What Is a Silent Heart Attack Peer Reviewed Article
Ann Transl Med. 2018 Nov; 6(Suppl 1): S35.
Silent myocardial infarction and risk of center failure
Timir K. Paul
iSectionalisation of Cardiology, Due east Tennessee State University, Johnson City, TN, United states;
Debabrata Mukherjee
2Sectionalization of Cardiovascular Medicine, Texas Tech University Wellness Sciences Eye, El Paso, Texas, The states
Received 2018 Sep 10; Accustomed 2018 Sep 17.
Center failure (HF) is a major public health problem with a electric current gauge of half-dozen.5 meg Americans of more 20 years of age having a diagnosis of HF (1). This is an increase from 5.7 meg U.s. adults with HF based on estimates from the National Health and Diet Test Survey (NHANES) conducted 2009 to 2012 (1). Furthermore, epidemiological projections propose that HF prevalence will increase 46% in the next two decades, resulting in more than 8 meg adults with HF in the The states (ii). The National Heart, Lung, and Claret Plant (NHLBI)-sponsored Chicago Center Clan Detection Projection in Industry (CHA), Atherosclerosis Gamble in Communities (ARIC), and Cardiovascular Wellness Study (CHS) data reported that HF incidence is shut to 21 per 1,000 population later on 65 years of age and is probable to exist a detail issue going forwards among our aging population (3). HF is also a mutual trouble throughout the world with estimates of prevalence as high equally vi.7% in some parts of the world (i).
To gainsay/preclude HF, it is of import to understand the risk or predisposing factors for HF. Information technology should be noted that take chances factors for HF vary substantially across different regions of the world, with hypertension having strong association with HF in Latin America, Eastern Europe, the Caribbean, and sub-Saharan Africa (four). On the other hand, ischemic middle affliction prevalence among HF patients is highest among Europeans and North Americans and is a central chance/predisposing factor in these regions (4). The Olmstead Canton, MN, data indicate that ischemic heart affliction, hypertension, diabetes mellitus, obesity, and smoking are responsible for more than than 50% of HF cases in their population (5). The odds ratios (ORs) or relative risk (RRs) and the population attributable risks (PARs) for the different take a chance factors are equally follows: ischemic centre illness OR, iii.ane and overall PAR, 20% (college in males, 23% versus 16% in females); cigarette smoking RR, one.4 and PAR, 14%; hypertension RR, i.four and PAR, 20% (higher in females, 28% versus 13% in males); obesity RR, ii.0 and PAR, 12%; diabetes mellitus OR, 2.seven and PAR, 12%; dietary sodium intake RR, 1.four and PAR, not available; and valvular heart disease RR, i.5 and PAR, ii% with ischemic eye affliction having the strongest association with HF (6). The chance of HF with a known history of prior myocardial infarction (MI) is well established (7) but the function of prior undiagnosed or silent MI remains poorly divers. The upshot is particularly important and challenging as silent MI may account for approximately half of the total number of MIs. Since prior MI or ischemic eye disease remains a key predisposing factor for HF, information technology is crucial that we diagnose these silent MIs prior to development of HF. There is also certainly a need to better define the risk of HF with silent MI equally well equally possible strategies to diagnose silent MI.
To this stop, a recent study analyzed ix,243 participants from the ARIC study who were free of cardiovascular affliction at baseline to examine the clan of silent MI and clinically manifested MI with HF, as compared with patients with no prior MI (8). The incidence rate of HF was college in both clinically manifested MI and silent MI compared to no prior MI (incidence charge per unit per i,000 person-years was 30.iv, 16.2, and 7.8, respectively; P value <0.001). Multivariable adapted Cox proportional risk models as well demonstrated both clinically manifested MI and silent MI, compared to no MI, were significantly associated with HF (incidence rate per one,000 person-years was 2.85 and ane.35 respectively) (8). This written report underscores the importance of silent/undiagnosed MI as an of import risk cistron for development of future HF.
The side by side important clinical question is whether screening for silent MI with tests is cost-constructive and whether preventative therapies in patients with silent MI would be beneficial in reducing the risk of futurity HF. In the ARIC report, silent MI was defined as electrocardiographic (ECG) evidence of new MI at subsequent visits that was not present at the outset visit. The presence of Q waves in an ECG has been used to diagnose prior MI for decades. One study assessed the how accurate an ECG is in detecting prior MI compared with cardiac magnetic resonance imaging (MRI) and reported a very small sensitivity of 48.iv%; specificity of 83.5%; a positive predictive accuracy of 72.0%; and a negative predictive accurateness of 64.2% with ECG. Sensitivity was reasonably high with large MI (64%), but specificity declined to 72% (9). These information would appear to advise that the poor sensitivity and the modest negative predictive value of ECG criteria may seriously curb its accuracy for diagnosis of prior MI. Furthermore, the presence of a correct parcel co-operative block (RBBB) while typically considered to interfere with the ECG diagnosis of prior MI, recent clinical studies have reported association between RBBB and both false-positive as well as false-negative ECG diagnoses of MI (10). Hence, the finding of a new Q wave in an asymptomatic individual with a RBBB design on ECG needs boosted testing to confirm the diagnosis of prior MI. Similarly, left anterior fascicular cake may besides confound the diagnosis of prior MI based solely on Q waves (11). Based on these and other prove, an aberrant ECG may not be necessarily diagnostic of a prior silent MI.
To confirm silent MI in a patient with Q waves on ECG, the commencement step should be to repeat another ECG to rule out lead malposition equally a cause of aberrant ECG. If repeat ECG confirms show of prior MI, several imaging tests may be considered to confirm MI or presence of significant coronary artery disease such as echocardiography, radionuclide ventriculography, myocardial perfusion scintigraphy, cardiac/coronary computed tomography (CT) angiography and cardiac MRI. Freeman et al. assessed the power of radionuclide ventriculography and echocardiography to appraise regional left ventricular wall motility in patients with healed prior MI (12). They reported a sensitivity in detecting wall motility abnormalities of 83% for echocardiography and 77% for radionuclide ventriculography in the anterolateral expanse and upmost (95%, and 84% respectively) segment and least for the inferior segment (48%, 48%) (12). Specificity of echocardiography and radionuclide ventriculography was quite adept, ranging from 94% in the anterolateral myocardial wall to 71% in the septal myocardial wall for echocardiography, and from 91% in the inferior wall to 81% in the posterobasal and septal wall for radionuclide ventriculography (12). Nikolaou et al. examined the diagnostic accuracy of multidetector cardiac CT for detecting significant coronary heart illness in patients with known coronary heart disease and no prior coronary middle illness on both per patient and per segment analyses (xiii). In this study, multidetector cardiac CT showed a sensitivity of 82% and 86%, respectively for the identification of stenoses of >50% and >75% per segment, and specificity and negative predictive value were as high as 95% and 97%, respectively.
Cardiac MRI offers high spatial resolution and, in contrast to other imaging modalities mentioned higher up, has better ability to discern myocardial fibrosis and distribution of infarct in the myocardium and across different myocardial layers. One study reported a sensitivity of contrast-enhanced Cardiac MRI for the detection of prior MI was 91% and a specificity of 100% (14). Another study to assess the diagnostic precision of CMR to detect coronary heart disease reported a sensitivity of CMR of 86.5% (95% CI, 81–ninety%), specificity of 83.4% (95% CI, 79–86%), a positive predictive value of 77% (95% CI, 72–81%), and negative predictive value of ninety.5% (95% CI, 87.1–93.0%) (15). Imaging modalities for the diagnosis of prior MI and meaning coronary artery affliction are summarized in Table 1 . The option of subsequent testing to confirm MI in those with aberrant ECG volition depend on several factors such as local expertise, availability, renal function and patient and physician preference.
Tabular array 1
Imaging modalities for the diagnosis of prior myocardial infarction and significant coronary artery illness
| Modality | Sensitivity (%) | Specificity (%) | Positive predictive value (%) | Negative predictive value (%) |
|---|---|---|---|---|
| Electrocardiography | 48.4 | 83.5 | 72 | 64.ii |
| Echocardiography | 48–95 | 71–94 | NA | NA |
| Radionuclide ventriculography | 48–84 | 81–91 | NA | NA |
| Cardiac CT | 82–86 | 97 | NA | 97 |
| Cardiac MRI | 91 | 100 | 77.2 | 90.5 |
NA, not available; CT, computerized tomography; MRI, magnetic resonance imaging.
It is obvious that the diagnosis of previous silent MI is clinically important every bit it is an important predisposing factor for HF and overall cardiovascular morbidity and mortality (16). Once a prior MI is detected/confirmed on testing, early initiation of therapies may potentially forbid overt HF and may improve the patient's long-term prognosis.
Of note, the United states Preventive Service Task Force currently recommends against screening with ECG for the prognostication of cardiac events in asymptomatic individuals who are at low run a risk for such events and concludes that the current evidence is not sufficient to appraise benefits and risks of screening with ECG for the prediction of cardiovascular events in asymptomatic individuals at intermediate or high chance given lack of do good and potential for impairment as a result of unnecessary follow-upwards tests and interventions (17). The 2017 Focused Update recommends utilizing B-blazon natriuretic peptide biomarker-based testing for individuals at perceived adventure of developing HF, followed by multidisciplinary care including a cardiovascular specialist directing guideline evidence-based medical therapy, to prevent the evolution of left ventricular dysfunction (systolic or diastolic) and/or incipient HF (xviii). Judicious employ of B-blazon natriuretic peptide biomarker screening for those at gamble for HF and use of ECG in those at least at intermediate or at loftier chance seems like a reasonable approach to prevent this life-threatening condition. Finally, in addition to pharmacotherapies such every bit angiotensin converting enzyme inhibitors, angiotensin receptor blockers, aldosterone antagonists (xix) and beta-blockers (20), lifestyle modifications such equally regular physical practice, maintaining a healthy trunk weight, not smoking, eating fruits and vegetables likewise will assistance to reduce risk of HF and should be recommended to all individuals at chance for ischemic heart disease and HF. Figure 1 provides a simplified algorithm for clinicians to use ECG and B-blazon natriuretic peptide levels to selectively identify individuals at high adventure for HF using the atherosclerotic cardiovascular disease (ASCVD) risk score and appropriately manage those with prior MI or elevated biomarkers.
Simplified algorithm for identification and management of individuals at high risk of heart failure. ASCVD, atherosclerotic cardiovascular disease; MI, myocardial infarction; CT, computerized tomography; MRI, magnetic resonance imaging.
Footnotes
Conflicts of Interest: The authors have no conflicts of interest to declare.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6291605/
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