Changes in the QRS complex and ST segment in transmural and subendocardial myocardial infarctions. A clinicopathologic study.

The QRS complex and ST segment in the ECGs of 80 patients who died of an acute myocardial infarction (MI) were studied in relation to the extent of the MI (subendocardial vs. transmural). Changes in the QRS complex developed in nine out of the 15 cases with an acute subendocardial MI. Five of these cases fulfilled the conventional QRS criteria for a myocardial infarction. A definite ST segment depression (a J point depression of 2 mm. or more in at least one lead, and a horizontal or downward sloping ST segment with a minimum duration of 0.08 sec.) occurred most frequently in connection with a circumferential subendocardial MI (88 per cent), but it was also found in a regional subendocardial (43 per cent) and transmural MI (43 per cent). In 17 per cent of the cases with a transmural MI, this was the only ECG abnormality. It is concluded that cases with a subendocardial MI cannot always be distinguished from transmural MI on the basis of the presence or absence of the QRS changes, and that an ST segment depression, as defined in this study, can give additional information in the evaluation of an acute phase of an MI.     

The relationship between electrocardiographic changes and early mortality rate in acute myocardial infarction

In 587 patients with acute myocardial infarction (AMI) and no previous MI, electrocardiographically estimated infarct size was related to three-month mortality. Mortality was found to be higher in patients with transmural MI (Q or R-wave changes in standard ECG) than in patients with subendocardial infarction (ST-T wave changes in standard ECG). In patients with anterior MI, precordial mapping with 24 chest electrodes was analyzed four days after arrival in hospital (n = 197). Neither the sum of R-waves, the sum of Q-waves, nor the number of Q-waves correlated significantly with early mortality, although there was a trend towards higher mortality among patients with more pronounced ECG changes. Finally, in patients with inferior AMI (n = 230), neither the sum of R-waves nor the sum of Q-waves in leads II, III and aVF on the fourth day influenced three-month mortality. However, when subtracting the sum of Q-waves from the sum of R-waves, there was a significant correlation between the estimated infarct size and the early mortality.     

Electrocardiographic prediction of the development and site of acute myocardial infarction in patients with unstable angina

BACKGROUND: ST-T changes on 12-lead electrocardiograms (ECGs) in patients with unstable angina (UA) have limited values for prediction of subsequent acute myocardial infarction (AMI). The aim of the present study is to obtain more useful ECG signs during UA in predicting the risk and the site of AMI. METHODS: ECGs were recorded from 238 consecutive patients with UA; 149 developed AMI, whereas 89 did not in the following 60 days after the UA episodes. P, ST-T and U wave changes in these AMI and non-AMI patients were analyzed retrospectively. Three groups of ECG leads were referred to reflect ischemic changes of anterior (V1-V5), lateral (I, aVL and V6) and inferior (II, III, and aVF) left ventricular walls. To explore the site-dependent predictors, the 149 AMI patients were divided into two groups; group A/L with anterior, antero-septal, apical or lateral AMI, versus group I/P with inferior or posterior AMI. RESULTS: ST depression > or =1 mm and abnormal T wave or U wave changes and P wave abnormalities were observed more frequently in AMI patients than non-AMI patients. On multivariate analysis, an independent ECG finding of the development of AMI was a biphasic U wave (odds ratio (OR) 5.4, 95% confidence interval (CI), 1.9-15.6, P=0.002) in the anterior leads. An inverted T wave (OR 5.1, 95%CI, 1.7-15.5, P=0.0036) and a biphasic U wave (OR 6.0, 95%CI, 2.2-16.1, P=0.0004) in the anterior leads were independent predictors of AMI in group A/L. There was no independent ECG predictor of group I/P. CONCLUSIONS: Biphasic U wave in anterior leads during UA is a useful ECG observation in the risk stratification of subsequent AMI. The independent ECG predictors of antero-lateral MI are inverted T wave and biphasic U wave.     

Left atrial transport function in myocardial infarction. Importance of its booster pump function.

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significane of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean +/- SD): (SEE ARTICLE). Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index less than or equal to 2.0 liters/min/m2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m2 (p less than 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p less than 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The "booster pump" function of the atrium cannot be ignored in assessing left ventricular performance.     

Significance of a terminal R wave in lead V1 of the electrocardiogram.

A terminal r wave in Lead V1 lower than 0.6 mV. was studied in the ECGs of four groups: (1) 104 healthy children, (2) 207 healthy young adults, (3) 171 patients with no autopsy evidence of a cardiopulmonary disease, and (4) 1,078 autopsy patients with a cardiopulmonary disease. Cases with a complete right bundle branch block were excluded. A terminal r wave occurred in 2.9 per cent healthy children, 1.4 per cent of healthy young adults, 0.6 per cent of patients without and in 5.9 per cent of patients with autopsy evidence of a cardiopulmonary disease. The occurrence of a terminal r wave was most common in pulmonary patients (10 per cent). But it was also found in patients with an anterior or a posterior myocardial infarction and in some cases of left ventricular hypertrophy. In the autopsy series RVH occurred in 57 per cent of patients with a Qr pattern, in 30 per cent of patients with a terminal r wave higher than the initial one, and in none of the patients with a terminal r wave lower than the initial one. It is concluded that the height of the terminal r wave has clinical significance. A terminal r wave higher than the initial one in Lead V1 is associated with a cardiopulmonary disease in subjects over 30 years of age, while an r wave lower than the initial one seems to be an innocent finding.     

Predictive value of electrocardiographic patterns in localizing left ventricular asynergy in coronary artery disease.

Transmural myocardial infarction by ECG (ECG-MI) was correlated with left ventricular asynergy by biplane left cineventriculography in 200 patients with coronary artery disease. The ability of individual ECG-MI patterns to predict and correctly localize asynergy was: anterior--98 per cent (43 of 44), inferior--82 per cent (36 of 44), true posterior--73 per cent (11 of 15). Of various combinations of criteria for true posterior ECG-MI, the pattern of an R wave and upright T wave in Lead V1 was most predictive of posterior asynergy--80 per cent (8 of 10). The LAO projection demonstrated a wall motion abnormality not appreciated in the RAO in 8 per cent (10 of 122) of cases of inferoposterior asynergy and enhanced assessment of asynergy in 30 per cent (36 of 122) of cases. It is concluded that: (1) ECG-MI has a high predictive accuracy for left ventricular asynergy, (2) an R-wave and upright T wave in Lead V1 is the best ECG predictor of posterior asynergy, and (3) the LAO projection makes an important contribution to the assessment of regional asynergy in coronary artery dieseas.     

Atrial flutter. Electrocardiographic,vectorcardiographic and echocardiographic correlation

The duration, contour, and amplitude of atrial flutter wave (f) was studied by electrocardiogram (ECG) and vectorcardiogram (VCG) in 32 patients and was related to the size of the left atrium (LA) measured by the echocardiogram (E). The following ECG parameters were analyzed: (1) the duration of left atrial depolarization, i.e., LA wave; (2) the amplitude of LA wave; (3) the surface area of LA wave; (4) maximum amplitude (A) of f in Leads 2 and V₁. There was good correlation between LA size and the duration of depolarization and surface area (p < 0.01), but the maximum amplitude of the f wave in Leads 2 and V₁ failed to predict LA size.The post-conversion sinus P wave showed abnormal LA depolarization time (P > 0.12 sec.) in 62 per cent of patients with enlarged left atrium (ELA) and in 43 per cent of patients with normal size LA (NLA).The VCG of the flutter wave revealed two patterns, (1) an eliptical smooth fsÊ loop in 63 per cent of patients with NLA, and (2) distorted fsÊ loop in 67 per cent of patients with ELA.Both VCG patterns were subdivided in two subgroups according to the number and location of conduction delays. The VCG of post-conversion P wave confirmed conduction delays in both groups.We conclude that both the size of the left atrium and conduction delays play a basic role in the duration and contour of left atrial wave.     

Electrocardiographic poor R wave progression. II: correlation with angiography.

Forty patients with "poor R wave progression" (PRWP) or "reversed R wave progression" (RRWP) on the electrocardiogram (ECG) who underwent coronary arteriography and left ventriculography within one month of electrocardiographic recording were analyzed. Patients were randomly selected from a population of catheterization proven predominant mitral stenosis with elevated right ventricular pressures (presumed right ventricular hypertrophy), predominant aortic stenosis with increased left ventricular mass (left ventricular hypertrophy) and anterior myocardial infarction (AMI). Application of criteria previously derived from vectorcardiographic (VCG) correlative data, as well as inclusion of right precordial lead repolarization abnormalities, correctly diagnosed 85% (11/13) of angiographic AMIs. It is clinically useful to note that 56% (15/27) of patients with either PRWP or RRWP who did not exhibit angiographic AMI could be identified by 12 lead ECG with only 12% (2/17) false negative AMIs. In comparison with Q wave anterior myocardial infarctions, those with only PRWP or RRWP exhibited a trend toward a less severe degree of contraction abnormality on contrast ventriculography.     

The mortality predictive power of discharge electrocardiogram after first acute myocardial infarction

The prognostic value of discharge ECG was studied in 457 patients after their first acute myocardial infarction. Thirteen different ECG variables were studied on the discharge ECG. When cumulative 4-year survival rates were calculated by standard life-table method for each variable individually, the following variables had statistically significant prognostic power: PTF (P terminal force), PTFA (P terminal frontal axis), AF (atrial fibrillation), ST depression, ST elevation, QRS duration, and the combination block (LBBB/RBBB + LAHB/LPHB). The variables with no statistically significant predictive power were: QTc, LBBB or RBBB, LAHB or LPHB, AV block, T wave angle, T negativity, and sigma R. The relative risks for the most important variables in the discrete life-table model were: PTF 3.4, QRS duration 3.3, ST depression 2.6, PTFA 2.5, and ST elevation 2.2. In further analysis a model with only three ECG variables (PTF, ST depression, and ST elevation) was developed which stratified the study population in categories with 1.9% to 75.5% estimated 4-year survival rates.     

The relationship between the electrocardiographically estimated infarct size and 1- and 2-year survival in acute myocardial infarction

In 587 patients with acute myocardial infarction (AMI) and no previous MI, electrocardiographically estimated infarct size was related to 1- and 2-year mortality. The overall mortality was higher in patients with transmural MI (Q- or R-wave changes in standard ECG) than in patients with subendocardial infarction (ST-T-wave changes in standard ECG) after 1 year (18.8% compared to 6.5% p less than 0.001) and after 2 years (22.2% compared to 13.8%, p = 0.049). When patients who were alive during primary hospitalization were analyzed separately, slightly higher mortality was found in patients with transmural MI than in subendocardial MI after 1 year (9.6% compared to 4.2%, p = 0.076) while no difference was found after 2 years (13.4% as compared to 11.7%, p greater than 0.2). In a subgroup of patients with anterior MI, precordial mapping with 24 chest leads was analyzed 4 days after arrival in hospital (n = 197). Patients were divided into quartiles according to the sum of R waves, the sum of Q waves, and the number of Q waves. There was a similar overall mortality in each quartile after 1 year and after 2 years regardless of ECG parameters studied. Neither did we find any correlation between the sum of R waves in leads II, III, and aVF on the fourth day in patients with inferior MI and overall 1- or 2-year mortality rate, although there was a trend towards higher mortality with more ECG changes.     

The cardiovascular manifestations of the hypereosinophilic syndrome. Prospective study of 26 patients, with review of the literature.

The major cause of morbidity and mortality in patients with the hypereosinophilic syndrome is cardiac dysfunction. A review of 65 cases from the literature (historic series) revealed the following cardiovascular manifestations to be most common: dyspnea (60 per cent), signs of congestive heart failure (75 per cent), murmur of mitral regurgitation (49 per cent), cardiomegaly (37 per cent), T wave inversions on electrocardiogram (37 per cent) and pathologic findings of endocardial fibrosis, myocardial inflammation and mural thrombus formation (57 per cent). We have prospectively followed 26 patients with the hypereosinophilic syndrome for up to nine years (average follow-up prospectively was 3.3 years, retrospectively 5.7 years). Common cardiac findings in our 26 patients were dyspnea (42 per cent), chest pain (27 per cent), signs of congestive heart failure (38 per cent), murmur of mitral regurgitation (42 per cent), cardiomegaly (35 per cent) and T wave inversions (35 per cent). Thus, these patients demonstrated cardiovascular manifestations similar to those in the historic series, although the literature review showed a higher incidence of overt congestive heart failure.Of 22 patients having echocardiograms, 55 per cent demonstrated some clinical, roentgenographic or electrocardiographic evidence of cardiac involvement, but 82 per cent had echocardiographic abnormalities. This suggests that the echocardiogram is a sensitive and perhaps early indicator of cardiac involvement in this disease. Common echocardiographic findings included increased left ventricular wall thickness (68 per cent), left ventricular mass (73 per cent) and left atrial size (37 per cent). Prospective echocardiographic follow-up of 18 patients (for up to four and a half years) revealed that seven of eight untreated or inadequately treated patients had increases in left ventricular wall thickness, whereas all 10 adequately treated patients had decreases (eight of 10) or no change (two of 10) in left ventricular wall thickness. This suggests that adequate antihypereosinophilic therapy (with prednisone and/or hydroxyurea) may stabilize and, in some cases, reverse the cardiac manifestations of the hypereosinophilic syndrome.In previous studies, congestive heart failure due to eosinophilic cardiomyopathy has been reported to be very resistant to therapy. In our patients with congestive heart failure, treatment has been almost invariably effective when digitalis and diuretics were combined with adequate antihypereosinophilic therapy.     

Prognosis in myocardial infarction survivors with left ventricular dysfunction is predicted by electrocardiographic RR interval but not QT dispersion

OBJECTIVES: The aim of the study was to assess if QT dispersion and RR interval on the standard 12-lead electrocardiogram (ECG) predict cardiac death and late arrhythmic events in postinfarction patients with low left ventricular ejection fraction (LVEF). QT dispersion on a standard electrocardiogram (ECG) is a measure of repolarization inhomogeneity, but its prognostic meaning in myocardial infarction (MI) survivors is unclear, especially in patients with left ventricular dysfunction. RR interval has been shown to predict mortality in post-MI patients, but its prognostic power has not been compared with other noninvasive risk factors. METHODS: Retrospective cohort study. Ninety patients were identified, from a series of 547 consecutive postinfarction patients admitted to our institution for phase II cardiac rehabilitation, as having a LVEF of <0.40 at two-dimensional echocardiography (mean LVEF 0.35+/-0.04; range 0.20-0.39). QT dispersion and RR interval were analyzed on the admission 12-lead electrocardiogram, 20+/-10 (range 8-45) days after MI, using specially designed software. Additional risk markers were collected from clinical variables, signal-averaged ECG and Holter recording. RESULTS: During 24+/-18 (range 1-63) months of follow-up, 10 of 90 patients (11%) died, all from cardiac causes, and there were 18 late arrhythmic events, defined as sudden death or the occurrence of a sustained ventricular arrhythmia > or =5 days after the index MI. QT interval and dispersion were not significantly prolonged in patients who died compared to survivors and not significantly different between patients with and without arrhythmic events. Mean RR interval from standard ECG was significantly shorter in patients with both cardiac death (682+/-99 vs. 811+/-134 ms; P=0.004) and arrhythmic events (720+/-100 vs. 818+/-139 ms; P=0.006). A Cox proportional hazards model identified RR interval from standard ECG (P<0.001) and a history of more than one MI (P=0.002) as significant predictors of cardiac death independent of thrombolytic therapy, LVEF, filtered QRS complex duration at signal-averaged ECG, mean RR and its standard deviation at 24-h Holter monitoring. CONCLUSIONS: Measurement of QT interval and dispersion 3 weeks after MI has no prognostic power in patients with LV dysfunction after a recent MI. RR interval on standard 12-lead ECG is as good a prognostic indicator as other, more expensive, noninvasive markers. These findings may be relevant in this era of limited health care resources.     

Morphologic significance of left atrial involvement

Left atrial involvement, defined as the terminal negativity of the P wave in Lead V₁ of 1 mm. or more in depth and a duration of 0.04 second or more, was evaluated in 270 autopsied cases with the use of a chamber dissection technique for the determination of atrial and ventricular hypertrophy. Left atrial involvement was present in the following: 35 (44.3 per cent) of 79 hearts with left atrial hypertrophy, 31 (34.8 per cent) of 89 hearts with right atrial hypertrophy, 32 (22.4 per cent) of 143 hearts without atrial hypertrophy, 52 (44.4 per cent) of 117 hearts with left ventricular hypertrophy, 17 (34.7 per cent) of 49 hearts with right ventricular hypertrophy, 9 (11.5 per cent) of 78 hearts without anatomic evidence of atrial or ventricular hypertrophy, and 3 (3.8 per cent) of 78 hearts without anatomic evidence of atrial or ventricular hypertrophy or any clinical or postmortem findings of cardiopulmonary disease. Left atrial involvement has a significant correlation with left atrial hypertrophy (p < 0.01) and left ventricular hypertrophy (p < 0.001). Left atrial involvement was frequently noted to be transient. The presence of left atrial involvement on the ECG appears to be the result of many factors including left-sided heart disease, left atrial hypertrophy, left ventricular hypertrophy, increases in left atrial volume or pressure, and possibly intra-atrial conduction delays.     

48-Lead Electrocardiogram in the Diagnosis of Non-Acute Myocardial Infarction

ABSTRACT. A 48-lead ECG including six extremity leads and seven vertical rows of six chest leads was registered in patients with myocardial infarction (MI) and controls. Patients with Wolff-Parkinson-White syndrome, bundle branch block or ventricular hypertrophy were excluded. The control group consisted of 75 healthy persons, aged 21–38, and 37 older patients who had never had MI, as verifed later at autopsy. The R wave amplitude was measured in each of the 42 chest leads and the normalized amplitude difference between each two adjacent leads (“quotient”) was calculated in horizontal and vertical direction. The ranges of these 71 quotients constituted, occasionally after exclusion of an extreme value, the reference to which 192 patients with MI were compared. The MIs were diagnosed by serum enzyme estimations, in 119 patients about one week and in 52 about one year prior to the ECG recording. In another 21 patients the diagnosis was subsequently confirmed at autopsy. The highest number of excluded extreme values in any control was three and, consequently, the presence of 4 quotients or more per ECG falling outside the reference range was used as the MI criterion of the 42 chest leads. Together with common Q wave criteria applied to the extremity leads it detected 70% of the 192 MIs. Fifty-nine per cent fulfilled the common criteria applied to the 13-lead ECG included in the 48-lead recording (extremity leads and CR_{4R–1–2–3–4–5–7}). In order to estimate the specificity of this 48-lead ECG, the control group was randomly divided into two halves. For one half, new reference ranges for the 71 quotients were estimated. The quotient values of the other half as well as of the MI patients were compared to this new reference range for each quotient. At 70% sensitivity—as found above—the specificity was 95%. The specificity of the 13-lead ECG was 96%.     

Accuracy of localization of acute myocardial infarction by 12 lead electrocardiography

Until recently, ECG accuracy in localizing acute myocardial infarction (AMI) could be assessed only by comparing the ECGs with autopsy findings. This approach, however, preselected patients, including only those who died. It is possible that this postmortem group of patients would be different from the whole population of patients with AMI. Myocardial imaging with 99mTc-pyrophosphate offers the advantage of directly localizing the region of injured myocardium in the acute phase of AMI. In 34 patients with confirmed AMI and focal uptake of 99mTc-pyrophosphate, serial ECGs were obtained and interpreted by two independent observers. The sensitivity and specificity of serial ECGs in determining the location of AMI in the five left ventricular (LV) wall segments were determined: (1) in the anterior wall sensitivity was 86.7% and specificity was 89.5%; (2) in the lateral wall sensitivity was 73.7% and specificity was 80.0%; (3) in the high lateral wall sensitivity was 80.0% and specificity was 87.5%; (4) in the inferior wall sensitivity was 87.5% and specificity was 100%; (5) in the "true" posterior wall sensitivity was 83.3% and specificity was 86.4%. Overall, in the 170 LV wall segments (five per patient) examined, scans localized with a sensitivity of 81.9% and a specificity of 88.8%. After four patients with LBBB were excluded, sensitivity increased to 87.1%. Overall, localization of AMI by serial ECG was accurate in 85.9% of the 34 patients included in the study.     

ST-segment monitoring with continuous 12-lead ECG improves early risk stratification in patients with chest pain and ECG nondiagnostic of acute myocardial infarction.

OBJECTIVES: The purpose of this study was to evaluate the prognostic importance of ischemic episodes detected by ST-segment monitoring with continuous 12-lead electrocardiography (ECG) in a nonselected coronary care unit (CCU) population with chest pain and ECG nondiagnostic of acute myocardial infarction (AMI). BACKGROUND: Patients with chest pain and ECG nondiagnostic of AMI constitute a heterogeneous group concerning both diagnosis and prognosis. Continuous 12-lead ECG is a rather new method not thoroughly studied in this population. METHODS: The ST-segment monitoring with continuous 12-lead ECG was performed for 12 h in 630 consecutive patients admitted to CCU due to chest pain and a nondiagnostic ECG, i.e., no ST-segment elevations. An ST-episode was defined as a transient ST-segment depression or elevation of at least 0.10 mV. The median follow-up time was six months. RESULTS: A total of 176 ST-episodes occurred in 100 (15.9%) patients. The median duration and maximal ST-segment deviation in patients with ST-episodes were 80 min and 0.20 mV, respectively. Presence of ST-episodes predicted worse outcome concerning cardiac death and cardiac death or myocardial infarction (MI) (log-rank p < 0.001). At 30 day follow-up procedure, 10% versus 1.5% died from cardiac causes or had an MI in the group with and without ST-episodes, respectively. In a multivariate analysis, only troponin T > or = 0.10 microg/l and the presence of ST-episodes came out as independent predictors of cardiac death or MI. CONCLUSIONS: Continuous 12-lead ECG monitoring provides prognostic information on-line and considerably improves early risk stratification in patients with ECG nondiagnostic of AMI and symptoms suggestive of acute coronary syndrome.     

P Wave Dispersion and P Wave Duration on SAECG in Predicting Atrial Fibrillation in Patients with Acute Myocardial Infarction

Background: Atrial fibrillation (AF) is a frequent complication of acute myocardial infarction (AMI), with reported incidence of 7% to 18%. The incidence of congestive heart failure, in‐hospital mortality, and long‐term mortality is higher in AMI patients with AF than in AMI patients without AF. P wave duration on signal‐averaged ECG (PWD) and P wave dispersion on standard ECG (Pd) are noninvasive markers of intra‐atrial conduction disturbances, which are believed to be the main electrophysiological cause of AF. Methods: In the present study we investigated prospectively whether P wave duration on SAECG and P wave dispersion on standard ECG can predict development of AF in a group of patients with AMI. One hundred and thirty patients (100 men and 30 women, aged 56.9 ± 12) with AMI were investigated. PWD, Pd, their clinical and hemodynamic characteristics were collected. Results: During the observation up to 14 days, 22 patients (16.9%) developed AF. Univariate analysis variables associated with development of AF: age > 65 years, Killip class III‐IV, PWD > 125 ms, and Pd > 25 ms. Stepwise logistic regression analysis showed that age > 65 years, PWD > 125 ms, and Pd > 25 ms were independently associated with AF. Conclusions: PWD and Pd both measured in a very early period of AMI are useful in predicting AF. A.N.E. 2002;7(4):363–368     

Clinical significance of changes in electrocardiographic R-wave voltage on chest leads in patients with acute anterior myocardial infarction

This article aims to clarify the clinical significance of changes in electrocardiographic (ECG) R-wave voltage on chest leads from 1 to 4 weeks in patients with acute anterior myocardial infarction (MI) in combination with echocardiographic findings and dual scintigraphic findings. Seventy-one patients with acute anterior MI who underwent emergency revascularization were subjected to ECG and echocardiography, at both 1 and 4 weeks, and to thallium-201 (TI) and iodine-123-beta-methyl-p-iodophenyl pentadecanoic acid (BMIPP) single-photon emission computed tomography (SPECT) about 1 week after the onset of MI. The total sum of ECG R-wave voltage on each chest lead was calculated. The mean defect ratio on TI and that on BMIPP derived from circumferential profile curve analysis were calculated. The percentage defect-discordant ratio of both SPECT images [(%) discordance on TI/BMIPP] was obtained. The percentage increase ratio of ECG R-wave voltage on chest leads [(%) increase of R wave] and the increase of left ventricular ejection fraction (DeltaEF) from 1 to 4 weeks were obtained. There were significant correlations between the (%) increase of R wave and the DeltaEF as well as between the (%) increase of R wave and the (%) discordance on TI/BMIPP (r =.63, P <.001; r =.74, P <.001). The reversibility of ECG R-wave voltage was related to cardiac functional improvement in addition to the discordance on the 2 images. Monitoring of changes in ECG R-wave voltage on chest leads is useful to detect the presence of myocardial viability and to evaluate functional evolution in patients with acute anterior MI.     

The non Q wave myocardial infarction in conventional valvular surgery. Diagnosis with cardiac troponin I

INTRODUCTION: Morbidity and mortality in elective valve surgery is still significant. The main cause of death in these patients is cardiogenic shock, of which the most frequent etiology is acute myocardial infarction (AMI) with Q wave in the ECG. However, there are patients with cardiogenic shock without Q wave in the ECG and with rises in CK-MB enzyme that makes us suspect non-Q wave AMI. OBJECTIVE: To analyze the use of the determination of cardiac troponin-I, a more specific marker of AMI than CK-MB after cardiac surgery, to detect perioperative non-Q wave AMI, and to establish its clinical significance. METHODS: A total of 147 patients without coronary artery disease scheduled for elective valve surgery were included. We used, based in anterior publications, ECG (presence or not of new Q wave) and cardiac troponin I to define perioperative AMI. Levels of cardiac troponin-I were analysed before surgery and 14 hours after. Non-Q wave AMI was diagnosed when troponin I was superior to 38.85 ng/ml and there was not a phatologic Q wave in ECG. RESULTS: One hundred twenty-three (83.67%) of patients did not have AMI, 9 (6.12%) suffered perioperative AMI with Q wave, and 15 (10.27%) carried out criteria of non-Q wave perioperative AMI. Morbidity and mortality in this last group was similar to that in the group with Q wave AMI. Morbidity and mortality were minimum in patients without AMI. CONCLUSIONS: This study suggest the possibility of in vivo identification of non-Q wave perioperative AMI, an entity with important morbidity and mortality in our series, with a simple determination of cardiac troponin I 14 hours after surgery.     

Computer analysis of the orthogonal electrocardiogram and vectorcardiogram in 939 cases with hypertensive cardiovascular disease

Orthogonal ECG's (Frank system) were recorded from 939 male patients with hypertensive cardiovascular disease (HCVD) and were compared with records from 229 normal subjects, matched for age, race, and sex. The hypertensive subjects were divided into three clinical groups: (1) patients without cardiac enlargement by chest x-ray and no history of congestive heart failure (CHF), (2) patients with cardiac enlargement but without past or present CHF, and (3) patients with cardiac enlargement and one or more episodes of CHF. A sustained blood pressure level of $\text{150}\text{90}\text{mm. Hg}$ or more was present in all cases.First an attempt was made to identify optimal scalar and vectorial ECG measurements for discriminating between HCVD and normal, testing a total of 333 variables. With four scalar measurements at a specificity level of 95 per cent, 24 per cent of Group 1, 37 per cent of Group 2, and 44 per cent of Group 3 could be correctly classified. Vector measurements were found mostly redundant.Using linear discriminant function analysis and a likelihood ratio test with 13 different ECG variables at a level of specificity of 95 per cent, it was possible to identify correctly 53 per cent, 75 per cent, and 87 per cent of Groups 1, 2, and 3, respectively.Comparison of results with other reports on ECG changes caused by left ventricular overload (LVO) suggested that the degree of LVO in HCVD, even in the most advanced Group 3, was considerably less than that reported in patients with valvular heart disease with the only exception of terminal cases with HCVD who had come to autopsy. Antihypertensive therapy was considered as one factor which might have contributed to this finding.Multivariate ECG analysis was found an efficient means for diagnostic classification, leading to results which equalled those reported for multiple dipole analysis. As compared to scalar or vector measurements, either used individually or in combination, the multivariate technique exceeded all of these methods for LVO diagnosis by a wide margin when specificity was kept at a constant level.