Massive T-wave inversion

Ippolito, Thomas L.; Blier, Julius S.; Fox, Theodore T.

doi:10.1016/0002-8703(54)90276-8

Cited by 24 publications

(6 citation statements)

References 2 publications

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“…In the other patient (Case 3), however, the etiology was less certain. In each instance there was marked bradycardia, substantiating previous observations on the conditions necessary for giant T wave formation (Scherf, 1944;Ippolito et al, 1954;Szilagyi and Solomon, 1959). The duration of the block before beginning steroid therapy was, however, variable and acute myocardial damage does not, therefore, seem essential for the development of these steroid-induced disturbances of repolarization.…”

Section: Methodssupporting

confidence: 88%

“…In most instances this electrocardiographic pattern has been associated either with acute myocardial infarction (Levine and Brown, 1929;Wood and Wolferth, 1934) or recent complete heart block (Ippolito, Blier, and Fox, 1954; Szilagyi and Solomon, 1959), and a slow ventricular rate is believed to be an important, but not invariable, determinant of this T wave configuration (Garcia-Palmieri et al, 1956). Stretching of areas of focally damaged myocardium by diastolic overloading and variations in vagal tone have been suggested as possible causes of this electrocardiographic abnormality (Scherf, 1944;Ippolito et al, 1954; Szilagyi and Solomon, 1959) which could in fact represent disturbance of the electrolyte flux and sodium-potassium pump across the cell membrane. Satisfactory confirmation of these hypotheses is, however, still lacking.…”

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confidence: 99%

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Steroid-Induced T Wave Changes in Heart Block

Cp¹,

Ew²

1965

Heart

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Giant T waves have previously been described by several observers. In most instances this electrocardiographic pattern has been associated either with acute myocardial infarction (Levine and Brown, 1929;Wood and Wolferth, 1934) or recent complete heart block (Ippolito, Blier, and Fox, 1954; Szilagyi and Solomon, 1959), and a slow ventricular rate is believed to be an important, but not invariable, determinant of this T wave configuration (Garcia-Palmieri et al., 1956). Stretching of areas of focally damaged myocardium by diastolic overloading and variations in vagal tone have been suggested as possible causes of this electrocardiographic abnormality (Scherf, 1944;Ippolito et al., 1954; Szilagyi and Solomon, 1959) which could in fact represent disturbance of the electrolyte flux and sodium-potassium pump across the cell membrane. Satisfactory confirmation of these hypotheses is, however, still lacking.We have made observations, during steroid treatment of patients with established heart block, which appear to support the concept that local ionic disturbances are responsible for this perversion of myocardial repolarization. As (Fig. lA) and the chest radiographs showed mild generalized cardiomegaly with marked calcification of the aortic valve. The serum electrolytes and SGOT were normal.Corticotrophin (40 units b.i.d.) was commenced 8 days after admission in an attempt to restore sinus rhythm, but a week later, despite considerable general improvement and resolution of mild congestive cardiac failure, the heart block persisted. In view of this general improvement betamethasone (0 5 mg. q.i.d.) was substituted and continued, with subsequent gradual withdrawal, for a further six weeks.Three days after commencing corticotrophin steep inversion of the T waves was noted (Fig. I B) and this electrocardiographic change persisted for two weeks after betamethasone had been withdrawn (Fig. 1C and D). No changes in heart rate, QRS complexes, systemic blood pressure, or serum electrolytes were observed during this time.Case 2. This 56-year-old woman was known to have had coronary artery disease and essential hypertension for seven years before developing heart block. Complete A-V block ( Fig. 2A) with left and right heart failure had been observed for 4 months before beginning steroid therapy. The SGOT at this time was 90 units/100 ml. and the serum electrolytes were normal. Chest radiograph showed generalized cardiomegaly. 56

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Section: Methodssupporting

confidence: 88%

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confidence: 99%

Steroid-Induced T Wave Changes in Heart Block

Cp¹,

Ew²

1965

Heart

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“…At first we attributed transient T inversion in patients admitted to the pacing unit to recent Adams-Stokes attacks (Ippolito, Blier, and Fox, 1954;Szilagyi and Solomon, 1959;Jacobson and Schrire, 1966), but recent attacks were excluded in the 31 patients chosen for the study. Underlying small or large coronary artery disease with a recent ischaemic episode was suggested (Wood and Wolferth, 1934;Silverman and Goodman, 1949;Garcia-Palmieri et al, 1956;Pruitt, Klakeg, and Chapin, 1955;Fisch, 1961), but the T inversion was too constantly present in a group of patients expected to have normal vessels and bilateral 776 Electrocardiographic Changes Subsequent to Artificial Ventricular Depolarization bundle-branch fibrosis as the cause of their heart block (Harris et aL., 1969).…”

Section: Resultsmentioning

confidence: 99%

Electrocardiographic changes subsequent to artificial ventricular depolarization.

Chatterjee¹,

Harris²,

Davies³

et al. 1969

Heart

161

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Massive T wave inversion and ST depression occur in the unpaced electrocardiogram subsequent to ventricular pacing, and persist for a varying length of time depending on the duration of pacing. That artificial depolarization of the ventricle causes changes in repolarization which persist after stopping pacing is of considerable theoretical and practical importance, and we describe the findings in 31 patients both with and without disease of the conduction tissue. Thirty-one patients were studied, 11 women, and 20 men, and their ages ranged from 42 to 84 years (mean 67 years): 30 were being paced from the endocardium by transvenous electrode wires, and one from the left ventricular epicardium by epicardial electrodes, all with external units at the time of investigation.Twenty-six patients were paced for chronic atrioventricular (AV) conduction disease with Adams-Stokes attacks. Three were paced after acute myocardial infarcts with temporary disturbance of AV conduction, in order to prevent Adams-Stokes attacks. The VI1 V2

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“…6,7 Our patient had Stokes-Adams attacks before hospitalization, but the ST-T changes appeared only after two days of ventricular pacing in the hospital.…”

Section: Discussionmentioning

confidence: 72%

Temporary cardiac pacing induced electrocardiographic changes simulating myocardial infarction

2017

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Temporary transvenous pacing is an immediate lifesaving measure in patients with Stokes-Adams syndrome and in patients with symptomatic bradycardia. Bradyarrhythmias are known to occur in acute myocardial infarction. But in a paced heart, it is difficult to diagnose myocardial infarction from electrocardiogram (ECG) because pacemaker rhythm causes distortion of natural wave forms. On the other hand, remarkable T wave inversions and ST depressions do occur in the ventricular paced ECG as secondary changes. The case report describes a patient who developed profound de novo T wave inversions and ST depressions in the unpaced ECG following temporary transvenous pacing simulating MI.

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Massive T-wave inversion

Cited by 24 publications

References 2 publications

Steroid-Induced T Wave Changes in Heart Block

Steroid-Induced T Wave Changes in Heart Block

Electrocardiographic changes subsequent to artificial ventricular depolarization.

Temporary cardiac pacing induced electrocardiographic changes simulating myocardial infarction

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