Several cardiac outcomes have been reported with West Nile-encephalitis; however, the underlying pathophysiology remains complex. We present a 42-year-old female, with multiple sclerosis, whose neurological symptoms and respiratory decline were finally explained by the diagnosis of West Nile-encephalitis. During her admission, the isolated peaked T-waves indicated the underlying stress-induced cardiomyopathy. The absence of all other causes of hyperacute T-waves, their subsequent resolution with the resolution of infection and improvement in wall motion abnormalities, further supported the association. This case highlights the importance of considering hyperacute T-waves in an approach towards the diagnosis of WNV-encephalitis related atypical variant of stress-induced cardiomyopathy.
West Nile virus (WNV) has been established to present with a spectrum of cardiac manifestations, including atrial fibrillation and atrioventricular (AV) node block in the setting of myocarditis and autonomous dysfunction [
A 42-year-old female with a history of seizures, multiple sclerosis, migraines, and anxiety presented to the emergency department with progressive left upper extremity weakness, lower extremity myalgias and altered mental status for 2 days, accompanied by headache and low-grade fever. She denied any history of sick contacts, traveling or changes in her medications.
On presentation, her blood pressure was 122/60 mmHg, a heart rate of 67 beats per minute, and saturating 99% on room air. Neurological examination revealed akathisia, decreased tone in the left lower extremity, 2+ reflexes in left upper extremity, 4+ patellar and mute plantar reflexes bilaterally. Ankle clonus noted in both lower limbs. Kernig’s and Brudzinski’s sign was negative. The rest of the examination was unremarkable.
An electrocardiogram (EKG) on day one showed a normal sinus rhythm and normal intervals. Labs were notable for hypokalemia (potassium 2.9 mmol/l), thrombocytopenia (Platelets 93000/mcl) and elevated C-reactive protein (CRP), other work-up as shown in
Neurology was consulted in the emergency department for the evaluation of stroke given left upper extremity weakness, which was ruled out with normal brain imaging. She was restless and agitated a night earlier and was kicking in bed while asleep. These findings along with hyperthermia and the use of multiple serotonergic medications including buspirone, fluoxetine, and trazodone raised concerns for serotonin syndrome. The patient had not been taking any medication for multiple sclerosis or headaches for a few years. Upon admission, all serotonergic medications were held, meanwhile, levetiracetam was resumed for seizure prophylaxis.
Given the constellation of symptoms with a 2-day onset into acute left arm pain and weakness, altered mentation, and akathisia, an infectious process was brought into consideration. A lumbar puncture was performed and based on the findings suggestive of viral meningitis, IV acyclovir was started. The Infectious Disease team was taken on board with concerns of aseptic meningitis, however,
| Initial investigations: | |
|---|---|
| CT scan | Stable periventricular white matter changes |
| Electroencephalogram | A moderate nonspecific generalized cerebral dysfunction. There were no epileptiform discharges or seizures recorded. |
| MRI brain | Increased demyelinating plaques since prior scan in 2015 |
| MRI cervical spine | Numerous new demyelinating plaques throughout the cervical spine |
| MRI upper extremities | There is bilateral symmetric muscle edema without fatty infiltration/atrophy. |
| Upper limb arterial doppler | Normal left arm pressures and waveforms. |
| Total Lymphocyte | 8400/mcl |
| ESR | 12 |
| CRP | 6 mg/l |
| Urine toxicology | Cannabinoids positive |
| CSF analysis | Elevated protein and WBC count of 128 (53% PMNs, 42% lymphocytes). Lyme CSF, CSF VDRL were negative. CSF ACE levels within normal limits. |
| CSF Myelin basic protein | 67.90 ng/mL |
| Lyme antibodies, HIV antibodies | Negative |
| Serum Vit B1, Vitamin B12, aldolase, serum copper, Serum immunoglobulins | Within normal limits |
| Immunological work-up | Negative |
| Blood, urine and sputum cultures | Negative |
| Cardiac work-up | |
| ECHO (Day 4) | LVEF 50%. Moderate basal hypokinesis with preserved to hyper-contractile apical function. Normal RV systolic function, as shown in |
| ECHO (Day 14) | EF 55% - 60%, mildly hypokinetic segments in basal region (improved from previous study), |
| High sensitivity troponin | 34 pg/ml à 37 pg/ml à 47 pg/ml |
given thrombocytopenia, Lyme disease work-up including CSF antibodies was ordered and doxycycline was started.
For the increased plaque burden on MRI and IgG in CSF, a 5-day course of intravenous immunoglobulin (IVIG) was started by neurology for MS flare and acyclovir was discontinued on day 3 after the CSF Biofire was negative for HSV. Negative Lyme serologies led to doxycycline discontinuation. On day 4 of admission, the patient was upgraded to the ICU due to worsening mentation and inability to protect the airway. She developed acute hypoxic respiratory failure, which was thought to be secondary to hospital-acquired pneumonia versus aspiration, given nasogastric tube was placed a day earlier and a repeat chest X-ray showed worsening bibasilar infiltrates (
With no evidence of clinical and neurological improvement, a 5-day course of methylprednisolone was initiated by neurology for autoimmune pathology. The
patient remained in the ICU, and multiple failed attempts at extubation were made, with subsequent tracheostomy formation. The mentation had improved by that time.
On day 12 of admission, the neurological exam was found consistent with a cervical cord lesion given normal mental function and intact cranial nerve examination, quadriparesis, (upper limbs affected more than lower limbs), lower motor signs in her upper limbs with hypotonia, and hyporeflexia and upper motor neuron signs in lower limbs with hypertonia, hyperreflexia, and upgoing plantar bilaterally. Difficulty in weaning from mechanical ventilation was also thought to be because of the cervical lesion affecting the diaphragm. MRI cervical spine was ordered, which showed some improving inactive demyelinating plaques. MRI of the brachial plexus bilaterally was also unremarkable. The serum antibodies for neuromyelitis optica were reported negative as well.
The etiology of the clinical presentation still remained unclear. It was this time when West Nile serology was sent, which came out positive on day 15 of admission. It was finally concluded that patient had acute encephalopathy and myelitis secondary to neuroinvasive West Nile virus in the context of positive IgM and IgG antibodies in the serum. However, patient's clinical condition had significantly improved as compared to the initial presentation and she was down-graded to intermediate care with supportive care, pressure support during the day and full vent overnight. She was transferred to long-term acute care facility on day 19 of admission, with subsequent complete recovery after a few weeks.
During the ICU stay, patient was found to have persistent asymptomatic bradycardia with hyper-acute T waves (
Our patient presented with a unique clinical presentation of West Nile encephalitis and myelitis, the presence of west nile IgM antibodies in the serum indicated acute infection, which had a prolonged, yet self-resolving course.
Cardiac involvement is not uncommon in patients with viral encephalitis. Some viruses have been associated with relative bradycardia [
Hyperacute T waves have commonly been associated with ST-segment elevation myocardial infarction [
In our case, the patient began to have a sudden onset of asymptomatic bradycardia with prominent tall peaked T waves several days later after the initial presentation. When the attention was driven to the significantly prominent T-waves, a broader differential was thought given the worsening respiratory status. In the absence of typical symptoms, and cardiac enzyme elevation, it was unlikely for this patient to have a transmural infarction. Along with excluding ischemic etiology, electrolyte imbalance was keenly monitored with daily labs. Although she presented initially with moderate hypokalemia and hypomagnesemia, she was never found to have electrolyte imbalance concomitantly with the appearance of EKG changes. A thorough medication review did not reveal any medication that could have been thought to contribute to her bradycardia or EKG changes. The transthoracic echocardiogram did not reveal significant left ventricular hypertrophy and there was the absence of pericardial effusion to suggest pericarditis, however, the basal hypokinesis with hypercontractile apex was indicative of an apical sparing variant of basal (inverted) stress-induced cardiomyopathy.
Although a lot has been known about WNV and its cardiac manifestations, our case reflects the unique electrophysiological presentation with isolated peaked T waves, which indicated the underlying atypical variant stress-induced cardiomyopathy associated with infection. The basal or inverted variant is found in <5% of patients and is usually not associated with isolated hyperacute T waves on EKG or severe hemodynamic compromise [
The authors declare no conflicts of interest regarding the publication of this paper.
Rafique, S., Khan, N. and Siddique, M. (2024) Isolated Hyperacute T-Waves in West Nile Encephalitis Indicating Atypical Variant of Stress-Induced Cardiomyopathy. Journal of Biosciences and Medicines, 12, 303-310. https://doi.org/10.4236/jbm.2024.122024