Appeal type: Medical necessity
Decision: Upheld

Diagnosis: Coronary Artery Disease. 
Treatment: Inpatient Hospital Stay. 

The insurer denied the inpatient hospital stay. 
The determination is upheld. 

The patient presented to the emergency department (ED) of the first hospital with imbalance and nausea for 3 days prior to presentation. 
The patient underwent a head computed tomography (CT) scan and it revealed encephalomalacia compatible with an old infarct of the right (R) occipital lobe. Chronic changes were found. 
The patient has a past medical history of coronary artery disease (CAD) and previously had 3 stents placed. He also suffered a recent stroke with no residual weakness. The patient had a history of hypertension (HTN) and hyperlipidemia (HLD). 
His vital signs were stable. Blood pressure (BP) was 147/78, heart rate (HR) 66 beats per minute (BPM), and oxygen saturation (O2 sat) 100% on room air (RA). 
His physical examination was unremarkable, including a neurologic exam. His troponin was 0.24. His electrocardiogram (ECG) revealed sinus bradycardia with left atrial (LA) enlargement, no acute ST-T changes. Neurology consulted on the phone and recommended computed tomography angiography (CTA) of the neck. 
His repeated troponin was 0.21. His CBC was unremarkable. The potassium was 3.4. A chest x-ray (CXR) revealed no acute disease. 
Computed tomography angiography (CTA) of his head revealed 50% stenosis in the distal right A2 anterior cerebral artery (ACA) segment and distal to that 80% segmental stenosis; 80-90% stenosis in 1 of the left M2 middle cerebral artery (MCA) branches within the sylvian cistern; multifocal high-grade stenosis throughout the left intracranial vertebral artery with possible occlusion in the region of the posterior inferior cerebellar artery (PICA) takeoff; multifocal high-grade stenosis in the basilar artery of greater than 90%; greater than 80% stenosis at the origin of the right posterior cerebral artery with non hemodynamically significant atherosclerotic luminal irregularity throughout the P2 segment. Neck computed tomography angiography (CTA) revealed no significant carotid stenosis. 

The patient was admitted to the hospital. He underwent a stress nuclear test and it revealed moderate stress induced ischemia in the large segment of the lateral wall, extending into the inferolateral region after the pharmacological stress. There was a small fixed defect in the distal inferolateral/apical region; mild ischemia in the inferoseptal and inferior region; slightly enlarged left ventricle; septal and mild lateral wall hypokinesis; ejection fraction (EF) 52%. 
Head magnetic resonance imaging (MRI) revealed "marked irregularity in the right occipital lobe. There appears to be mild laminar necrosis at this level". 
His echocardiogram revealed a normal EF with grade 1 diastolic dysfunction. The patient underwent cardiac a catheterization and was found to have severe 3 vessel disease. The left main was patent. The left anterior descending (LAD) had diffuse 80% tubular stenosis involving proximal, mid and distal segments. There was distal stenosis at the site of a prior stent. The circumflex (Cx) had 70% tubular stenosis. The obtuse marginal (OM) 1 was occluded and supplied by collateral from the LAD. The right coronary artery (RCA) was calcified and occluded at the site of prior stent. The distal vessel was collateralized from the LAD. 
The patient's condition was stable. His troponin came down to normal. The patient was loaded with Brilinta. 
Cardiothoracic surgery was consulted and accepted the patient for surgery. The patient was transferred to another hospital for a possible coronary artery bypass graft (CABG). 
During transfer, his vital signs were stable, and his physical examination was unremarkable. His review of system was abnormal because of cough. After transfer, the patient underwent routine labs. 

The patient's lab results were positive for coronavirus disease (COVID)-19. The patient was complaining of a cough. He had a fever of 101.9 degrees Fahrenheit. His O2 saturation was 94-96% on room air (RA). His physical examination, including the lungs and cardiovascular exam, were unremarkable. His troponin was 0.19. His brain (or B-type) natriuretic peptide (BNP) was 11. A chest x-ray (CXR) was unremarkable. 
The patient was treated with intravenous (IV) Regeneron. The patient also received subcutaneous (S/Q) Lovenox. 
An echocardiogram was repeated and it revealed an EF of 31-35%. There was mild to moderate septal left ventricular hypertrophy. 
The patient was seen by cardiothoracic surgery and recommended to be discharged to follow up in few weeks. 
At issue is the medical necessity of an inpatient level of care. 

The requested health service/treatment of inpatient stay was not medically necessary for this patient. 
The patient initially presented to another hospital with neurologic complaints. His troponin was elevated, he had history of coronary artery disease. The patient underwent initially non-invasive evaluation for ischemia. His stress test was positive. His coronary angiography revealed severe 3 vessel CAD. The patient was recommended for surgery.
His condition was stable, without chest pain, arrhythmia or heart failure. There were no cardiac complaints. The patient was loaded with Brilinta prior to transfer. 
The patient, after he was transferred to second hospital for CABG, was diagnosed with COVID. He had mild symptoms and was treated per the protocol for COVID. His surgery was postponed. The patient was discharged in stable condition. 
Inpatient stay from was not medically necessary. The patient was transferred for a CABG, but CABG was not done due to COVID diagnosis. The surgery was postponed and that confirms that the patient was stable from cardiovascular standpoint. If he was not stable, the surgery would not be delayed. The patient was hemodynamically stable, with normal vital signs and a normal physical examination. He was treated with oral medications, Lovenox injections for deep vein thrombosis (DVT) prophylaxis with COVID and intravenous (IV) treatment for COVID. The management of this patient for the above dates could have been accomplished at a lower level of care. 
Per a paragraph from first reference: "As indicated in the Third Universal Definition of Myocardial Infarction consensus document, acute myocardial infarction (AMI) is defined by the detection of a rise and/or fall of cardiac biomarkers (preferably cardiac troponin levels) with at least 1 value above the 99th percentile upper reference limit and with at least one of the following: (a) symptoms of ischemia; (b) new or presumed new significant ST-segment-T wave changes or new left bundle branch block; (c) development of pathological Q waves in the electrocardiogram (ECG); (d) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality; (e) identification of an intracoronary thrombus by angiography or autopsy. The Third Universal Definition of Myocardial Infarction consensus document, published in 2012, classifies MI into 5 types, based on pathological, clinical, and prognostic differences, along with different treatment strategies. The performance and quality measures described in the current document are predominantly pertinent to patients with spontaneous MI, or MI type 1. MI type 1 is an event related to atherosclerotic plaque disruption (eg, rupture, ulceration, erosion) with superimposed thrombus formation in a coronary artery, resulting in acute reduction in myocardial blood supply and/or distal embolization with subsequent myonecrosis. MI type 2 is myocardial injury caused by conditions other than coronary artery disease that results in an imbalance between myocardial oxygen supply and/or demand (eg, coronary artery embolism or spasm, tachyarrhythmias, anemia, respiratory failure, profound hypotension)."