A 66-year-old man (body height, 168 cm; body weight, 88.5 kg) experienced dyspnea, a sensation of chest tightness, and back pain for a few days before he was brought to our hospital on an emergency basis. His symptoms became aggravated suddenly as he was about to get off a taxi on his way home from work. He presented with a history of close contact with a coworker with COVID-19 and was waiting for instructions from a public health center.
In the ambulance, the following conditions were documented: Glasgow Coma Scale score, E4V5M6; heart rate, 80/min and irregular; blood pressure, 100/60 mmHg; body temperature, 38.4ºC; oxygen saturation, 98% (O2 delivered with reservoir mask at a rate of 15 L/min). On admission, his white blood cell count was 22,300/µL; hemoglobin, 14.7 g/dL; platelet count, 35 × 104/µL; creatinine level, 2.23 mg/dL; creatine kinase level, 2582 IU/L; creatine kinase myocardial band level, 164 ng/mL; low-density lipoprotein cholesterol level, 97 mg/dL; high-density-lipoprotein cholesterol level, 19 mg/dL; triglyceride level, 173 mg/dL; hemoglobin A1c level, 7.9%; C-reactive protein level, 13.8 mg/dL; troponin T level, 9.640 ng/mL; N-terminal pro-brain natriuretic peptide level, 11753 pg/mL; procalcitonin level, 0.62 ng/mL; d-dimer level, 16.34 µg/mL; and soluble fibrin level, 113.1 µg/mL. An electrocardiogram showed atrial fibrillation; ST-elevation in II, III, aVF, and V2–V6 leads; and ST depression in aVR leads (Figure ). Echocardiography revealed severe hypokinesis extending from the anterior wall to the apex and the inferior wall in left ventricle, with an approximate ejection fraction of 20%. We diagnosed STEMI and decided to perform emergency coronary angiography (CAG). A chest radiograph showed infiltrative shadows in both lungs and tracheal intubation was performed in the emergency outpatient unit (Figure ). Continuous infusion of noradrenaline (0.1 μg/kg/min) was started because his systolic blood pressure dropped below 80 mmHg. After heparin (5,000 U) was administered intravenously, the patient was transferred to the cardiac catheterization room.
CAG was performed by cardiologists, emergency physicians, clinical engineers, nurses, and radiological technologists who donned appropriate personal protective equipment before entering the room. CAG revealed total occlusion of the middle of the right coronary artery (RCA) and left anterior descending artery (LAD; Figure ). After a loading dose of dual antiplatelet therapy (aspirin, 162 mg; clopidogrel, 300 mg), an intra-aortic balloon pump catheter was inserted, and a 7-Fr guiding catheter was inserted into the left coronary artery. We removed white material, which did not at a first glance appear to be a typical thrombus, with an aspiration catheter, but blood flow did not improve. The onset-to-device time and door-to-device time were 116 and 84 minutes, respectively. Subsequent intravascular ultrasonography (IVUS) revealed several structures, which were thought to be thrombi; therefore, we performed plain old balloon angioplasty (Figure ). After the balloon was expanded, blood flow improved slightly in the LAD but not distally. Next, we placed an everolimus-eluting stent (4.0 × 38 mm) in the middle of the LAD, but peripheral blood flow was still not observed. Repeated IVUS revealed severe stenosis caused by plaque with thrombi. An additional balloon was inflated at the distal site, and a cutting balloon was also used. Another everolimus-eluting stent (2.25 × 38 mm) was placed at the distal site, but no blood flow improvements were seen angiographically.
We moved a double-lumen catheter to the distal LAD and performed CAG from the distal LAD, which revealed retrograde blood flow up to the middle of the LAD and collateral circulation from the septal branch to the RCA. Repeated IVUS examination revealed thrombi and plaque at the distal end of the stent and no intrastent blood flow (Figure ). Then, we tried to perform PCI for the total occlusion of RCA, but it was unsuccessful. At this point, 7 hours passed since the patient entered the cardiac catheterization room, and so we finished the procedure. The levels of activated clotting time during PCI were maintained at 280–310 seconds. After PCI, pathological examination proved the aspirated white material was white thrombi. Chest computed tomography performed after PCI showed ground-glass opacities distributed unevenly in both the lungs, as well as left-sided pleural effusion (Figure ). After the patient was transferred to the intensive care unit, he showed pulseless electrical activity, and cardiopulmonary resuscitation (CPR) was initiated. Return of spontaneous circulation was achieved with 1 mg of epinephrine and one cycle of CPR. Veno-arterial extracorporeal membrane oxygenation was considered, but his family decided against it. The blood pressure was maintained through the continuous administration of noradrenaline, dobutamine, and adrenaline. His nasopharyngeal swab was tested with polymerase chain reaction for SARS-CoV-2, and COVID-19-related pneumonia was diagnosed. Remdesivir treatment was initiated at a dose of 200 mg/day on the 5th day of hospitalization and continued at 100 mg/day. Because of the possibility of concomitant bacterial pneumonia, ampicillin sodium/sulbactam sodium (9 g/day) was also administered. However, the patient's oxygenation level worsened, and he died on the 7th day. It was difficult to confirm a main cause of death because we were not permitted to dissect patients due to COVID-19. We assumed that he had died from both cardiogenic shock due to myocardial infarction and septic shock due to covid-19 infection.
The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 66 years old. 
The concentration of creatinine is 2.23 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 88.5 kg. The patient's bmi is therefore 88.5 kg / (1.68 m * 1.68 m) = 31.356 kg/m^2.The patient's BMI is 31.4, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Male.
The patient's height is 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.142 in. 
For males, the ideal body weight (IBW) is calculated as follows:
IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 50 kg + 2.3 kg * (66.142 (in inches) - 60) = 64.127 kg.
Hence, the patient's IBW is 64.127 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 64.127 kg + 0.4 * (88.5 kg  - 64.127 kg) = 73.876 kg. The patient's adjusted body weight is 73.876 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 66) * 73.876 * 1) / (2.23 * 72) = 34.048 mL/min. Hence, the patient's creatinine clearance is 34.048 mL/min.