WINSTON SALEM, NC — New silent MI at electrocardiography predicted future onset of heart failure (HF) independently of age, sex, and a range of clinical HF risk factors, although not as strongly as it predicted clinical MI, in a diverse observational cohort study[1].
The results from the multiethnic, population-based Atherosclerosis Risk in Communities (ARIC) cohort, published January 1, 2018 in the Journal of the American College of Cardiology, strengthen and extend decades of evidence from that longitudinal study as well as other research that silent or unrecognized MIs are common and raise the risk of clinical coronary heart disease (CHD).
“An accidental finding of silent MI, or manifestations of silent MI on the ECG, should not be taken lightly,” senior author Dr Elsayed Z Soliman (Wake Forest School of Medicine, Winston Salem, NC) told theheart.org | Medscape Cardiology.
“Previously in ARIC[2] we showed that [silent MI] is associated with an increase in all-cause death,” he said. The current finding that it is also associated with HF suggests that silent MI “is as bad as clinical myocardial infarction.”
Yet, despite such consistent and generally well-regarded evidence from ARIC, the Multi-Ethnic Study of Atherosclerosis (MESA) study, the Rotterdam Study, and other observational studies, silent or unrecognized MIs aren’t standard end points in randomized trials and so may not get due consideration in clinical practice.
An accompanying editorial emphasizes that point[3]. The current study “provides new and consistent evidence regarding the consequences of silent MI,” it notes.
“The growing body of evidence on ECG-defined silent MI over the past 10 years,” write the editorialists, led by Dr C Michael Gibson (Beth Israel Deaconess Medical Center, Boston, MA), “supports its use as a meaningful clinical end point.”
The new ARIC analysis, with first author Dr Waqas T Qureshi (Wake Forest School of Medicine), is based on 9243 participants who were deemed free of cardiovascular disease at their baseline workup, which included ECG, conducted during 1987 to 1989.
Of the cohort, 10.6% had a first HF hospitalization over a median follow-up of 13 years. The cumulative rate among patients with incident clinical MI was 31.4% and among those with new silent MI by ECG was 17.7%.
Both rates were significantly higher than the 9.5% rate of HF among those without signs of any MI during the follow-up (P<0.001).
Silent MI was defined in this analysis as ECG evidence of MI, without clinical evidence of MI, that wasn’t present at baseline but was observed at any follow-up visit in ARIC. Clinical MIs were determined by physician review of ECG, biomarkers, symptoms, and other standard criteria. Silent MIs were adjudicated at a central ECG laboratory.
The adjusted hazard ratio (HR) for HF for participants developing silent MI compared with those who didn’t show any kind of MI was 1.35 (95% CI 1.02–1.78, P=0.035). For those developing clinical MI, it was 2.85 (95% CI 2.31–3.51, P<0.001).
Multivariates in the analysis included age, sex, race, body mass index, smoking status, heart rate, systolic blood pressure, use of antihypertensives, and diabetes status.
The authors acknowledge a few limitations of their analysis, including the exclusion of about 40% of ARIC participants because of missing ECG data, and the lack of information from other ways to define silent MI, such as perfusion scans, wall-motion studies, or other assessments of myocardial viability.
The current study obviously can’t show that silent MIs are a cause of some HF, observe Gibson et al, but “the association between myocardial damage leading to electrically inert tissue (a Q-wave) and subsequent heart failure would be apparent to any cardiologist.”
It remains, therefore, that “Early identification of patients with an increased risk of heart failure is crucial because early initiation of treatment may improve the patient’s prognosis and may reduce the related healthcare costs.” But the group also notes there isn’t much clinical trial evidence supporting that approach.
Silent MI should be managed as a risk factor for clinical CHD, according to Soliman, and “taken seriously” whenever its signs appear on an ECG that is part of a standard workup for heart disease.
Soliman has no relevant disclosures. Qureshi discloses serving as a consultant for Medicure and owning Medtronic stock in the past 12 months. The remaining authors had no relevant disclosures. Gibson reports he has received consulting honoraria from Novo Nordisk; disclosures for the other editorialists are listed in their report.
Follow Steve Stiles on Twitter: @SteveStiles2. For more from theheart.org | Medscape Cardiology, follow us on Twitter and Facebook.
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