American Heart Journal
Volume 151, Issue 4 , Pages 768-770, April 2006

The clinically unrecognized Q-wave myocardial infarction: What does it mean and what should we do?

  • David Aguilar, MD

      Affiliations

    • Corresponding Author InformationReprint requests: David Aguilar, MD, Cardiovascular Division, Baylor College of Medicine, 1709 Dryden Street-BCM 620, Suite 500, Box 13, Houston, TX 77030.

Division of Cardiology, Baylor College of Medicine, Houston, TX 77030

Article Outline

 

Since the original description of clinically unrecognized myocardial infarction in 1912 by Herrick,1 several epidemiologic studies have shown that clinically unrecognized myocardial infarctions, as detected by the presence of abnormal Q waves on surveillance electrocardiograms, may represent between 20% and 40% of all myocardial infarctions.2, 3, 4, 5, 6, 7, 8, 9, 10, 11 Importantly, these clinically unrecognized Q-wave myocardial infarctions carry a prognosis similar to those infarctions that are clinically recognized.4, 5, 7, 8, 11

Despite significant data describing the prevalence and adverse prognosis associated with clinically unrecognized Q-wave myocardial infarctions, there are several unresolved issues regarding the clinical entity of unrecognized Q-wave myocardial infarction. The prevalence estimates derived from epidemiologic studies vary substantially, a finding that is likely attributed to the heterogeneity in the definitions used. A gold standard for the definition of a clinically unrecognized Q-wave myocardial infarction does not exist, and multiple diagnostic criteria have been applied in epidemiologic studies. In addition, the reliance of Q waves on the electrocardiogram to establish the diagnosis limits the ability to identify clinically unrecognized non–Q-wave infarctions, which comprise a significant proportion of all myocardial infarctions.12 Alternatively, Q-wave abnormalities may be seen in a variety of conditions other than a myocardial infarction, including conduction abnormalities, ventricular hypertrophy, myocardial infiltration, anatomical rotation of the heart, and electrocardiographic lead placement errors.

Not much is known regarding the predisposing conditions that are associated with clinically unrecognized Q-wave myocardial infarction. Although certain cardiac risk factors such as age,3, 8, 13 hypertension,2, 3, 13 and diabetes14, 15 have been suggested to predispose to the development of unrecognized Q-wave myocardial infarctions, multivariable analyses suggest that these risk factors are simply the traditional risk factors for coronary artery disease. Using multivariable analyses of data from the Cardiovascular Health Study, independent predictors of unrecognized myocardial infarction include the absence of angina, the absence of congestive heart failure, and reduced FEV1 (although the latter predictor was of borderline significance, P = .07).11 The identification of reduced anginal symptoms in those with clinically unrecognized myocardial infarction has been suggested as evidence of a “defective anginal warning system,” but the potential for diagnosis bias must be considered (ie, those patients with angina are more likely to be treated by a physician and may be more likely to be evaluated for atypical symptoms). Similarly, those with congestive heart failure may be more likely to be under the care of a physician and be evaluated for cardiac symptoms. Finally, those with pulmonary disease may be more likely to have cardiac symptoms attributed to pulmonary disease than a cardiac origin.

Despite these areas of uncertainty, multiple epidemiologic studies have demonstrated that clinically unrecognized Q-wave myocardial infarctions have significant clinical implications.4, 5, 6, 7, 8, 11, 13 In the Framingham Study, within 10 years of the detection of unrecognized Q-wave myocardial infarction, 58% of men and 48% of women had died, a rate similar to those who had recognized myocardial infarctions.13 In a more recent analysis from the Cardiovascular Health Study, the 7-year mortality was similar between those with clinically unrecognized and those with recognized myocardial infarctions (21% vs 25%, respectively).11

In this issue of the Journal, Ammar et al16 provide further insight into the relationship of clinically unrecognized Q-wave myocardial infarctions, echocardiographic abnormalities, and cardiopulmonary symptoms. Using a cross-sectional study design, the authors used 2042 Olmstead County residents enrolled in the Olmstead County Heart Function Study to identify 81 individuals with unrecognized Q-wave myocardial infarctions (according to the Minnesota code) and 101 individuals with recognized myocardial infarctions. Consistent with prior studies, most traditional cardiac risk factors were similarly elevated in both those with clinically unrecognized Q-wave myocardial infarction and recognized myocardial infarction. The authors demonstrate that those individuals with unrecognized Q-wave myocardial infarctions had more structural echocardiographic abnormalities than those without myocardial infarction, but to a lesser degree than those with recognized myocardial infarction. The level of brain natriuretic peptide for those with clinically unrecognized Q-wave myocardial infarction was also intermediate between those without myocardial infarction and those with recognized myocardial infarction. Upon this background of clinical and echocardiographic differences, the authors show that certain cardiopulmonary symptoms such as dyspnea on exertion, orthopnea, palpitations, and history of fluid overload tended to increase across the spectrum of infarct recognition. These findings suggest that clinically unrecognized Q-wave myocardial infarctions likely represent underlying cardiac pathology that is somewhat intermediate in severity between those without myocardial infarction and those with recognized myocardial infarction.

The presence of these cardiopulmonary symptoms was associated with increased mortality. Using multiple logistic regression models, the authors demonstrate that the associations of exertional dyspnea and fluid overload with unrecognized Q-wave myocardial infarction were independent of age, sex, and pulmonary disease and that the effects were markedly reduced when adjusted for global echocardiogram parameters of cardiac function, particularly diastolic dysfunction, with minimal impact when adjusted for regional wall motion abnormalities alone. The authors also suggest that the increased risk of mortality associated with these symptoms is partially mediated by clinically unrecognized Q-wave myocardial infarction, as there is mild attenuation of the hazard ratio (HR) associated with these symptoms when accounting for clinically unrecognized Q-wave myocardial infarction.

Finally, the presence of clinically unrecognized Q-wave myocardial infarction increased the risk of death when compared with those without myocardial infarction (HR = 3.67, P = .0001), a finding that was of borderline statistical significance after adjusting for potential clinical confounders (age, sex, diabetes, hypertension, and smoking) (HR = 1.82, P < .059) or when adjusted for diastolic dysfunction (HR = 1.94, P = .08). When stratified by abnormalities on echocardiogram, the subset of individuals with clinically unrecognized Q-wave myocardial infarction and echocardiographic abnormalities had increased risk of death; on the contrary, in the small subset of patients (n = 20) with clinically unrecognized myocardial infarction and no echocardiographic abnormality, the hazard was not increased (HR = 0.99, P = .99).

The incorporation of echocardiographic information in this article adds several novel features to the body of literature regarding clinically unrecognized Q-wave myocardial infarction. Despite the presence of Q waves on an electrocardiogram, the presence of echocardiographic regional wall abnormalities was identified in only 12% of those with clinically unrecognized Q-wave myocardial infarction and 53% of those with recognized Q-wave myocardial infarction. Importantly, despite the absence of regional wall motion abnormalities, those individuals with clinically unrecognized Q-wave myocardial infarction, in the presence of other echocardiographic abnormalities such as left atrial and left ventricular enlargement and/or global systolic or diastolic dysfunction, had increased risk compared with those without myocardial infarction. This finding is important because clinicians, upon discovering a previously undocumented Q-wave myocardial infarction on an electrocardiogram, will often order an echocardiogram to evaluate for regional wall motion abnormalities. In the absence of regional wall motion abnormalities, a clinician might dismiss electrocardiographic findings as a false positive. The adverse prognosis associated with clinically unrecognized Q-wave myocardial infarction in the setting of other echocardiographic abnormalities suggests that this dismissal would be premature. Whether these Q-wave abnormalities represent infarcts that are too small for recognition by echocardiogram or represent other myocardial pathology than pure myocardial infarction remains unclear. Future population studies using more sensitive techniques such as nuclear perfusion imaging or magnetic resonance imaging assessing for myocardial scar may shed more insight into the underlying pathology of clinically unrecognized Q-wave myocardial infarction.

One area that deserves further attention relates to the interplay of diastolic dysfunction, clinically unrecognized myocardial infarction, and prognosis. The most common echocardiographic abnormality in those with unrecognized Q-wave myocardial infarction was diastolic dysfunction, which was seen in 57% of individuals. Although the exact definition for diastolic dysfunction was not reported in the article, the presence of diastolic dysfunction markedly attenuated the hazard associated with clinically unrecognized Q-wave myocardial infarction and attenuated the relationship between cardiopulmonary symptoms and clinically unrecognized Q-wave myocardial infarction. The presence of diastolic dysfunction on echocardiogram has been previously associated with increased all-cause mortality, after adjusting for age, sex, and ejection fraction.17 The presence of underlying coronary artery disease and diastolic dysfunction may portend an even worse prognosis.18 Although the relationship of diastolic function, cardiopulmonary symptoms, and prognosis was explored in the article, the independent relationships of age, diastolic dysfunction, and prognosis were not fully addressed.

The authors conclude that measures of secondary coronary prevention should be instituted in subjects with clinically unrecognized Q-wave myocardial infarction with subtle echocardiographic abnormalities. Although the exact underlying pathology in mechanisms and pathology by which clinically unrecognized Q-wave myocardial infarction is represented remains unclear, these individuals with echocardiographic abnormalities are at a higher risk. Clinical trials have led to beneficial therapies in those with recognized myocardial infarction. Whether these same therapies will reduce the risk associated with clinically unrecognized Q-wave myocardial infarction is yet to be determined. Until these issues are fully resolved, we feel that it is reasonable to implement aggressive strategies of secondary prevention in individuals with unrecognized Q-wave myocardial infarctions as determined by electrocardiogram, even in the absence of obvious regional wall motion abnormalities. These strategies include screening and treatment of conventional cardiac risk factors and further noninvasive testing for risk stratification, particularly if other abnormalities are identified on an echocardiogram.

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References 

  1. Herrick JB. Clinical features of sudden obstruction of the coronary arteries. By James B. Herrick, Landmark article (JAMA 1912) JAMA. 1983;250:1757–1765
  2. Rosenman RH, Friedman M, Straus R, et al. Coronary heart disease in the Western Collaborative Group Study. A follow-up experience of 4 and one-half years. J Chronic Dis. 1970;23:173–190
  3. Medalie JH, Goldbourt U. Unrecognized myocardial infarction: five-year incidence, mortality, and risk factors. Ann Intern Med. 1976;84:526–531
  4. Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction. An update on the Framingham study. N Engl J Med. 1984;311:1144–1147
  5. Grimm RH, Tillinghast S, Daniels K, et al. Unrecognized myocardial infarction: experience in the Multiple Risk Factor Intervention Trial (MRFIT). Circulation. 1987;75(3 Pt 2):II6–II8
  6. Yano K, MacLean CJ. The incidence and prognosis of unrecognized myocardial infarction in the Honolulu, Hawaii, Heart Program. Arch Intern Med. 1989;149:1528–1532
  7. Nadelmann J, Frishman WH, Ooi WL, et al. Prevalence, incidence and prognosis of recognized and unrecognized myocardial infarction in persons aged 75 years or older: The Bronx Aging Study. Am J Cardiol. 1990;66:533–537
  8. Sigurdsson E, Thorgeirsson G, Sigvaldason H, et al. Unrecognized myocardial infarction: epidemiology, clinical characteristics, and the prognostic role of angina pectoris. The Reykjavik Study. Ann Intern Med. 1995;122:96–102
  9. de Bruyne MC, Mosterd A, Hoes AW, et al. Prevalence, determinants, and misclassification of myocardial infarction in the elderly. Epidemiology. 1997;8:495–500
  10. Jonsdottir LS, Sigfusson N, Sigvaldason H, et al. Incidence and prevalence of recognised and unrecognised myocardial infarction in women. The Reykjavik Study. Eur Heart J. 1998;19:1011–1018
  11. Sheifer SE, Gersh BJ, Yanez ND, et al. Prevalence, predisposing factors, and prognosis of clinically unrecognized myocardial infarction in the elderly. J Am Coll Cardiol. 2000;35:119–126
  12. Furman MI, Dauerman HL, Goldberg RJ, et al. Twenty-two year (1975 to 1997) trends in the incidence, in-hospital and long-term case fatality rates from initial Q-wave and non–Q-wave myocardial infarction: a multi-hospital, community-wide perspective. J Am Coll Cardiol. 2001;37:1571–1580
  13. Kannel WB, Cupples LA, Gagnon DR. Incidence, precursors and prognosis of unrecognized myocardial infarction. Adv Cardiol. 1990;37:202–214
  14. Boland LL, Folsom AR, Sorlie PD, et al. Occurrence of unrecognized myocardial infarction in subjects aged 45 to 65 years (the ARIC study). Am J Cardiol. 2002;90:927–931
  15. Aguilar D, Solomon SD, Kober L, et al. Newly diagnosed and previously known diabetes mellitus and 1-year outcomes of acute myocardial infarction: the VALsartan In Acute myocardial iNfarcTion (VALIANT) trial. Circulation. 2004;110:1572–1578
  16. Ammar KA, Jacobsen SJ, Makwana R, et al. Unrecognized myocardial infarction: the association with cardiopulmonary symptoms and mortality is mediated via echocardiographic abnormalities of global dysfunction instead of regional dysfunction. The Olmstead County Heart Function Study. Am Heart J. 2005;
  17. Redfield MM, Jacobsen SJ, Burnett JC, et al. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA. 2003;289:194–202
  18. O'Connor CM, Gattis WA, Shaw L, et al. Clinical characteristics and long-term outcomes of patients with heart failure and preserved systolic function. Am J Cardiol. 2000;86:863–867

PII: S0002-8703(05)00982-8

doi:10.1016/j.ahj.2005.10.015

American Heart Journal
Volume 151, Issue 4 , Pages 768-770, April 2006