Electrocardiogram Markers Research Articles

Deriving a reduced lead system from the 80-lead body surface map in the electrocardiographic determination of acute myocardial infarction

BackgroundBody surface mapping (BSM) involves the application of extra electrodes or “nonstandard lead sets” over a larger area of the thorax than the routine 12-lead electrocardiogram (ECG). The number of electrodes can range from 15 to more than 250, and the optimum number and placement of leads is a major topic of research. We used a novel retrospective approach, analyzing the records from patients admitted to our center with acute ischemic-type chest pain, to determine optimum lead number and placement.MethodsWe analyzed 576 patients with acute myocardial infarction (MI) (242 anterior, 173 inferior, 69 lateral, 69 posterior, and 23 right ventricular; peak cardiac troponin T > 0.09 nmol/L) and 279 controls (normal ECG and cardiac markers). Infarct location was verified by 2 cardiologists not involved in the study. Initially, an 80-lead (64 anterior, 16 posterior) BSM (Prime ECG) was recorded on all patients prior to revascularization. A combined method of analysis for a reduced lead set was used—analysis of variance (ANOVA) determined which leads had the greatest mean ST elevation (ST0 [mm]), logistic regression analysis of the ST0 ranked each lead in terms of MI diagnosis, and a computer algorithm determined which leads in combination produced the greatest sensitivity and specificity for MI diagnosis.ResultsThus, a 30-lead set (20 anterior, 10 posterior) was derived from the combined method of analysis. The sensitivity and specificity of the 30-lead set for MI was 84% and 97%, respectively, compared with the 80-lead BSM of 91% and 93%. Receiver operating characteristic (ROC) c statistic for the 30 lead set was 0.825 (95% confidence interval, 0.797-0.852), which was within the 95% confidence intervals for the 80 lead ROC c statistic of 0.850 (0.824-0.875). The data set was split equally into training and validation set. The training set ROC c statistic for the 30-lead set was 0.860 (0.825-0.896) and 0.908 (0.881-0.935) for the 80-lead set. The validation set ROC c statistic was 0.821 (0.782-0.860) for the 30-lead set and 0.782 (0.739-0.825) for the 80-lead set.ConclusionUsing the ROC c statistic, we showed that the 30-lead BSM was noninferior to the 80-lead model.

Electrocardiographic Evaluation of Cardiovascular Status

The electrocardiogram (ECG) is indispensable for the diagnosis and management of patients with a wide variety of cardiac and noncardiac diseases. The purpose of this paper is focused on recent research that used ECG, specifically the long-QT interval and microvolt T wave alternans, for the evaluation of life-threatening ventricular arrhythmias. Although remaining to be validated, QT prolongation along with other emerging electrocardiographic indices such as T wave morphology, T peak-to-T end time, or beat-to-beat QT variability may be sensitive indicators of malignant polymorphic ventricular tachyarrhythmia, torsade de pointes. Microvolt T wave alternans may provide important information in identifying a low-risk group with left ventricular dysfunction who is unlikely to benefit from unnecessary prophylactic implantable cardioverter defibrillator therapy. These ECG markers have the potential to aid in the safe administration of individualized medications, avoidance of sudden cardiac death, and provision of a noninvasive strategy to identify patients who are most and least likely to benefit from expensive prophylactic implantable cardioverter defibrillator placement.

The early risk stratification of the patients with acute chest pain

Objective This investigation was designed to stratify patients with acute chest pain based on their symptoms, electrocardiogram (ECG), cardiac injury markers and the number of accompanying traditional risk factors(smoking, obesity, hyperlipemia, hypertension, diabetes), and to assess the effect of the above factors to obtain a risk stratification for patients with chest pain. Methods We identified 139 patients with acute chest pain, including 45 myocardiac infarction patients, 65 unstable angina patients and 29 chest pain patients without identified acute coronary syndrome(ACS) admitted to our Coronary Heart Center during December 2004 to February 2005. All patients accepted coronary angiography. All data was collected using questionnaires. Based on reported symptom, electrocardiogram (ECG), cardiac injury markers and the number of the accompanying traditional risk factors, we stratified all patients into four groups: Group 1, patients with acute chest pain, ECG changes and abnormal cardiac injury biomarkers. Group 2, patients with acute chest pain and ECG changes(without abnormal cardiac injury biomarkers). Group 3, patients with acute chest pain, normal ECG, normal cardiac injury biomarkers and > 2 traditional risk factors. Group 4, patients with acute chest pain, normal ECG and normal cardiac injury biomarkers, but only ≤ 2 traditional risk factors. From this data we examined the difference of ACS incidence in the four groups. Results After stratification the ACS incidence of the grouped patients in turn was 100%, 84%, 69.6% and 53.3%. The combination of early phase ECG and cardiac injury markers identified 70.9% patients with ACS(the specificity being 90.7%). The mortality of group 3 was higher compared with group 4(69.6% vs 53.3%), however the P value was more than 0.05 and didn't show significant statistical difference. The correlation analysis found the number of the traditional risk factors had a significant positive correlation ( r = 0.202, P = 0.044) with the number of stenosis being more than 50% of the artery diameter. Multiple linear regression showed the hypertension had a significant correlation with the number of the diseased regions(P = 0.014). Conclusions The risk stratification based on the symptom, ECG, cardiac injury markers and accompanying traditional risk factors is both important and available in practice. It is unsuitable for patients with a normal ECG and cardiac injury markers to differentiate ACS from non-cardiac chest pain relying only on the number of the accompanying traditional risk factors. However we found the number of the risk factors can indicate the disease severity.

Acute oppressive chest pain in a 66-year-old woman with a recent Amplatzer device closure of patent foramen ovale

bpm); cardiac sounds were valid and rhythmic, without pathologic rumours. Peripheral pulses were symmetrically present and no carotid or femoral bruits were found. The electrocardiogram (ECG) revealed left axis deviation. A chest X-ray showed no pathologic findings. Considering the features of the chest pain, which was acute, oppressive, transmitted to the interscapular region and irradiated to the neck, the initial differential diagnosis was between acute coronary syndrome, pulmonary embolism and aortic dissection. Acute coronary syndrome was ruled out by ECG and myocardial damage markers, which were repeatedly negative. A pulmonary angioCT was performed and ruled out both pulmonary embolism and aortic dissection. Nevertheless the thoracic CT scan revealed a dense, circular, homogeneous mass with a maximum transverse diameter of 4 cm (Fig. 1a) located in a retrocardiac paracaval position, extended from the confluence of the inferior vena cava in the right atrium to the retrohepatic portion of the inferior vena cava, at the level of the confluence of the suprahepatic veins (Fig. 1b). A differential diagnosis among pleuro-pericardial cyst, iatrogenic paracaval haematoma (after device positioning) of the interatrial septum or pseudoaneurysm of the inferior vena cava wall was considered. Thoracic CT scan was performed with contrast medium and no enhancement of the pericaval lesion was observed after injection of contrast medium both in the arterial and venous phases. These findings were consistent with a lack of direct communication between right atrium or inferior vena cava and the pericaval lesion. The magnetic resonance imaging (MRI) confirmed the presence of the pericaval lesion with a density consistent with a liquid cyst (Fig. 1C). No additional information for the differential diagnosis could be obtained by MRI, thus the image was given a diagnosis of pleuro-pericardial cyst. Interestingly enough, standard and transoesophageal echocardiography performed at admission and repeated in the following days showed the Amplatzer on site without residual shunt, left ventricular of normal dimension and function, and in particular failed to detect the pericaval lesion, possibly because of the peculiar position of the cyst. The patient remained asymptomatic during the days following admission. Contrast CT scan was repeated twice (at day +3 and day +7) and no variation in the size and density of the lesion was observed. Given the absence of symptoms, the age, the dimension of the mass and co-morbidity, the patient is simply being followed on a regular basis. She has a clinical examination every two months and the latest thoracic CT scan, performed five months after discharge, was unchanged. Intern Emerg Med (2007) 2:229–230 DOI 10.1007/s11739-007-0064-4

Yield of Early Rest and Stress Myocardial Perfusion Single-Photon Emission Computed Tomography and Electrocardiographic Exercise Test in Patients With Atypical Chest Pain, Nondiagnostic Electrocardiogram, and Negative Biochemical Markers in the Emergency Department

There are no studies in which diagnostic yield of early rest myocardial perfusion gated single-photon emission computed tomography (SPECT), electrocardiographic exercise testing, and stress SPECT were compared in patients with atypical chest pain, nondiagnostic electrocardiograms (ECGs), and negative markers of myocardial damage in the emergency department. A prospective study of 96 patients who presented with atypical chest pain and nondiagnostic ECG, but without elevated markers of necrosis, was performed. All underwent rest gated SPECT using technetium-99m methoxyisobutyl isonitrile within 6 hours after pain subsided followed by an electrocardiographic exercise test to obtain stress-rest SPECT images. After 1 year, there were no deaths and coronary artery disease was confirmed in only 5 patients. Negative predictive values of the 3 techniques were high (99%, 96%, and 100%, respectively), but positive predictive values were low (27%, 22%, and 14%, respectively). Sensitivities of early SPECT (80%) and stress SPECT (100%) were higher than for the electrocardiographic exercise test (40%). In conclusion, in patients with atypical chest pain, nondiagnostic ECG, and negative biochemical markers, negative predictive values of the 3 tests analyzed are very high. The sensitivity of radionuclide tests is higher, but their widespread use does not appear warranted because their positive predictive value and incidence of complications is low.

An electrocardiogram marker to detect paroxysmal atrial fibrillation

An electrocardiogram marker to detect patients who have paroxysmal atrial fibrillation (PAF) is reported. The data set of ECG records made available by PhysioNet for Cardiology Challenge 2001 was used. The method uses a filtered time series with a frequency range between 3 and 9 Hz obtained from the electrocardiogram record. Typically, frequencies observed when a patient is in atrial fibrillation and atrial flutter is within this frequency range. Filtering was done using wavelets. Thereafter, the temporal properties of this filtered time series are studied. The temporal properties studied are the standard deviation, standard deviation of successive differences, and the length of the ellipse in the Poincare plot. The results indicate that these temporal properties of patients with PAF are depressed compared to the healthy group. A marker based on these temporal properties shows promise in detecting PAF when patients are in normal sinus rhythm. Results also show that the values for these temporal properties for a patient with PAF show little variation with time, and its measure is not dependent on the time of occurrence of a PAF episode.

Relationship between electrocardiographic and biochemical variables in coronary artery disease

Background ECG (electrocardiogram) markers reflecting abnormal heart rate variability and abnormal repolarization as well as several biochemical markers reflecting inflammation, endothelial dysfunction, and procoagulation states were reported to show an association with increased cardiovascular mortality. ECG and biochemical markers could operate independently or they could interrelate in pathogenetic pathways of coronary disease. In this study, we aimed to explore the relationship between ECG and biochemical markers in a longitudinal study of coronary patients. Methods A total of 499 observations from 52 patients with up to 12 repeated measurements were collected providing data on series of ECG (heart rate variability and repolarization) parameters and biochemical parameters. Generalized estimating equation models adjusting for repeated measurements were used for the analyses. Results There was a significant association between ECG parameters reflecting abnormal repolarization (prolonged QT interval, lower T wave amplitude) and elevated levels of C-reactive protein and fibrinogen. Abnormal heart rate variability, increased sympathetic tone (low-frequency power) was associated with increased concentrations of soluble E-selectin, a marker of endothelial cell activation. There was no association between ECG markers and parameters reflecting increased procoagulation states. Conclusion These results indicate that there is an association between ECG parameters and blood markers reflecting endothelial function and inflammation in coronary artery disease patients. The pathophysiologic mechanisms of these associations remain to be elucidated.

Superiority of ST abnormalities as electrocardiogram markers of heart failure

Left ventricular hypertrophy (LVH) and obesity are important cardiovascular risk factors. This study evaluates the influence of obesity on the diagnostic performance of the most used electrocardiographic criteria for LVH in hypertensive patients.One thousand two hundred four outpatients from the Hypertensive Unit of the Hospital São Paulo, São Paulo, SP, Brazil, were studied. All underwent 12-lead electrocardiogram and echocardiogram. The most known electrocardiographic criteria for LVH were assessed and compared with the left ventricular mass index obtained by echocardiogram in obese and nonobese groups of hypertensive patients.The population's mean age was 57.4 ± 4.7 years; 351 were men (29.1%) and 853 women (70.8%). Cornell voltage, Cornell duration, Sokolow-Lyon voltage, Romhilt-Estes criteria, and R wave in aVL 11 mm or higher showed a positive correlation with left ventricular mass index (P < .05). Notwithstanding, there were no changes regarding specificity for obese or nonobese characteristics. However, sensitivity had a statistically significant decrease in obese patients in regard to Sokolow-Lyon voltage and Romhilt-Estes criteria and strain pattern (P < .05).Cornell voltage and Cornell duration criteria, Perugia score, R wave in aVL, and QTc variable had no significant changes in diagnostic sensitivity in the obese patients.

Abnormal intra-QRS potentials associated with percutaneous transluminal coronary angiography–induced transient myocardial ischemia

This article introduces a novel concept of abnormal intra-QRS potentials (AIQPs) associated with myocardial ischemia. AIQPs are microvolt-level potentials—subtle alterations in the QRS of the high-resolution electrocardiogram (ECG)—isolated from the unfiltered signal-averaged ECG (SAECG) by a method of mathematical modeling. The aims of the study were (1) to determine the characteristics of potentials in the SAECG related to ischemically altered activation during percutaneous transluminal coronary angiography (PTCA), (2) to determine their relationship with standard 12-lead ECG variables, and (3) to investigate whether AIQPs have a specific pathophysiologic basis in myocardial ischemia. Continuous high-resolution ECG data were acquired from 12 patients before, during, and after PTCA. SAECGs were computed every 60 seconds using an enhanced method of signal averaging. AIQP, ST-segment deviation, and changes in standard ECG QRS duration were measured in each 1-minute SAECG. AIQP amplitudes increased significantly during balloon inflation, compared with the preinflation state. AIQPs exhibited a greater prevalence (12 of 12 patients) than ST-segment deviation changes of more than 100 μV (7 of 12 patients), or measurable changes in standard QRS duration (4 of 12 patients). In patients with significant changes in 12-lead ECG variables during balloon inflation, AIQPs were strongly correlated with both ST-segment and QRS-duration changes. AIQP timing was correlated with the artery occluded, suggesting a specific, ischemia-influenced origin of the signal. AIQPs show promise as a time-localized, sensitive new ECG marker of ischemically altered ventricular activation.

We-W30:1 Genetic determinants of plasma lipoproteins

The independent predictive value of d-dimer and inflammatory markers for the risk of recurrent adverse events in patients with acute chest pain but normal levels of cardiac troponin I (cTnI) remains unclear.We studied 391 patients admitted to the hospital in 1 year with acute ischemic-type chest pain. Creatine kinase-myocardial band isoenzyme (CK-MB) mass and cTnI levels were measured in initial and 12-hour samples. Soluble intercellular adhesion molecule (sICAM)-1, vascular cell adhesion molecule (sVCAM)-1, sP-selectin, sE-selectin, high sensitivity C-reactive protein (hsCRP), interleukin-6 (IL6), fibrinogen, and d-dimer levels were measured in initial samples. A 1-year incidence of death, myocardial infarction (MI), revascularization, or readmission with chest pain was determined (with death/MI as the primary end point).Patients with normal levels of CK-MBmass and cTnI (195/391[50%]) were at a lower risk than patients with elevated levels of CK-MBmass or cTnI, but still had an important incidence of events (77/195[39%]). Marker elevation was defined as >75th percentile (upper quartile). Elevated d-dimer levels (>580 ng/mL) was predictive of death/MI (odds ratio, 5.4; 95% CI, 1.5-20.2; P = .005). Elevated sP-selectin levels (>152 ng/mL; odds ratio, 3.2; 95% CI, 0.9-11.6; P = .06) trended to increased death/MI rates, with weaker trends for elevated levels of hsCRP (>7.1 mg/L), IL6 (>10.7 pg/mL), and ST depression. Other markers, other electrocardiogram changes, or classic risk factors were not predictive of death/MI. With a multivariate analysis, d-dimer and sP-selectin were found to be of independent significance for death/MI after adjustment for inflammatory, hemostatic, and electrocardiogram markers and d-dimer after adjustment for classic risk factors.Normal cTnI levels after acute chest pain does not confer absence of future risk. Concurrent assessment of d-dimer and inflammatory markers may improve risk stratification.

1072-217 QRS intrinsicoid in lead I: A novel surface electrocardiogram marker for left sided conduction system disease in patients with a right bundle branch block pattern

1072-217 QRS intrinsicoid in lead I: A novel surface electrocardiogram marker for left sided conduction system disease in patients with a right bundle branch block pattern

Exercise-induced prolongation of the infarct-related Q-waves as a marker of myocardial viability in the infarcted area

Objective: It is known that exercise-induced ischemia in patients with coronary artery disease (CAD) may produce QRS prolongation in the surface electrocardiogram (ECG). To investigate the presence of exercise-induced Q-wave prolongation in patients with single-vessel CAD and Q-wave myocardial infarction (MI), in association with the presence of reversible perfusion defects during thallium scintigraphy in the infarcted area. Methods: 107 consecutive patients (89 males, mean age 56±8 years) were evaluated. All patients underwent coronary arteriography, maximal treadmill exercise testing and thallium-201 scintigraphy. Q-wave duration was measured both before exercise testing and during maximal heart rate from 12-lead ECGs recorded with a paper speed of 50 mm/s. Results: Only 57 out of the 107 studied patients showed reversible perfusion defects in the infarcted area during thallium scintigraphy. Q-wave duration was significantly increased from the resting to the stress ECG (ΔQ-wave duration) in patients with reversible perfusion defects in the infarcted areas (10±13 ms), but not in patients with fixed defects in the infarcted zone (−2.0±5 ms, p<0.01). The sensitivities and the specificities of Q-wave prolongation, ST segment elevation, and the combination of ST segment elevation with ST segment depression in the reciprocal leads for the detection of myocardial viability in the infarcted area were 82%, 48%, 29% and 88%, 50%, and 90%, respectively. Conclusions: Exercise-induced Q-wave prolongation is demonstrated in those patients with single-vessel CAD and a recent MI who show reversible perfusion defects in thallium scintigraphy. Exercise-induced Q-wave prolongation was found to be a sensitive and specific ECG marker for the detection of myocardial viability in the infarcted area.

Noninvasive risk stratification in postinfarction patients with severe left ventricular dysfunction and methodology of the MADIT II noninvasive electrocardiology substudy

Sudden cardiac death occurs as a result of a complex interplay of changes in myocardial substrate, imbalance of autonomic regulation of the heart, and myocardial vulnerability. Noninvasive electrocardiology serves as a comprehensive tool for investigating factors representing mechanistic pathways leading to cardiac events. Heart rate variability, nonlinear dynamics of heart rate, and heart rate turbulence provide insight into autonomic control of the heart. Prognostic value of these parameters in postinfarction patients is well established for predicting cardiac death, but there is less evidence for their association with sudden death or arrhythmic events. Electrical manifestation of changes in myocardial substrate include QRS and QTc prolongation, presence of conduction disturbances, presence of late potentials, abnormalities of repolarization morphology, and presence of nonsinus rhythm, namely atrial fibrillation. Electrocardiogram (ECG) measures reflecting myocardial vulnerability to arrhythmias include frequent ventricular premature beats, T wave alternans, or QT variability. Prognostic significance of these parameters is documented in studies focused mostly on them as individual markers of risk. The noninvasive electrocardiology substudy of the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) allows for simultaneous analysis of several of the above ECG markers of risk and will provide insight about relative contribution of mechanistic pathways leading to cardiac death in postinfarction patients with severe left ventricular dysfunction. Combination of a standard 12-lead ECG and 10-minute high-resolution Holter recordings serves to evaluate the prognostic significance of noninvasive electrocardiology parameters for mortality in patients randomized to conventional treatment and for arrhythmic events in patients randomized to implantable cardioverter defibrillator therapy.

Intermittent Noninfarction Q Waves: A Finding Suggestive of Latent Preexcitation

To describe 3 patients who presented with chest pain and intermittent Q waves on the electrocardiogram (ECG) and were subsequently found to have latent preexcitation. During a span of 8 years, 3 patients were evaluated because of atypical chest pain and pathologic Q waves in the inferior leads; in all 3 patients, the Q waves were intermittent. No patient had a history of arrhythmia or had Wolff-Parkinson-White pattern on the ECG. Diagnostic and therapeutic interventions for suspected myocardial infarction included cardiac catheterization in 2 patients, intravenous thrombolytic therapy in 1 patient, and heparin in 2 patients. Ischemic heart disease was excluded in all. Patients underwent pharmacological testing and/or electrophysiologic study for suspected preexcitation. Despite the absence of ECG markers of preexcitation, the presence of a latent accessory atrioventricular connection was confirmed in each patient by pharmacological or electrophysiologic studies. In patients who present with intermittent noninfarction Q waves, the most likely diagnosis is latent preexcitation. Clinicians need to be educated about this clinical diagnosis and encouraged to pursue confirmatory testing. Such patients should be informed about the nature and importance of their electrocardiographic abnormality.

Prediction of Recurrent Events by D-Dimer and Inflammatory Markers in Patients with Normal Cardiac Troponin I (PREDICT) study

Background The independent predictive value of d-dimer and inflammatory markers for the risk of recurrent adverse events in patients with acute chest pain but normal levels of cardiac troponin I (cTnI) remains unclear. Methods We studied 391 patients admitted to the hospital in 1 year with acute ischemic-type chest pain. Creatine kinase-myocardial band isoenzyme (CK-MB) mass and cTnI levels were measured in initial and 12-hour samples. Soluble intercellular adhesion molecule (sICAM)-1, vascular cell adhesion molecule (sVCAM)-1, sP-selectin, sE-selectin, high sensitivity C-reactive protein (hsCRP), interleukin-6 (IL6), fibrinogen, and d-dimer levels were measured in initial samples. A 1-year incidence of death, myocardial infarction (MI), revascularization, or readmission with chest pain was determined (with death/MI as the primary end point). Results Patients with normal levels of CK-MB mass and cTnI (195/391[50%]) were at a lower risk than patients with elevated levels of CK-MB mass or cTnI, but still had an important incidence of events (77/195[39%]). Marker elevation was defined as >75th percentile (upper quartile). Elevated d-dimer levels (>580 ng/mL) was predictive of death/MI (odds ratio, 5.4; 95% CI, 1.5-20.2; P = .005). Elevated sP-selectin levels (>152 ng/mL; odds ratio, 3.2; 95% CI, 0.9-11.6; P = .06) trended to increased death/MI rates, with weaker trends for elevated levels of hsCRP (>7.1 mg/L), IL6 (>10.7 pg/mL), and ST depression. Other markers, other electrocardiogram changes, or classic risk factors were not predictive of death/MI. With a multivariate analysis, d-dimer and sP-selectin were found to be of independent significance for death/MI after adjustment for inflammatory, hemostatic, and electrocardiogram markers and d-dimer after adjustment for classic risk factors. Conclusion Normal cTnI levels after acute chest pain does not confer absence of future risk. Concurrent assessment of d-dimer and inflammatory markers may improve risk stratification.

C-reactive protein, clinical presentation, and ischemic activity in patients with chest pain and normal coronary angiograms

ObjectivesWe sought to investigate the relationship among C-reactive protein (hs-CRP), clinical characteristics, exercise stress test responses, and ST-segment changes during daily life in patients with typical chest pain and normal coronary angiograms (CPNCA). BackgroundPatients with CPNCA have coronary microvascular endothelial dysfunction and myocardial ischemia. Elevated hs-CRP levels have been related to atherogenesis and endothelial dysfunction. The relationship between hs-CRP and disease activity has not been previously investigated in CPNCA patients. MethodsWe studied 137 consecutive CPNCA patients (mean age, 57 ± 9; 33 men). All completed standardized angina questionnaires, underwent exercise stress testing, 24-h ambulatory electrocardiogram (ECG) monitoring (Holter), and hs-CRP measurements at study entry. ResultsC-reactive protein levels (mg/l) were higher in patients with frequent (2.9 ± 3.3) and prolonged (3.9 ± 4.1) chest pain episodes, and in those with ST-segment depression on exercise testing (2.6 ± 2.8) and Holter monitoring (3.4 ± 3.1) compared with patients with occasional (1.3 ± 1.2; p = 0.002) or shorter chest pain (1.5 ± 1.3; p < 0.001) episodes, negative exercise stress testing (1.1 ± 1.1; p < 0.001), and no ST-segment shifts on Holter monitoring (0.9 ± 0.7; p < 0.001). Moreover, we found a correlation between hs-CRP concentration and number of ischemic episodes during Holter monitoring (r = 0.65; p < 0.001) and with the magnitude of ST-segment depression on exercise testing (r = −0.43; p < 0.001). The hs-CRP was the only independent variable (multivariate logistic regression) capable of predicting positive findings on Holter monitoring (odds ratio [OR], 3.8; confidence interval [CI], 2.3 to 6.2) and exercise testing (OR, 1.7; CI, 1.2 to 2.2). ConclusionsThe hs-CRP correlates with symptoms and ECG markers of myocardial ischemia in CPNCA patients. Whether hs-CRP is related to the pathogenesis of angina in these patients deserves further investigation.

A randomized comparison of direct stenting with conventional stent implantation in selected patients with acute myocardial infarction

ObjectivesWe sought to determine whether direct stenting might prevent the adverse events associated with stent implantation during primary angioplasty and to compare it with conventional stent implantation in patients with acute myocardial infarction (AMI). BackgroundNo trial has demonstrated that stents favorably influence mortality rate. Recent studies have even suggested a negative impact of stents on coronary blood flow and clinical outcome. MethodsOf 409 patients treated by primary angioplasty with stent implantation in our center, 206 (50%) were enrolled in this randomized, single-center trial and allocated to direct stent implantation (n = 102) or stent implantation after balloon pre-dilation (n = 104). The study end points included angiographic results (final corrected Thrombolysis In Myocardial Infarction [TIMI] frame count and a composite end point of slow and no-reflow or distal embolization), an electrocardiogram marker of myocardial reperfusion assessment (ST-segment resolution) and in-hospital clinical outcome (death and recurrent infarction). ResultsDirect stent implantation failed in eight patients but succeeded after pre-dilation in all. A non-significant increase in TIMI flow grade 3 was achieved after direct stenting (95.1% vs. 93.3%, p = 0.74) without significant difference in the corrected TIMI frame count (31.5 ± 17 and 35.2 ± 20 frames after direct and conventional stent, respectively, p = 0.42). The composite angiographic end point was significantly reduced by direct stent implantation (11.7% vs. 26.9%, p = 0.01). ST-segment resolution was also significantly improved after direct stent (no ST-segment resolution in 20.2% vs. 38.1% after direct and conventional stent, respectively, p = 0.01). Death and/or recurrent infarction occurred in six patients after conventional stent implantation and in two patients after direct stenting (p = 0.28). ConclusionsIn selected patients with AMI, direct stenting can be applied safely and effectively. This strategy may result in a significant reduction of microvascular injury, as suggested by improved ST-segment resolution after reperfusion with major potential clinical consequences.

Plasma amino-terminal pro-brain natriuretic peptide levels in subjects presenting to the Emergency Department with suspected acute coronary syndrome: possible role in selecting patients for follow up?

Plasma amino-terminal pro-brain natriuretic peptide (NT-proBNP) level is a sensitive and specific indicator of cardiac dysfunction. To determine whether plasma NT-proBNP level is elevated at the time of presentation with acute coronary syndrome (ACS) and whether it may assist in the diagnosis of heart failure and myocardial ischaemia in the Emergency Department. Plasma NT-proBNP levels were measured prospectively in 201 unselected presentations to the Emergency Department with suspected ACS where cardiac injury markers were requested by clinicians as part of routine assessment. NT-proBNP levels were correlated with clinical, electrocardiogram (ECG), biochemical and radiological findings. Elevated NT-proBNP level detected heart failure with high sensitivity (95-96%). Among patients without heart failure, NT-proBNP levels were increased more frequently in patients with previously diagnosed ischaemic heart disease. Elevated NT-proBNP level predicted cardiomegaly and a cardiac cause of presentation. However, the NT-proBNP level was not associated with ECG or biochemical markers of myocardial ischaemia, and only one-third of patients with ACS showed an increase of 40% or more in NT-proBNP level at repeat measurement of cardiac injury markers 5 h after presentation. Although elevated NT-proBNP level detected heart failure with high sensitivity, NT-proBNP level did not assist in the diagnosis of acute myocardial ischaemia. These findings indicate that the major determinant of elevated NT-proBNP level on presentation with suspected ACS was underlying cardiac dysfunction rather than acute myocardial ischaemia. This suggests that NT-proBNP measurement in patients with a suspected cardiac reason for presentation to the Emergency Department may identify a previously unrecognized group of patients without acute ischaemia who may nevertheless benefit from further investigation of cardiac function.

The spatial QRS-T angle as a marker of ventricular repolarisation in hypertension.

Ventricular repolarisation abnormalities are important in arrhythmia provocation. The dispersion of repolarisation duration is not the only aspect of repolarisation heterogeneity. Spatial vectorcardiographic descriptors constitute a novel approach to quantify ventricular repolarisation. To test the ability of vectorcardiographic descriptors to discriminate between hypertensives with high or low blood pressure (BP), 110 treated hypertensives (mean age 63.6 +/- 12.1 years) were classified in the high (systolic BP > or = 160 mm Hg or diastolic BP > or = 95 mm Hg) (n = 67), or the low (systolic BP < 160 mm Hg and diastolic BP <95 mm Hg) (n = 43) BP group. The maximum QT, JT, and T peak-T end intervals and the QT, JT, and T peak--T end dispersion were calculated from a digitally recorded 12-lead electrocardiogram (ECG). X, Y, and Z leads were reconstructed from the 12-lead ECG. The amplitude of the maximum spatial T vector (spatial T amplitude), the angle between the maximum spatial QRS and T vectors (spatial QRS-T angle) and the frontal plane QRS-T angle were calculated. The spatial QRS-T angle was higher in patients with high compared to those with low BP (P = 0.025). All conventional ECG markers of the dispersion of ventricular repolarisation duration failed to demonstrate significant differences between hypertensives with high or low BP. In conclusion, the spatial QRS-T angle was significantly increased in those treated hypertensive patients who showed repeatedly high BP values. Hence, we may suggest that the angle between the directions of ventricular depolarisation and repolarisation is a sensitive marker of the repolarisation alterations in systemic hypertension. Journal of Human Hypertension (2001) 15, 63-70

Prediction of right ventricular and posterior wall ST elevation by coronary care nurses: The 12-lead electrocardiograph versus the 18-lead electrocardiograph

Objective To determine the value of routine versus selective use of the 18-lead electrocardiogram in determining the size of an acute inferior myocardial infarction (MI). Design Prospective, quasi-experimental, random assignment. Setting The coronary care unit (CCU) of a major teaching hospital in South Australia. Patients Fifty-two patients admitted to the CCU with acute evolving inferior MI. Outcome measures Correlation and comparison of the predictions of right ventricular (RV) and posterior wall (PW) lead ST elevation with prospectively chosen markers on the 12-lead electrocardiogram—ST elevation in lead III>II and precordial ST depression, and the predictions by coronary care nurses. Procedure The results of 18-lead electrocardiograms of 52 consecutive patients admitted to the CCU with acute evolving inferior MI were classified according to prospectively chosen criteria. Coronary care nurses were randomly assigned four 12-lead electrocardiograms and asked to “blindly” predict ST elevation in the concurrent RV and PW leads. Results ST elevation in lead III>II demonstrated a sensitivity and positive predictive accuracy of 86% to 1 mm of ST elevation in the RV leads. ST depression in V 1, V 2, and V 3 similarly demonstrated a 75% sensitivity and 89% positive predictive accuracy to 1 mm of ST elevation in the PW leads. In comparison, coronary care nurses proved to be as accurate in their predictions of additional PW ST elevation ( p=0.73), but were significantly less able to predict RV ST elevation ( p=0.049). These predictions were independent of the level of experience and qualifications. Conclusions Discriminating between smaller and larger types of inferior MIs has the potential to alter patient management: Thirty-two percent of patients in the study demonstrated additional ST elevation in both the RV and PW leads. Both of the 12-lead electrocardiogram markers used in this study proved reasonably accurate in predicting additional ST elevation in the leads that normally comprise the 18-lead electrocardiogram. Recognition of these markers has the potential to expedite the need for the additional 18-lead electrocardiogram when rapid assessment of infarction size is required. However, the routine use of the 18-lead electrocardiogram is supported by this study.