pre-contraction, ventricular fibrillation, and sick sinus syndrome
.

The most common ECG charts for subarachnoid hemorrhage are T-wave high-tip, flat, and inverted, QT interval prolongation, ST-segment elevation and downward shift, pronounced u-wave, P-wave high tip, and pathological Q-wave
.
Occasional J waves
are visible.
Among them, the incidence of acute arrhythmias in the acute phase of subarachnoid hemorrhage is high, with ventricular arrhythmias such as torsades de pointes, ventricular flutter, and ventricular fibrillation
occurring in 14%.
About 52% of patients with ventricular arrhythmias have a QTc interval extension of 1>470 ms
.

ECG manifestations and management of subarachnoid hemorrhage:

(1) The QTc interval is often prolonged in the acute phase of subarachnoid hemorrhage;

(2) Female patients with subarachnoid hemorrhage and hypokalemia are independent risk factors for the occurrence of a significant prolongation of the QTc interval;

(3) Clinically, for patients with acute stage of subarachnoid hemorrhage, intravenous infusion should pay attention to potassium chloride supplementation, especially female patients;

(4) For patients with acute stage of subarachnoid hemorrhage, ECG monitoring should be done to detect serious arrhythmias as much as possible, and avoid the use of drugs
that prolong ventricular repolarization.

3 ECG manifestations of acute cerebral infarction

In patients with acute transient ischemic attacks, the incidence of short-term cardiovascular events is high and an ECG should be routinely done to detect new episodes of atrial fibrillation, atrioventricular block, and myocardial ischemia
.
One study showed
.

The incidence of atrial fibrillation is 25% in elderly patients with acute stroke and transient ischemic attacks, especially in elderly women, and the incidence of myocardial ischemia is also high
.
Population-based studies such as Jensen JK have shown that 13% to 16% of patients with acute cerebral infarction have ST-segment downward movement and T-wave inversion, and often have QT interval prolongation and increased
QT interval dispersion.

4 Effects of acute stroke site on electrocardiogram

Depending on the site of acute stroke, ECG findings vary:

(1) More patients with temporal, frontal and parietal stroke have ECG changes;

(2) Ischemic T wave inversion often occurs in patients with left parietal lobe and right frontal lobe cerebral infarction;

(3) The incidence of arrhythmias in cerebral hemisphere stroke is higher than that in patients with brainstem stroke;

(4) Acute stroke of the insula of the brain may cause sinus tachycardia, pre-stage contraction, and ST-segment elevation
.

Atrial fibrillation, AV block, and prephase contraction can occur in right insula stroke, and QTc interval prolongation and left bundle branch block occur at a high
rate.
Patients with right insula stroke have a 15-fold
higher risk of myocardial injury than patients with strokes at other sites.
In addition, the right insula plays a very important role in the autonomic regulation of the heart, and when stroke occurs in the right insula of the brain, it is more likely to develop complex and malignant arrhythmias than any other part of the stroke
.

5 Mechanisms of ECG abnormalities in acute stroke

Acute stroke often causes ECG changes, but the mechanism is not fully understood
.
In both acute cerebral hemorrhage and cerebral infarction, there is a marked increase in the concentration of catecholamines in the blood plasma, which may be from the nervous system rather than the adrenal glands
.
In addition, sympathetic activity increases after stroke, especially the right insula belongs to the sympathetic nervous system, which is involved in the regulation of heart rate and heart rhythm
.
The left insula is associated with the vagus nerve of the
heart.
When the left insula is stroked, the sympathetic-vagus nerve is out of balance, and the sympathetic excitability is also enhanced
.

Catecholamines can induce cyclic adenosine phosphate-mediated intracellular calcium overload that damages the myocardium and causes arrhythmias, and catecholamines can induce coronary arteries and/or cardiac microvasospasm
.

In the acute phase of subarachnoid hemorrhage, the activity of both the sympathetic and vagus nerves is enhanced, which can cause ECG changes
.
Adrenergic nervous system activation, by the action of catecholamines on the potassium channel of cells causes hypokalemia, which causes torsades de pointes ventricular tachycardia
.
In addition, in patients with subarachnoid hemorrhage, other factors can also cause hypokalemia, such as diuretics, adrenal hyperfunction, exogenous corticosteroids, respiratory alkalosis
due to mechanical ventilation.

6 Predictive value of ECG abnormalities in acute stroke

1.
Atrial pre-period contraction (early atrioventric period)

99% of people over the age of 50 have had at least 1 early
room after 24-hour Holter ECG.
Moreover, an increase in the number of early atrial episodes is a strong independent risk factor
for the development of atrial fibrillation.
Patients with frequent early atrial episodes (> 100 beats per day) are at high risk of new atrial fibrillation and other adverse cardiovascular events, including ischemic stroke, heart failure, and mortality, and therefore require close follow-up and management
.
The atrial morning increases by 10 beats per hour, the risk of stroke and death increases by 27%, and the risk of atrial fibrillation increases by 50%.

As the number of early atrial cases increases, so does the risk of atrial fibrillation, stroke, and death
.

2.
Preventricular contraction (ventricular early)

Early frequent ventricular disease is also a high risk factor for stroke in patients with nonhypertension and diabetes, suggesting that early ventricular remodeling is associated with atrioventricular remodeling and may be a risk factor
for cerebral embolism.
If 4 episodes are recorded in 2 minutes early, the risk of stroke is significantly increased, suggesting that the ventricular early is a "criminal arrhythmia" with cardiomyopathy, and there are reports that ventricular early can predict the risk of new atrial fibrillation and cardiovascular death
.

3.
P wave dispersion

Measuring P-wave dispersion on a 12-lead ECG within 24 hours of acute stroke can guide physicians in predicting paroxysmal atrial fibrillation in high-risk patient populations and help reduce the risk of recurrent
strokes.
P-wave dispersion > 57.
5 ms predicts paroxysmal atrial fibrillation, with a sensitivity of 80%.

Specificity 73%.

7 Examples of central electrograms of acute stroke

1.
Case l

The patient, a 64-year-old male, presents with weakness of the left limb for days
.
Physical examination: BP: 120/80mmHg, drowsy state, left upper and lower extremity muscle strength grade 0, left Pap sign positive
.
CT of the skull: cerebral infarction in the right basal ganglion
.
ECG examination shows that the chest leads are Niagara waterfall-like T-wave inverted, with a wide basal base, two asymmetrical branches, and a QT interval extension (600 ms) (Figure 1).

2.
Case 2

The patient, a 62-year-old male, was admitted to the emergency department
due to coma.
The patient's ECG showed atrial fibrillation, I, AVL, V
.
～V
。 Lead ST segment elevation and II.
, HI, aVF lead ST segment depression, suggesting acute anterior wall myocardial infarction
.
Cardiac enzymatic examination shows that troponin I is elevated by 32 ng/mLCiE and CK-MBl 14 ng/mL (normal 5.
0 ng/mL).

CT of the skull shows subarachnoid hemorrhage in the left parietal occipital area, subcap-like aponeurotic and subdural hematoma
.
Coronary angiography shows that the three coronary veins of the anterior descending branch, the gyratory branch and the right coronary artery are completely normal (Figures 2 to 4).

3.
Case 3

The patient, 65 years old, was admitted to the hospital with an ECG showing sinus tachycardia and nonspecific ST-T changes; A few minutes after stroke, the ECG showed sinus tachycardia, the sT segment of the inferior wall lead was elevated by 2 to 4 mm, and the high lateral lead and the chest lead showed corresponding changes
.
CT of the skull shows cerebral infarction in the right middle cerebral artery area, with normal
myocardial enzyma.
Autopsies did not reveal severe coronary artery lesions and myocardial infarction (Figure 5
).

4.
Case 4

The patient, female, 74 years old, series of ECG changes in subarachnoid hemorrhage: pathological Q waves, ST-segment elevation, and T-wave inversion, showing ECG changes in acute myocardial infarction (Figure 6).

5.
Case 5

The patient, 36 years old, has hemiparesis of the right limb and MRI of the skull shows acute large-scale cerebral infarction caused by occlusion of the left middle cerebral artery and the proximal anterior artery, and the electrocardiogram II, III, aVF leads show J waves (Figure 7).

6.
Case 6

The patient, male, 57 years old, developed left bundle branch block in the acute phase of subarachnoid hemorrhage
.
ECG without atrioventricular block in human hospital, QRS wave group time limit l00ms, sinus rhythm 88bpm, electric axis-20
.
(Figure 8)
。

7.
Case 7

The patient, female, 70 years old, had an acute cerebral infarction of the right parietal lobe for 1 day, and the ECG showed a broad lead with a large inverted T-wave and QT interval prolongation (Figure 9
).

8

Summary

1.
The incidence of acute cerebral infarction and cerebral hemorrhage ECG abnormalities is very high, which can be as high as 60%; Prolonged QT on the ECG in stroke patients, pathological Q waves, and left bundle branch block suggest a poor prognosis
.

2.
Acute cerebral infarction and cerebral hemorrhage can all have ECG manifestations
of myocardial ischemia and myocardial infarction.

3.
The incidence of atrial fibrillation in patients with acute cerebral infarction is higher than that in patients with
acute cerebral hemorrhage.

4.
The incidence of QTc interval prolongation and malignant ventricular arrhythmias in patients with acute cerebral hemorrhage is higher than that in patients with
acute cerebral infarction.

5.
Stroke of the island lobe of the right cerebral hemisphere is more prone to complex
arrhythmias.

6.
For patients in the acute stage of subarachnoid hemorrhage, attention should be paid to potassium chloride supplementation during intravenous infusion, especially in female patients, and avoid the use of drugs
that prolong ventricular repolarization.

7.
Patients with acute stroke have a high incidence of cardiac events, which may be related
to central autonomic nerve injury.
In addition, it is also associated with an increase in the concentration of catecholamines in the blood circulation in the early stages of
stroke.