Electrocardiographic Repolarization Abnormalities Research Articles

Combined rest and exercise electrocardiographic repolarization findings in relation to structural and functional abnormalities in asymptomatic aortic regurgitation

The relationship of combined rest and exercise electrocardiographic (ECG) repolarization abnormalities to left ventricular geometry and function was examined in 48 patients with asymptomatic chronic pure aortic regurgitation and no recent use of digitalis. Echocardiographic and radionuclide cineangiographic findings were compared in groups defined by the presence or absence of the “strain” pattern of repolarization abnormality on the resting ECG and also by the presence or absence of standard positive repolarization changes during upright treadmill exercise (>0.1 mV additional horizontal or downsloping ST depression). These hierarchic groups demonstrated trends toward progressively abnormal left ventricular dimensions, mass, wall stress, and change in ejection fraction with exercise. Although the presence of the strain pattern on the resting ECG alone was most strongly correlated with underlying functional and geometric abnormalities, an abnormal exercise test response was independently associated with abnormal left ventricular systolic dimension. The large group of patients with no symptomes and normal resting repolarization had only 0% to 4% prevalences of markedly increased systolic dimension (>55 mm), reduced ejection fraction at rest (<45%), or reduced ejection fraction during exercise (<40%), whereas the small group of patients with abnormal resting repolarization and a positive exercise test response had 50% to 83% prevalences of these findings. These data suggest a possible role for rest and exercise ECG in the serial evaluation of patients with aortic regurgitation.

Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage

Mayer, S A; LiMandri, G; Sherman, D; Lennihan, L; Fink, M E; Solomon, R A; DiTullio, M; Klebanoff, L M; Beckford, A R; Homma, S.

Influence of left ventricular hypertrophy on detection of coronary artery disease using exercise echocardiography

This study examined the influence of left ventricular hypertrophy on the accuracy of exercise electrocardiography and echocardiography for detection of coronary artery disease. Electrocardiographic repolarization abnormalities caused by left ventricular hypertrophy compromise the diagnostic accuracy of exercise electrocardiography but not of exercise echocardiography. The relative merits of these investigations are less well defined in patients with hypertrophy but without electrocardiographic (ECG) changes. We prospectively evaluated 147 consecutive patients without prior myocardial infarction undergoing both exercise echocardiography and coronary arteriography. Coronary stenoses > 50% diameter were present in 62 patients (42%). Positive test results were defined by a new or worsening wall motion abnormality or > 0.1 mV of ST depression. Echocardiographic left ventricular hypertrophy (mass > 131 g/m2 in men, > 100 g/m2 in women) was identified in 68 patients. A subgroup with clinically suspected hypertrophy was defined according to the presence of ECG evidence of hypertrophy, hypertension or aortic stenosis. The overall sensitivity of exercise echocardiography exceeded that of exercise electrocardiography (71% vs. 54%, p = 0.06). Echocardiographic hypertrophy had no significant effect on the sensitivity of either test. The specificity of exercise echocardiography exceeded that of exercise electrocardiography (91 vs. 74%, p = 0.01). In patients with hypertrophy, the specificity of exercise echocardiography exceeded that of exercise electrocardiography (95% vs. 69%, p < 0.01), whereas among patients without hypertrophy, the specificities (respectively, 87% and 78%) were more comparable. The accuracy of exercise echocardiography exceeded that of the exercise ECG in the overall group (82% vs. 65%, p = 0.002) and in patients with hypertrophy (85% vs. 60%, p = 0.004), but this difference was less prominent in patients without hypertrophy (80% vs. 69%, p = NS). In patients with clinically suspected hypertrophy, exercise echocardiography demonstrated a higher sensitivity, specificity and accuracy than exercise electrocardiography. The cost incurred in the identification of coronary disease was least with a strategy involving use of the exercise echocardiogram instead of routine exercise testing in patients with known or clinically suspected left ventricular hypertrophy. Exercise echocardiography is more accurate than exercise electrocardiography for the detection of coronary artery disease in patients with known or clinically suspected left ventricular hypertrophy.

Relation between ECG strain pattern and left ventricular morphology, left ventricular function, and DPTI/SPTI ratio in patients with aortic regurgitation

The relative contributions of left ventricular structural changes, dysfunction, and subendocardial ischemia in determining electrocardiographic repolarization abnormalities were assessed in 53 patients with chronic, pure aortic regurgitation and no evidence of coronary artery disease. Thirty-six patients with an abnormal electrocardiographic pattern of repolarization showed larger end-diastolic (154 ± 46 vs 120 ± 32 mL/m 2; P < .001) and end-systolic (80 ± 40 vs 52 ± 30 mL/m 2; P = .016) volumes, higher end-diastolic pressure (22 ± 11 vs 15 ± 10 mmHg; P = .021), lower ejection fraction (52 ± 12 vs 59 ± 13%; P < .05) and greater mass (168 ± 48 vs 140 ± 44 g/m 2; P < .05) of the left ventricle compared to 17 patients with normal repolarization. Furthermore, patients with repolarization abnormalities also showed higher peak meridian (217 ± 68 vs 153 ± 92 Kdyne/cm 2; P < .001) and circumferential (358 ± 110 vs 259 ± 153 Kdyne/cm 2; P < .001) stress and a more spherical shape (end-diastolic shape: 1.4 ± 0.1 vs 1.5 ± 0.2, P = .046; end-systolic shape: 1.7 ± 0.3 vs 1.9 ± 0.3, P = .026) of the left ventricle. Patients with secondary repolarization abnormalities were also older than patients with normal repolarization (56 ± 10 vs 40 ± 11 years; P < .001). However, the diastolic pressure-time index/systolic pressure-time index, which is an estimate of the myocardial oxygen supply-to-demand ratio, was similar in both groups of patients (0.74 ± 0.3 vs 0.8 ± 0.2; P = NS). Multiple logistic regression analysis selected age ( P < .001), end-systolic volume ( P = .0149), and peak circumferential wall stress ( P = .0369) as factors independently related to the pattern of repolarization. These results suggest that in patients with chronic aortic regurgitation, the presence of secondary repolarization abnormalities on the resting electrocardiogram reflect left ventricular dysfunction and long-standing volume overload.

Terfenadine-Ketoconazole Interaction

To examine prospectively the effects of ketoconazole on the pharmacokinetics and electrocardiographic repolarization pharmacodynamics (corrected QT intervals) of terfenadine in men and women. Prospective cohort study with each subject serving as his or her own control. Outpatient cardiology clinic and inpatient telemetry unit for monitoring period. Six healthy volunteers (four men and two women, aged 24 to 35 years) not taking any prescription or over-the-counter medications. After achieving a steady state while taking terfenadine (60 mg every 12 hours for 7 days), daily concomitant oral ketoconazole (200 mg every 12 hours) was added to the subjects' regimen. Pharmacokinetic profiles were obtained while subjects were taking terfenadine alone and after the addition of ketoconazole. Electrocardiograms were obtained at baseline, after 1 week of taking terfenadine alone, and at the time of the second pharmacokinetic profile after the addition of ketoconazole to the regimen. Terfenadine and its acid metabolite serum concentrations and corrected QT intervals. All subjects had detectable levels of unmetabolized terfenadine after the addition of ketoconazole, which was associated with QT prolongation. Only two of the six subjects could complete the entire course of ketoconazole coadministration. Four subjects received a shortened duration of ketoconazole therapy because of significant electrocardiographic repolarization abnormalities. There was a significant change in the area under the curve of the acid metabolite of terfenadine after the addition of ketoconazole administration. Ketoconazole alters the metabolism of terfenadine in normal men and women and results in the accumulation of unmetabolized parent drug, which is associated with significant prolongation of the corrected QT interval. This drug combination should be avoided.

Geometric and functional correlates of electrocardiographic repolarization and voltage abnormalities in aortic regurgitation

Although electrocardiographic left ventricular hypertrophy is a recognized marker of disease severity in patients with chronic aortic regurgitation, the quantitative relations of repolarization abnormalities and QRS voltage to measurements of cardiac structure and function have not been established. The presence or absence of the "strain" pattern of repolarization and QRS voltage was compared with echocardiographic and radionuclide cineangiographic findings in 95 adults with sever, pure, chronic aortic regurgitation and no evidence of coronary artery disease. In contrast to 54 patients with normal repolarization, 41 patients with an abnormal repolarization pattern had greater left ventricular end-diastolic and end-systolic dimensions (7.2 +/- 1.1 versus 6.6 +/- 0.8 cm, p less than 0.002 and 5.2 +/- 1.2 versus 4.4 +/- 0.7, p less than 0.001, respectively), greater left ventricular mass (431 +/- 138 versus 303 +/- 89 g, p less than 0.001), higher end-systolic stress (128 +/- 46 versus 95 +/- 27 dynes-cm2 X 10(3), p less than 0.001), lower fractional shortening (28 +/- 8 versus 34 +/- 5%, p less than 0.001) and lower exercise ejection fraction (39 +/- 11 versus 51 +/- 8%, p less than 0.001). Multiple logistic regression analysis revealed that left ventricular mass and end-systolic stress were independently related to the presence of repolarization abnormalities (p less than 0.005). Among the 73 asymptomatic patients, those with normal repolarization had significantly lower prevalences of fractional shortening less than 25% (1 of 45 versus 5 of 27, p less than 0.05), left ventricular systolic dimension greater than 5.5 cm (1 of 45 versus 8 of 27, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Spectrum of cardiac involvement in Friedreich's ataxia: Clinical, electrocardiographic and echocardiographic observations

Combined 2-dimensional and M-mode echocardiography was used to assess the cardiac status of 22 patients with Friedreich's ataxia, and the findings were correlated with the clinical and electrocardiographic (ECG) data. Mean age at onset of Friedreich's ataxia was 8 years (range 3 to 18); mean age at echocardiography was 18 years (range 8 to 39). Echocardiographic findings were abnormal in 19 patients (86%). The 3 patients with normal echocardiographic findings did not have cardiac symptoms, but 1 had ECG repolarization abnormalities. Concentric left ventricular (LV) thickening, the most common echocardiographic finding, was found in 15 patients (68%) and in all 15 the papillary muscles were thickened. These 15 patients had ECG repolarization abnormalities and 5 had left-axis deviation; however, only 3 satisfied ECG criteria for LV or right ventricular hypertrophy. Two of the 15 patients (9%) had symptoms of heart failure. Two patients had asymmetric septal thickening without clinical evidence of LV outflow tract obstruction; neither had cardiac symptoms, but both had ECG repolarization abnormalities. Two patients showed a dilated cardiomyopathy pattern; both had heart failure and atrial flutter. One of these patients died, and necropsy revealed 4-chamber cardiac dilatation, biventricular hypertrophy and histologic findings of diffuse interstitial fibrosis, myocellular hypertrophy and necrosis. This study revealed a wide spectrum of cardiac abnormalities in patients with Friedreich's ataxia.

Electrocardiographic Changes Suggestive of Cardiac Ischemia in a Patient With Esophageal Food Impaction

MANY patients presenting with chest pain initially believed to be cardiac in etiology may, in fact, have esophageal disease as an alternative or additional cause of their complaints. Although electrocardiographic (ECG) repolarization abnormalities have been well described in gastroenterologic processes, such as pancreatitis and cholecystitis,¹and have been reported in esophageal disease,^2-9the ECG is generally thought to be a reliable means of distinguishing between esophageal and cardiac pain.^10,11In this report, we describe a patient who developed ECG changes suggestive of cardiac ischemia secondary to esophageal food impaction. <h3>Report of a Case</h3> A 57-year-old woman was admitted to the George Washington University Medical Center, Washington, DC, with a chief complaint of chest discomfort and dysphagia. She had a history of intermittent epigastric and substernal burning discomfort with meals, alleviated by antacids, and in 1979 was found to have a hiatal hernia with reflux by upper gastrointestinal