Introduction: Despite normal ejection fraction, nonobstructive hypertrophic cardiomyopathy (nHCM; rest and provoked gradients <30 mmHg) is associated with high rates of angina, arrhythmias and heart failure symptoms, as well as abnormalities of echo-based myocardial strain. Using Myocardial Work (MW) analysis, we investigated the potential mechanisms contributing to exercise-induced symptoms in nHCM. Methods and Results: Using validated methods (EchoPAC), longitudinal strain and non-invasive blood pressure were integrated to generate normalized left ventricular pressure curves and pressure-strain loops to derive global and segmental MW data in 14 nHCM patients with normal ejection fraction (>55%) who underwent treadmill stress testing. Global myocardial work efficiency was expressed as the ratio of global constructive work over the sum of global constructive and wasted work. A total of 9 of 14 patients reported symptoms during exercise (chest pain, dyspnea, and palpitations) and this group had reduced global myocardial work efficiency compared to those without exercise-induced symptoms (85% vs 90%, respectively, p = 0.04, Figure 1). No statistical differences were noted in age, % men, maximal wall thickness, ejection fraction, E/e’ ratio, resting blood pressure, resting global strain and exercise performance between symptomatic and asymptomatic patients. Conclusions: Despite similar ventricular morphology, resting mechanics and exercise performance, nHCM patients with symptoms during exercise have worse myocardial work efficiency. Our data suggest that mechanisms potentially impacting global strain may be distinct from those affecting myocardial work efficiency. Understanding these differences may offer insights into management of exercise-induced symptoms.
A woman in her 80s presented to the emergency department with altered mental status, weakness, slurred speech, emesis, and headache. Emergency medical services found her pulse rate in the 20s, so transcutaneous pacing was initiated. Her initial vital signs in the emergency department were blood pressure of 100/73 mm Hg, heart rate of 49 beats/min, respiratory rate of 27 breaths/min, and oxygen saturation of 95% on a nonrebreather mask. Computed tomography of the head showed no acute pathology, and chest radiography showed a pulmonary consolidation. She was intubated for airway protection. An electrocardiogram (ECG) obtained subsequently, after her transient bradycardia had resolved, is shown in the Figure.Question: Is the transcutaneous pacemaker (TCP) failing to capture or sense, or both?
Introduction: Syncope describes a brief, sudden loss of consciousness and tone, with spontaneous return to baseline. Although episodes arise from a transient interruption of cerebral blood flow, work-up identifying an underlying is critical, as it can determine the proper treatment for cessation of these episodes. In this case, we describe a patient who was later diagnosed with stretch syncope of adolescence (SSA), a rarely reported cause of syncope. Case Presentation A 16-year-old male presented to the E.R. after experiencing a syncopal event immediately after looking up. He endorsed a similar episode one week earlier, after standing and looking up. The patient also revealed that he commonly would crack his neck and would often sleep with his head extended over the arm of his couch. In the E.R., the patient was hypotensive to 107/62 mmHg, but physical exam and lab work-up did not reveal any significant pathology. EKG and a CT head without IV Contrast showed no acute intracranial abnormality. Soon after admission, he became bradycardic, hypotensive, and lightheaded. Due to concern for carotid artery dissection, bilateral carotid duplex scan and CT of the head and neck were completed, and given the reproducibility of the patient’s symptoms with neck dorsiflexion, an MRI to evaluate for carotid sinus syndrome was completed. All imaging, however, returned unremarkable. Given the patient’s age, symptom onset with movement, and exclusion of other etiologies, a diagnosis of SSA was made. The patient was discharged with strict instructions to avoid stretching, especially when standing. Discussion SSA is characterized by episodic loss of consciousness triggered by a combination of stretching and neck hyperextension. It is a rarely reported phenomenon, with only 14 case reports published on SSA as of 2014, and is often confused with more common syndromes, most commonly epileptic seizures. Our case is especially unique because the patient’s presentation was initially most consistent with carotid artery dissection and coronary sinus syndrome, a previously unreported presentation. By continuing to recognize and report cases such as ours, patients with SSA may receive more prompt diagnosis, avoid extraneous work-up, and ultimately, prevent future syncopal events.
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