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ECHOCARDIOGRAPHY IN DIAGNOSIS OF AORTIC DISSECTION
1201 stool (without gross bleeding). The patient’s haemoglobin fell to 84
unarguably gives
mg/dl, and four units of packed erythrocytes were transfused.
presence
The patient was discharged, still on parenteral nutrition via her original Hickman catheter, and there has been no recurrence of
group
thrombosis in the 12 months since recanalisation.
Superior vena cava syndrome is caused by extrinsic compression (usually from a tumour) or, much more rarely, by intrinsic thrombosis.1 However, with the increase in use of long-term indwelling catheters the incidence of thrombosis is likely to increase. When the syndrome is due to pressure from a tumour obstruction radiotherapy is usually effective. In this case of intrinsic thrombosis an attack on the occluding thrombus itself seemed the logical
approach. have been used not only to treat acute on the venous side of the circulation,2--4 and patients with superior vena cava syndrome due to thrombotic occlusion might be helped by this type of treatment. At first we were reluctant to try a thrombolytic agent because our patient had a history of radiation enteritis-induced gastrointestinal bleeding. However, heparin therapy was not effective and prolonged heparinisation itself carries a significant risk of haemorrhage. We chose alteplase because it is more "clot-specific" than streptokinase or urokinases and is better than streptokinase in patients with older thrombian important factor in our patient. The agent was infused directly into the thrombus because we assumed that systemic administration would have resulted in a significant amount of the agent bypassing the thrombus via the extensive collateral system. A direct infusion was expected to achieve a high local concentration of the agent after a lower total dose. The large bolus followed by a rapid tapering customary in coronary artery therapy was thought to be unnecessary because speed in the lysis of a clot already 8 days old was not a priority. Continuing the heparin infusion alone might have been sufficient, but a long time in hospital would have been required and
Thrombolytic agents
a definite diagnosis. Here the question is the absence of aortic dissection. Thus confirmation of by surgery or necropsy in their group A is acceptable. In since CT and aortography results are compared with or
diagnosis B,
echocardiography (echocardiography being deemed to have 100% values for sensitivity, specificity, and positive and negative predictive values) it appears that echocardiography is being used as the gold standard. This is unacceptable because this is the primary procedure under assessment. Hence data gained from group B analyses and also that from analysis of the combined results of group A and B are questionable. Group A data are probably also suspect since patients were not randomly allocated to group A or B. There is a definite predominance of positive diagnoses in group A and negative diagnoses in group B.
coronary artery occlusion but also
nutritional deficits would have ensued. The restored patency in less than a day. Division of Cardiovascular Diseases and Internal Medicine and Department of Diagnostic Radiology, Mayo Clinic and Mayo Foundation, Rochester, Minnestoa 55905, USA
thrombolytic agent
DAVID G. FINE ROGER F. J. SHEPHERD TIMOTHY J. WELCH
DE, Lee RE. Etiologic considerations in superior syndrome. Mayo Clin Proc 1981; 56: 407-13. 2. Marder VJ. The use of thrombolytic agents: choice of patient, drug administration, laboratory monitoring. Ann Intern Med 1979; 90: 802-08. 3. A Cooperative Study. Urokinase-streptokinase embolism trial: phase 2 results. JAMA 1974; 229: 1606-13. 4. Verstraete M, Miller GAH, Bounameaux H, et al. Intravenous and intrapulmonary recombinant tissue-type plasminogen activator in the treatment of acute massive pulmonary embolism. Circulation 1988; 77: 353-60. 5. Hoylaerts M, Rijken DC, Lijnen HR, Collen D. Kinetics of the activation of plasminogen by human tissue plasminogen activator: role of fibrin. J Biol Chem 1. Parish JM, Marschke RF Jr, Dines vena cava
1982; 257: 2912-19. 6. Chesebro
JH, Knatterud G, Roberts R, et al. Thrombolysis in myocardial infarction (TIMI) trial, phase I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase: clinical findings through hospital discharge. Circulation 1987; 76: 142-54.
ALICE V. STANTON MIRIAM CASEY EOIN T. O’BRIEN
Department of Cardiology, Beaumont Hospital, Dublin, Ireland
* Thisletter has been shown follows.-ED. L.
Professor Erbel, whose reply
to
SjR,—The aim of our study was to test the accuracy of echocardiography in the diagnosis of aortic dissection. In previous studies the gold standards were surgery/necropsy and angiography. We regarded surgery and necropsy (group A) as the gold standard. In this group the angiographic methods we used did not give optimum results. A diagnosis was retrospectively regarded as true only when it was confirmed by at least one additional method (combined diagnosis); we recorded higher sensitivity and specificity than with angiography alone. Thus this combined diagnosis was regarded as the adequate standard in cases without surgery and necropsy. Of course the results in these patients (group B) are not as reliable as those of group A. But we could not ignore the results of the
surgery/necropsy
necropsy
cases.
In all
cases
without surgery and
echocardiography was confirmed by at least one (of two)
additional methods. As we described for initial entry criteria, patients were consecutively included on the basis of clinical signs, usually with chest X-ray. The order of diagnostic procedures was decided by the physician (and a surgeon). Different persons did the diagnostic studies. The examiners usually worked with the information "suspected aortic dissection", but because of the emergency situation in some cases they possibly had more information. To some extent this restricts the interpretation. Thus we did not state that echocardiography is better than angiographic methods and CT in general. But there is no longer any evidence that echocardiography (including the transoesophageal approach) is inferior to the other methods in the first diagnosis of aortic dissection. Under these circumstances we use echocardiography as the primary method in the emergency room because of its noninvasiveness and short time needed for examination. In 17 additional emergency cases (not included in the study) surgery was done based on echocardiographic diagnosis alone (16 dissections, 1 true aneurysm). The surgeons confirmed the diagnosis in all these cases.
ECHOCARDIOGRAPHY IN DIAGNOSIS OF AORTIC DISSECTION
SiR,— Professor Erbel and colleagues (March 4,
II, Johannes Gutenberg University, 6500 Mainz, West Germany
RAIMUND ERBEL
457)
argue strongly in favour of the use of echocardiography as a sole investigation in the diagnosis of aortic dissection before surgery. Their results for sensitivity, specificity, and negative and positive predictive values indicate that echocardiography had an advantage over aortography and computed tomography (CT), except in a few situations. We are concerned about several aspects of this study and hesitate to implement its recommendations. Erbel and colleagues give no information about the entry criteria upon which the patients were diagnosed as having aortic dissection. Were the doctors examining the echocardiographs blinded to the results of the aortography and CT? The opportunity for bias without blinding is obvious. Most worrying is the analysis of data for sensitivity, specificity, and predictive values. To estimate sensitivity and specificity one needs a gold standard test, a test which p
Medical Clinic
CANDIDATE GENE APPROACH TO TYPE IIa HYPERCHOLESTEROLAEMIA
SiR,—If an individual genetically predisposed to coronary heart disease can be identified before lipid and lipoprotein concentrations become raised, prophylaxis can be started. There are now at least two well-defined single-gene disorders causing isolated hypercholesterolaemia that have been characterised at the DNA level. Familial hypercholesterolaemia (LDL receptor deficiency) accounts for less than 5% of the hypercholesterolaemia seen in developed countries.’ Sorai et al2 have described ApoB 100 defective mutations in the receptor-binding domain of the apolipoprotein B gene, in families with an autosomal dominant form of moderate hypercholesterolaemia. The contribution of this type to primary
unarguably gives
mg/dl, and four units of packed erythrocytes were transfused.
presence
The patient was discharged, still on parenteral nutrition via her original Hickman catheter, and there has been no recurrence of
group
thrombosis in the 12 months since recanalisation.
Superior vena cava syndrome is caused by extrinsic compression (usually from a tumour) or, much more rarely, by intrinsic thrombosis.1 However, with the increase in use of long-term indwelling catheters the incidence of thrombosis is likely to increase. When the syndrome is due to pressure from a tumour obstruction radiotherapy is usually effective. In this case of intrinsic thrombosis an attack on the occluding thrombus itself seemed the logical
approach. have been used not only to treat acute on the venous side of the circulation,2--4 and patients with superior vena cava syndrome due to thrombotic occlusion might be helped by this type of treatment. At first we were reluctant to try a thrombolytic agent because our patient had a history of radiation enteritis-induced gastrointestinal bleeding. However, heparin therapy was not effective and prolonged heparinisation itself carries a significant risk of haemorrhage. We chose alteplase because it is more "clot-specific" than streptokinase or urokinases and is better than streptokinase in patients with older thrombian important factor in our patient. The agent was infused directly into the thrombus because we assumed that systemic administration would have resulted in a significant amount of the agent bypassing the thrombus via the extensive collateral system. A direct infusion was expected to achieve a high local concentration of the agent after a lower total dose. The large bolus followed by a rapid tapering customary in coronary artery therapy was thought to be unnecessary because speed in the lysis of a clot already 8 days old was not a priority. Continuing the heparin infusion alone might have been sufficient, but a long time in hospital would have been required and
Thrombolytic agents
a definite diagnosis. Here the question is the absence of aortic dissection. Thus confirmation of by surgery or necropsy in their group A is acceptable. In since CT and aortography results are compared with or
diagnosis B,
echocardiography (echocardiography being deemed to have 100% values for sensitivity, specificity, and positive and negative predictive values) it appears that echocardiography is being used as the gold standard. This is unacceptable because this is the primary procedure under assessment. Hence data gained from group B analyses and also that from analysis of the combined results of group A and B are questionable. Group A data are probably also suspect since patients were not randomly allocated to group A or B. There is a definite predominance of positive diagnoses in group A and negative diagnoses in group B.
coronary artery occlusion but also
nutritional deficits would have ensued. The restored patency in less than a day. Division of Cardiovascular Diseases and Internal Medicine and Department of Diagnostic Radiology, Mayo Clinic and Mayo Foundation, Rochester, Minnestoa 55905, USA
thrombolytic agent
DAVID G. FINE ROGER F. J. SHEPHERD TIMOTHY J. WELCH
DE, Lee RE. Etiologic considerations in superior syndrome. Mayo Clin Proc 1981; 56: 407-13. 2. Marder VJ. The use of thrombolytic agents: choice of patient, drug administration, laboratory monitoring. Ann Intern Med 1979; 90: 802-08. 3. A Cooperative Study. Urokinase-streptokinase embolism trial: phase 2 results. JAMA 1974; 229: 1606-13. 4. Verstraete M, Miller GAH, Bounameaux H, et al. Intravenous and intrapulmonary recombinant tissue-type plasminogen activator in the treatment of acute massive pulmonary embolism. Circulation 1988; 77: 353-60. 5. Hoylaerts M, Rijken DC, Lijnen HR, Collen D. Kinetics of the activation of plasminogen by human tissue plasminogen activator: role of fibrin. J Biol Chem 1. Parish JM, Marschke RF Jr, Dines vena cava
1982; 257: 2912-19. 6. Chesebro
JH, Knatterud G, Roberts R, et al. Thrombolysis in myocardial infarction (TIMI) trial, phase I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase: clinical findings through hospital discharge. Circulation 1987; 76: 142-54.
ALICE V. STANTON MIRIAM CASEY EOIN T. O’BRIEN
Department of Cardiology, Beaumont Hospital, Dublin, Ireland
* Thisletter has been shown follows.-ED. L.
Professor Erbel, whose reply
to
SjR,—The aim of our study was to test the accuracy of echocardiography in the diagnosis of aortic dissection. In previous studies the gold standards were surgery/necropsy and angiography. We regarded surgery and necropsy (group A) as the gold standard. In this group the angiographic methods we used did not give optimum results. A diagnosis was retrospectively regarded as true only when it was confirmed by at least one additional method (combined diagnosis); we recorded higher sensitivity and specificity than with angiography alone. Thus this combined diagnosis was regarded as the adequate standard in cases without surgery and necropsy. Of course the results in these patients (group B) are not as reliable as those of group A. But we could not ignore the results of the
surgery/necropsy
necropsy
cases.
In all
cases
without surgery and
echocardiography was confirmed by at least one (of two)
additional methods. As we described for initial entry criteria, patients were consecutively included on the basis of clinical signs, usually with chest X-ray. The order of diagnostic procedures was decided by the physician (and a surgeon). Different persons did the diagnostic studies. The examiners usually worked with the information "suspected aortic dissection", but because of the emergency situation in some cases they possibly had more information. To some extent this restricts the interpretation. Thus we did not state that echocardiography is better than angiographic methods and CT in general. But there is no longer any evidence that echocardiography (including the transoesophageal approach) is inferior to the other methods in the first diagnosis of aortic dissection. Under these circumstances we use echocardiography as the primary method in the emergency room because of its noninvasiveness and short time needed for examination. In 17 additional emergency cases (not included in the study) surgery was done based on echocardiographic diagnosis alone (16 dissections, 1 true aneurysm). The surgeons confirmed the diagnosis in all these cases.
ECHOCARDIOGRAPHY IN DIAGNOSIS OF AORTIC DISSECTION
SiR,— Professor Erbel and colleagues (March 4,
II, Johannes Gutenberg University, 6500 Mainz, West Germany
RAIMUND ERBEL
457)
argue strongly in favour of the use of echocardiography as a sole investigation in the diagnosis of aortic dissection before surgery. Their results for sensitivity, specificity, and negative and positive predictive values indicate that echocardiography had an advantage over aortography and computed tomography (CT), except in a few situations. We are concerned about several aspects of this study and hesitate to implement its recommendations. Erbel and colleagues give no information about the entry criteria upon which the patients were diagnosed as having aortic dissection. Were the doctors examining the echocardiographs blinded to the results of the aortography and CT? The opportunity for bias without blinding is obvious. Most worrying is the analysis of data for sensitivity, specificity, and predictive values. To estimate sensitivity and specificity one needs a gold standard test, a test which p
Medical Clinic
CANDIDATE GENE APPROACH TO TYPE IIa HYPERCHOLESTEROLAEMIA
SiR,—If an individual genetically predisposed to coronary heart disease can be identified before lipid and lipoprotein concentrations become raised, prophylaxis can be started. There are now at least two well-defined single-gene disorders causing isolated hypercholesterolaemia that have been characterised at the DNA level. Familial hypercholesterolaemia (LDL receptor deficiency) accounts for less than 5% of the hypercholesterolaemia seen in developed countries.’ Sorai et al2 have described ApoB 100 defective mutations in the receptor-binding domain of the apolipoprotein B gene, in families with an autosomal dominant form of moderate hypercholesterolaemia. The contribution of this type to primary