Background: Myocardial infarction with non-obstructive coronary arteries (MINOCA) occurs in 6-15% of MI and disproportionately affects women. Scientific statements recommend multi-modality imaging in MINOCA to define the underlying cause. We performed coronary optical coherence tomography (OCT) and cardiac magnetic resonance imaging (CMR) to assess mechanisms of MINOCA. Methods: In this prospective, multicenter, international, observational study, we enrolled women with a clinical diagnosis of MI. If invasive coronary angiography revealed <50% stenosis in all major arteries, multi-vessel OCT was performed, followed by CMR (cine imaging, late gadolinium enhancement, and T2-weighted imaging and/or T1 mapping). Angiography, OCT, and CMR were evaluated at blinded, independent core laboratories. Culprit lesions identified by OCT were classified as definite or possible. The CMR core laboratory identified ischemia-related and non-ischemic myocardial injury. Imaging results were combined to determine the mechanism of MINOCA, when possible. Results: Among 301 women enrolled at 16 sites, 170 were diagnosed with MINOCA, of whom 145 had adequate OCT image quality for analysis; 116 of these underwent CMR. A definite or possible culprit lesion was identified by OCT in 46.2% (67/145) of participants, most commonly plaque rupture, intra-plaque cavity or layered plaque. CMR was abnormal in 74.1% (86/116) of participants. An ischemic pattern of CMR abnormalities (infarction or myocardial edema in a coronary territory) was present in 53.4% of participants undergoing CMR (62/116). A non-ischemic pattern of CMR abnormalities (myocarditis, takotsubo syndrome or non-ischemic cardiomyopathy) was present in 20.7% (24/116). A cause of MINOCA was identified in 84.5% of the women with multi-modality imaging (98/116), higher than with OCT alone (p<0.001) or CMR alone (p=0.001). An ischemic etiology was identified in 63.8% of women with MINOCA (74/116), a non-ischemic etiology was identified in 20.7% (24/116), and no mechanism was identified in 15.5% (18/116). Conclusions: Multi-modality imaging with coronary OCT and CMR identified potential mechanisms in 84.5% of women with a diagnosis of MINOCA, three-quarters of which were ischemic and one-quarter of which were non-ischemic, alternate diagnoses to MI. Identification of the etiology of MINOCA is feasible and has the potential to guide medical therapy for secondary prevention. Clinical Trial Registration: URL: https://clinicaltrials.gov Unique Identifier: NCT02905357

SUMMARYDose-dependent PR interval prolongation has been reported in preclinical studies of lacosamide (LCM), a recently U.S. Food and Drug Administration (FDA)-approved antiepileptic drug (AED). Here we report a case of second-degree atrioventricular block (AV) block caused by the addition of LCM to other AEDs known to prolong the PR interval, resulting in hypotension and bradycardia, with consequent seizure exacerbation. The patient recovered completely after withdrawal of LCM. This case demonstrates the need for caution and interval cardiac testing when adding LCM to other AEDs known to prolong the PR interval. KEY WORDS: Lacosamide, Heart block, Arrhythmia. Case ReportA 45-year-old man with frontal lobe epilepsy, seizurefree for 1 year, developed palpitations, dyspnea, and exercise intolerance 1 week prior to hospitalization for recurrent seizure. En route to the hospital, he was noted to have bradycardia (44 bpm) with hypotension (83/64 mm Hg).His medical history included craniopharyngioma at age 6, treated with right frontal craniotomy, resection, radiation, and ventriculoatrial shunting. His course was complicated by right eye blindness and panhypopituitarism with diabetes insipidus, hypothyroidism, and adrenal insufficiency. At age 21, he developed acute lymphocytic leukemia, treated with chemotherapy. At age 23, he developed frontal lobe epilepsy featuring generalized tonic-clonic seizures beginning with stereotyped right arm extension. There was no personal or family history of cardiac conduction disorders.His medications included desmopressin, hydrocortisone, levothyroxine, somatropin, alfuzosin, risedronate, Carbatrol 100 mg po qAM and 200 mg po qPM, oxcarbazepine 600 mg po qAM, 600 mg po qPM, and 1200 mg po qHS, and LCM 200 mg nightly. His only medication change over the last year was LCM replacing zonisamide (ZNS) for unclear reasons 3 months previously, reaching 200 mg 2 months prior to presentation.Initial laboratory evaluation with blood counts, electrolytes, and hepatic enzymes was unremarkable; carbamazepine (CBZ) level was 3.8 lg/ml. Head computerized tomography showed stable right frontal encephalomalacia. Electrocardiography (ECG) showed second-degree AV block (Mobitz I/Wenckebach) with frequent dropped beats and bradycardia. A transvenous pacemaker was placed. After three further seizures, Carbatrol was increased to 200 mg twice daily, continuous intravenous lorazepam was added, and he was transferred to our institution.At our institution, physical examination revealed prior craniotomy, depressed consciousness, and right afferent pupillary defect. Echocardiography, urinalysis, urine toxicology, and endocrine evaluation [including sodium, thyroxine, and morning cortisol] were unremarkable. Thyroid-stimulating hormone was undetectable, as expected. His antiepileptic drugs (AEDs) were continued except for ZNS replacing LCM. Initial cardiac monitoring showed a markedly prolonged PR interval, frequent Mobitz I AV block, and right bundle branch block. Continuous videoelectroencephalography (EEG) ...

Sixty-five cases of chronic low back pain were studied. Infrared thermography (IRT) was abnormal in 92%, magnetic resonance imaging (MRI) in 89%, computerized tomography (CT) in 87% and myelography in 80%. IRT correlated with MRI in 94% of cases, and with CT in 87% of cases. Of 22 MRI positive disc and root cases, 21 (95%) had significant leg abnormalities on IRT. All 19 cases with radicular involvement on CT and all 18 with radicular involvement on myelography demonstrated significant leg changes on IRT.

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