Increased R-wave Amplitude Research Articles

Electrocardiographic and Vectorcardiographic Diagnosis of Posterior Wall Myocardial Infarction: Significance of the T Wave

The electrocardiographic diagnosis of posterior wall myocardial infarction remains elusive. To determine discriminating criteria a group of 27 patients with posterior infarction proven by biplane angiocardiography were compared to 97 controls. All patients had single-vessel obstruction of the circumflex artery or one of its major branches (greater than or equal to 75 percent area stenosis) without occlusive disease in the other coronary arteries. High-frequency, high-gain electrocardiograms and Cube and McFee vectorcardiograms were analyzed. Pathologic Q waves in the inferior leads were present in only 22 percent (six) of the patients; increased R-wave amplitude or duration in the right precordial leads was found in 17 to 26 percent, and an R/S ratio greater than or equal to I in lead V1 or greater than or equal to 1.5 in lead V2 was present in 22 percent (six) of patients. Vectorcardiographic criteria which improved the diagnostic yield were: (1) the presence of a QRS loop mostly anterior to the E point, and (2) the presence of an abnormally anterior T wave. This abnormal T-wave shift was present in over 70 percent of the patients with posterior infarctions and was clearly discernible from the 12-lead ECG, as manifested by tall T waves in lead V2 and flat T waves in lead V6. To approximate the T-wave angle in the 12-lead scalar ECG, an index was calculated by subtracting the amplitude of the T wave in lead V6 from its amplitude in lead V2 (T2-T6 index). An index of 0.38 mV or more yielded a sensitivity of 81 percent and a specificity of 75 percent; however, this was not as discriminating as the vectorcardiogram where a T angle of 60 degrees or more in the horizontal plane yielded a sensitivity of 70 percent and a specificity of 97 percent.

Relation of electrocardiographic R-wave amplitude to changes in left ventricular chamber size and position in normal subjects

Although exercise-induced changes in electrocardiographic R-wave amplitude have been ascribed to changes in left ventricular (LV) size, QRS axis, heart rate and ischemia, the physiologic mechanism remains unclear. To clarify the relation between R-wave amplitude and changes in LV size and position, simultaneous 9-lead electrocardiograms and targeted M-mode echocardiograms were recorded from 15 normal subjects. Recordings were made at rest, during Valsalva maneuver and during methoxamine infusion. LV diastolic dimension increased with methoxamine and decreased with Valsalva maneuver (p < 0.001). R-wave amplitude in leads V 5 and V 6 varied directly with LV dimensions (p < 0.001). The correlation coefficient between the change in R-wave amplitude in V 5 or V 6 and the change in LV dimension was 0.81 (p < 0.001). No significant changes in R-wave amplitude were seen in electrocardiographic leads I, II, III, aVR, aVL, aVF or V 1. Distance from the chest wall to the LV posterior wall correlated with change in R-wave amplitude (r = 0.79, p < 0.001). Change from supine to left lateral position moved the left ventricle closer to the lateral chest wall in association with a 41 ± 8% increase in R-wave amplitude in V 5 and V 6 (p < 0.001). In conclusion, there is a direct and a dynamic relation between R-wave amplitude and LV chamber size. Chamber size and distance from the left ventricle to leads V 5 or V 6 interact as major determinants of R-wave amplitude.

Increased R-wave amplitude induced by acute myocardial ischemia in the dog: A predictor of malignant ventricular arrhythmias

The ability of an increase of 25 % or greater in the sum of R-wave amplitudes in leads X, Y, Z, L 2, and V 5 to predict the occurrence of malignant ventricular arrhythmias (10 or more ventricular premature beats/min, ventricular tachycardia [5 or more consecutive premature beats], and/or fibrillation) was evaluated in 17 dogs during experimental acute myocardial ischemia. Each dog underwent a 15 minute ligation of the left anterior descending coronary artery followed by reperfusion and after recovery, 2 hours later, a 15 minute ligation of the circumflex coronary artery. During ligation of the left anterior descending coronary artery, 12 of 17 dogs (71%) showed no R-wave increase and no arrhythmias (true-negative response). In 5 (29%) of 17 dogs malignant ventricular arrhythmias developed: 2 of 5 (40%) dogs with arrhythmias had a concomitant R-wave increase (true-positive response), and 3 of 5 (60%) with arrhythmias had a less than 25% increase in R-wave amplitude (false-negative results). During circumflex coronary artery ligation, 13 of 17 (76%) dogs showed both R-wave increases and arrhythmias (true-positive response). Four (24%) of 17 dogs had no arrhythmias: 3 of 4 (75%) with no arrhythmias also had a less than 25% increase in R-wave amplitude (true-negative response), whereas 1 of 4 (25%) dogs with no arrhythmias had an increase in R-wave amplitude (false-positive response). In dogs with both arrhythmias and R-wave increases, R-wave changes preceded the onset of arrhythmias by a mean (± standard deviation) of 1 minute 27 seconds (± 43 seconds). Overall, R-wave increases were highly sensitive (83%), specific (94%), and predictive (94%) for the occurrence of malignant ventricular arrhythmias during experimental acute myocardial ischemia.

Increase in R-wave amplitude during transient epicardial injury (prinzmetal type)

An increase in QRS amplitude with S-T elevation occurs during the acute phase of myocardial infarction, coronary ligation and variant angina. Ischemic conduction delay, postulated as the cause, has not been well characterized. Six patients with transient chest pain, S-T elevation and increase in R-wave voltage also displayed concomitant shift of the frontal QRS axis toward the locus of injury. Electrocardiographic considerations suggest that regional ischemic block, not true hemiblock as has been suggested, offers the most inclusive explanation, providing previously neglected clinical confirmation of experimental observations.

Predicting coronary artery disease with treadmill stress testing: Changes in R-Wave amplitude compared with ST segment depression

Coronary angiograms and treadmill stress tests were reviewed independently in 108 nonconsecutively selected cases. There were 16 patients (15%) with infarcts on ECG. Changes in R-wave amplitude and ST segments during exercise were evaluated to determine the sensitivity and specificity of each as a predictor of coronary artery disease (CAD). ST segment changes had a sensitivity of 49%, and a specificity of 74%. The sensitivity increased to 55% when infarcts were excluded. R-wave amplitude changes had a sensitivity of 68% and a specificity of 84%. The sensitivity increased to 78% when infarcts were excluded. An index formed by the sum of the change in R-wave amplitude and the magnitude of ST segment change yielded a sensitivity of 76% and specificity of 78%. The sensitivity increased to 84% when infarcts were excluded. There was no statistical difference between specificities for each criteria. Of those patients with an R-wave amplitude decrease, 69% had no coronary artery atherosclerosis, while 31% had significant lesions. Of those patients with no change or an increase in R-wave amplitude, 83% had coronary artery atherosclerosis, while 17% were normal. Of the 83% with coronary artery atherosclerosis, 81% had two and three vessel disease, while only 19% had single vessel disease. No change or an increase in R-wave amplitude during treadmill stress testing is a more reliable indicator of CAD in our laboratory than ST segment changes.

Electrocardiographic QRS changes induced by acute coronary ligation in the isolated rabbit heart

The electrical fields associated with augmented R- and decreased S-wave amplitudes during acute, severe myocardial ischemia were studied in fifteen isolated rabbit heart preparations. Hearts were suspended in a spherical tank and perfused with oxygenated electrolyte solution. Electrocardiographic signals were recorded from electrodes on the tank's surface and processed by computerized methods. Fifteen minutes after suture ligation of the left anterior descending coronary artery, records from electrodes overlying the lesion demonstrated increased R-wave amplitude and ST-segment elevation. Fitting a single moving dipole to pre- and post-ligation potentials demonstrated that the ligation increased the dipolarity of the field and shifted the terminal QRS dipole to a position topographically related to the location of the ischemic lesion. The effects of injury were further assessed by study of fields computed by subtracting control from post-ligation data. This generated a dipolar field at the instant of maximal dipole moment whose strength directly correlated (r=0.74) with the area of non-perfused epicardium, as determined by post-ligation methylene blue infusion. These results suggest that the electrical fields generated during mid to late dipolarization by coronary ligation are qualitatively similar to those generated during repolarization, and may therefore be of similar clinical and/or experimental value.

A mechanism for the electrocardiogram response to left ventricular hypertrophy and acute ischemia.

A proposed mechanism for explaining the electrocardiographic response in left ventricular hypertrophy and in subendocardial and epicardial acute ischemia was incorporated in a mathematical model of electrical heart activity. The model of hypertrophy was simply an increase in cell size, and the principal effect on the computer-generated 12-lead electrocardiograms (ECGs) was an increase in R-wave amplitude and ventricular activation time and a flattening or polarity reversal of the T wave. The model of acute ischemia was a reduction between plateau and resting potential of the transmembrane action potential. The principal effect on the computer-generated 12-lead ECGs was an S-T segment displacement up or down depending on the location of the lesion. This shift was linearly proportional to the severity of the ischemia, i.e., the reduction in electrical activity of the ischemic cell, and for a lesion of given severity the S-T segment shift was a measure of the area, not the volume, of ischemic tissue. Therefore, this model suggests that a direct correlation does not necessarily exist between volume-measuring tests such as serum enzyme values in the case of necrosis and S-T segment shifts.

The Effect of Ingested Lead Shot on the Electrocardiogram of Canada Geese

SUMMARY Myocardial degeneration and necrosis is a common finding in lead-poisoned waterfowl. An attempt was made to detect this damage electrocardiographically. The lead-II electrocardiograms of six Canada geese were recorded daily for 2 weeks before five of the birds were dosed with lead shot via stomach tube. The ECG's were recorded daily until the poisoned birds died. Myocardial necrosis was demonstrated histologically in three of the geese. The ECG's of two of these geese contained abnormalities consisting of increased Rwave amplitude, changes in ST-segment elevation and shape, and T-wave inversion.

Electrocardiographic Effects of Glucose Ingestion

To assess the influence of glucose ingestion on resting and exercise electrocardiograms, 35 subjects were tested after ingestion of a glucose solution and a placebo on separate days. Graded submaximal exercise tests (GXTs) were performed to 90% predicted maximal heart rate. Computer-processed ECGs taken at rest showed a decrease in T-wave amplitude, more ST-segment depression, increased R-wave amplitude, and increased heart rate after glucose. Minnesota code classifications of these same ECGs were more abnormal after glucose. Computer-processed exercise ECGs showed a decrease in T-wave area after glucose ingestion during and after exercise. ST-segment area showed the most variability at one minute after exercise. Three subjects had normal exercise ECGs after placebo and abnormal ECGs after glucose ingestion (ST area >7.5μv/sec). Both resting and exercise ECGs should be made fasting to avoid this significant source of variability.

Electrocardiographic findings among the total adult population of a large religious isolate.

Electrocardiograms were recorded as part of a survey of 1,303 men and 1,348 women past 15 years of age belonging to a large religious isolate inhabiting regions of northwestern U.S.A. and southwestern Canada. The ECGs were classified according to the Minnesota Code and the abnormalities were related to constitutional characteristics, blood pressure, and serum cholesterol. Major codable ECG items included abnormal Q waves (54 cases), abnormal left axis deviation (44 cases), bundle-branch block (left 10, right 10), T-wave abnormalities (257 cases), prolonged P-R interval (80 cases), and occasional premature beats (143 cases) and showed no significant sex differences. ST-segment depressions were more common among females ( P &lt; 0.005). The males showed a significantly higher frequency of increased R-wave amplitude ( P &lt; 0.005) and more qualitative T-wave changes ( P &lt; 0.005). In general, abnormal ECG features were associated with age, sex, and blood pressure, but not with serum cholesterol, body weight and height, skin-fold thickness, or arm girth. A notable exception was the negative relationship of body weight to high amplitude R waves in young males. In clinical practice, age and sex stratifications will improve the diagnostic power of the ECG.

Relationship of Phospholipin metabolism to thromboangiitis obliterans and its treatment: Rabinowitz, H. M., and Kahn, J.: Am. J. Surg. 31: 329, 1936

Poor R-wave progression (PRWP) is a common electrocardiographic phenomenon in which the anticipated increase in R-wave amplitude in successive precordial leads, V1 to V5, fails to occur. PRWP is prevalent in approximately 10% of hospitalized adult patients, predominantly in those with coronary artery disease. Debate is ongoing on its association with myocardial infarction (MI). However, studies that showed no association failed to appraise the significance of the QRS axis in relation to PRWP among such patients with MI. In our retrospective study, we consecutively identified 150 unselected adult patients with PRWP among 660 successive admissions to the general medical floors of a tertiary care teaching hospital (Saint Vincent Hospital, Worcester, Massachusetts). After excluding patients with anterior wall Q-wave MI (defined as the presence of a QS complex or Q-wave ≥1 mm deep in V2 or V3), sudden unexpected death, MI after percutaneous coronary interventions or coronary artery bypass grafting during this hospitalization, Wolff-Parkinson-White syndrome, pacemakers, bundle branch blocks, and electrocardiograms that were of poor quality or affected by severe motion artifact, inconsistencies with patient identification, or errors in lead placement, 137 patients remained. The patients were then screened for non–ST-segment elevation MI (NSTEMI) during the present admission. The DePace criteria for PRWP were systematically used for all patients, and the QRS axis was calculated using limb leads based on Einthoven's equilateral triangle (normal was considered −30° to 100°). Of the 137 study patients screened with PRWP, 38 had NSTEMI (25.3%). Thirty-one had a normal QRS axis (mean age ± standard deviation 71.3 ± 12 years), and 7 showed either right or left axis deviation (mean age ± standard deviation 64.3 ± 15 years). This proved to be statistically significant (p <0.0001) within this cohort of NSTEMI patients. In conclusion, PRWP determined using the DePace criteria in the presence of a normal QRS axis appears to be more significantly associated with the presence of overall MI within this cohort of NSTEMI patients.