Value of electrocardiogram in predicting and estimating infarct size in man.

The value of the electrocardiogram in assessing infarct size was studied using serial estimates of the MB isomer of creatine kinase (CK MB) in plasma, serial 35 lead praecordial maps in 28 patients with anterior myocardial infarction, and serial 12 lead electrocardiograms in 17 patients with inferior myocardial infarction. In patients with anterior infarcts, sigma ST, sigma R, sigma Q, sigma R/(Q+S), and the number of sites with ST elevation more than 2 mm or with QS waves, were obtained from each map. Correlation between both maximum sigma Q and maximum sigma ST with cumulative CK MB was highly significant. There was also a significant correlation between sigma R and sigma R/(Q+S) with cumulative CK MB. There was no significant correlation between maximum number of sites with ST elevation or with Q or QS waves and cumulative CK MB. Maximum sigma ST and number of sites with ST elevation predicted maximum sigma Q and number of sites with QS or Q waves at a time when infarction was not complete. In patients with inferior infarcts, there was a significant correlation between maximum sigma Q and maximum sigma ST in leads II, III, and a VF, and cumulative CK MB. This study shows that all the waves in the electrocardiogram are useful in assessing infarct size. The fact that maximum sigma ST predicts final sigma Q may be used to assess the efficacy of interventions designed to salvage ischaemic myocardium.     

ECG findings after myocardial infarction in children after Kawasaki disease

Standard 12-lead ECGs were evaluated in 17 children with myocardial infarction and 78 children without myocardial infarction after Kawasaki disease; sensitivity and specificity of the ECG infarction criteria were determined. The presence or absence of myocardial infarction was determined from either clinical examination results (coronary angiography, ventriculography, and thallium-201 myocardial imaging) or autopsy findings. Of seven patients with inferior infarction, abnormally deep Q waves in lead II, III, or aVF were observed in six, but the duration was greater than 0.04 second in only one (14%). The sensitivity and specificity of inferior infarction criteria based on Q wave amplitude were 86% and 97%, respectively. Of eight patients with anterior infarction, seven (88%) had abnormally deep and wide (greater than or equal to 0.04 second) Q waves in anterior chest leads. The sensitivity and specificity of the infarction criteria based on the amplitude and duration of the Q wave were 75% and 99%, respectively. Of seven patients with lateral infarction, Q waves were observed in lead I, aVL, or both in four patients, and in all of these patients Q waves were wider than 0.04 second. In two patients with both inferior and anterior infarction, Q waves were observed only in leads II, III, and aVF; in only one patient were the Q waves wider than 0.04 second. Thus deep Q waves in lead II, III, or aVF that are not wider than 0.04 second may indicate inferior infarction in children. Q waves in lead I, aVL, and chest leads associated with anterolateral infarction are in most instances deep and wide.     

Reliability of standard electrocardiogram in detecting left ventricular asynergy in 315 patients with recent myocardial infarction

The relationship between asynergy of the left ventricular wall detected by two-dimensional echocardiography and ECG signs of necrosis (number of Q waves greater than or equal to 40 ms, Wagner's score) was evaluated in 315 patients (NYHA I-II) 23-90 days after a first Q-wave myocardial infarction (MI). Poor correlations were found between asynergy and ECG parameters. An ECG anterior MI is an apicoseptal MI by echo (independently of the ECG extent of Q waves) and the ECG is of little or no help in predicting the extent of asynergy to the inferior wall and proximal segments of the septum. An ECG inferior MI is inferoposterior by echo and the ECG has very limited value in predicting the extent of asynergy to the apex and septum. Patients with Q waves in leads II, III, and aVF had more extensive asynergy than those with either 2Q or greater than 3Q. R/S greater than or equal to 1 in V1 and/or V2 was present in 44% of patients with inferior MI while asynergy of at least one segment of the posterior wall was observed in 94%. In conclusion, standard ECG is sensitive in identifying anterior versus inferior infarct but it is unreliable in predicting the real extent of asynergy of the left ventricle, particularly in inferior infarcts.     

Diagnostic value of electrocardiogram and vectorcardiogram in postinfarction ventricular asynergy

The ability of ECG-VCG to predict the severity of postinfarction LV asynergy was evaluated in 152 patients with previous myocardial infarction who underwent left cineventriculography in the right anterior oblique view. Various ECG and VCG signs were examined in order to predict the existence of severe asynergy in general (dyskinesia or akinesia or severe hypokinesia) and of dyskinesia in particular. In patients with inferior myocardial infarction (Group A) persistent ST segment elevation was the only specific ECG sign (100%) of severe asynergy; it had a poor sensitivity (6.2%). Four frontal VCG signs (presence of terminal bite, y- greater than 0.18 mV, maximum early superior vector along x axis = MESV greater than or equal to 1.3 mV, duration of initial superior forces = DISF greater than 50 msec) increased the sensitivity of the ECG-VCG method to 75.8% while maintaining a 100% specificity. Regarding the diagnosis of dyskinesia, only the ECG sign of persistent ST segment elevation and the VCG sign of y- greater than or equal to 0.3 mV had a 100% specificity. The sensitivity of the ECG-VCG method was 33.3% (16.6% ECG and 16.6% VCG). In patients with anterior myocardial infarction (Group B), concerning the diagnosis of severe asynergy, the ECG signs of sigma ST greater than 3 mm in anterior leads; pathologic Q wave in four or more anterior leads (including D1 and aVL); and the presence of LAH or LAH + RBBB, had a 100% specificity and a good sensitivity (60.5%). The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 71% while maintaining a 100% specificity. As for the diagnosis of dyskinesia, the ECG signs with a 100% specificity were sigma ST greater than or equal to 5 mm in anterior leads, a pathologic Q wave in more than five anterior leads (including I and a VL) and RBBB + LAH; these variables had a sensitivity of 48.3%. The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 79.3% while maintaining a 100% specificity. In patients with inferior plus anterior myocardial infarction (Group A + B) the signs mentioned above for each group were evaluated, confirming a 100% specificity. Regarding the diagnosis of severe asynergy, the ECG signs had a sensitivity of 61.3%, while VCG increased the sensitivity of the ECG-VCG method to 90.3%.(ABSTRACT TRUNCATED AT 400 WORDS)     

Left ventricular asynergy in electrocardiographic "posterior" myocardial infarction

P2 300 selected patients, scalar electrocardiograms and contemporaneous radionuclide angiograms were analyzed retrospectively to assess the association between prominent right precordial R waves (duration greater than or equal to 0.04 second, R greater than or equal to S in lead V1 or V2), traditionally considered diagnostic of "posterior" infarction, and asynergy in various left ventricular segments. Mathematical methods for analysis of association between nonparametric variables clearly demonstrated that prominent right precordial R waves were strongly associated with asynergy of the basal lateral left ventricular wall, although asynergy of adjacent inferior and lateral segments was common. With the exclusion of right ventricular hypertrophy and bundle branch block, a prominent R wave in lead V1 exhibited a high specificity (greater than to 99%), a high positive predictive value (91%) and a low sensitivity (36%) for diagnosing basal lateral myocardial infarction. A prominent R wave in lead V2 exhibited a higher sensitivity (61%), a somewhat lower specificity (95%) and a significantly lower positive predictive value (76%). A newly developed criterion for such infarction--a prominent R wave in lead V2 and a Q wave inferior infarction--had intermediate characteristics and may be more clinically useful. The most common reasons for the decreased sensitivities of all three criteria were left ventricular hypertrophy or associated anterior myocardial infarction. These data demonstrate that prominent right precordial R waves are clinically useful in identifying inferior and lateral wall infarctions that involve the basal lateral left ventricular segment. Confusion results primarily from inappropriate use of the electrocardiographic term "posterior" for such infarctions.     

Value of electrocardiogram in diagnosing right ventricular involvement in patients with an acute inferior wall myocardial infarction

To study the value of the electrocardiogram in diagnosing right ventricular involvement in acute inferior wall myocardial infarction, the electrocardiographic findings were analysed in 67 patients who had had scintigraphy to pin-point the infarct. All 67 patients were consecutively admitted because of an acute inferior wall infarction. A 12 lead electrocardiogram with four additional right precordial leads (V3R, V4R, V5R, and V6R) was routinely recorded on admission and every eight hours thereafter for three consecutive days. Thirty-six to 72 hours after the onset of chest pain a 99mtechnetium pyrophosphate scintigraphy and a dynamic flow study were performed to detect right ventricular involvement, which was found in 29 of the 67 patients (43%). ST segment elevation greater than or equal to 1 mm in leads V3R, V4R, V5R, and V6R is a reliable sign of right ventricular involvement. ST segment elevation greater than or equal to 1 mm in lead V4R was found to have the greatest sensitivity (93%) and predictive accuracy (93%). The diagnostic value of a QS pattern in lead V3R and V4R or ST elevation greater than or equal to 1 mm in lead V1 was much lower. ST segment elevation in the right precordial leads was short lived, having disappeared within 10 hours after the onset of chest pain in half of our patients with right ventricular involvement. When electrocardiograms are recorded in patients with an acute inferior wall infarction within 10 hours after the onset of chest pain, additional right ventricular infarction can easily be diagnosed by recording lead V4R.     

Value of electrocardiogram in diagnosing right ventricular involvement in patients with an acute inferior wall myocardial infarction.

To study the value of the electrocardiogram in diagnosing right ventricular involvement in acute inferior wall myocardial infarction, the electrocardiographic findings were analysed in 67 patients who had had scintigraphy to pin-point the infarct. All 67 patients were consecutively admitted because of an acute inferior wall infarction. A 12 lead electrocardiogram with four additional right precordial leads (V3R, V4R, V5R, and V6R) was routinely recorded on admission and every eight hours thereafter for three consecutive days. Thirty-six to 72 hours after the onset of chest pain a 99mtechnetium pyrophosphate scintigraphy and a dynamic flow study were performed to detect right ventricular involvement, which was found in 29 of the 67 patients (43%). ST segment elevation greater than or equal to 1 mm in leads V3R, V4R, V5R, and V6R is a reliable sign of right ventricular involvement. ST segment elevation greater than or equal to 1 mm in lead V4R was found to have the greatest sensitivity (93%) and predictive accuracy (93%). The diagnostic value of a QS pattern in lead V3R and V4R or ST elevation greater than or equal to 1 mm in lead V1 was much lower. ST segment elevation in the right precordial leads was short lived, having disappeared within 10 hours after the onset of chest pain in half of our patients with right ventricular involvement. When electrocardiograms are recorded in patients with an acute inferior wall infarction within 10 hours after the onset of chest pain, additional right ventricular infarction can easily be diagnosed by recording lead V4R.     

Mechanisms of abnormal Q waves in hypertrophic cardiomyopathy assessed by intracoronary electrocardiography

INTRODUCTION: To clarify the mechanisms of abnormal Q waves in hypertrophic cardiomyopathy (HCM), local epicardial electrical activities were assessed by intracoronary electrocardiography (ECG). METHODS AND RESULTS: Unipolar intracoronary ECG was recorded by introducing a guide wire for angioplasty into the left anterior descending artery (LAD) in 20 patients with HCM and 10 control subjects. Intracoronary ECG showed no Q waves in any control subjects. Intracoronary ECG showed no Q waves in 8 HCM patients without abnormal Q waves on surface ECG. In 12 HCM patients with abnormal Q waves on surface ECG, 4 showed Q waves on intracoronary ECG associated with regional wall-motion abnormalities, suggesting Q waves are formed by loss of electrical forces due to transmural myocardial fibrosis. The remaining 8 patients, who did not have Q waves on intracoronary ECG, showed greater thickening of the basal free wall than the apical free wall, with no wall-motion abnormalities. Intracoronary ECG was characterized by increased R or R' waves and prolonged R peak times at the proximal LAD, suggesting Q waves are formed by increased electrical forces of hypertrophied basal septal and/or ventricular free wall, unopposed by apical forces. CONCLUSION: The study findings provide evidence for two mechanisms of abnormal Q waves in HCM: (1) loss of electrical forces due to transmural myocardial fibrosis, and (2) altered direction of resultant initial QRS vector due to increased electrical forces of disproportionate hypertrophy of the basal septal and/or ventricular free wall, unopposed by apical forces.     

Reassessment of Q waves in left bundle branch block.

This study disputes a number of recent reports claiming that abnormal Q waves or a QS configuration in inferior leads (II, III and AVF) coexisting with left bundle branch block is highly suggestive of, and indeed specific for, myocardial infarction. Five patients reported herein demonstrate disappearance of Q waves in inferior leads on spontaneous reversal of LBBB to normal conduction. This necessitates the conclusion that these Q waves represent a postdivisional conduction variant most closely equivalent to left anterior fascicular block coexisting with predivisional LBBB. Absence of inferior R waves in the five patients demonstrating LBBB is explicable by as little as a 20 msec conduction delay in the posterior fascicle coexisting with a higher grade conduction defect in the anterior fascicle. It is concluded that LBBB with a QS configuration in II, III and AVF cannot be considered diagnostic of inferior wall infarction since it regularly results from impaired conduction of the left anterior and possibly the left posterior fascicle (to a lesser extent), which may be reversible.     

On the relationship between Q waves in leads II and VF and inferior-posterior wall motion abnormalities

Twelve electrocardiographic criteria, based on various combinations of Q wave morphology in leads II and aVF, were tested in 235 cases for their diagnostic value in detecting inferoposterior wall motion abnormality (presumably reflecting infarction in the area) as demonstrated on left ventriculogram. The most reliable indicator of inferoposterior wall motion abnormality was found to to a QR complex with a Q wave width greater than or equal to .03 or greater than or equal to .04 sec associated with a Q/R ratio greater than .25. Using as criterion a QR complex with a Q wave width greater than or equal to .04 sec and a Q/R ratio greater than .25, the sensitivity was 41.9% in the cases with akinetic-dyskinetic wall motion and 3.7% in the cases with hypokinesis with an associated specificity of 100%. By lowering the Q wave duration to greater than or equal to .03 sec, the sensitivity increased to 51.6% and 9.3%, respectively, while retaining a very high specificity (96%). The exclusion of cases with a Q and R of less than 5 mm markedly lowered the sensitivity with a negligible increase in specificity. QS complexes in leads II or aVF were not found to be reliable indicators of inferoposterior wall motion abnormality.     

Insensitivity of the electrocardiogram in apical myocardial infarction

The ability of the standard ECG to identify myocardial infarction (MI) involving primarily the left ventricular (LV) apex is controversial. Therefore, the ECGs of 62 consecutive patients with acute infarction and isolated akinesia or dyskinesia of the LV apex on gated blood pool scintigraphy performed at rest 9 +/- 4 days after MI, were reviewed. The following distribution of Q waves was found: none, 26%; inferior leads only, 23%; anterior leads only, 32%; inferior + 1 or more V leads, 13%; lead I and/or aVL + 1 or more V leads, 6%. Only 12 patients (19%) demonstrated one of the "combination" Q-wave patterns thought to indicate apical infarction. Although the 20 patients with a history of MI did not differ in age or ejection fraction from those with a first MI, the combination of inferior and anterior Q waves was present in 6 of them (30%), vs only 2 of the remaining 42 patients (5%) (p less than 0.02). The 24 patients with apical dyskinesia had a lower ejection fraction (36 +/- 14 vs 48 +/- 12, p less than 0.001), a lower prevalence of isolated inferior Q waves (8 vs 32%, p less than 0.05) and a greater prevalence of isolated anterior Q waves (46 vs 24%, p = 0.09) than those with akinesia. Thus, in patients with recent MI localized to the LV apex on radionuclide ventriculography, pathologic Q waves are commonly confined to the anterior or inferior leads or absent altogether. The insensitivity of the various proposed criteria for the electrocardiographic diagnosis of apical MI emphasizes the value of imaging techniques in detecting this common clinical entity.     

Relation between the extent of the myocardial lesion and the state of the coronary bed in acute myocardial infarction

The probability of combined lesion of both ventricles in acute myocardial infarction (AMI) is discussed. In cases of proximal stenosis or occlusion of the right coronary artery, both inferior and right-ventricular (RV) AMI may develop. ECG recordings from the V3R-V6R, V3RIII, V4RIII leads were used for the diagnosis of RV AMI. Elevated ST segment plus the formation of Q waves and a negative T wave in the recordings from these leads indicate RV AMI in the presence of inferior AMI. The extent of myocardial lesion, estimated on the basis of maximum plasma MB CPK activity, is greater in cases of inferior AMI with electrocardiographic signs of RV AMI, as compared to inferior AMI free of such signs.     

Use of initial ST-segment deviation for prediction of final electrocardiographic size of acute myocardial infarcts

The decision to administer thrombolytic therapy for limitation of acute myocardial infarction (AMI) size must occur when only the history, physical examination and 12-lead electrocardiogram of a patient are available. A method that could quickly assess the amount of jeopardized myocardium would greatly aid the physician. This study developed formulas from 68 anterior and 80 inferior AMI patients using the extent of initial ST-segment deviation (ST delta) to predict the final AMI size estimated by the Selvester QRS score in a population not receiving reperfusion therapy. Inclusion required: initial anterior or inferior AMI; admission electrocardiogram less than or equal to 8 hours after the onset of symptoms with evidence of epicardial injury; elevated creatine kinase-MB; a predischarge electrocardiogram taken greater than or equal to 72 hours after admission; and no AMI extension before the predischarge electrocardiogram. The extent of epicardial injury was quantified by counting the number of leads with greater than or equal to 0.1 mm ST delta, by the sum (sigma) of ST delta in all leads and by the sigma ST delta in the lead groups associated with each AMI location. These results were compared to the AMI size estimated from the predischarge electrocardiogram. Univariable and multivariable analyses generated these formulas for AMI size: anterior = 3[1.5 (number leads ST increases) - 0.4]; inferior = 3[0.6 (sigma ST increases II, III, aVF) + 2.0]. Thus, formulas based on quantitative measurements of ST delta on the admission electrocardiogram are predictive of final QRS-estimated AMI size, and may be useful in determining the efficacy of acute reperfusion therapy.     

Use of integral indicators of precordial mapping in differential diagnosis of focal-cicatricial lesions of the myocardium

The paper proposes new criteria for differential diagnosis of myocardial "focal scarring" and "++pseudo-scarring" changes in various cardiac abnormalities and homogeneous morphological alterations in the ventricular complex on ECG (the QS, Qr-type abnormalities of the R line) by using the findings of 35 lead ECG mapping (PM-35). ECG-12 and PM-35 were analysed in 427 patients, including those with coronary heart disease (n-122), arterial hypertension and aortic malformations (n-130), dilated cardiomyopathy, congenital cardiac disease (n-175). Electrocardiographic signs of focal scarring lesions were revealed in all the cases with coronary heart disease and 66 with myocardial hypertrophy. The total value of ST segment depression and the sum of Q wave squares in three to five vertical mapping columns were found to be the most significant differential and diagnostic criterion. When scars and ++pseudo-scars were differentiated, a sensitivity of 75% was obtained at a specificity of 87%.     

Computerized orthogonal electrocardiogram: relation of QRS forces to left ventricular ejection fraction

Several studies have suggested a relation between Q wave or R wave amplitude in the standard 12 lead electrocardiogram and the left ventricular ejection fraction. Accordingly, we analyzed the relation between Q wave and R wave amplitudes obtained with computerized orthogonal (Frank) electrocardiography and the angiographically determined left ventricular ejection fraction. A computerized orthogonal electrocardiogram was obtained before cardiac catheterization in 52 consecutive patients being evaluated for chest pain. The electrocardiographic diagnosis indicated 14 normal tracings, 20 inferior, 12 anterior and 6 lateral myocardial infarctions. Linear correlations were made between X, Y and Z axis lead voltages and ejection fraction. A significant correlation was obtained between the voltages of the R waves in the X, Y and Z leads (Rx, Ry, Rz) and of the Q waves in lead Z (Qz) as well as total amplitude Qx + Rx, Qy + Ry and ejection fraction (P <0.01). Arithmetic summation of Rx + Ry + Qz (∑R) significantly augmented the correlation with ejection fraction (r = 0.78, P <0.001); this was only slightly improved by multivariate analysis of Rx, Ry, Qz (r = 0.80, P <0.001) or Rx, Ry, Rz, Qx, Qy, Qz (r = 0.82, P <0.001). ∑R, utilized as a means of predicting whether an ejection fraction was more or less than 50 percent, had an accuracy rate of 92 percent. Thus, ∑R contains important information that can be used practically in the precatheterization evaluation of patients with chest pain and follow-up evaluation of patients with myocardial infarction.     

Correlation between the ST/heart rate slope and the severity of coronary disease in inferior infarcts. A new criterion of positivity of the ergometric test

We reviewed a group of 80 patients who had bicycle exercise stress testing and cardiac catheterization: 60 patients with known coronary artery disease (CAD) had a remote myocardial infarction, anterior, inferior, Q and no Q wave (post MI), 20 patients evaluated for suspected CAD resulted to have normal coronary arteries or lesions less than 50%. Patients were divided into three groups according to the extent of CAD. Group I with anatomically or functionally high risk CAD: left main (LM) stenosis greater than or equal to 50%, 3 vessels CAD greater than or equal to 70%, proximal left anterior descending stenosis (PLAD) greater than or equal to 90% with another vessel CAD; group II with one or two vessels CAD greater than or equal to 70%; group III with no or insignificant CAD. Linear regression analysis of the heart rate (HR)--related change in ST segment depression (ST/HR slope) was compared with six conventional electrocardiographic exercise test criteria to evaluate whether ST/HR slope can identify with improved accuracy group I. When all 80 patients are assessed together, ST/HR slope greater than or equal to 60 mm/beat/min 10(3) compared with standard electrocardiographic criteria failed to discriminate significantly between high-risk CAD (group I) and less extensive (group II) or insignificant CAD (group III). When only Q wave inferior post MI are considered, ST/HR slope greater than or equal to 60 mm/beat/min. 10(3) compared with ST segment depression greater than or equal to 1 mm identifies group I with 90% +/- 4 versus 75% +/- 6 overall predictive accuracy (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Diagnostic value of abnormal Q waves for identification of preclinical carriers of hypertrophic cardiomyopathy based on a molecular genetic diagnosis.

AIMS: There are currently no established diagnostic criteria for the identification of abnormal Q waves in patients with hypertrophic cardiomyopathy (HCM), resulting in various definitions being applied in each previous study. The aim of this study was to determine the most accurate diagnostic definition of abnormal Q waves for HCM based on a molecular genetic diagnosis, and also to apply abnormal Q waves to the identification of preclinical carriers. METHODS AND RESULTS: We applied three different criteria used in previous reports for abnormal Q waves in 148 genotyped subjects. Of the three criteria, Criterion 3 (Q wave >3mm in depth and/or >0.04s in duration in at least two leads except aVR) showed the highest sensitivity (50% in the young, 29% in adults) while retaining a high specificity (90% in the young, 97% in adults), resulting in the highest accuracy (69% in the young, 52% in adults). Using Criterion 3, abnormal Q waves were present 27.6% of preclinical carriers, and in 5.4% of non-carriers (P<0.01). CONCLUSIONS: These findings suggest that Criterion 3 may be the most accurate diagnostic definition for HCM. Understanding the diagnostic value of abnormal Q waves may be useful in screening preclinical carriers of HCM.     

Body surface distribution of abnormally low QRST areas in patients with left ventricular hypertrophy. An index of repolarization abnormalities.

BACKGROUND. QRST isointegral maps (I-maps) have been useful in detecting repolarization abnormalities. We investigated the body surface distribution of abnormally low QRST areas in patients with left ventricular hypertrophy (LVH) and the relation of the abnormalities in I-map to the severity of LVH as assessed by echocardiography. METHODS AND RESULTS. QRST area departure maps were constructed from electrocardiographic (ECG) data recorded in patients with LVH and precordial negative T waves resulting from aortic stenosis (AS) (10 patients), aortic regurgitation (AR) (12 patients), or hypertrophic cardiomyopathy (HCM) with asymmetric septal hypertrophy (22 patients). Fifty normal subjects served as controls. The I-map was constructed from 87 body surface electrocardiograms recorded simultaneously at a sampling interval of 1 msec. The area where the QRST area was smaller than normal limits (mean -2 SD) was designated the "-2 SD area." The echocardiographic left ventricular (LV) mass was calculated by Devereux's method. Patients with large LV masses due to AS or AR had 2 SD areas located over the left anterior chest or the midanterior chest, respectively. The 2 SD area was located over the left shoulder and left anterior chest and had a lingual shape in patients with HCM. The sum of QRST area values less than the normal range (sigma QRST) was significantly correlated with LV mass in patients with AS or AR (r = 0.83 and r = 0.69, p less than 0.01 and p less than 0.05). However, there was no significant correlation between sigma QRST and the severity of LVH in patients with HCM. sigma QRST divided by the number of electrodes in the 2 SD area was significantly greater in patients with HCM than in those with AS or AR. CONCLUSIONS. These findings suggest that abnormalities in patients with HCM are manifest even in mild LVH and that there is a greater disparity of repolarization in hypertrophied left ventricles due to HCM than in LVH due to aortic valve disease. QRST isointegral departure maps may provide ECG evidence of LV mass of patients with AS or AR and of susceptibility to malignant arrhythmias in patients with HCM.     

Clinical Analysis of 42 Patients With Hypertrophic Cardiomyopathy

Objectives To investigate the clinical manifestations of hypertrophic cardiomyopathy (HCM), and to find out the clinical clues to avoid misdiagnosis and provide reference for future clinical diagnosis and treatment. Methods A retrospective analysis of 42 consecutive patients with HCM hospitalized in our hospital between January 1995 and December 2002 was explored. Based on the family history of HCM, clinical manifestations, electrocar-diogram, echocardiogram, coronary angiography and left ventriculography, the clinical characteristics between HCM patients with left ventricular outflow tract obstruction (HOCM) and HCM patients without obstruction (HNOCM) were compared. The causes of misdiagnosis and losing diagnosis were analysis. Results 13 patients were in HOCM group and 29 patients were in HNOCM group. More patients with syncope were in HOCM group than in HNOCM group (6/13 vs. 2/29, P < 0.05). Patients with ejective murmur were in HOCM group only (P < 0.01). Left ventricular outflow tract pressure gradient (LVOTPG) only observed in HOCM group (P < 0.01). Ventricular tachycardia was seen in both groups. 28 out of 42 patients (66.67%) had misdiagnosis, and 4 out of 42 patients (9.53%) had losing diagnosis. Thus, coronary heart disease (CHD) had the highest rate of misdiagnosis. There were 20 CHD patients (71.43%) among 28 patients with misdiagnosis. Hypertension was in 3, congenital heart in 2, cerebro-embolism in 2, and myocarditis in 1. Conclusions For a patient with family history or sudden death history of HCM, unexplained syncope episodes, chest pain (angina), especially in young, an ejection murmur along the left sternum border, the presence of narrow and deep Q waves, or inversion of giant T waves in V3-V6, atrial fibrillation and /or cerebra-embolism echocardiogram should be given. CAG and LVG are necessary only if the result of echo is negative, and the patients with suspected HCM or CHD.     

Can the surface electrocardiogram be used to predict myocardial viability?

OBJECTIVE—To investigate whether QRS morphology on the surface ECG can be used to predict myocardial viability.
DESIGN—ECGs of 58 patients with left ventricular impairment undergoing positron emission tomography (PET) were studied. ¹³N-Ammonia (NH₃) and ¹⁸F-fluorodeoxyglucose (FDG) were the perfusion and the metabolic markers, respectively. The myocardium is scarred when the uptake of both markers is reduced (matched defect). Reduced NH₃ uptake with persistent FDG uptake (mismatched defect) represents hibernating myocardium. First, the relation between pathological Q waves and myocardial scarring was investigated. Second, the significance of QR and QS complexes in predicting hibernating myocardium was determined.
RESULTS—As a marker of matched PET defects, Q waves were specific (79%) but not sensitive (41%), with a 77% positive predictive accuracy and a poor (43%) negative predictive accuracy. The mean size of the matched PET defect associated with Q waves was 20% of the left ventricle. This was not significantly different from the size of the matched PET defects associated with no Q waves (18%). Among the regions associated with Q waves on the ECG, there were 16 regions with QR pattern (group A) and 23 regions with QS pattern (group B). The incidence of mismatched PET defects was 19% of group A and 30% of group B (NS).
CONCLUSIONS—Q waves are specific but not sensitive markers of matched defects representing scarred myocardium. Q waves followed by R waves are not more likely to be associated with hibernating myocardium than QS complexes.


Keywords: electrocardiography; myocardial viability; positron emission tomography; myocardial scarring