Evidence-based medical therapy after percutaneous coronary intervention

Evidence-based medical therapy after percutaneous coronary intervention

ARTICLE IN PRESS Evidence-based Cardiovascular Medicine (2006) 10, 79–80 Evidence-based CARDIOVASCULAR MEDICINE www.elsevier.com/locate/ebcm GUEST ...

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ARTICLE IN PRESS Evidence-based Cardiovascular Medicine (2006) 10, 79–80

Evidence-based

CARDIOVASCULAR MEDICINE www.elsevier.com/locate/ebcm

GUEST EDITORIAL

Evidence-based medical therapy after percutaneous coronary intervention Wissan A Jaber, Charanjit S Rihal Mayo Clinic, Rochester, Minnesota, USA Percutaneous coronary intervention (PCI) with or without stenting alleviates symptoms and ischaemia among people with coronary artery disease and improves clinical outcomes after a myocardial infarction, but it does not mitigate the systemic atherosclerotic process. Indeed, PCI alone has not been found to lower long-term mortality or the rate of myocardial infarction (MI) in people with chronic stable angina.1 This editorial describes the importance of evidence-based medical treatment following PCI.

What is the problem? Recently a large trial found no benefit from an early invasive strategy when compared to a conservative approach in the presence of optimal medical treatment for people with unstable angina.2 In other studies, however, early revascularisation in people with non-ST elevation MI decreased mortality3 and repeat MI.4–6 These observations suggest that regional and systemic therapies are complementary. Optimal outcomes may be obtained by treating ischaemia and aggressive risk factor modification. In our opinion, the comparisons of medical therapies versus revascularisation have now become a distraction from what clinicians are trying to do – improve quality of life, improve the likelihood of survival, and prevent non fatal cardiac events such as myocardial infarction.

What is the solution? People admitted for PCI, particularly those presenting with acute coronary syndromes, may be Corresponding author.

particularly well motivated to undertake lifestyle modification, smoking cessation, and secondary prevention – so these non procedural aspects of care need to be emphasised. Aspirin, ACE inhibitors, beta-blockers and lipid lowering agents have all been found to improve survival and decrease cardiovascular events in people with coronary artery disease.7 Using a combination of all these cardioprotective agents may also be beneficial after PCI.8 Yet, in practice, prescription rates of these medications at discharge is still unacceptably low. In the Global Registry of Acute Coronary Events, in people with a non STelevation MI, aspirin was used in 86%, beta-blockers in 69%, ACE inhibitors in 49% and statins in 46% at discharge.9 Prescription rates may be increasing over time,1 but the numbers remain poor. We recently examined the PCI prospective database at the Mayo Clinic in Rochester, Minnesota, and collected information about medication use at discharge.8 Everyone who underwent a successful PCI for the first time was included. We calculated a simple score (medication score, or MEDS) for each person based on how many of the cardioprotective medication classes were prescribed, namely aspirin, ACE inhibitors, betablockers and lipid lowering agents. A MEDS score of 0 means that the patient was discharged with none of these medications, a score of 1 means they were discharged on one of them, and so forth up to a score of 4. A total of 7,745 people were followed up for an average of three years. Only 28% of people had a score of 4 and 71% had a score of either 3 or 4.

1361-2611/$ - see front matter & 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.ebcm.2006.04.013

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Fig. 1 Kaplan-Meier curve for adjusted MI-free survival by MEDS score.

Compared with people with lower scores, patients with higher scores were sicker at baseline, with more frequent history of recent MI, heart failure at presentation, and comorbid illnesses. Despite this, they had a lower mortality at follow up (7.5% for MEDS 4 group and 13% for MEDS 0 and 1 groups, p ¼ 0.014). In multivariable analysis that corrected for baseline characteristics, MI-free survival curves for the MEDS 3 and 4 groups had significant divergence from those of lower score groups (Fig. 1). The difference in outcome starts appearing early, and persists through follow up. The adjusted hazards ratio for death or MI was 0.67 (95% CI 0.52 to 0.86) for MEDS 4 and 0.72 (95% CI 0.57 to 0.91) for MEDS 3, when MEDS 0 or 1 was the reference group. Being discharged on more medications was beneficial whether an individual had a history of MI or not, although those with a history of MI had the largest benefit. Of note is that MEDS did not correlate with the target vessel revascularisation rate, corroborating that these medications do not reduce restenosis. Their benefit is due to effects on the generalised atherosclerotic process, which is not limited to the specific lesion or lesions targeted by PCI.

Implications These data reinforce the need for more aggressive evidence-based medical management in people with cardiovascular disease. While prior studies focused on people with a history of MI or heart failure, and on one specific medication, our analysis underscores the importance of combining these evidence-based medications in people undergoing PCI.

At the Mayo Clinic we use the index PCI procedure as an opportunity to institute aggressive secondary prevention with follow up through a systematic link with the Cardiovascular Health Clinic. Part of the responsibility of the interventional cardiologist is to ensure each person eligible to receive these drugs does in fact receive them. In our centre, everyone undergoing PCI is systematically referred to the preventive cardiology programme, risk factors are reviewed, preventive measures optimised, and follow up arranged. As a corollary, the simple MEDS score may be useful as a quality indicator following PCI.

References 1. Bucher HC, Hengstler P, Schindler C, Guyatt GH. Percutaneous transluminal coronary angioplasty versus medical treatment for non-acute coronary heart disease: metaanalysis of randomised controlled trials. BMJ 2000; 321(7253):73–7 2. de Winter RJ, Windhausen F, Cornel JH et al. Early invasive versus selectively invasive management for acute coronary syndromes. N Engl J Med 2005;353:1095–104. 3. Wallentin L, Lagerqvist B, Husted S et al. Outcome at 1 year after an invasive compared with a non-invasive strategy in unstable coronary-artery disease. Lancet 2000;356(9223): 9–16. 4. Invasive compared with non-invasive treatment in unstable coronary-artery disease: FRISC II prospective randomised multicentre study. FRagmin and Fast Revascularisation during InStability in Coronary artery disease Investigators. Lancet 1999;354(9180):708–15. 5. Cannon CP, Weintraub WS, Demopoulos LA et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med 2001;344(25): 1879–87. 6. Fox KA, Poole-Wilson PA, Henderson RA et. al. Interventional versus conservative treatment for patients with unstable angina or non-ST-elevation myocardial infarction: the British Heart Foundation RITA 3 randomised trial. Randomized Intervention Trial of unstable Angina. Lancet 2002;360(9335): 743–51. 7. Mukherjee D, Fang J, Chetcuti S et al. Impact of combination evidence-based medical therapy on mortality in patients with acute coronary syndromes. Circulation 2004;109(6): 745–49. 8. Jaber WA, Lennon RJ, Mathew V et al. Application of evidence-based medical therapy is associated with improved outcomes after percutaneous coronary intervention and is a valid quality indicator. J Am Coll Cardiol 2005;46(8):1473–8. 9. Steg PG, Goldberg RJ, Gore JM et al. Baseline characteristics, management practices, and in-hospital outcomes of patients hospitalized with acute coronary syndromes in the Global Registry of Acute Coronary Events (GRACE). Am J Cardiol 2002;90(4):358–63. 10. Rogers WJ, Canto JG, Lambrew CT et al. Temporal trends in the treatment of over 1.5 million patients with myocardial infarction in the US from 1990 through 1999: The National Registry of Myocardial Infarction 1, 2 and 3. J Am Coll Cardiol 2000;36:2056–63.