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A 47-year-old man was referred from an outside facility with complaints of recurrent falls. He had been referred to a neurologist for evaluation of recurrent unexplained syncope. Each event was non-convulsive, random, and preceded by a sudden loss of balance that would progress to falling due to altered mental status. There was no apparent triggering factor, post-event confusion, or loss of either bowel or urinary continence. He had been evaluated twice at a local healthcare facility for these falls, but no cause was identified.He was referred to us on the third presentation after suffering multiple facial and thoracic injuries. He had no evident cardiopulmonary symptoms. Because he was adopted, he had no knowledge of any family history history of cardiac events. His past medical history included bipolar disorder, tobacco abuse, alcohol dependence, and atypical facial pain. His home medications were carbamazepine, lamotrigine, olanzepine, diazepam, and venlafaxine. The only recent change in his medications was a carbamazepine dose reduction because a provider at an outside facility had thought that this might be contributing to his symptoms. On review of his past medical records (more than 10 years prior), left ventricular hypertrophy had been mentioned, but it had not been followed-up in subsequent evaluations. Previous computerized tomography (CT) of the head and neck had been unremarkable.Clinically, the patient was alert, awake, and oriented. Blood pressure was 123/63 mmHg, pulse 83 beats/minute, temperature 99.6ºF, respirations 20 breaths/ minute, and oxygen saturation 95% on room air. He had no orthostatic hypotension. The physical examination was normal except for the multiple facial swellings and left-sided chest wall tenderness he had sustained from the falls. Apical hypertrophic cardiomyopathy (AHC) is a rare variant of hypertrophic cardiomyopathy. Since its description by Sakamoto in 1976 in Japanese patients, our understanding of this entity has evolved. Although cardiac magnetic resonance imaging has emerged as the gold standard for diagnosing AHC, clinical attention must be drawn to the unique electrocardiographic features that provide the initial clues to making the diagnosis. In this case, we present a 47-year-old man with AHC who presented with recurrent syncope, but anomalies on his electrocardiogram went unnoticed on two clinical encounters. He was subsequently admitted to our service and rapidly diagnosed after we observed the very classical findings in the plain twelve lead electrocardiogram done at the time of admission. In a clinical encounter involving a patient presenting with recurrent syncope, special attention must be focused on the electrocardiogram to decipher the unique diagnostic features it might show.

Two types of pulmonary edema occur in clinical medicine: cardiogenic pulmonary edema (or hydrostatic pulmonary edema) and noncardiogenic pulmonary edema, better known as acute lung injury or acute respiratory distress syndrome (ARDS). Their clinical manifestations are very similar, so the differentiation between them, based only on clinical grounds, may be very difficult, and knowing the precise etiology of the episode of acute pulmonary edema has major implications in the treatment plan. Cardiogenic pulmonary edema is usually due to systolic and/or diastolic left ventricular dysfunction and is typically treated with diuretics, nitrates, and afterload reduction medications such as angiotensin converting enzyme inhibitors, although some cases also require coronary revascularization. Noncardiogenic pulmonary edema is usually secondary to a more systemic severe medical or surgical pathology that triggers the event, and the treatment should be directed to treat that pathology. Oxygen supplementation in the form of mechanical ventilation (invasive or non-invasive) is always required. A rapid diagnosis of the cause of the episode of acute pulmonary edema facilitates a timely and appropriate therapeutic intervention.Electroconvulsive therapy (ECT) is recognized as a well-established, highlyeffective, safe psychiatric treatment. It is estimated that 100,000 patients per year receive a course of ECT across the United States, with an average of 8 to 10 treatments per course of therapy. Severe complications are very infrequent and generally reported as transitory cardiac arrhythmias and severe transitory Acute pulmonary edema complicating electroconvulsive therapy is an extremely uncommon event that has rarely been described in the literature. Different theories, including one suggesting a cardiogenic component, have been proposed to explain its genesis. The present report describes a classic presentation of this condition with review of its potential mechanisms and diagnostic approach. After successful completion of a session of electroconvulsive therapy, a 42-year-old woman with major depressive disorder developed acute systemic high blood pressure, shortness of breath, and hemoptysis. A chest radiograph demonstrated diffuse bilateral pulmonary infiltrates. Initially cardiogenic pulmonary edema was presumed, but an extensive diagnostic work-up demonstrated normal systolic and diastolic left ventricular function, and with only supportive measures, a complete clinical and radiographic recovery was achieved within 48 hours. The present case does not support any cardiogenic mechanism in the genesis of this condition.

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Case PresentationA previously healthy woman, age 26 years, presented with abdominal pain, progressive fatigue, and purpuric skin rash over the extremities that began 7 days after beginning a treatment with trimethoprim-sulfamethoxazole (TMP-SMX) for a Klebsiella pneumoniae urinary tract infection. She also complained of exertional shortness of breath with no cough, hemoptysis, or other cardiopulmonary symptoms. No history of bleeding gums or hematochezia was present. A detailed interrogation did not demonstrate any other recent clinical complaints or the administration of any other type of medication beyond TMP-SMX. Physical examination revealed a young woman in no obvious distress, with a body mass index of 27 and stable vital signs. She had pallor and icterus of the mucus membranes but had no bleeding gums or rectal bleeding. She had a non-itchy, purpuric skin rash over her extremities, as well as petechiae. The rest of her physical examination was unremarkable. Thrombotic thrombocytopenic purpura (TTP) is a hematological disease characterized by microangiopathic hemolytic anemia and thrombocytopenia. Although the link between ADAMTS13 deficiency and idiopathic TTP has been well-established, the role of trimethoprimsulfamethoxazole (TMP-SMX) in the pathogenesis of TTP is not yet well elucidated. To the best of our knowledge, there have been only two previous reports linking this medication with the development of TTP. We present the case of a healthy woman, age 26 years, who developed TTP during TMP-SMX therapy for urinary tract infection. She was found to have ADAMTS13 deficiency with anti-ADAMTS13 antibodies. Her condition responded to discontinuation of the TMP-SMX, plasmapheresis, and rituximab therapy. We speculate that the acquired ADAMTS13 deficiency might have been triggered by the TMP-SMX therapy.