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P terminal force in lead V1
READERS’ COMMENTS P Terminal Force in Lead V1
The P wave in valvular heart disease was analyzed by Morris et al.1 They first described the use of the P terminal force in lead V1 and elegantly showed that this method of P-wave analysis had a high positive predictive value and a sensitivity of 92% for left atrial (LA) abnormality in the presence of leftsided heart disease. Although this is now an accepted criterion for LA enlargement,2 the P terminal force in V1 has a lower sensitivity of 69% when used for LA enlargement than for LA abnormality.3 Mehta et al4 clearly showed the usefulness of LA abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block. The criterion that most effectively distinguished between normal and left ventricular hypertrophy was the P terminal force in V1. Morris et al1 detail and demonstrate the calculation of this P terminal force: the product of the duration of the terminal portion of the P wave in V1 (in seconds) and its amplitude (in millimeters). A value more negative than ⫺0.03 mm 䡠 s is considered abnormal. Thus, the units of millivolts/s as used by Mehta et al4 are incorrect and should not be perpetuated.5 An argument could be made that not all electrocardiographic recordings use the standard recording speed of 25 mm/s or amplitude measurement of 10 mm/mV, and that the cutoff value for the P terminal force in V1 should be standardized to ⫺0.003 or ⫺3.0 mV 䡠 ms. Andrzej M. Okreglicki,
MBChB, MMed
Cape Town, South Africa 20 April 2000 1. Morris JJ, Estes EH, Whalen RE, Thompson HK, McIntosh HD. P-wave analysis in valvular heart disease. Circulation 1964;24:242–252. 2. Chou T. Electrocardiography in Clinical Practice,
Letters (from the United States) concerning a particular article in The American Journal of Cardiology姞 must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 doublespaced typewritten pages. Two copies must be submitted.
4th ed. Philadelphia, PA: WB Saunders, 1996:23– 36. 3. Munuswamy K, Alpert MA, Martin RH, Whiting RB, Mechlin NJ. Sensitivity and specificity of commonly used electrocardiographic criteria for left atrial enlargement determined by M-mode echocardiography. Am J Cardiol 1984;53:829 – 832. 4. Mehta A, Jain A, Mehta MC, Billie M. Usefulness of left atrial abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block. Am J Cardiol 2000;85:354 –359. 5. Mehta A, Jain A, Mehta MC, Billie M. Left atrial abnormality in acute myocardial infarction. Am J Cardiol 1997;79:807– 811. PII S0002-9149(00)01064-X
Appropriate Treatment of Aortic Intramural Hematoma
We read with interest the report of Shimizu et al1 on the prognosis of aortic intramural hemorrhage compared with classic aortic dissection. The authors evaluated 96 consecutive patients with “acute aortic dissection” of whom 51 were considered to have aortic intramural hematoma (IMH). The diagnosis of IMH was made by computer tomography scan features (eccentric or circumferential thickening on unenhanced computer tomography imaging and no intimal flap on contrast studies). No confirmatory evidence is included to support the diagnosis in these 51 cases. The incidence of IMH in 53% of a patient population presenting with symptoms consistent with aortic dissection is in stark contrast to that noted in previous large studies using transesophageal echocardiographic imaging (13% to 23%) or magnetic resonance imaging (17%).2– 4 Perhaps the inclusion of patients not having confirmation of IMH explains their discrepant incidence and outcome. The authors suggest that the patients in their study have a more benign prognosis than earlier studies and further suggest that ascending aortic IMH may not require surgical therapy. However, of the 13 patients with ascending IMH, 2 were treated surgically, and 3 (27%) of the 11 remaining with ascending IMH treated medically died suddenly. Early reports including 49 patients with ascending aorta IMH in whom only 47% of
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 86 July 15, 2000
patients were treated medically describe a mortality rate of 57% with medical management.2– 4 Thus, the mortality rate for patients with ascending aorta IMH in this series is high and reaffirms data established in larger earlier series, which led to recommendations that an aggressive surgical approach was indicated for ascending IMH, similar to that used for ascending aortic dissection.2– 4 The authors also claim that the incidence of tamponade is not well known. However, pericardial effusions have been reported to occur in 75% to 100% of patients with ascending IMH, some of whom developed tamponade.2,3 In the report by Shimizu, 38% of patients with ascending IMH developed tamponade. Of 16 patients with cardiac tamponade due to either ascending IMH or dissection, 8 underwent pericardiocentesis. Three of the 8 patients (38%) undergoing pericardiocentesis died! It is not stated why some patients underwent pericardiocentesis and whether the fluid was hemorrhaghic, nor is it stated how many survivors of tamponade went on to have urgent surgery. We are very concerned with the suggestion that pericardiocentesis may be an adequate treatment for cardiac tamponade in these patients with ascending IMH. In fact, although there may be a role for pericardiocentesis in the acute stabilization of a critically hypotensive patient, it has been well recognized that this procedure can be harmful in patients with an acute aortic dissection.5 We believe that cardiac tamponade associated with acute aortic catastrophes requires urgent surgical therapy. In summary, we are concerned that the patients described in this report are not representative of acute IMH as has been described in the literature to date. This may be due to the fact that their series may include some patients with other diagnoses. Thus, while the authors data are intriguing, we agree that the incidence of the diagnosis may be related to the diagnostic test performed. When the 255
The P wave in valvular heart disease was analyzed by Morris et al.1 They first described the use of the P terminal force in lead V1 and elegantly showed that this method of P-wave analysis had a high positive predictive value and a sensitivity of 92% for left atrial (LA) abnormality in the presence of leftsided heart disease. Although this is now an accepted criterion for LA enlargement,2 the P terminal force in V1 has a lower sensitivity of 69% when used for LA enlargement than for LA abnormality.3 Mehta et al4 clearly showed the usefulness of LA abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block. The criterion that most effectively distinguished between normal and left ventricular hypertrophy was the P terminal force in V1. Morris et al1 detail and demonstrate the calculation of this P terminal force: the product of the duration of the terminal portion of the P wave in V1 (in seconds) and its amplitude (in millimeters). A value more negative than ⫺0.03 mm 䡠 s is considered abnormal. Thus, the units of millivolts/s as used by Mehta et al4 are incorrect and should not be perpetuated.5 An argument could be made that not all electrocardiographic recordings use the standard recording speed of 25 mm/s or amplitude measurement of 10 mm/mV, and that the cutoff value for the P terminal force in V1 should be standardized to ⫺0.003 or ⫺3.0 mV 䡠 ms. Andrzej M. Okreglicki,
MBChB, MMed
Cape Town, South Africa 20 April 2000 1. Morris JJ, Estes EH, Whalen RE, Thompson HK, McIntosh HD. P-wave analysis in valvular heart disease. Circulation 1964;24:242–252. 2. Chou T. Electrocardiography in Clinical Practice,
Letters (from the United States) concerning a particular article in The American Journal of Cardiology姞 must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 doublespaced typewritten pages. Two copies must be submitted.
4th ed. Philadelphia, PA: WB Saunders, 1996:23– 36. 3. Munuswamy K, Alpert MA, Martin RH, Whiting RB, Mechlin NJ. Sensitivity and specificity of commonly used electrocardiographic criteria for left atrial enlargement determined by M-mode echocardiography. Am J Cardiol 1984;53:829 – 832. 4. Mehta A, Jain A, Mehta MC, Billie M. Usefulness of left atrial abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block. Am J Cardiol 2000;85:354 –359. 5. Mehta A, Jain A, Mehta MC, Billie M. Left atrial abnormality in acute myocardial infarction. Am J Cardiol 1997;79:807– 811. PII S0002-9149(00)01064-X
Appropriate Treatment of Aortic Intramural Hematoma
We read with interest the report of Shimizu et al1 on the prognosis of aortic intramural hemorrhage compared with classic aortic dissection. The authors evaluated 96 consecutive patients with “acute aortic dissection” of whom 51 were considered to have aortic intramural hematoma (IMH). The diagnosis of IMH was made by computer tomography scan features (eccentric or circumferential thickening on unenhanced computer tomography imaging and no intimal flap on contrast studies). No confirmatory evidence is included to support the diagnosis in these 51 cases. The incidence of IMH in 53% of a patient population presenting with symptoms consistent with aortic dissection is in stark contrast to that noted in previous large studies using transesophageal echocardiographic imaging (13% to 23%) or magnetic resonance imaging (17%).2– 4 Perhaps the inclusion of patients not having confirmation of IMH explains their discrepant incidence and outcome. The authors suggest that the patients in their study have a more benign prognosis than earlier studies and further suggest that ascending aortic IMH may not require surgical therapy. However, of the 13 patients with ascending IMH, 2 were treated surgically, and 3 (27%) of the 11 remaining with ascending IMH treated medically died suddenly. Early reports including 49 patients with ascending aorta IMH in whom only 47% of
©2000 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 86 July 15, 2000
patients were treated medically describe a mortality rate of 57% with medical management.2– 4 Thus, the mortality rate for patients with ascending aorta IMH in this series is high and reaffirms data established in larger earlier series, which led to recommendations that an aggressive surgical approach was indicated for ascending IMH, similar to that used for ascending aortic dissection.2– 4 The authors also claim that the incidence of tamponade is not well known. However, pericardial effusions have been reported to occur in 75% to 100% of patients with ascending IMH, some of whom developed tamponade.2,3 In the report by Shimizu, 38% of patients with ascending IMH developed tamponade. Of 16 patients with cardiac tamponade due to either ascending IMH or dissection, 8 underwent pericardiocentesis. Three of the 8 patients (38%) undergoing pericardiocentesis died! It is not stated why some patients underwent pericardiocentesis and whether the fluid was hemorrhaghic, nor is it stated how many survivors of tamponade went on to have urgent surgery. We are very concerned with the suggestion that pericardiocentesis may be an adequate treatment for cardiac tamponade in these patients with ascending IMH. In fact, although there may be a role for pericardiocentesis in the acute stabilization of a critically hypotensive patient, it has been well recognized that this procedure can be harmful in patients with an acute aortic dissection.5 We believe that cardiac tamponade associated with acute aortic catastrophes requires urgent surgical therapy. In summary, we are concerned that the patients described in this report are not representative of acute IMH as has been described in the literature to date. This may be due to the fact that their series may include some patients with other diagnoses. Thus, while the authors data are intriguing, we agree that the incidence of the diagnosis may be related to the diagnostic test performed. When the 255