INTRODUCTION — Incidental findings are common in medicine and often lead to diagnostic and management dilemmas. This topic discusses one such patient group: asymptomatic individuals who are found to have a previously undiagnosed myocardial infarction (MI).
DEFINITIONS — According to the Fourth Universal Definition of MI, criteria for silent/unrecognized MI include any one of the following criteria [1] (see "Diagnosis of acute myocardial infarction", section on 'Prior MI'):
●Pathological Q waves with or without symptoms in the absence of non-ischemic causes
●Imaging evidence of loss of viable myocardium in a pattern consistent with ischemic etiology
●Pathoanatomical findings of a prior MI
The term "previously undiagnosed" MI is used synonymously to describe either a "silent" MI, when no symptoms are recalled by the patient, or an "unrecognized" MI in a patient who, despite experiencing atypical symptoms related to their MI, did not seek medical attention at that time as they did not recognize their symptoms to be harmful. The literature has used both of these terms interchangeably over the last few decades. In either case, owing to a lack of classic symptoms, there is an invariable delay in diagnosis and treatment of these patients, and often the MI will go undiscovered for months or even years.
Patients who present with symptoms or late complications of a "missed" MI (a term that refers to an individual with chest pain that is inappropriately managed as a noncardiac cause and subsequently found to have sustained an acute MI within the next 24 to 48 hours) represent a different patient cohort [2-4]. The approach to these patients is discussed separately. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the nonacute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction".)
CLINICAL PRESENTATION — There are two principal clinical scenarios in which a previously undiagnosed MI might be suspected. This diagnosis is most commonly associated with the finding of an abnormal electrocardiogram (ECG) with significant abnormalities, usually pathological Q waves, discovered incidentally during a routine health checkup [5,6]. Persistent ST-segment and T wave ECG abnormalities, though less specific for MI than Q waves, can also be signs of prior MI in asymptomatic patients. In this scenario, ECG patterns suggestive of prior MI are often identified by ECG machines with automated interpretation (eg, "cannot exclude anterior MI").
Previously undiagnosed MIs might also be detected by cardiac imaging. For example, this diagnosis could be inferred by the presence of regional wall motion abnormalities observed incidentally on an echocardiogram (obtained for a different reason) [7]. Similarly, sub-endocardial or transmural myocardial scarring detected by cardiac magnetic resonance imaging with late gadolinium enhancement (image 1) [8], intramyocardial fatty scars on cardiac computed tomography scans, or an irreversible perfusion defect found on myocardial perfusion scanning [9,10] are additional findings that can be unexpected. An initial noninvasive imaging strategy is recommended for many patients with suspected stable coronary disease [11]. We predict that in the future, as more tests are performed, incidental detection of previously undiagnosed MIs by cardiac imaging is likely to become an increasingly common occurrence.
PREVALENCE — It is not uncommon for prior undiagnosed MIs to be found in otherwise asymptomatic patients in community or outpatient settings. Observational studies conducted primarily in White males between 1976 and 1998 estimated between 20 to 40 percent of MIs are unrecognized [12-15]. For example, in a Framingham analysis (1990), unrecognized MI represented 30 percent of all infarctions [12]. Studies of the Reykjavik cohort demonstrated that 35 percent of MIs in males and 33 percent of MIs in females escaped clinical detection, with a prevalence of >5 percent in individuals aged 75 to 79 years [16,17]. Similarly, in the Honolulu Heart study, one-third of all Q wave MIs were clinically unrecognized [14]. In the Bronx Aging Study, which evaluated individuals at least 75 years of age, 43.5 percent of MIs were clinically unrecognized [18].
More contemporary population-based cohort studies, performed after 2000, confirm that up to one-fifth of MIs defined by electrocardiograph (ECG) Q wave criteria are clinically undetected. In the Cardiovascular Health study (2000), 901 of the 5888 (15.3 percent) participants, who were all ≥65 years of age, had ECG evidence of prior MI at baseline, of which 201 (22.3 percent) were classified as clinically unrecognized MI [19]. In the ICELAND MI study (2012), the prevalence of unrecognized MI by ECG criteria in a community dwelling cohort of older individuals in Iceland was 5 percent [20]. Isolated minor Q waves were also present in 377 of 6551 (5.8 percent) individuals in the Multi-Ethnic Study of Atherosclerosis (MESA) study (2013) [21]. Data from the Atherosclerosis Risk in Communities (ARIC) study (2002), where serial ECGs were reviewed before and after incident MIs diagnosed by hospital records in patients aged 45 to 65 years, showed that 20 percent of incident MIs were unrecognized, with African Americans having a slightly higher incidence than White Americans (23 versus 19 percent) [22].
In a case control study of 5869 patients with verified sudden cardiac death, 42.4 percent of patients without a clinical history of coronary artery disease had silent MI at autopsy, and 67 percent of these individuals had abnormal premorbid ECGs [23]. However, many MI patients do not develop Q waves or indeed any other persistent ECG abnormalities. In fact, up to 20 percent of patients with nonrecurrent MI have been noted to have normal ECGs four years after their event [24]. Thus, a highly sensitive imaging modality such as cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) has the potential to identify more undiagnosed MIs than screening with ECG. When compared with CMR, the overall sensitivity of Q wave ECG criteria for MI is roughly 50 percent, despite its high specificity of 85 to 95 percent [25,26]. Of 936 individuals studied in ICELAND-MI, 157 (17 percent) had unrecognized MI diagnosed by CMR, which was significantly higher than the 46 (5 percent) detected by ECG [20]. Similarly, the prevalence of CMR-detected unrecognized MI was 20 percent in another study of 259 selected 70-year-olds in Sweden [27]. Myocardial scarring was also reported in 146 of 1840 (8 percent) individuals in the MESA cohort who underwent CMR with LGE at year 10 of follow-up, of which 114 (78 percent) were undetectable by ECG or clinical adjudication [28]. In contrast to the high prevalence of CMR-detected MI in unselected older adult populations, perhaps unsurprisingly, undiagnosed MI was found to be very low (0.2 percent) in a study of 5000 middle-age patients without prior cardiovascular disease and with low- to intermediate-risk scores who underwent CMR imaging [29].
CLINICAL RISK PREDICTORS — Several clinical risk factors have been associated with an increased likelihood of undiagnosed MI. Older age [30], female gender [31,32], hypertension [33], and diabetes mellitus [34] are all associated with atypical MI symptoms, providing at least theoretical rationale that presence of these clinical factors might help predict which patients are more likely to have undiagnosed MI. Whether or not significant clinical benefit is gained from routine ECG screening for unrecognized MI in asymptomatic patients with clinical cardiovascular risk factors remains to be determined.
While it remains unclear why some patients with MI do not experience overt chest pain, it is likely that silent myocardial ischemia results from several mechanisms in these individuals, including autonomic dysfunction, cardiovascular autonomic neuropathy, abnormalities in afferent pain gating mechanisms, and central factors leading to altered pain perception [35-39]. (See "Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis".)
Age — Undiagnosed MI is more common in older patients. In the Reykjavik study discussed above, the prevalence of unrecognized MI increased steeply after age 60 years; it was 0.5 percent at age 50 years and exceeded 5 percent at age 75 years [16].
Sex — Sex-based differences have also been reported in some studies. Data from ARIC and ICELAND-MI [40,41], published in 2016, as well as the Rotterdam study [42] showed that undetected MI was more common in males than females, a finding that contrasts earlier reports where either no sex difference was observed [22] or increased prevalence was seen in females [43].
Hypertension — Although hypertension has been identified as an independent risk factor for undiagnosed MI in some studies [13,44], this relationship has not been consistently observed [14,16]. In a study that directly compared risk factors in older adult patients with unrecognized MI versus recognized MI, age, female gender, and hypertension were all significant predictors of unrecognized MI (odd ratios 1.18, 1.45, and 1.06, respectively, p<0.05 for all) [19].
Chronic kidney disease — The prevalence of MI has also been shown to be increased in patients with chronic kidney disease and microalbuminuria compared with those without [45]. In the Irbesartan Diabetic Nephropathy Trial, 14 percent of all first nonfatal MIs were clinically unrecognized in patients with diabetes mellitus, hypertension, and nephropathy during a mean follow-up of 2.5 years [46].
Diabetes — Diabetes mellitus is an important clinical risk factor for undiagnosed MI [47]. The prevalence of unrecognized Q wave MI at baseline in the Rosiglitazone Evaluated For Cardiac Outcomes and Regulation of Glycaemia in Diabetes (RECORD) study was 1.9 percent [48] and, similarly, in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study, the prevalence was 2.7 percent [49]. A slightly higher prevalence of silent MIs detected by ECG criteria were observed in patients with diabetes in the Fremantle cohort from Australia at 4 percent, which amounted to 44 percent of all Q wave MIs in this study [50]. In the United Kingdom Prospective Diabetes Study, 17.5 percent of patients with diabetes had Q waves identified on their ECG at baseline, rising to 30 percent at 12 years [51]; however, the ECG criteria used in this study might not have been specific enough to exclude a high proportion of false positives [52]. Undiagnosed MI also appears to be more common in patients with impaired fasting glucose compared with those with normal fasting glucose [53], and diabetes mellitus has been identified as an independent predictor of silent MI in patients referred for myocardial perfusion imaging [9]. However, among patients with type 2 diabetes, no clinical factor significantly increased the odds ratio for silent versus clinically recognized MI in the FIELD study that included analysis of 31,390 serial ECGs from 9795 patients aged 50 to 75 years over an average five-year follow-up [49]. In a retrospective analysis of 732 patients with diabetes mellitus and no known history of coronary heart disease from the DISCO cohort who underwent CT coronary artery calcification (CAC) scanning, 83 (21 percent) had intramyocardial fat suggestive of previous MI on their CT scan, including 28 (11.6 percent) patients with CAC score of 0 and 55 (37.6 percent) with CAC ≥300 [10].
PROGNOSIS — Data from large observational cohort studies show that patients with asymptomatic Q wave MI diagnosed by ECG criteria have a similar [19,40], or worse [14,18], long-term prognosis compared with those with clinically apparent MI in whom prompt treatment is initiated. The risk of incident cardiovascular events, including MI and cardiovascular death, for isolated minor Q waves in asymptomatic individuals was observed to be greater than in those without isolated Q waves in the MESA cohort (16.1 versus 10.4 per 1000-person year; p = 0.01) [21]. However, after adjusting for demographics, cardiovascular risk factors, socioeconomic status, and other electrocardiographic (ECG) abnormalities, the presence of minor isolated Q waves was strongly associated with incident cardiovascular events in Hispanic individuals (hazard ratio [HR] 2.62) but not in White or Black individuals. Evidence from the ARIC study showed that silent MI also increases the risk of heart failure by 35 percent compared with patients without MI [54]. Silent MI diagnosed by Q wave ECG criteria was an independent predictor of subsequent ischemic stroke in the Cardiovascular Health Study [55] and of sudden cardiac death in a meta-analysis of the ARIC and Cardiovascular Health Study cohorts [56].
Asymptomatic patients with cardiac magnetic resonance (CMR)-detected MI also have significantly increased risk for future cardiovascular disease (CVD) events compared with individuals without CMR-evidence of prior MI. In a study of 248 unselected 70-year-olds followed up for a mean 11 years, CMR-detected unrecognized MI was associated with >twofold risk of major adverse cardiac events (MACE) compared with those with no MI [57]. In another study, diabetic patients with prior MI detected by CMR had an even higher fourfold increase in MACE over a period of 17 months compared with those without [58]. Clinically unrecognized MI detected by CMR (but not ECG criteria) was also associated with increased mortality in ICELAND-MI after adjustment for covariates (HR 1.45; 8 percent increased absolute risk) [20]. Further evidence demonstrating the prognostic implications of CMR-detected undiagnosed MI is provided by two prospective longitudinal studies of patients with suspected stable coronary artery disease who lacked Q waves on their ECGs [59,60]. Moreover, the Strong Heart Study showed that echocardiographic segmental left ventricular wall motion abnormalities indicative of previous MI in adults without overt cardiovascular disease were associated with a 2.5-fold increased risk of cardiovascular events or death, independent of established risk factors [61].
The relatively high number of CVD events may be attributable to multiple factors, including a lower rate of the use of proven preventive therapy, such as aspirin and statins (see "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk" and "Management of low density lipoprotein cholesterol (LDL-C) in the secondary prevention of cardiovascular disease" and "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease"). In a post-hoc analysis of the MESA study, it was observed that both non-zero coronary artery calcification (CAC) score and CAC ≥100 were more common in patients with evidence of silent MI on ECG compared with those without, linking incidental ECG abnormalities with a prognostic imaging biomarker [62]. Moreover, the high prevalence of comorbid conditions observed in patients with silent MIs (including diabetes mellitus, chronic kidney disease, and systemic hypertension), as well as the fact that these patients are less likely to undergo percutaneous coronary artery stenting within the recommended 24- to 72-hour window following their event, are additional factors that potentially contribute the increased risk observed in this patient cohort.
DIFFICULTIES WITH ELECTROCARDIOGRAM DIAGNOSIS — The Fourth Universal definition of MI [1] defines pathological Q waves by the following criteria:
●Any Q wave in leads V2-V3 >0.02 seconds or QS complex in leads V2-V3
●Q wave ≥0.03 seconds and ≥0.1 mV deep or QS complex in leads I, II, aVL, aVF or V4-V6 in any two leads of a contiguous lead grouping
●R wave >0.04 seconds in V1-V2 and R/S >1 with a concordant positive T wave in absence of conduction defect
Q waves are more likely to be diagnostic of a prior MI when an inverted T wave is also present in the same lead. However, it is important to recognize that the finding of pathological Q waves, when combined with giant negative T waves, could indicate presence of an underlying inherited cardiomyopathy (eg, hypertrophic cardiomyopathy) rather than a true MI (see "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation"). In patients with hypertrophic cardiomyopathy, abnormal depolarization due to septal hypertrophy often results in Q waves in the inferior and lateral leads. A pseudoinfarct electrocardiographic (ECG) pattern with QS waves in two consecutive leads is also observed in approximately 50 percent of individuals with cardiac amyloidosis. Overall, the Q and QS wave patterns have moderate specificity (75 percent) and sensitivity (58 percent) for MI when compared with myocardial scintigraphy [63]. While the ECG criteria for MI listed above are more sensitive and have greater negative predictive value than previously recommended criteria, this comes at the cost of lower specificity and positive predictive value [64].
There are a number of situations in which a Q wave is present on an ECG but does not represent true MI. A QS complex in lead V1 is normal. A narrow (<0.03 seconds) and shallow (<25 percent of R wave) Q wave in lead III is normal if the frontal QRS axis is between -30 and 0 degrees. Similarly, a Q wave in aVL may be normal if the frontal QRS axis is between 60 and 90 degrees. Septal Q waves in leads I, aVL, aVF, or V4-V6 that are <0.03 seconds and <25 percent of the R wave amplitude in these leads are nonpathologic.
Although the presence of right bundle branch block (RBBB) is not usually thought to interfere with the ECG diagnosis of Q wave MI in clinical practice, several reports have shown associations between RBBB and both false-negative and false-positive ECG diagnoses of Q wave MI [65]. Therefore, the finding of a new Q wave in an asymptomatic individual with a RBBB pattern on ECG warrants further corroboration to establish the diagnosis of transmural infarction. Similarly, left anterior fascicular block (LAFB) poses a diagnostic challenge when Q waves are present in leads V2 or V3, which occurs in 5 percent of patients with LAFB [66].
Other situations that can mimic the ECG diagnosis of prior MI include respiratory Q waves in lead III arising from chest wall motion [67] and electrolyte abnormalities. Incorrect lead placement, left ventricular hypertrophy, and presence of left bundle branch block may also lead to a false positive ECG.
Finally, the ECG may represent MI, but there are multiple causes of MI that are not caused by obstructive coronary artery disease. Examples include nonischemic cardiomyopathies or myocarditis associated with scarring or coronary artery dissection.
FURTHER DIAGNOSTIC TESTING — The challenge for the general clinician is to determine which patients with abnormal or borderline ECG criteria for previously undiagnosed MI require further cardiac testing to confirm MI. Referral to a specialist may be useful in situations where the diagnosis remains in doubt. (See 'Referral to a specialist' below.)
To confirm MI in an asymptomatic patient with Q waves on ECG, the ECG should first be repeated to ensure that lead malposition or respiratory changes are not the cause (algorithm 1). The next step is to assess the cardiovascular risk profile of the patient and to inquire about the presence of cardiac symptoms in order to determine the clinical likelihood of an MI. From a practical point of view, in asymptomatic patients, clinical risk stratification tools designed to guide primary prevention treatment strategies, such as the "ASCVD" score that provides sex- and race-specific 10-year cardiovascular disease risk estimates based on pooled cohort data from studies performed in the United States [68] or the "QRISK3" [69] score based on general practice registry data from the United Kingdom, may be applied here. (See "Cardiovascular disease risk assessment for primary prevention: Risk calculators".)
For most patients in whom a repeat ECG has confirmed the presence of worrisome abnormalities, we consider troponin testing when a recent event is suspected because of symptoms recalled by the patient or evolving changes on serial ECGs.
In most patients, we obtain additional diagnostic (and prognostic) information using stress or anatomical imaging (eg, coronary computed tomography angiography [CCTA]) (see "Cardiac imaging with computed tomography and magnetic resonance in the adult", section on 'Cardiac CT'). For those patients at very low risk of a prior infarction based on the ECG, we may evaluate regional left ventricular function with echocardiography only.
The ischemic cascade paradigm indicates that myocardial ischemia predictably progresses through a series of steps to produce clinical disease by causing coronary flow maldistribution, hypoperfusion, diastolic dysfunction, systolic dysfunction, stress-induced ECG changes, and, ultimately, angina. Thus, a range of noninvasive imaging techniques that detect cardiac perfusion, wall thickness, and function can be used, with or without stress testing, to confirm presence of atherosclerotic coronary artery disease or infarcted myocardium in patients with suspected MI based on the ECG.
In an otherwise asymptomatic patient, echocardiography, myocardial perfusion scintigraphy, and cardiac magnetic resonance imaging (CMR) are functional tests that can be used to detect prior infarction. CCTA is another useful test with very high sensitivity to exclude the presence of obstructive atherosclerotic coronary artery disease in appropriately selected patients, particularly when the ECG diagnosis is uncertain. Unlike functional tests, CCTA directly interrogates coronary atherosclerotic plaque and can inform about the anatomical distribution and burden of disease, stenosis severity, and plaque morphological characteristics associated with adverse prognosis. CCTA is the recommended first-line imaging test for many patients with stable chest pain and ECG abnormalities. Aside from diagnosing coronary disease, evidence of prior MI on CCTA includes myocardial thinning, regional wall motion abnormalities on retrospectively gated cine imaging, and focal intramyocardial fat deposition (defined by low attenuation) due to healed MI.
Beyond standard transthoracic echocardiography, choice of first-line noninvasive testing for suspected coronary disease will be guided by local expertise and availability and should be directed by specialist input.
The strength of echocardiography is the ability to assess cardiac structure and function without the need for potentially nephrotoxic contrast or exposure to ionizing radiation. Regional myocardial function can be assessed with conventional two-dimensional imaging, three-dimensional imaging, tissue Doppler, or myocardial strain imaging using speckle tracking. A normal, good quality echocardiogram without wall motion abnormality and normal myocardial strain pattern in a patient with asymptomatic Q waves on ECG decreases the likelihood that there is a true prior MI. Use of echo contrast can also enhance detection of potentially scarred myocardium. Stress testing (with echocardiography, radionuclide imaging, or magnetic resonance imaging [MRI]) can also be used in such instances when the clinical suspicion remains high or the patient is otherwise at increased risk for having coronary artery disease. Myocardial global longitudinal strain, for example, increases during exercise stress echocardiography in healthy adults without MI [70] and is attenuated in those with coronary artery disease [71].
Radionuclide imaging can detect myocardial viability and inducible perfusion abnormalities. Radionuclide imaging can also identify myocardial motion, thickening, and ejection fraction; however, this technique has poor spatial resolution compared with echocardiography or MRI.
CMR offers high spatial resolution, the option for stress perfusion imaging, and is particularly useful for tissue characterization. Unlike echocardiography and radionuclide imaging, CMR can identify the pattern and severity of myocardial fibrosis throughout the myocardium and across myocardial layers (see "Clinical utility of cardiovascular magnetic resonance imaging", section on 'CMR after myocardial infarction'). The last point is especially relevant to patients presenting with asymptomatic Q waves on ECG because MRI can distinguish between subendocardial patterns of fibrosis versus other patterns of fibrosis (eg, mid-wall scarring due to myocarditis) that can mimic prior myocardial infarction. While CMR has advantages, echocardiography may be more accessible to many clinicians.
MANAGEMENT AFTER CONFIRMATION OF THE DIAGNOSIS — Long-term management of patients with previously undiagnosed MI due to obstructive coronary artery disease should not differ from that of clinically recognized MI, as lack of overt clinical symptoms at the time of presentation has no relation to the severity of underlying atherosclerotic coronary artery disease or indeed long-term prognosis. However, none of the clinical trials of MI were specifically designed to test efficacy of drug intervention in asymptomatic patients in whom the diagnosis was incidental.
Young females with MI who present without symptoms are a particularly high-risk group [72,73], in whom prompt treatment is critical [74]. (See "Clinical features and diagnosis of coronary heart disease in women" and "Coronary artery disease and myocardial infarction in young people" and "Management of coronary heart disease in women".)
The diagnosis and prognosis should be discussed with all patients.
Secondary prevention — Secondary preventive therapies should be started in all patients with MI. Secondary prevention begins with risk factor modification, including lifestyle intervention (eg, healthy eating, weight reduction, regular exercise, and smoking cessation), and treatment to correct high blood pressure, reduce low density lipoprotein cholesterol, and improve glycemic control in diabetic patients. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)
All patients with confirmed MI, regardless of whether or not they experienced symptoms at the time of presentation, should be prescribed long-term aspirin as the first-line antiplatelet agent to reduce the risk of death and nonfatal MI, provided there is no contraindication. (See "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease", section on 'Summary and recommendations'.)
Unless contraindicated, dual antiplatelet therapy with aspirin and a PY212 receptor inhibitor (eg, clopidogrel or ticagrelor) is recommended for 12 months after MI. While the timing of the event is often unknown in patients with previously undetected MI, a practical approach would be to consider a treatment strategy including dual antiplatelet therapy for one year in patients with recent symptoms or who are found to have an elevated troponin at the time of diagnosis. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy", section on 'Summary and recommendations' and "Acute non-ST-elevation acute coronary syndromes: Early antiplatelet therapy", section on 'Summary and recommendations'.)
High intensity statin therapy is recommended for all patients with MI, unless contraindicated, as this has been shown to improve mortality. This issue is discussed separately. (See "Low-density lipoprotein-cholesterol (LDL-C) lowering after an acute coronary syndrome", section on 'Summary and recommendations' and "Management of low density lipoprotein cholesterol (LDL-C) in the secondary prevention of cardiovascular disease", section on 'Summary and recommendations'.)
Long-term treatment with beta blockers (eg, bisoprolol) is recommended for all patients with MI. This issue is discussed separately. (See "Acute myocardial infarction: Role of beta blocker therapy", section on 'Long-term therapy'.)
Angiotensin converting enzyme (ACE) inhibitors are recommended for patients after MI with left ventricular systolic impairment ≤40 percent, heart failure (HF), hypertension, or diabetes. Moreover, there is also some prognostic evidence to support the use of ACE inhibitors in patients with stable atherosclerotic disease without HF or left ventricular systolic dysfunction [75]. An angiotensin receptor blocker may be used when there is a contraindication or intolerance to ACE inhibitor. This issue is discussed separately. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use".)
Mineralocorticoid receptor antagonists (eg, eplerenone) are also indicated in patients with left ventricular systolic impairment ≤40 percent and either HF or diabetes after an MI, who are receiving therapeutic doses of ACE inhibitor and beta blocker, and who lack significant renal dysfunction or hyperkalaemia [76,77].
Angiotensin receptor-neprilysin inhibitor (as a replacement for ACE inhibitor) and SGLT2 inhibitors are recommended in patients with symptomatic HF and reduced ejection fraction to reduce the risk of HF hospitalization and death. (See "Overview of the management of heart failure with reduced ejection fraction in adults".)
Pharmacologic management of patients with prior MI who develop symptoms of stable angina is discussed elsewhere [78]. (See "Chronic coronary syndrome: Overview of care".)
Patients with Q waves on their ECG who are determined to not have MI nevertheless have an increased risk of future cardiovascular events compared with the general population and should therefore be considered for aggressive primary prevention. However, there are no randomized trials or comparative effectiveness research studies to inform long-term management for patients with Q waves on ECG that do not represent true MI.
Prognostic evaluation — Similar to patients with a new diagnosis of stable ischemic heart disease, we refer the patient for stress testing or noninvasive anatomical imaging with computed tomographic coronary angiography to screen for severe coronary artery disease. (See "Chronic coronary syndrome: Overview of care", section on 'Determining disease severity'.)
For patients with stress evidence of severe disease or prognostically significant anatomical disease, we proceed with optimal medical therapy and diagnostic coronary angiography and revascularization if indicated. (See "Chronic coronary syndrome: Overview of care", section on 'Identifying patients for angiography and revascularization'.)
Routine follow-up — Patients with confirmed undiagnosed MI who are asymptomatic, have normal cardiac function, who lack prognostically significant coronary disease (ie, left main stem or multi-vessel disease), and do not have functional myocardial ischemia can be followed by their primary care clinician without the need for ongoing specialist care. This routine follow-up should include regular monitoring of modifiable cardiovascular risk factors to ensure good blood pressure, lipid, and glycemic control. Provided there are no concerns, we suggest these checks are performed on a six monthly to yearly basis.
REFERRAL TO A SPECIALIST — Patients with prior MI who develop symptoms of stable angina, heart failure, arrhythmias, or other MI complications should be referred for specialist opinion.
As such, patients with previously undiagnosed MI should be educated about the risks of their condition and made aware of symptoms (typical and atypical) that might indicate the need for urgent medical attention. Similarly, asymptomatic patients who are identified on noninvasive testing to have impaired left ventricular systolic dysfunction, significant myocardial ischemia, or anatomically prognostic coronary artery disease should also be referred to specialist input. In this context, invasive coronary angiography might be indicated to define the anatomy, even in asymptomatic patients, to guide management decisions, including the need for coronary revascularization. Specialist input might also be required in cases where, after initial assessment, alternative diagnoses (eg, cardiomyopathy, myocarditis, or cardiac amyloidosis) are suspected.
Even if asymptomatic, patients with pathological Q waves and giant negative T waves should be referred to a specialist center for evaluation of a possible inherited cardiomyopathy if a diagnosis of old MI has been excluded.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic coronary syndrome".)
SUMMARY AND RECOMMENDATIONS
●Definitions – The term "previously undiagnosed" myocardial infarction (MI) is used synonymously to describe either a "silent" MI, when no symptoms are recalled by the patient, or an "unrecognized" MI in a patient who, despite experiencing atypical symptoms related to their MI, did not seek medical attention at that time. (See 'Definitions' above.)
●Clinical presentation – There are two principal clinical scenarios in which a previously undiagnosed MI might be suspected: an abnormal electrocardiogram (ECG) with significant abnormalities, usually pathological Q waves, discovered incidentally during a routine health checkup, and an abnormal noninvasive cardiac imaging test obtained for another reason.
●Prognosis – Patients with previously undiagnosed MI have a similar or worse long-term prognosis compared with those with clinically apparent MI in whom prompt treatment is initiated. (See 'Prognosis' above.)
●Risk stratification – Patients with previously undiagnosed MI should undergo risk stratification using available risk score and should have additional testing with stress or anatomical imaging. (See 'Further diagnostic testing' above and 'Prognostic evaluation' above.)
●Long-term medical management – In patients with previously undiagnosed MI due to obstructive coronary artery disease, long-term medical management is similar to that of clinically recognized MI and should include long-term aspirin, beta blocker, and statin. (See 'Management after confirmation of the diagnosis' above.)
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