TABLE 2.
Clinical application of lipid-lowering drugs in patients with HF and T2DM.
| Drug | Clinical application | References | |||||
|---|---|---|---|---|---|---|---|
| Clinic types of experiments | Patients | Number of examinees (n) | Drug usage and dosage | Usage time | Main results and conclusion | ||
| Atorvastatin | A randomized controlled clinical trial | Patients with asymptomatic HF after myocardial infarction | n = 162; observation group (n = 81), control group (n = 81) | p.o., 20 mg per night | 12 months | TNFα, hs-CRP, IL-6, and other factors were improved in both groups, but the observation group showed greater results than the control group. Atorvastatin exerted a great effect in treating asymptomatic HF after myocardial infarction, which can evidently improve cardiac function and vascular endothelial function. | Wang et al. (2020) |
| A follow-up study | Patients hospitalized for ischemic HF | n = 155; atorvastatin therapy group (n = 92) | / | / | The most frequent rehospitalization was in patients without statin therapy (66.7%), followed by patients on rosuvastatin (64.1%) and atorvastatin (13.2%). It confirms that statin therapy is associated with substantially better long-term outcomes in patients with HF. | Faris et al. (2018) | |
| A randomized controlled clinical trial | Non-ischemic chronic HF patients | n = 40; control group (n = 20), experimental group (n = 20) | p.o., 40 mg/day | 6 weeks | In patients, atorvastatin improved heart function E/A velocity ratio; decreased LV-end diastolic diameter (LV-EDD) and LV-end systolic diameter (LV-ESD), and significantly reduced serum lipid profiles, cTnT, hs-CRP, and MDA versus patient controls. | Elmadbouh et al. (2015) | |
| Rosuvastatin | A randomized, double-blind, placebo-controlled trial | Patients with chronic HF | n = 4,574; rosuvastatin therapy group (n = 2,285), placebo group (n = 2,289) | p.o., 10 mg/day | Followed up for a median of 3.9 years | 1,305 (57%) patients in the rosuvastatin group and 1,283 (56%) in the placebo group died or were admitted to the hospital for cardiovascular reasons. It confirms that rosuvastatin 10 mg daily did not affect clinical outcomes in patients with chronic HF of any cause. | Mitrohina and Kuryata (2008) |
| / | Non-diabetic participants | n = 8,749; participants on statin treatment (n = 2,142) | / | / | Participants on statin treatment had a 46% increased risk of T2DM. Insulin sensitivity was decreased by 24% and insulin secretion by 12% in individuals on statin treatment compared with individuals without statin treatment. | Cederberg et al. (2015) | |
| / | Patients with systolic HF (age ≥60 years) | n = 5,011 | / | / | Rosuvastatin was shown to reduce the risk of HHF by approximately 15%–20%, equating to approximately 76 fewer admissions per 1,000 patients treated over a median 33 months of follow-up. | Rogers et al. (2014) | |
| Fluvastatin | / | Patients with ischemic HF and hyperlipidemia | n = 29 | p.o., 80 mg/day | 3 months | Compared with those of healthy subjects, the heart rate recovery (HRR) values were significantly lower in the HF patients in both the 1st and 3rd minutes. The results revealed an improvement in HRR in HF patients by fluvastatin treatment. | Katircibasi et al. (2005) |
| A prospective uncontrolled study | Patients with ischemic HF | n = 29 | p.o., 80 mg/day | 12 weeks | After fluvastatin therapy, levels of IL-10 in the plasma were significantly increased and plasma TNF-α levels were significantly decreased. Fluvastatin therapy significantly improved HRR at 1 min after 12 weeks compared with baseline. | Tekin et al. (2016) | |
| An open label and prospective study | HF patients with idiopathic dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM) | n = 40; DCM group (n = 20), ICM group (n = 20) | p.o., 80 mg/day | 12 weeks | After fluvastatin therapy, functional capacity and LVEF improved and the levels of TNF-α and IL-6 decreased. The results revealed fluvastatin improved cardiac functions and the clinical symptoms in HF patients with either idiopathic dilated or ischemic etiology. | Gürgün et al. (2008) | |
| Simvastatin | A randomized, double-blind, placebo-controlled trial | Patients with coronary heart disease without evidence of HF | n = 4,444; placebo group (n = 2,223), simvastatin therapy group (n = 2,221) | p.o., 20 mg–40 mg | Followed for more than 5 years | Mortality was 31.9% in the placebo group and 25.5% in the simvastatin group among patients who developed HF. There were 45 hospitalizations because of acute HF in the placebo group and 23 in the simvastatin group. This indicates that long-term prevention with simvastatin reduces the occurrence of HF in a cohort of patients with coronary heart disease without previous evidence of CHF. | Kjekshus et al. (1997) |
| An open non-randomized study | Patients with diastolic chronic HF | n = 125; main group (n = 66), control group (n = 59) | / | 6 months | Significant increase in E (peak early diastolic left ventricular filling velocity) value by 14.1% and E/A (A peak left ventricular filling velocity at atrial contraction) ratio by 18.7% was found in the main group. It confirms that simvаstatin therapy resulted in significant improvement in the left ventricle diastolic function. | Pinchuk et al. (2015) | |
| A randomized, double-blind, controlled trial | Patients with chronic HF and preserved systolic function | n = 34; study group 1 (n = 20), control group 2 (n = 14) | p.o., 10 mg/day | 12 weeks | After 12 weeks of treatment with simvastatin, insulin levels in 30% patients have decreased in group 1 by 26.47% and HOMA index by 28.78% and in 19% patients in group 2 by 9.47 and 9.76%, respectively. It confirms that simvastatin is effective and safe for patients with chronic HF and preserved systolic function and reduces IR. | Mitrohina and Kuryata (2008) | |
| Fenofibrate | / | Patients with chronic HF | ICM patients (n = 57), DCM patients (n = 71) | / | / | In circulating angiogenic cells (CACs), fibronectin adhesion function was reversed by FF treatment, suggesting that FF reversed CACs and late EPC dysfunction in chronic HF patients. | Huang et al. (2020) |
| A randomized, double-blind, controlled trial | Patients with chronic HF | n = 70; standard therapy group (n = 35), FF therapy group (n = 35) | p.o., 0.2 g q.d. | 6 months | After FF combined with standard therapy, the patients’ serum PC Ⅰ, PC Ⅲ, LN, and HA concentrations decreased significantly, and the decrease was greater than that in the standard therapy alone. At the same time, the systolic and diastolic functions of the patient were significantly improved. | Xiaoyan et al. (2013) | |
| A randomized controlled clinical trial | Elderly patients with chronic HF(age 62–75 years) | n = 32; FF therapy group (n = 16), control group (n = 16) | 200 mg every night | 6 months | After 90 days of treatment, the NYHA classification, 6MWD, TG, and BUA levels of the FF group improved better than those in the control group. The LVEF and LVEDD of the FF group were significantly improved compared with those in the control group after 180 days of treatment. | Zhiming and Zhonghua (2011) | |