Myocarditis is associated with a wide range of infections, most commonly viral (cytomegalovirus), bacterial, and parasitic (Trypanosoma cruzi). Epstein-Barr virus (EBV) rarely causes myocarditis, which is a lifethreatening complication. Autoantibodies against cardiac myocytes activate the complement system and cause diffuse myocyte necrosis. Myocarditis has a variable presentation from asymptomatic to cardiogenic shock. Over time, untreated myocarditis can progress and result in dilated ventricles. Continued dilation of ventricles leads to systolic dysfunction, conduction abnormalities, ventricular arrhythmia, heart failure, valvular abnormalities, and thromboembolism. So, we are emphasizing the importance of early diagnosis and treatment of EBV to prevent mortality. This case study represents a rare case of mortality secondary to EBV infection with resultant DCM and congestive heart failure (CHF).

Posterior reversible encephalopathy syndrome (PRES) refers to white matter vasogenic edema primarily affecting the brain's posterior occipital and parietal lobes, causing acute neurological symptoms like headaches, visual symptoms, seizures, and altered mental status. We present the case of a 32-year-old male with uncontrolled hypertension, altered mental status, and left-sided weakness. He had a rapid neurological decline, and a computed tomography (CT) head showed blurring of gray-white matter interfaces in the right posterior parietal lobe, suggesting infarction or PRES. Magnetic resonance imaging (MRI) of the brain suggested worsening with acute-early subacute infarction involving the right temporal, parietal, and occipital lobes and diffuse cerebral edema causing compression of the right ventricle with diffuse sulcal effacement and central downward herniation. There were flair hyperintensities in the bifrontal, pons, and cerebellum. Given the history of uncontrolled hypertension, the right hemispheric infarction and edema were thought to be due to secondary complications of severe PRES. He underwent urgent bilateral craniectomies with dural augmentation and external ventricular drain placement to control the intracranial pressure the next day. His mental status, as well as neurologic function, showed gradual improvement in the next few months. A high index of suspicion and rapid treatment can pave the way for a quick recovery and help reduce morbidity and death.

Hemoglobin A1c (HbA1c) can be unreliable (falsely elevated or lowered) in certain conditions, including hemoglobinopathies, anemia, lead poisoning, chronic alcoholism, and opioid use. Hemoglobin Wayne is a rare variant of hemoglobin (Hgb) that can also result in a false elevation of HbA1c. Hence, clinicians should be aware of these underlying causes before diagnosing and treating diabetes mellitus to avoid unexpected consequences. We are reporting a case of falsely elevated HbA1c in a female in her early 60s due to a rare variant of Hgb called hemoglobin Wayne. The patient presented with a consistently elevated HbA1c ranging from 10.3% to 10.7% for two years, which did not correlate with her fasting blood glucose levels ranging between 80 and 100. The continuous glucose monitoring (CGM) profile was also within the normal range. The hemoglobin electrophoresis technique was used to confirm the diagnosis of hemoglobin Wayne in this patient and the initial treatment of metformin was discontinued upon confirmation.

Aldosterone is a mineralocorticoid hormone that maintains sodium and potassium homeostasis. Excess aldosterone secretion causes sodium influx and potassium outflow, leading to hypertension and in some cases hypokalemia. Conn's syndrome, or primary aldosteronism, is the most common cause of secondary hypertension, accounting for 20% or more of people with resistant hypertension. We present a young male with hypertension, blurry vision in the right eye, and hypokalemia who was on further investigation found to have an aldosterone-secreting adrenal adenoma. He was treated with retroperitoneoscopic right-sided adrenalectomy and his blood pressure improved. Conn's syndrome should be suspected in any hypertensive patient with hypokalemia. Adrenal venous sampling is the best investigation to measure aldosterone levels and also to lateralize the source. Surgical resection is the treatment of choice.