Résumé
Heart failure with preserved ejection fraction (HFpEF) accounts for 15–20% of patients with heart failure (HF) in India. Diagnosis is by clinical features supported by biomarkers and echocardiography. Lifestyle modifications, control of risk factors to optimum levels, and treatment of comorbidities are essential in the management of HFpEF. Spironolactone and sacubitril-valsartan [angiotensin receptor neprilysin inhibitor (ARNI)] are beneficial in subsets of HFpEF, especially with lower range of ejection fraction (EF). Sodium-glucose co-transporter-2 inhibitors (SGLT2i)—empagliflozin and dapagliflozin and probably sotagliflozin are the only currently available drugs which have shown benefits in HFpEF, mostly by reducing hospitalizations. The benefit of SGLT2i is evident in both diabetic and nondiabetic subsets. Heart failure with preserved ejection fraction is defined as patients with HF with documented left ventricular ejection fraction (LVEF) equal to or more than 50%.1 Globally, HFpEF accounts for close to 50% of patients presenting with HF. As per the registry data like Trivandrum Heart Failure Registry2 and ASIAN-HF,3 the proportion of HFpEF in our country is approximately 19–25%, which is much lower as compared to that of western population. There is a possibility that many cases go undiagnosed in developing countries like India. The mean age of presentation of patients from India was around 58–68 years, which is about 10 years younger than the data reported from the west. Heart failure with preserved ejection fraction is characterized by elevated left ventricular filling pressures and/or reduced cardiac output either at rest or on exertion. Cardiac output is maintained at the cost of abnormally elevated filling pressure which is responsible for the symptoms and signs. Neurohumoral activation (sympathetic and renin-angiotensin-aldosterone system activation) is present only in a group of HFpEF patients unlike in patients with heart failure with reduced ejection fraction (HfrEF).
Résumé
OBJECTIVE: We investigated the safety and efficacy of combination therapy of extended release (ER) niacin and atorvastatin in patients with low HDL-C and compared the results with atorvastatin monotherapy. METHODS: This open label study recruited consecutive men and women who had coronary artery disease with HDL-C levels <35 mg/dL. These patients were already on atorvastatin therapy targeted to lower low density lipoprotein cholesterol (LDL-C), for a minimum period of 6 months. Group 1, n = 104 (mean age 52.7 years) received ER niacin in addition to atorvastatin and group 2 (n = 106) continued on atorvastatin (mean age 52.3 years). ER niacin dose was built up to a maximum of 1.5 g and atorvastatin dose titrated according to LDL levels in both the groups. The lipoprotein levels at baseline were similar (p = NS). RESULTS: At 9 +/- 1.8 months of follow-up, the mean dose of ER niacin was 1.3 g and atorvastatin 13.2 mg in group 1. In comparison, group 2 patients had mean atorvastatin dose of 15.9 mg. Patients in group 1 had significant elevation in HDL-C cholesterol (39.5 +/- 5.5 vs 35.7 +/- 4.5 mg/dL), reduction in total cholesterol (156.4 +/- 31 vs 164.5 +/- 39.3 mg/dL) and also LDL-C (88.9 +/- 28.3 vs 99.8 +/- 35.4 mg/dL) compared to group 2 (all p < 0.05). The magnitude of reduction in triglyceride levels was not significant between the groups (140.1 +/- 40.4 vs 145.2 +/- 46.5 mg/dL) (p = NS). No major adverse events or clinical myopathy occurred in either groups. Four patients (4%) discontinued ER niacin (2 due to gastro-intestinal symptoms and 2 due to worsening of diabetes). Flushing occurred in 3% patients, but none felt it to be troublesome. CONCLUSION: Adding ER niacin to atorvastatin exhibited beneficial effects on lipid profile with significant elevation of HDL-C cholesterol and further lowering of LDL-C compared to monotherapy. This treatment offered better targeted therapy and was well tolerated with proper monitoring in Indian patients.