Serial P wave changes in acute myocardial infarction

Grossman, James I.; Delman, Abner J.

doi:10.1016/0002-8703(69)90189-6

Cited by 26 publications

(6 citation statements)

References 25 publications

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“…There was no correlation between left atrial size and pulmonary artery wedge pressure at rest or during exercise. Discussion P wave abnormalities in ischaemic heart disease have been studied in acute myocardial infarction (Master, 1933;Grossman and Delman, 1969;Heikkila and Luomanmaki, 1970;Chandraratna and Hodges, 1973) but few studies have been done in patients with stable angina pectoris. Bethell and Nixon (1972) noted that in 152 patients with angina the incidence of a P terminal force more negative than -0-02 s was 18 per cent compared with an incidence of 0 5 per cent in 206 normal subjects.…”

Section: Resultsmentioning

confidence: 99%

“…Morphological changes in the P wave of the electrocardiogram have been seen in valvular heart disease (Morris et al, 1964;Gooch et al, 1966;Kasser and Kennedy, 1969;Rubler et al, 1976), hypertension (Ross, 1963;Tarazi et al, 1966), heart failure (Wood and Selzer, 1939;Sutnick and Soloff, 1962;, acute myocardial infarction (Master, 1933;Grossman and Delman, 1969;Heikkila and Luomanmaki, 1970;Chandraratna and Hodges, 1973), and ischaemic heart disease (Bethell and Nixon, 1972;Rios et al, 1974). P wave abnormalities have been correlated with atrial hypertrophy caused by pressure overload and atrial enlargement resulting from volume overload.…”

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confidence: 99%

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P wave analysis in ischaemic heart disease. An echocardiographic, haemodynamic, and angiographic assessment.

Shettigar¹,

Barry²,

Hultgren³

1977

Heart

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Fifty-two men with stable angina pectoris, without associated valvular heart disease or congestive failure, were studied to assess the electrocardiographic P wave abnomalities and their relation to left atrial size, pressure, and left ventricularfunction. Their mean age was 52years. Duration ofP waves in leads II, III, and aVF and the P terminalforce in Vl were examined. Echocardiograms were obtained to assess left atrial size and left atrial-aortic ratio. These measurements were also made in 33 normal subjects. Mean pulmonary artery wedge pressure at rest and exercise, left ventricular asynergy, ejectionfraction, and severity of coronary artery disease were determined in all 52 patients. P terminal force more negative than -002 mm s was noted in 69 per cent of coronary artery disease patients but in none of the normal subjects. P terminalforce correlated with exercise pulmonary artery mean wedge pressure but not with left atrial size. P wave duration in lead II did not correlate withpulmonary artery mean wedge pressure or left atrial size. P terminal force correlated with left ventricular contraction abnormality but not with ejection fraction or number of vessels diseased. It is suggested that chronic intermittent increases in left atrial pressure in association with angina pectoris result in left atrial hypertrophy which is responsible for the increased magnitude of P terminalforce in Vl in patients with ischaemic heart disease.Morphological changes in the P wave of the electrocardiogram have been seen in valvular heart disease (Morris et al

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

P wave analysis in ischaemic heart disease. An echocardiographic, haemodynamic, and angiographic assessment.

Shettigar¹,

Barry²,

Hultgren³

1977

Heart

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“…The clinical significance of P‐wave duration has been investigated in many clinical conditions such as left atrial enlargement, 19 , 22,23 left atrial hypertension, 24–26 exercise, or angioplasty‐induced myocardial ischemia, 27–29 acute MI, 25 , 30,31 stable angina pectoris, 25 , 32–34 and in patients with paroxysmal AF 9,10 , 17 , 35 …”

Section: Discussionmentioning

confidence: 99%

Effects of P‐wave Dispersion on Atrial Fibrillation in Patients with Acute Anterior Wall Myocardial Infarction

Baykan¹,

Çelık²,

Erdöl³

et al. 2003

Noninvasive Electrocardiol

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“…The second possible mechanism is tbat tbe shift is the result of a chtuige in conduction out of the mxle that changes the site of earliest extracellular activation. Mapping data in the sinus node of rabbits suggest that the earliest sites do move with changes V "111 20 in tbe rate eaused by neurotransmitters.-' Furthermore, studies have also suggested that autonomic transmitters have significant dromotropic effects.'' Therefore, it appears that both mechanisms play a role in shifts of the earliest impulse initiation witlun the atrium.…”

Section: Complexity Of Conduction Out Of the Sinus Nodementioning

confidence: 99%

Origin of the Sinus Impulse

Schuessler

Boineau

Bromberg

1996

Cardiovasc electrophysiol

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It was generally accepted that the site of normal impulse origin within the atria was a single static focus within the sinus node. This review will examine how this model of impulse origin came about and has evolved. Early on, conflicting data suggested that the sinus node focus was not static and changed with interventions that changed heart rate, such as vagal stimulation. Furthermore, even with removal of the sinus node, a normal atrial rhythm was generated. High-resolution mapping in humans and dogs showed that the initiation of the impulse was dynamic and could be multicentric, with more than one focus initiating a single beat. Shifts in the site of origin correlated with changes in rate and were consistent with P wave changes routinely observed in the standard ECG. These studies suggested multiple pacemakers were responsible for impulse initiation. However, it was not clear how these widespread pacemakers were coordinated to function synchronously. Recent canine data suggest that the node may be partially insulated from the surrounding atrium, resulting in multicentric origin starting from a single site within the node. What has evolved is a model of impulse origin with a sinus node having discrete exit sites and a dominant pacemaker within the node that can shift to other nodal sites. Complex and changing conduction out of the node, coupled with extranodal pacemakers, which can assume dominance over the node, combine with the autonomic nervous system to control heart rate and the pattern of impulse origin within the atria.

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Serial P wave changes in acute myocardial infarction

Cited by 26 publications

References 25 publications

P wave analysis in ischaemic heart disease. An echocardiographic, haemodynamic, and angiographic assessment.

P wave analysis in ischaemic heart disease. An echocardiographic, haemodynamic, and angiographic assessment.

Effects of P‐wave Dispersion on Atrial Fibrillation in Patients with Acute Anterior Wall Myocardial Infarction

Origin of the Sinus Impulse

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