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What caused this previously healthy thirty-something to have vertigo, slurred speech, vomiting and left-sided weakness for the past 6 hours? The source of these symptoms puzzled Tong Liu, MD, PhD, of the Second Hospital of Tianjin Medical University in China, and colleagues, as they reported in .

The patient presented with normal vital signs and no dyspnea or chest pain. Initial assessment with a CT brain scan revealed a large infarction of the left cerebellar hemisphere and left pontine. Clinicians admitted the patient and followed up with an ECG, with the following findings: "Sinus rhythm at a rate of 83 bpm with a 3-mm upsloping ST segment depression at the J points along with tall, symmetrical T waves in leads V2 through V5, a slight ST-segment elevation in lead aVR, and a 1-mm ST-segment depression in inferior leads."

Findings of subsequent blood tests included a troponin T level of 1,349 pg/mL (reference range <14 pg/mL) and N-terminal pro B-type natriuretic peptide (NT-proBNP) level of 1,674 pg/mL (reference range <125 pg/mL).

There was no evidence of thrombophilia, vasculitis, or antiphospholipid syndrome.

The patient underwent an echocardiogram, which revealed regional wall-motion abnormalities of the left ventricle and an ejection fraction (LVEF) reduced to 36%. Based on these findings, clinicians diagnosed the patient with acute ischemic stroke and ST-segment elevation myocardial infarction (STEMI).

The findings of the ECG taken at the time of admission, along with the elevated troponin T level and the abnormal left ventricular wall motion, indicated de Winter ECG pattern. This abnormality occurs in just 2% of patients whose proximal left anterior descending coronary artery (LAD) suddenly becomes blocked, case authors noted.

This confirmation that the patient had a significant infarction of the cerebellar hemisphere and pontine, as well as the strong possibility of STEMI, left clinicians with what they described as "a huge diagnostic and treatment challenge."

A cerebral angiogram revealed occlusion of the left posterior cerebellar artery; arterial dissection had caused severe stenosis of the left vertebral artery. Just 90 minutes after hospital admission, the patient received a coronary stent.

The following day, clinicians performed a coronary CT angiography. This showed only a superficial myocardial bridge in the mid-left anterior descending artery, which the team considered was not likely to have caused such extensive heart damage.

Given extent of the patient's stroke and myocardial injury, the team suspected the patient had stroke-heart syndrome from stroke-induced heart injury (SIHI).

Physicians prescribed dexamethasone, sacubitril/valsartan (Entresto), and a statin. After 3 days of treatment with those medications, ECG showed that the previously observed abnormalities had resolved.

On day 6 after admission, another echocardiogram showed improvement in the left ventricular wall motion, increase in the patient's LVEF to 66%, and normalization of NT-proBNP and troponin T levels. The team discharged the patient to home in stable condition.

Discussion

Clinicians reporting this case of stroke-heart syndrome -- "considered a perfect storm for patients with stroke" -- suggested that this is the first report of de Winter ECG pattern observed in a patient with stroke-induced heart injury. The case demonstrated that de Winter ECG pattern is not necessarily always associated with acute coronary artery occlusion but may also occur due to stroke-induced heart injury.

The case illustrated coexistence of large ischemic stroke and suspected STEMI, which is a huge challenge to diagnose and to treat, Liu's group wrote, "because it is not entirely clear which comes first (the stroke causing myocardial infarction, or sometimes in the opposite sequence)."

They described the five categories of stroke-heart syndrome:

• Asymptomatic presentation of elevated troponin in the setting of ischemic and nonischemic acute myocardial injury
• Acute myocardial infarction
• Left ventricular dysfunction
• Neurogenic sudden cardiac death
• ECG changes

The group cited a 2020 Journal of the American College of Cardiology stating that new ECG abnormalities may occur in about nine of 10 people with acute ischemic stroke and in 32% of people who do not have any preexisting cardiac conditions.

In acute ischemic stroke, the group noted that potential ECG changes include the following:

• ST-segment elevation
• ST-segment depression
• Unspecified ST-T changes
• QT prolongation
• T inversion
• Abnormal T wave morphology
• Bundle branch block
• Pathologic Q waves

Of these, the most are unspecified ST changes and ST depression.

Liu's group wrote that the "de Winter pattern has been widely as an equivalent of STEMI...with a high predictive value (95.2%-100%) for acute coronary occlusion," frequently requiring urgent coronary angiography followed by revascularization.

So while clinicians should consider patients with de Winter pattern to have STEMI until proven otherwise, the case authors cautioned that the de Winter pattern may also occur in patients with SIHI, which has also been in a case of de Winter pattern observed in a patient with myocarditis.

Catheterization and use of antiplatelet and anticoagulant therapies could cause a catastrophic cerebral hemorrhage in such patients, the group noted. They suggested that "because coronary angiography would cause risk, but it is imperative to exclude STEMI, in these cases, coronary CT angiography is appropriate, but cannot really exclude spasm." Thrombolytic treatment may have a role in other thromboembolic strokes in which STEMI is suspected, authors noted, but more data are needed to support this.

"The electrophysiological mechanism of de Winter pattern is still obscure," case authors wrote. Possible explanations include "ischemic adenosine triphosphate (ATP) depletion leading to lack of activation of sarcolemmal ATP sensitive potassium channels, and subendocardial ischemia owing to intermittent or incomplete coronary artery occlusion."

Overall, stroke-induced heart injury induces stroke-heart syndrome via autonomic dysregulation, catecholamine surge and amplified inflammation, mechanisms that can lead to a wide range of changes to the myocardium, said Liu's group. These include "myocardial ischemia, loss of ATP synthesis, impaired contractility, and nonischemic cardiomyocyte necrosis, which could, at least partially, explain the mechanisms of de Winter pattern seen in this patient," they wrote.

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