Table 2.

Case study: a patient with HF who is a potential candidate for SGLT2i therapy in clinical practice

Patient  A.K. is a 59-year-old man with a 10-year history of hypertension, initially managed with lisinopril 20 mg/day. Last year, he experienced an anterior wall MI, after which his LVEF has been 30%. During hospitalization for the MI, A.K. was started on carvedilol, and lisinopril was discontinued and replaced by sacubitril/valsartan. Spironolactone was added at a subsequent clinic visit. His other medications include low-dose aspirin and high-intensity statin therapy  His family history is notable for CAD and CHF in his father; A.K. remembers his father being hospitalized several times after his diagnosis  On exam, A.K. is clinically euvolemic and tolerating all of his current cardiac medications

Medical history  Hypertension, CAD status post-MI, CKD stage 2, and HFrEF  BP 145/85 mmHg  Heart rate 75 bpm  LDL cholesterol 68 mg/dL  BMI 28.1 kg/m2 (weight, 91 kg/height, 1.8 m)  HbA1c 6.1%  eGFR 65 mL/min/1.73 m2  Lifestyle (regular exercise/healthy dietary practices/nonsmoker)  Family history of CAD (father had experienced ACS at age 54 years and died of CHF at age 71)

Medications  Sacubitril/valsartan, 97/103 mg BID  Carvedilol, 25 mg BID  Furosemide, 20 mg QD  Spironolactone, 25 mg QD  Aspirin, 81 mg QD  Atorvastatin, 80 mg QD

ACS acute coronary syndrome, BID twice daily, BMI body mass index, BP blood pressure, CAD coronary artery disease, CHF congestive heart failure, CKD chronic kidney disease, eGFR estimated glomerular filtration rate, HbA1c glycated hemoglobin, HF heart failure, HFrEF heart failure with reduced ejection fraction, LDL low density lipoprotein, LVEF left ventricular ejection fraction, MI myocardial infarction, QD once daily, SGLT2i sodium–glucose cotransporter 2 inhibitor