Effects of atorvastatin pretreatment on infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

Hahn, Joo‐Yong; Kim, Hyun‐Joong; Choi, Yu Jeong; Jo, Sang‐Ho; Kim, Hak Jin; Lee, Sahng; Ahn, Kyoung-Ju; Song, Young Bin; Choi, Jin‐Ho; Choi, Seung–Hyuk; Choi, Young–Jin; Lee, Kyung-Han; Lee, Sang Hoon; Gwon, Hyeon‐Cheol

doi:10.1016/j.ahj.2011.08.011

Cited by 50 publications

(58 citation statements)

References 28 publications

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“…Several studies on the protective effects related to the use of statins seem to focus on the lipid-lowering and other properties of these drugs [19,20,21], such as improvement in endothelial function, homeostasis and inflammation, which result in the stabilization of coronary plaque. A variety of physiologic perturbations induced by the perioperative status may precipitate plaque instability and thrombosis specifically during emergency surgical procedures.…”

Section: Discussionmentioning

confidence: 99%

Patients with Stable Coronary Artery Disease Receiving Chronic Statin Treatment Who Are Undergoing Noncardiac Emergency Surgery Benefit from Acute Atorvastatin Reload

Xia

Shen³

et al. 2014

Cardiology

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Objective: This study was designed to investigate whether patients with stable coronary artery disease (CAD) receiving chronic statin treatment who are undergoing noncardiac emergency surgery benefit from acute atorvastatin reload. Methods: A total of 500 patients with stable CAD and regular administration of statin before noncardiac emergency surgery were randomized to atorvastatin reload (n = 250) or placebo (n = 250). All patients received atorvastatin treatment thereafter. The primary end point was a 30-day incidence of major adverse cardiac events (MACE). Secondary end points were the incidence of atrial fibrillation (AF) during hospitalization and length of hospital stay. Results: The primary end point occurred in 2.4% of patients treated with atorvastatin reload and in 8% in the placebo arm (p = 0.0088). The incidence of AF during hospitalization was 6.8% in patients treated with atorvastatin reload and 17% in the placebo arm (p = 0.0003). Compared with the placebo arm, the atorvastatin reload arm shortened the length of stay (9.8 ± 3.3 vs. 10.6 ± 3.5 days, p = 0.009). Multivariable analysis suggested that atorvastatin reload conferred a 65% risk reduction of 30-day MACE (odds ratio 0.35, 95% confidence interval 0.18-0.86; p = 0.005). Conclusion: The trial suggests that atorvastatin reload may improve the clinical outcome of patients with stable CAD receiving chronic statin treatment who are undergoing noncardiac emergency surgery.

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Section: Discussionmentioning

confidence: 99%

Patients with Stable Coronary Artery Disease Receiving Chronic Statin Treatment Who Are Undergoing Noncardiac Emergency Surgery Benefit from Acute Atorvastatin Reload

Xia

Shen³

et al. 2014

Cardiology

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“…A number of studies about the protective effects of statins seem to be based on both the lipid-lowering properties of these drugs and their capacity to improve endothelial dysfunction, inhibit inflammatory responses, increase nitric oxide bioavailability, serve as antioxidants, and stabilize atherosclerotic plaques [17,18,19]. The cholesterol-independent effects of statins can occur immediately after a single dose of these drugs.…”

Section: Discussionmentioning

confidence: 99%

Preoperative Rosuvastatin Protects Patients with Coronary Artery Disease Undergoing Noncardiac Surgery

Xia

Yin

et al. 2015

Cardiology

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Objectives: We explored whether preoperative rosuvastatin could protect the cardiac health of patients with coronary artery disease undergoing emergency, noncardiac surgery. Methods: We randomized 550 noncardiac emergency surgery patients with stable coronary artery disease on long-term statin therapy to treatment with and without preoperative rosuvastatin. All patients received rosuvastatin after surgery. We evaluated the incidence of myocardial necrosis and major adverse cardiovascular and cerebrovascular events (MACCE) 30 days and 6 months after surgery. Results: Creatinine kinase-myocardial band (CK-MB) isoform elevations occurred less frequently 12 and 24 h after noncardiac emergency surgery in the experimental group than in the control group (p = 0.029). After surgery, the incidence of MACCE was also lower in the experimental group than in the control group (p = 0.019). The difference was mainly due to the incidence of perioperative myocardial infarction (p = 0.029). Multivariable analysis found that rosuvastatin reload reduced the incidence of MACCE 52% 6 months after surgery (p = 0.03). Conclusions: Preoperative rosuvastatin reload therapy decreases the incidence of myocardial necrosis and MACCE after noncardiac emergency surgery in patients with stable coronary artery disease on long-term statin therapy.

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“…Acute high dose statin before PCI did not reduce infarct compared to low dose 70 ; prior statin exposure in patients with non-STEMI did reduce infarct size 71 …”

Section: Statinsmentioning

confidence: 99%

“…There are few clinical trials that have focused on the issue of whether statins can reduce myocardial infarct size in humans. Hahn et al 70 randomized 173 patients undergoing PCI for STEMI to high-dose atorvastatin (80 mg before PCI and for 5 days after) or to low dose (10 mg daily after PCI). Patients were included when PCI was performed within 12 hours of symptoms.…”

Section: Statinsmentioning

confidence: 99%

Current State of Clinical Translation of Cardioprotective Agents for Acute Myocardial Infarction

Kloner

2013

Circulation Research

138

112

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Abstract:There is continued interest in the concept of limiting myocardial infarct size with adjunctive agents administered along with reperfusion injury; however, there remains considerable controversy in the literature. The purpose of this article is to review the medical literature on clinical trials performed during the past 3 years that have attempted to reduce myocardial infarct size by administration of adjunctive therapies along with reperfusion therapy. A PubMed-driven literature search revealed a host of clinical trials focusing on the following prominent types of therapies: endogenous conditioning (postconditioning and remote ischemic conditioning); rapid cooling; pharmacological therapy (cyclosporine, abciximab, clopidogrel, tirofiban, erythropoietin, thrombus aspiration, adenosine, glucose-insulin-potassium, statins, antidiabetic agents, FX06, iron chelation, and ranolazine). Although there remains some controversy, quite a few of these studies showed that adjunctive therapy further reduced myocardial infarct size when coupled with reperfusion. Antiplatelet agents are emerging as some of the newest agents that seem to have cardioprotective capabilities. Postconditioning has become a bit more controversial in the clinical literature; remote conditioning, early and rapid cooling, adenosine, and ranolazine are intriguing therapies deserving of larger studies. Certain agents and maneuvers, such as erythropoietin, protein kinase C δ inhibitors, iron chelation, and intra-aortic balloon counterpulsation, perhaps should be retired. The correct adjunctive therapy administered along with reperfusion has the capability of further reducing myocardial injury during ST-segment-elevation myocardial infarction. ( infarct size reducing agents in clinical trials. Some of these disappointing agents included antibodies that prevent white blood cell adhesion to the endothelium; eniporide, a sodium/hydrogen exchange inhibitor; caldaret, an intracellular calcium-handling modulator; nicorandil, a potassium ATP channel opener/vasodilator; glucose-insulin-potassium (GIK); delcasertib (a protein kinase C δ inhibitor); and erythropoietin. 5 However, some agents and maneuvers that were observed to work in experimental models did show promise in clinical trials of MI under the right circumstances: postconditioning; remote conditioning; cyclosporine (maintains the mitochondrial permeability transition pore closed); intravenous adenosine infusions; atrial natriuretic peptide; mild hypothermia induced before reperfusion; supersaturated oxygen therapy and others. [4][5][6][7] The reasons for discrepancies between experimental findings and clinical trials have been reviewed in detail. 6,7 Since these reviews were written there have been a large number of new clinical trials recently published during the past 3 years, on the basis of literature searches through PubMed. These trials cover additional new studies on therapies, such as conditioning, abciximab, clopidogrel, erythropoietin, hypothermia, thrombectomy, intracoronary adenosine...

show abstract

Effects of atorvastatin pretreatment on infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

Cited by 50 publications

References 28 publications

Patients with Stable Coronary Artery Disease Receiving Chronic Statin Treatment Who Are Undergoing Noncardiac Emergency Surgery Benefit from Acute Atorvastatin Reload

Patients with Stable Coronary Artery Disease Receiving Chronic Statin Treatment Who Are Undergoing Noncardiac Emergency Surgery Benefit from Acute Atorvastatin Reload

Preoperative Rosuvastatin Protects Patients with Coronary Artery Disease Undergoing Noncardiac Surgery

Current State of Clinical Translation of Cardioprotective Agents for Acute Myocardial Infarction

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