Chiefs’ Inquiry Corner

April 29, 2019

Being an outstanding physician and lifelong learner requires stoking the flames of clinical curiosity.  In Chiefs’ Inquiry Corner (CIC) we attempt to succinctly answer actual clinical questions that have been raised on the wards and in the clinics of NYU’s teaching hospitals.  Our answers are not meant to be all encompassing or practice changing but rather to serve as springboards for further exploration.  For those of us with short attention spans, we hope CIC satisfies that craving for a morsel of knowledge in a digestible format.


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Myocardial infarction in the absence of obstructive coronary artery disease, or MINOCA, is found in approximately 5-6% of all patients with acute myocardial infarction (AMI). However, the diagnostic and therapeutic approach to MINOCA is not standardized given varying provider awareness, practices, and resources. A scientific statement from the American Heart Association was recently published to set forth a formal definition for MINOCA and to provide a clinically useful framework for the diagnosis and management of MINOCA patients. Key takeaways include a revision of the MINOCA term (in accordance with the “Fourth Universal Definition of Myocardial Infarction”) — MINOCA should only be used for patients with an ischemic basis for their presentation; providers should exclude patients with (1) other overt causes for elevated troponin (i.e. pulmonary embolus, sepsis), (2) overlooked obstructive coronary disease (i.e. distal stenosis), and (3) nonischemic causes for myocyte injury (i.e. myocarditis). Of note, the “Fourth Universal Definition of Myocardial Infarction” does not consider Takotsubo syndrome an AMI, therefore it is not considered under the umbrella of MINOCA. For patients in whom MINOCA remains in the working-diagnosis, the group recommends further evaluation with cardiac MRI, optical coherence tomography or intravascular ultrasound imaging to further elucidate the etiology. Additionally, if there is any evidence of atherosclerosis from the above, modifiable coronary artery disease risk factors should be treated aggressively.

References: MINOCA  
Malignant pleural effusions (MPE) are most often caused by cancers of the lung and breast;  in addition to infectious etiologies, MPEs represent a common cause of exudative, lymphocytic pleural effusions. Diagnosis of MPE primarily relies on cytological analysis, though the sensitivity of pleural fluid cytology for the diagnosis of malignant effusions is only approximately 60%. Given these diagnostic challenges, recent studies have attempted to identify biochemical tests to assist in diagnosing malignant pleural effusions. A retrospective study examined 163 patients with exudative effusions in an attempt to identify both pleural fluid and serum biochemical markers that may be suggestive of malignant effusions. This study collected data on common serum biomarkers such as LDH as well as pleural fluid studies including adenosine deaminase (ADA) – an enzyme implicated in purine metabolism previously shown to have a role in diagnosing tuberculous effusions. This study found that the ratio of serum LDH to pleural fluid ADA could be used to help diagnose malignant effusions, with a cut-off value of >20 yielding a sensitivity of 98% and specificity of 94% for this diagnosis. Given some of the existing challenges in diagnosing MPE, these biochemical tests may offer an additional method for diagnosing these effusions and helping to distinguish them from other common etiologies.

References: Diagnosing MPE  
It is well known that regular use of NSAIDs such as ibuprofen, naproxen, and diclofenac lead to an increased risk of gastrointestinal bleeding. Whether individual NSAIDs carry a higher risk of gastrointestinal bleeding than others, is less well understood. There are some data to suggest slight differences in risk of gastrointestinal bleeding for patients taking the various non-selective COX inhibitors.  In a case-control study examining over 600,000 patients, there were 726 hospitalizations for an upper gastrointestinal bleed, 234 of which were in patients using NSAIDs.  Among the different non-selective COX inhibitors, naproxen had the highest adjusted odds ratio (3.6; CI 2.2-5.7).  Other NSAIDs had more intermediate OR’s, including diclofenac (OR 2.1; CI 1.1-4.1), ibuprofen (OR 1.7; CI 0.7-4.4), and indomethacin (OR 1.5; CI 0.6-3.5).  These data suggest there are potentially small differences in the relative rates of bleeding complications with NSAIDs, with naproxen representing highest risk, though further direct comparisons are necessary.

References: NSAIDs and GIB