Effects of telmisartan on markers of ventricular remodeling in patients with acute myocardial infarction: comparison with enalapril

Abstract

Enalapril is effective in the suppression of left ventricular remodeling after acute myocardial infarction (AMI), but the effect of telmisartan is unclear. The consecutive 163 AMI patients underwent primary percutaneous coronary intervention and were randomized to telmisartan (n = 82) or enalapril (n = 81). Left ventriculography was performed in the acute and chronic (6 months) phases. Matrix metalloproteinase (MMP)-2 and MMP-9 activities were measured by zymography in the acute (days 1, 7, and 14) and chronic (6 months) phases. Plasma pentraxin3 (PTX3), a marker of vascular inflammation, was also measured. There were no adverse effects in the telmisartan group. The analysis of the left ventriculograms in the acute and chronic phases revealed no difference between the two groups. MMP-9 activities at days 7 and 14 and in the chronic phase were decreased compared to that at day 1 in both groups. MMP-2 activity was also decreased in the acute phase, but increased in the chronic phase in both groups. There was no difference in the plasma PTX3 level in the acute phase, but in the chronic phase, PTX3 was significantly lower in telmisartan than in enalapril group (2.6 ± 1.4 vs. 3.2 ± 1.6 ng/ml, p = 0.04). Telmisartan is well tolerated, shows similar effects on the markers of left ventricular remodeling to those of enalapril, and suppresses vascular inflammation more effectively than enalapril in AMI patients. Telmisartan can be an alternative to angiotensin converting enzyme inhibitor in patients with AMI.

High fat diet induced atherosclerosis is accompanied with low colonic bacterial diversity and altered abundances that correlates with plaque size, plasma A-FABP and cholesterol: a pilot study of high fat diet and its intervention with Lactobacillus rhamnosus GG (LGG) or telmisartan in ApoE−/− mice

“…The inhibitory effects of TLM on A-FABP [64, 65] and monocytic cell adhesions [66] may have been mediated by PPARƔ activation; and on MMP-9 [67–72] by Elk-1 phosphorylation inhibition [67]. While TLM was previously shown to lower cholesterol [73, 74], possibly through inhibiting intestinal cholesterol absorption [74], such reduction was not seen in the current study.…”

Serum Levels of IL‐1β, IL‐6, TGF‐β, and MMP‐9 in Patients Undergoing Carotid Artery Stenting and Regulation of MMP‐9 in a New In Vitro Model of THP‐1 Cells Activated by Stenting

“…However, the molecular mechanism of telmisartan on MMP-9 expression has not been fully clarified. There are several reports showing that overexpression of MMP-9 could be downregulated by telmisartan in various pathological conditions [30–34], while losartan, a non-PPAR- γ agonistic ARB, does not decrease MMP-9 activity [33]. What is more, the decrease of MMP-9 after incubation with telmisartan can be inhibited by addition of PPAR- γ antagonist GW9662 [30, 33].…”

“…Recent clinical trials found that telmisartan reduced inflammation, late lumen loss, and neointimal tissue proliferation in patients who underwent coronary artery stenting [27–29]. The inhibitory effects of telmisartan on MMP-9 expression are also well documented [30–34]. Additionally, PPAR- γ agonists are reported to suppress MMP-9 expression by blocking activator protein-1 (AP-1) activity, which could be regulated by ERK1/2/Elk-1 pathway [35–37].…”

The effects and mechanism of ginsenoside Rg1 on myocardial remodeling in an animal model of chronic thromboembolic pulmonary hypertension

“…MMPs are typical enzymes involved in myocardial remodeling, of which MMP-2 and MMP-9 play the mostimportant role [18]. MMP-2 and MMP-9 are gelatinases, which can degrade gelatin and normal collagen, causing the normal myocardial interstitium to be replaced by a fibrous myocardial interstitium, enlarging the ventricles and decreasing cardiac function.They haverecently aroused wide attention fortheir possible involvement in myocardial remodeling [19,20]. …”