Abnormal Q-waves Research Articles

Association Between ECG Abnormalities and Mortality in a Low-Risk Population.

The ECG is a simple, noninvasive screening method for cardiovascular disease and arrhythmia. The impact of ECG abnormality on mortality is not certain in low-risk populations. To address this, we evaluated the association between ECG abnormality and mortality. We retrospectively assessed baseline ECG and all-cause mortality and cardiovascular mortality in 660 383 patients presenting for medical check-ups. Baseline ECG abnormalities were classified according to the Minnesota Code. Among the total 660 383 participants, 23 609 (3.6%) had major and 110 038 (16.7%) had minor ECG abnormalities. All-cause mortality occurred in 7751 patients (1.1%) and cardiovascular mortality in 1180 (0.18%) over a median follow-up period of 8.8 years. Major ECG abnormalities were associated with all-cause mortality (hazard ratio [HR], 1.11 [95%, 1.03-1.2]) and cardiovascular mortality (HR, 1.92 [95% CI, 1.63-2.27]) compared with no ECG abnormalities. All-cause mortality was associated with right atrial enlargement (HR, 2.11 [95% CI, 1.1-4.07]), left atrial enlargement (HR, 1.76 [95% CI, 1.1-2.84]), sinus tachycardia (HR, 1.52 [95% CI, 1.15-2.01]), complete atrioventricular block (HR, 2.1 [95% CI, 1.05-4.2]), atrial fibrillation (HR, 1.52 [95% CI, 1.26-1.84]), and left ventricular hypertrophy (HR, 1.15 [95% CI, 1.02-1.3]). Cardiovascular mortality was associated with left atrial enlargement (HR, 4.52 [95% CI, 2.15-9.5]), atrial fibrillation (HR, 3.22 [95% CI, 2.33-4.46]), left ventricular hypertrophy (HR, 1.72 [95% CI, 1.35-2.19]), major Q-wave abnormality (HR, 1.6 [95% CI, 1.08-2.39]), and major ST-T abnormality (HR, 1.76 [95% CI, 1.01-3.04]). ECG abnormalities, including left atrial enlargement, left ventricular hypertrophy, atrial fibrillation, and major Q-wave and ST-T abnormalities, were associated with cardiovascular mortality in a low-risk population.

Abstract 16516: CMR-ECG Imaging in Hypertrophic Cardiomyopathy Detects Electrophysiological Abnormalities Before Hypertrophy or ECG Changes

INTRODUCTION: In hypertrophic cardiomyopathy (HCM), ventricular arrhythmia associates with severity of LVH and scar, and presence vs absence of a sarcomeric gene mutation (G+LVH+ vs G-LVH+). Also, ECG changes in subclinical HCM (G+LVH-) signal increased risk of phenotype progression. HYPOTHESES: ECG Imaging (ECGI) can detect: i) subtle electrophysiological (EP) abnormalities in subclinical HCM (pre-LVH). ii) EP abnormalities related to genetic status (G+ vs G-LVH+) and structural changes (late gadolinium enhancement [LGE], max. wall thickness [MWT]) in overt disease. METHODS: 200 participant multicenter study: 70 G+LVH-, 51 G+LVH+, 53 G-LVH+ and 26 healthy volunteers (HV) underwent 12-lead ECG (to detect abnormal Q-waves, repolarization changes, LVH criteria) and CMR-ECGI computing epicardial unipolar electrograms (UEGs) to derive: activation time (AT), activation-recovery intervals (ARIc), spatial gradients (activation: G AT , repolarisation: G RT ) and fractionation. RESULTS: Compared to HV, G+LVH- had prolongation of AT (40.3±7.3 vs 35.4±6.1 ms p=0.003) and steeper G RT (mean: 1.12±0.27 vs 1.00±0.23 ms/mm p=0.042, max: 11.7±2.8 vs 10.0±1.9 ms/mm p=0.005). AT was prolonged even in G+LVH- with a normal 12-lead ECG (p<0.004). Compared to G+LVH-, G+LVH+ had similar AT but a more prolonged ARIc (275±29 vs 245±26 ms p<0.001). Compared to G-LVH+, G+LVH+ had similar MWT and LGE, but more signal fractionation (0.02±0.02 vs 0.01±0.03% UEGs with ≥2 deflections p=0.002). In overt HCM (all LVH+), MWT associated with AT ( r s 0.25 p=0.011) while LGE burden associated with G AT ( r s=0.27 p=0.006) and fractionation ( r s=0.22 p=0.025). CONCLUSION: Cardiac activation prolongation and repolarization abnormalities occur in subclinical HCM (before hypertrophy). Activation is prolonged even in subclinical HCM with normal 12-lead ECG. In overt HCM, ECGI abnormalities track adverse structural changes and reveal greater fractionation in those with a sarcomeric mutation.

Differentiating primary sarcomeric hypertrophic cardiomyopathy from Noonan syndrome: can the electrocardiogram be of use?

Noonan syndrome is a multi-system genetic disorder and patients may suffer from hypertrophic cardiomyopathy. Previous studies have identified electrocardiographic features that may support a diagnosis of Noonan syndrome. In this two-centre retrospective study, we analysed typical Noonan syndrome-related electrocardiographic features in 30 patients with Noonan syndrome with hypertrophic cardiomyopathy and compared these with the electrocardiographic features in 15 children with sarcomeric hypertrophic cardiomyopathy. Typical Noonan syndrome-related electrocardiographic features are a negative aVF, small left precordial R-waves, large right precordial S-waves, and abnormal Q-wave. We also analysed electrocardiographic features of hypertrophic cardiomyopathy: ST-segment abnormalities and T-wave abnormalities. A negative aVF was seen in 83% of patients with Noonan syndrome-related hypertrophic cardiomyopathy in contrast to 27% of patients with primary sarcomeric hypertrophic cardiomyopathy (p < 0.001). An extreme QRS axis in the north-west was seen only in patients with Noonan syndrome-related hypertrophic cardiomyopathy. This QRS axis deviation is likely to be determined by the Noonan syndrome-related hypertrophic cardiomyopathy and not by the type of hypertrophic cardiomyopathy. There were no differences between the two groups in the frequency of large right precordial S-waves and small R-waves in the left precordial leads V5 and V6. However, an abnormal R/S ratio was more often seen in patients with Noonan syndrome-related hypertrophic cardiomyopathy (p < 0.001). Pathologic Q-waves were seen statistically more frequently in patients with sarcomeric hypertrophic cardiomyopathy (p = 0.009). The occurrence of ST-segment and T-wave pathology did not statistically differ between the two groups. Electrography can be of use in differentiating sarcomeric hypertrophic cardiomyopathy from Noonan syndrome-related hypertrophic cardiomyopathy.

Electrophysiological, structural, and functional disorders in patients with inflammatory cardiomyopathy secondary to inflammatory myopathy.

BackgroundInflammatory cardiomyopathy (IC) is a syndrome with chronic myocarditis and cardiac remodeling. This study aimed to explore predicting factors of adverse outcomes in patients with IC secondary to idiopathic inflammatory myopathy (IIM‐IC).MethodsBy means of a single‐center retrospective study, 52 patients with IIM‐IC at Peking Union Medical College Hospital were identified from January 1999 to June 2019. Electrocardiogram and echocardiography data were analyzed for the primary outcome (defined as all‐cause death) and secondary outcomes (defined as re‐hospitalization of heart failure and all‐cause death), using regression and survival analysis.ResultsThe prevalence of atrial fibrillation, ventricular tachycardia, Q‐wave abnormality, left ventricular conduction abnormalities, and reduced left ventricular ejection fraction (LVEF) (≤40%) were 65.4%, 67.3%, 67.3%, 61.6%, and 50.5%. After a median follow‐up of 2 years (IQR 0.8–3.0), 26 cases were readmitted due to heart failure. Twenty‐two deaths were recorded, including 20 cardiogenic deaths. Among the patients with adverse events, the incidence of poor R‐wave progression, low‐voltage of the limb leads, Q‐wave abnormality, QRS duration >130 ms, left ventricular enlargement, and impaired systolic function were higher. Kaplan–Meier analysis showed that Q‐wave abnormality, limb leads low‐voltage, LVEF ≤40%, and left ventricular end‐diastolic dimension >60 mm were correlated with shorter survival. However, multivariate Cox regression analysis revealed that only Q‐wave abnormality (HR = 12.315) and LVEF ≤40% (HR = 5.616) were independent risk factors for all‐cause death.ConclusionQ‐wave abnormality and reduced LVEF are predictive of poor prognosis in patients with IIM‐IC.

Prevalence of major and minor electrocardiographic abnormalities and their relationship with cardiovascular risk factors in Angolans.

AimsTo identify the prevalence of major and minor electrocardiographic abnormalities and their association with the main risk factors for cardiovascular disease in a population in the province of Bengo, northern Angola.MethodsA cross-sectional community-based study was conducted and a representative random sample stratified by sex and age was selected. In total, 2379 black individuals were included in the final analysis. A standard 12-lead ECG were recorded from all participants, analyzed and processed by the University of Glasgow software and coding by the Minnesota code.Results22.3% of participants had minor electrocardiographic abnormalities and 4.58% major ECG abnormalities. The most common minor ECG abnormalities were abnormal T wave inversion, minor isolated ST abnormalities and premature beats. The most common major ECG abnormalities were Left ventricular hypertrophy with major ST-T abnormalities, Ventricular conduction defects and major Q-wave abnormalities. Hypertension, diabetes mellitus, hypercholesterolemia, alcohol consumption and smoking, were significantly associated with major and minor electrocardiographic abnormalities.ConclusionsIn this study several participants had minor and major electrocardiographic abnormalities. Minor electrocardiographic abnormalities were more prevalent in men and major abnormalities in women. The electrocardiographic abnormalities had significant associations with the main cardiovascular risk factors.

The added value of the electrocardiogram in Noonan syndrome.

Noonan syndrome is a genetic disorder characteried by short stature, typical facial features, developmental delay, and CHD. In this single-centre retrospective study, we analysed typical Noonan syndrome-related electrocardiographic features in 95 patients with clinically and molecularly confirmed Noonan syndrome. Typical Noonan syndrome-related electrocardiographic features are left axis deviation, small left precordial R-waves, large right precordial S-waves, abnormal Q-wave, and abnormal wide QRS complex. In this representative cohort, CHD was found in 59 patients (62.1%) and typical Noonan syndrome-related electrographic features in 60 patients (63.2%). The typical Noonan syndrome-related electrographic features were also increased over baseline in patients without CHD (41.7%). Of all 95 patients, left axis deviation was seen in 46.3%, small left precordial R-waves in 30.5%, large right precordial S-waves in 5.3%, and abnormal Q-wave and wide QRS complex in 2.1%. There was no significant difference in the frequency of the individual-specific electrographic features between the group with CHD and the group without CHD. However, there were significantly more patients with a small left precordial R-wave in the subgroup with pulmonary stenosis compared to patients without pulmonary stenosis. Conclusion: Specific Noonan syndrome-related electrographic features are frequently present in patients with Noonan syndrome, also in the absence of CHD. These results suggest that there may be a continuum of cardiac anomalies from overt CHD to milder abnormalities that are only seen on electrocardiogram.

The utility of silent myocardial infarction on electrocardiogram as an ASCVD risk enhancer for primary prevention: The multi-ethnic study of atherosclerosis

BackgroundThe 2018 AHA/ACC cholesterol guidelines introduced a new list of markers called “risk enhancers” that, if present, confer an increased risk of atherosclerotic cardiovascular disease (ASCVD). Silent myocardial infarction (SMI) on electrocardiogram (ECG) is notably absent, even though it associated with future ASCVD. MethodsWe assessed the utility of SMI on ECG as a risk-enhancer in intermediate-risk participants in MESA (Multi-Ethnic Study of Atherosclerosis) – those with 10-year ASCVD risk of 5–20% by the pooled cohort equation (PCE). SMI was defined as major Q-wave abnormality or minor Q/QS waves in the setting of major ST-T abnormalities without prevalent clinical cardiovascular disease. ResultsAmong 2946 participants (mean age 63.1 ± 7.6, 53.9% women, 36% white, 11% Chinese-American, 33% African-American, 19% Hispanic), 66 (2.2%) had SMI at baseline. After a median 15.8 years of follow-up, incident ASCVD events occurred in 431/2876 (15.0%) of those without SMI and 16/66 (24.2%) of those with SMI. In a multivariable-adjusted Cox proportional hazards model, baseline SMI was associated with an increased risk of incident ASCVD events (HR 1.68, 95% CI 1.02–2.77, p = 0.04). However, adding SMI to the PCE did not improve discrimination and reclassification was modest—net reclassification improvement was 0.0161 (95% CI 0.002–0.034, p = 0.08). ConclusionOur findings suggest that the prevalence of SMI is 2.2% among those without known clinical cardiovascular disease considered intermediate-risk by the PCE. In our analysis, SMI only modestly improved classification of risk, suggesting that it may not be very useful as an ASCVD risk enhancer.

Pattern of electrocardiographic abnormalities in pediatric HIV/AIDS clients at Federal Medical Center, Abeokuta

Background: Sub-Saharan Africa presently contributes about 70% of global HIV/AIDS population with little or no emphasis on the contribution of cardiovascular abnormalities to the associated morbidity and mortality in the region. Objectives: The objective is to determine the prevalence of electrocardiographic (ECG) abnormalities and association of such abnormalities with HIV/AIDS severity in terms of clinical manifestations and level of CD4 depletion. Design: A hospital-based cross-sectional case-control study. Methodology: One hundred and five (105) HIV-infected children attending HIV clinic and equivalent age- and sex-matched HIV un-infected controls attending pediatrics General Outpatient Clinics at FMCA were consecutively recruited over 8 months. They were evaluated clinically and had CD4 count, hematocrit, plasma calcium and potassium, and standard 12-lead ECG done. Results: Thirty-five (33.3%) of the subjects had ECG abnormalities compared with four (3.8%) in the controls (χ 2 = 28.34, P &lt; 0.05). The left ventricular hypertrophy was the commonest (13.3%) among other detected abnormalities such as Q-wave abnormalities, right ventricular hypertrophy, and ventricular repolarization abnormalities. The detected abnormalities were not significantly associated with advanced clinical or immunological stage of HIV/AIDS (χ 2 &lt; 4.0, P &gt; 0.05). Conclusion: There was a high prevalence of ECG abnormalities in children with HIV/AIDS. These abnormalities occurred irrespective of the extent of the disease advancement. There is therefore a need for at least an ECG to identify from among HIV infected children those who may subsequently require echocardiography since the cost of echocardiography is presently too high and precludes its routine use in the Sub-Saharan Africa.

Abstract 13196: The Utility of Silent Myocardial Infarction on Electrocardiogram as an ASCVD Risk Enhancer for Primary Prevention: The Multi-Ethnic Study of Atherosclerosis

Introduction: The 2018 AHA/ACC cholesterol guidelines introduced a new list of markers called “risk enhancers” that, if present, confer an increased risk of atherosclerotic cardiovascular disease (ASCVD). Notably absent is silent myocardial infarction (SMI) on electrocardiogram (ECG), even though SMI has been shown to be associated with future ASCVD. Hypothesis: Adding SMI to the pooled cohort equation (PCE) will improve risk discrimination and classification in those with intermediate ASCVD risk (5 - 20% 10-year risk). Methods: SMI was defined as a major Q-wave abnormality or minor Q/QS waves in the setting of major ST-T abnormalities in the absence of history of clinical cardiovascular disease. Incident ASCVD events included myocardial infarction, coronary heart disease death, and fatal and non-fatal stroke. Results: Among 2,278 intermediate-risk MESA participants, 48 (2.1%) had SMI at baseline. Over 32,150 person-years (median 15.8), incident ASCVD events occurred in 297/2,230 (13%) of those without SMI and 13/48 (27%) of those with SMI. In a Cox proportional hazards model that was adjusted for calculated 10-year ASCVD risk based on the PCE, SMI was associated with increased risk of ASCVD (HR 2.22, 95% CI 1.27 - 3.87, p = 0.005). Adding SMI to the PCE did not improve discrimination, with areas under the receiver operating characteristic curves for models without and with SMI of 0.5812 and 0.5874, respectively (p-value for difference 0.22; Figure 1a). The net reclassification improvement for adding SMI as a risk enhancer to reclassify participants from intermediate-risk to high-risk was 0.0242 (95% CI 0.0011 - 0.0472, p = 0.04; Figure 1b). Conclusions: Our findings suggest that the prevalence of SMI is 2.1% among those without known clinical cardiovascular disease considered intermediate-risk by the pooled cohort equation. In our analysis, SMI only modestly improved classification of risk, suggesting that it may not be very useful as an ASCVD risk enhancer.

Electrocardiographic Risk Markers for Heart Failure in Women Versus Men

Heart failure (HF) is one of the leading causes of hospitalization in the Western world. Women have a lower HF hospitalization rate and mortality compared with men. The role of electrocardiography as a risk marker of future HF in women is not well known. We studied association of electrocardiographic (ECG) risk factors for HF hospitalization in women from a large middle-aged general population with a long-term follow-up and compared the risk profile to men. Standard 12-lead ECG markers were analyzed from 10,864 subjects (49% women), and their predictive value for HF hospitalization was analyzed. During the follow-up (30 ± 11 years), a total of 1,743 subjects had HF hospitalization; of these, 861 were women (49%). Several baseline characteristics, such as age, body mass index, blood pressure, and history of previous cardiac disease predicted the occurrence of HF both in women and men (p <0.001 for all). After adjusting for baseline variables, ECG sign of left ventricular hypertrophy (LVH) (p <0.001), and atrial fibrillation (p <0.001) were the only baseline ECG variables that predicted future HF in women. In men, HF was predicted by fast heart rate (p = 0.008), T wave inversions (p <0.001), abnormal Q-waves (p = 0.002), and atrial fibrillation (p <0.001). Statistically significant gender interactions in prediction of HF were observed in ECG sign of LVH, inferolateral T wave inversions, and heart rate. In conclusion, ECG sign of LVH predicts future HF in middle-aged women, and T wave inversions and elevated heart rate are associated with HF hospitalization in men.

P3427Prognostic performance of echocardiography, electrocardiogram, albuminuria, plasma proBNP and hs-TnI in patients with type 2 diabetes

Abstract Background A range of diagnostic tests including echocardiography, albuminuria, electrocardiogram (ECG), plasma measurement of high sensitivity troponin T (hs-TnI) and pro-brain natriuretic peptide (proBNP) have been suggested as cardiovascular (CV) risk predictors in patients with type 2 diabetes. In this study we examined prognostic yield from these risk markers. Methods A total of 1,030 out-patients followed at a large secondary care diabetes clinic were recruited. Echocardiography was considered feasible in patients in sinus rhythm with adequate image quality (n=886). Abnormal echocardiography was defined as a left ventricular ejection fraction (LVEF) &lt;50%; a ratio of early diastolic mitral inflow velocity to early diastolic septal annular velocity (E/e'septal) ≥15; increased left ventricular mass index (&gt;95 g/m2 for women and &gt;115 g/m2 for men) or left atrial volume index &gt;34 ml/m2. ECG was performed in 983 patients and was considered abnormal in the presence of abnormal Q-waves; ST-T segment deviation or bundle branch block. We measured urine albumin (n=1,009) and proBNP/hs-TnI (n=933). The end-point of CV event was a composite of CV death and hospitalization with myocardial infarction/revascularization, stroke, peripheral artery disease or heart failure. Results The median follow-up was 4.7 years (interquartile range: 4.0 to 5.3) and 174 patients suffered an CVD event. All markers except hs-TnI were significantly (p&lt;0.001) associated with the composite outcome: Abnormal echocardiogram: Hazard ratio (95% confidence interval): 2.39 (1.69–3.37); albuminuria 2.01 (1.47–2.76); abnormal ECG 2.35 (1.72–3.21); log2(proBNP) 1.60 (1.47–1.75) and hs-TnI 1.05 (0.92–1.19). The findings persisted after adjusting for clinical variables, but after adjusting for the other markers, only log2(proBNP) remained associated with the composite outcome (1.50 (0.20–1.73), p&lt;0.001), figure. Measured by C-index model performance was highest with proBNP (0.70 (0.65–0.75)) and similar to clinical variables (0.71 (0.67–0.76)). Combining risk markers only resulted in very limited increase in C-index (echocardiogram, albuminuria, ECG and proBNP: 0.71 (0.66–0.76)). Uni- and multivariables Conclusions This study identifies proBNP measurement in plasma over echocardiography, ECG and albuminuria for risk prediction in patients with type 2 diabetes. The diagnostic yield in considering more than one risk marker was limited in this population.

Coronary artery involvement in chronic graft‐versus‐host disease presenting as sudden cardiac arrest

Graft-versus-host disease (GVHD) is related to considerable morbidity and mortality after allogeneic hematopoietic stem cell transplantation (HSCT). Cardiac complications associated with GVHD are uncommon, and coronary artery involvement is even more unusual. We report on a male pediatric patient with chronic GVHD who developed a fatal ventricular arrhythmia caused by coronary artery obstruction after HSCT. At 30months after HSCT, he suddenly collapsed with ventricular fibrillation. After resuscitation, electrocardiography showed abnormal q-wave and ST changes in the inferior leads, suggesting a coronary event. Coronary angiography revealed complete obstruction of the proximal left anterior descending artery, subtotal obstruction of the mid left circumflex artery, and mild narrowing at the right coronary artery. This boy had none of the risk factors for coronary artery disease, and the only possible explanation for the cardiac event is GVHD. Coronary artery disease only rarely occurs as a cardiac event in children. However, coronary artery involvement should be recognized as one of the important manifestations of chronic GVHD in children.

Abstract 12323: Effect of Prompt Revascularization on Outcomes in Diabetic Patients With Stable Ischemic Heart Disease Depends on Prior Myocardial Infarction Status and Mode of Revascularization

Introduction: The Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) trial found no benefit from prompt revascularization in addition to optimal medical therapy (PR+OMT) compared with OMT alone in diabetics with stable ischemic heart disease (SIHD). However, diabetics with prior myocardial infarction (PMI) are a higher risk group. Thus, we examined whether PMI status altered the effect of PR+OMT versus OMT alone on outcomes in diabetics with SIHD. Methods: BARI 2D randomized 2368 diabetics with SIHD to either PR+OMT with PCI or CABG or OMT alone. PMI was defined by reported history of MI or abnormal Q-waves on ECG. For patients with PMI and no PMI, we used Kaplan-Meier analysis to compare the rate of death, MI, stroke, congestive heart failure (CHF) and a composite of death/MI/stroke between patients randomized to PR+OMT versus OMT alone. Results: Of 2280 patients with known PMI status, 936 (41%) had PMI and 1344 (59%) did not. Baseline variables including age, sex, race, BMI, history of CHF, hypertension, hyperlipidemia, tobacco use, abnormal ejection fraction, prior revascularization, CAD severity, creatinine, glycemic control and use of guideline-directed medical therapy were similar between the two treatment strategies within each group. In patients with PMI, PR+OMT had no effect on any outcome compared with OMT alone. In those without PMI, PR+OMT was associated with higher 5-year event free rates of MI (91% vs. 85%, P = 0.002) and death/MI/stroke (81% vs. 76%, P = 0.04) compared with OMT alone, although these differences were limited to patients treated with CABG. Conclusions: In diabetics with SIHD and PMI, PR+OMT did not improve outcomes compared with OMT alone. However, in those without PMI, PR+OMT reduced the rate of MI and a composite of death/MI/stroke when treated with CABG, but not PCI. These findings, if confirmed in a prospective study, may improve outcomes in diabetics with SIHD through appropriate selection of a revascularization strategy.

Usefulness of ECG to differentiate Takotsubo cardiomyopathy from acute coronary syndrome

ObjectiveWe aimed to describe the evolution of ECG changes in TC compared with MI, and evaluate ECG features which might help to distinguish between these conditions. BackgroundTakotsubo cardiomyopathy (TC) can mimic both ST-elevation (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) but management is different. Several electrocardiographic (ECG) abnormalities have been identified which might help to differentiate TC with and without ST-elevation, from STEMI and NSTEMI, respectively. MethodsWe prospectively identified 100 consecutive patients with TC and 100 MI patients. They were divided into 2 groups according to the presence of ST-segment elevation (STE). Serial ECGs from admission to Day 2 were compared. ResultsThirty-five TC patients had STE on admission. Compared with STEMI patients they had less prominent STE (median peak elevation 2mm vs. 3mm, P<0.05), less reciprocal ST-segment depression and no abnormal Q-waves. By Day 2 all STEMI patients had pathological Q-waves but none of the TC patients.Compared with NSTE-TC patients, NSTEMI patients had more ST-segment depression (28.2% vs. 0%, P<0.05), but less T-wave inversion (33.8% vs. 11.3%, P<0.05) on admission. By Day 2 the ECG criterion which best distinguished NSTE-TC from NSTEMI was the presence of T-wave inversion in ≥6 leads (sensitivity 74%, specificity 92%). ConclusionECG changes seen in TC within two days of presentation are distinctive and important clues for clinicians to suspect the diagnosis.

Sex Differences in Biological Markers of Health in the Study of Stress, Aging and Health in Russia.

BackgroundThe apparent contradiction that women live longer but have worse health than men, the so called male-female health-survival paradox, is very pronounced in Russia. The present study investigates whether men in Moscow are healthier than women at the level of biomarkers, and whether the associations between biomarkers and subjective health have sex-specific patterns.MaterialsPreviously collected data in the study of Stress, Aging, and Health in Russia (SAHR, n = 1800) were used to examine sex differences in biomarkers and their associations with physical functioning and self-rated health.ResultsThe present study found mixed directions and magnitudes for sex differences in biomarkers. Women were significantly disadvantaged with regard to obesity and waist circumference, whereas men had a tendency toward higher prevalence of electrocardiographic abnormalities. No sex differences were indicated in the prevalence of immunological biomarkers, and mixed patterns were found for lipid profiles. Many biomarkers were associated with physical functioning and general health. Obesity and waist circumference were related to lower physical functioning among females only, while major Q-wave abnormalities with high probabilities of myocardial infarction and atrial fibrillation or atrial flutter were associated with physical functioning and self-rated health among males only.ConclusionNo clear patterns of sex differences in prevalence of high-risk levels of biomarkers suggest that the male-female health-survival paradox is weaker at the level of health biomarkers. We found some evidence that certain biomarkers reflecting pathophysiological changes in the organism that do not possess acute health risks, but over many years may lead to physical disability, are associated with physical functioning and self-rated health in women, whereas others reflecting more serious life-threatening pathophysiological changes are associated with physical functioning and self-rated health in men.

Differences in ST-elevation and T-wave amplitudes do not reliably differentiate takotsubo cardiomyopathy from acute anterior myocardial infarction

BackgroundPrevious efforts to distinguish acute anterior ST-elevation myocardial infarction (anterior-STEMI) from various forms of takotsubo cardiomyopathy (TTC) by electrocardiography (ECG) have produced differing results. MethodsWe performed a retrospective comparison of acute ECGs between 48 apical and 9 mid-ventricular TTC patients, with 96 anterior-STEMI patients. ECG was recorded in acute phase (<24h from onset of pain), and analyzed for ST-changes, negative T-waves, abnormal Q-waves and QT-interval duration. Time from onset of pain to ECG was gathered from patient records. ResultsAnterior-STEMI patients had ST-elevation in lead V1 more frequently than apical (70% vs 15%, p<0.0001) or mid-ventricular TTC patients (70% vs 0%, p<0.0001), and higher ST-elevation amplitudes in leads V2–V5 (p<0.02). Lack of ST-elevation in lead V1 and ST-elevation amplitude <2mm in lead V2 distinguished TTC from anterior-STEMI patients with 63% sensitivity and 93% specificity, with 79% predictive value. ConclusionsIn patients with anterior ST-elevation and acute chest pain, lack of ST-elevation in lead V1 and ST-elevation amplitude <2mm in lead V2 suggests a TTC diagnosis. However, this criterion is not reliable enough in clinical practice to distinguish between TTC and anterior-STEMI patients.

Utility of a novel risk score for prediction of ventricular tachycardia and cardiac death in chronic Chagas disease - the SEARCH-RIO study

The SEARCH-RIO study prospectively investigated electrocardiogram (ECG)-derived variables in chronic Chagas disease (CCD) as predictors of cardiac death and new onset ventricular tachycardia (VT). Cardiac arrhythmia is a major cause of death in CCD, and electrical markers may play a significant role in risk stratification. One hundred clinically stable outpatients with CCD were enrolled in this study. They initially underwent a 12-lead resting ECG, signal-averaged ECG, and 24-h ambulatory ECG. Abnormal Q-waves, filtered QRS duration, intraventricular electrical transients (IVET), 24-h standard deviation of normal RR intervals (SDNN), and VT were assessed. Echocardiograms assessed left ventricular ejection fraction. Predictors of cardiac death and new onset VT were identified in a Cox proportional hazard model. During a mean follow-up of 95.3 months, 36 patients had adverse events: 22 new onset VT (mean±SD, 18.4±4‰/year) and 20 deaths (26.4±1.8‰/year). In multivariate analysis, only Q-wave (hazard ratio, HR=6.7; P<0.001), VT (HR=5.3; P<0.001), SDNN<100 ms (HR=4.0; P=0.006), and IVET+ (HR=3.0; P=0.04) were independent predictors of the composite endpoint of cardiac death and new onset VT. A prognostic score was developed by weighting points proportional to beta coefficients and summing-up: Q-wave=2; VT=2; SDNN<100 ms=1; IVET+=1. Receiver operating characteristic curve analysis optimized the cutoff value at >1. In 10,000 bootstraps, the C-statistic of this novel score was non-inferior to a previously validated (Rassi) score (0.89±0.03 and 0.80±0.05, respectively; test for non-inferiority: P<0.001). In CCD, surface ECG-derived variables are predictors of cardiac death and new onset VT.

Non–Q-Wave Myocardial Infarction

Since the invention of electrocardiogram (ECG or EKG), its significance in the diagnosis of acute ischemic disease, chronic ischemic disease, and its contribution to cardiology has been no less than remarkable. The pathophysiology of acute coronary syndromes in most cases correlates with the clinical outcomes, biochemical findings (cardiac biomarkers), and electrocardiographic patterns. Electric activity in the myocardium is registered in the ECG describing positive deflections when the depolarization potential orientates positive charges to the recording electrode (approaches to it) and negative deflections when the depolarization potential orientates negative charges to the recording electrode and gets away from it. The abnormal Q-wave is the cornerstone of the myocardial infarction diagnosis after several days of the ischemic event. Findings in the ECG suggestive of ischemia and necrosis are ST elevation/depression and deep Q-waves, respectively, and the presence of a deep abnormal Q-wave in the ECG is evidence of necrotic areas and an inert myocardium, which is not capable to depolarize. Non-Q-wave myocardial infarction has been defined as acute myocardial infarction without a new-onset deep Q-wave on the ECG after day(s) of evolution, and because of the anatomopathological concept of infarction is usually related to necrosis, it results paradoxical to consider this widely known clinical and biochemical entity as a myocardial infarction when there is no evidence of necrosis in the ECG.

THROMBOLYSIS IN MYOCARDIAL INFARCTION FRAME COUNT IN TAKOTSUBO CARDIOMYOPATHY

Takotsubo cardiomyopathy (TC) in its typical form, is characterizedby transient systolic dysfunction of the apical and/or mid segments ofthe left ventricle that mimic myocardial infarction (MI), but in the ab-sence of significant coronary artery disease [1–3]. Common triggeringfactorsincludeacutemedicalillness,severeemotionalorphysicalstresse.g., unexpected death of relatives, domestic violence, arguments, cata-strophic medicaldiagnoses,financialor gambling losses and naturaldi-sasters [2,3]. Pathogenesis remains unclear although catecholamine-mediated myocardial stunning, multivessel coronary vasospasm andabnormalities in coronary microvascular function have been proposedas possible explanations [2,3]. TC has strong female preponderancewith nearly 90% cases involvingpostmenopausal women [3,4]. Patientscommonly present with substernal chest pain. Electrocardiographicchanges include ST-segment elevation, T-wave inversion, QT-intervalprolongation, abnormal Q-waves or non-specific abnormalities [1–3].Elevations in cardiac biomarkers are typically less pronounced than inacute anterior ST-segment elevation myocardial infarction (STEMI)and coronary angiography does not revealobstructive coronary diseaseor plaquerupture correspondingto thewall motion abnormalitiesseenin this condition [1–4].MayoCliniccriteriaiscommonlyusedfordiagnosisandrequiresfol-lowing four conditions: a) transient hypokinesis, akinesis or dyskinesisoftheleftventricularmidsegmentswithorwithoutapicalinvolvement,b) absence of obstructive coronary disease or acute plaque rupture,c) new electrocardiographic abnormalities (ST-segment elevation and/orT-waveinversion)ormodestelevationincardiactroponin,andd)ab-sence of pheochromocytoma or myocarditis [5,6]. However thesecriteria are considered outmoded and newer versions have been pro-posed which suggest that myocarditis and TC can coexist and don'thave to be mutually exclusive [5,6]. Supportive measures are themain-stay of management. Patients generally receive aspirin, β-blockers,angiotensin-converting-enzyme inhibitors, and intravenous diuretics ifneeded. Hypotension in the setting of left ventricular outflow tract ob-struction may warrant use of beta-blockers and phenylephrine. In se-vere left ventricular dysfunction, inotropic agents or an intraaorticballoonpumpmayberequired [1–4].Prognosisisexcellent,withnearly95%ofpatientsexperiencingcompleterecoverywithin4–8weeks[3,4].Gibson et al. [7] introduced the TIMI frame count (TFC) method formeasuring coronary flow velocity from coronary angiograms. It is de-fined as ‘the number of frames required for contrast material to travelfrom the coronary ostium to the distal landmark’ [7]. The objective ofour study isto determineif TFC isa useful tool in determiningthecoro-nary flow in TC patients [8].Sixteen patients were identified at our institute with an apparentacute anterior-STEMI presentation but were subsequently diagnosedwith TC. They were retrospectively compared with randomly chosencontrolswithout coronary artery disease on angiography. Microcircula-tory analysis was done via calculation of TFC (Gibson technique) in allthree major vessels. Left anterior descending (LAD) artery values wereadjusted (by applying a correction factor) to get ‘corrected TIMI-Frame-Count’ (CTFC). This was done to compensate for the longerlengthofLADandcalculatedbydividingthenumberofframesrequiredfor the dye to pass through the LAD by 1.7. Data was analyzed usingExcel-2007 software. Mean ± Standard Deviation are given for quanti-tative variables (Table 1). Frequencies, percentages and graphs aregiven for qualitative variables (Table 2). Two-independent sample t-test was applied to observe group mean differences. p-Value of b0.05was considered to be statistically significant.Patients were divided into two groups viz. cases and controls. Caseshad 16 patients (all females), while controls had 15 (9 females; 6males). Mean ages of the cases and control groups were 68.31 ±10.88 years and 66.5 ± 14.28 years respectively. Mean-CTFC for LADin cases was 19.61 ± 5.77 and in controls it was 16.65 ± 2.41 (statisti-cally significant difference, p-value = 0.04 (table/Fig. 1)). Mean-CTFCfor Circumflex artery was 18.93 ± 3.87 and 18.06 ± 3.95 in cases andcontrols respectively (no statistically significant difference p-value =

Clinically silent myocardial infarctions in the CKD community

Burden of clinically silent myocardial infarction in patients with kidney disease Patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) are at a greater risk for incident myocardial infarction and death from coronary heart disease (CHD) compared with the general population [1]. The presence of CKD may accelerate the formation of vulnerable plaques, increase the frequency of plaque disruption and may increase thrombogenicity of the blood, making patients with CKD at high risk for myocardial infarction and mortality. Once diagnosed with CHD, patients with CKD have a greater incidence of recurrent cardiovascular events and mortality [2]. Research has suggested that CHD is unique in patients with CKD and ESRD compared with the general population with early onset, more rapid progression, atypical symptoms and higher rates of death. Although it is estimated that ∼13% of patients with CKD have suffered an acute myocardial infarction [3], it is likely that many patients with CKD have clinically silent CHD, which may have serious clinical implications on long-term cardiovascular morbidity and mortality. In a provocative study in this issue of NDT, Rizk et al. examine the prevalence and long-term impact of unrecognized myocardial infarctions among patients with CKD. In this large study of 18 864 patients with and without CKD enrolled in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort, 12-lead ECGs were used to identify the presence of Q-wave abnormalities [4]. Recognized myocardial infarction was defined as the concurrence of self-reported myocardial infarction as well as Q-wave abnormalities on ECG, whereas unrecognized myocardial infarction was defined as the presence of diagnostic Q-wave abnormalities without self-report. The investigators report that, in patients with eGFR <30 mL/min/1.73 m 2 , the prevalence of unrecognized myocardial infarction was 13% compared with 4% in those without CKD [4]. The presence of macroalbuminuria was associated with a 10% risk of unrecognized myocardial infarction compared with 4% in patients without albuminuria. After 4 years of follow-up, the investigators found that among patients with CKD, the risk of death was similar in those with unrecognized versus recognized myocardial infarctions [4]. These compelling results suggest that unrecognized myocardial infarction appears to be more common in patients with CKD; and notably, unrecognized myocardial infarction conveys a similar negative prognosis compared with a clinically recognized myocardial infarction. This study makes an important contribution in being one of the first to define the burden of clinically silent myocardial infarctions in the CKD community. Several limitations of this study must be noted. The study cohort was primarily African-American (by design) so results may not be generalizable to other populations. This was a cohort that oversampled from the ‘stroke belt’ so participants likely had a higher prevalence of risk factors for stroke and thus CHD. The authors chose to utilize Q-wave abnormalities on baseline ECGs and self-report