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More on high school health curricula
Letters to the Editor Reply To the Editor: Dr. Loeliger and associates criticize the intensity of the anticoagulant treatment reported in my paper,* where the therapeutic range was considered to be from 5 to 15 per cent of normal coagulation activity as measured by Thrombotest (TT).’ I agree that the therapy is optimal when the TT is kept between 5 and 10 per cent, and this level is now propagated by the producer and is the accepted one in our country. The slightly higher values had, however, been allowed mainly for two reasons. Firstly, because the hazard of strict anticoagulation in such patients is severe bleeding, and fatal intracranial or other types of hemorrhage are not rare.?-” Two patients in my study died from bleeding that occurred on TT values of 5 and 11 per cent. Patients with prosthetic ball valves might be particularly susceptible to hemorrhage because they have a considerably reduced platelet adhesiveness and a prolonged bleeding:time.‘” The recommendation by Dr. Loeliger and associates that valve patients should have particularly intensive anticoagulation could therefore have serious consequences, and I fear that an increased number of bleeding episodes would more than counterbalance a possibly better effect on thrombus formation. Secondly, slightly higher values were used because of the practical difficulties connected with control of anticoagulant therapy in patients living in all parts of Norway, often very far from the control laboratories. Nevertheless, the intensity of anticoagulation was consistently satisfactory in approximately half of the patients, even after the standards outlined by Dr. Loeliger and associates, and higher levels are accepted by several centers.” Furthermore, I have later collected information of all TT values throughout the period, since the distribution of the values reported in the paper reflected only the levels at follow-up. This demonstrated that 86 per cent of the values fell between 5 and 15, and 55 per cent fell between 5 and 10 per cent of normal activity. To my knowledge, a more consistently intensive anticoagulant therapy in materials concerning patients with prosthetic valves has not been presented. The relation between the intensity of the therapy and the incidence of arterial thromboembolic complications has been evaluated further. The rate of thromboembolism was, however, not lower in the patients with the majority of their ‘IT values at 10 per cent or lower than in the others. This supports my conclusion that such complications represent a major threat to the patients in spite of intensive anticoagulant treatment. Dr. Loeliger and associates seek support for their assertion that intensive anticoagulation can effectively prevent arterial thromboembolism in patients with prosthetic heart valves from a Canadian study.’ This is surprising, since they stress the importance of prothrombin-time standardization, because in that paper not even the type of thromboplastin used is mentioned. A direct comparison is therefore not possible, but it is not improbable that the majority of my patients received what was considered satisfactory anticoagulation in that study. Furthermore, only 33 patients received what was defined as adequate therapy, and one had a thromboembolic complication. Moreover, most patients had mitral or tricuspid valve replacement, which would predispose for thrombi of a more “venous” composition. That this type of thrombosis can be effectively prevented by anticoagulants is well established.
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It is astonishing that Dr. Loeliger and associates build their assertion on this study alone, since only 12 of the patients with single aortic valves had received adequate anticoagulation. Dr. Loeliger and associates state that they very seldom see thromboembolic complications in patients with artificial heart valves. A better documentation of the intensity of the treatment, its antithrombotic effect, and the rate of bleeding complications would, however, be more valid. Finally, their assumption does not take into consideration the role of the platelets for the thrombotic process. While the dominant mechanism for venous thrombosis is plasma coagulation, platelet aggregation is important for the formation of arterial thrombi. Although adequate anticoagulation certainly is of some benefit, it does not affect the reactivity of the platelets. Therefore, arterial thrombosis on prosthetic aortic valves will most probably represent a problem even during very intensive anticoagulant therapy.
Jon Dale Institute for Thrombosis Research Rikshospitalet, Oslo 1 Norway REFERENCES 1.
2. 3.
4.
5.
6.
7.
8.
9.
10. 11.
More
Dale, J.: Arterial thromboembolic complications in patients with Starr-Edwards aortic ball valve prostheses, AM.HEART J. 91:653,1976. Owren, P. A.: Thrombotest: A new method for controlling anticoagulant therapy, Lancet 2:754, 1959. Cleland, J., and Molloy, P. J.: Thrombo-embolic complications of the cloth-covered Starr-Edwards prostheses no. 2300 aortic and no. 6300 mitral, Thorax 28:41, 1973. Friedli, B., Aerichide, N., Grondin, P., and Campeau, L.: Thromboembolic complications of heart valve prostheses, AM. HEART J. 81:702, 1971. Duvoisin, G. E., Wallace, R. B., Ellis, F. H., Andersson, M. W., and McGoon, D. C.: Late results of cardiac-valve replacement, Circulation 37 and 38 (Suppl. 11):75, 1968. Akbarian, M., Austen, W. G., Yurchak, P. M., and Scannell, J. G.: Thromboembolic complications of prosthetic cardiac valves, Circulation 37:826, 1968. Matloff, J. M., Collins, J. J., Sullivan, J. M., Gorlin, R., and Harken, D. E.: Control of thromboembolism from prosthetic heart valves, Ann. Thorac. Surg. 8:133, 1969. Reed, G. E., Claus+ R. H., Tice, D. A., and Acinapura, A. J.: Five-year experience with Magovern aortic prostheses, Circulation 43 and 44 (Suppl. 1):73, 1971. Bjbrk, V. O., Henze, A., and Holmgren, A.: Five years experience with the Bjerk-Shiley tilting disc valve in isolated aortic valvular disease, J. Cardiovasc. Surg. 16:451, 1975. Dale, J., and Myhre, E.: Platelet functions in patients with aortic ball valves, AM. HEART J. 94:359, 1977. Lam-PO-Tang, P. R. L. C., and Potter, L.: Oral anticoagulant therapy and its control: An international survey, Thromb. Diath. Haemorrh. 34:419, 1975.
on high
school
health
curricula
To the Editor: I was relieved to discover that the problem of an inadequate and inappropriate high school health curricula was at last cited by Dr. Mroczek in the AMERICAN HEART JOURNAL." I would lie to add three points to his editorial.
February, 1978,Vol. 95, No. 2
Letters to the Editor My first point is to label high school health textbook material as also being inadequate and inappropriate. If you will observe the contents of most high school (and some college) health texts, you will discover an imbalance in subject matter favoring subjects other than cardiovascular disease and cancer. The one thing that I can remember from my high school health education is the proper procedure for brushing my teeth. Cardiovascular disease was not even mentioned in high school curriculum at this time (early 1960’s). I believe high school health care texts should be joint-authored by the physician, exercise physiologist, and health educator alike. My second point is more specific to my own profession. High school physical education classes are often an unstructured and non-educational experience. Inappropriate curricula is the culprit here as well. Overemphasis on superior athletic performance, body physique, and non-dynamic forms of exercise have been the rule rather than the exception. Cardiovascular endurance types of exercises and recreation should be at least 60 per cent of the emphasis. If secondary school curriculum specialists would just wake up and start reading even a portion of current medical literature relating to exercise physiology, the problem would be partially solved. Finally, my last point is what I believe to be the crux of the problem. The training of health educators at the college level is far out of line. Speaking from my own experiences, some of the nation’s largest and supposedly most prestigious universities are the most misaligned with regard to the training of secondary school health educators. Regardless of how well we improve college-level health education textbooks, we still see the type of professor who remains bolted to a few 40-year-old ideas. I’m speaking specifically about neglecting to teach lifelong cardiovascular endurance exercise habits and how they frequently have a positive effect on CHD-related risk factors. Nearly every significant piece of research that has been published in the last 6 years has been either ignored or is contrary to what is presently taught in many high school physical education classes. There is no excuse for ignorance regarding the proper forms of exercise when you consider the availability of current publications.‘-’ My suggestion is that we re-educate some of the professors who are responsible for instilling (or not instilling) health care information into our secondary health education teachers. One step further-evaluate the chairmen of university health, physical education, and recreation departments.
Ralph L. LaForge, M.&Y. Physiologist Lovelace-Bataan Medical Center Preventive Medicine 5400 Gibson Blvd. SE Albuquerque, N. M. 87108 REFERENCES Committee on Exercise, American Heart Association: Exercise testing and training of apparently healthy individuals, New York, 1972, American Heart Association, pp. l-6, 40. American College of Sports Medicine: Guidelines for graded exercise testing and exercise prescription, Philadelphia, 1975, Lea & Febiger, Publishers, pp. 28-49. Pollock, M.: The quantification of endurance training programs, in Exercise and sport sciences reviews, vol. 1, Wilmore, J., ed., New York, 1973, Academic Press, Inc., pp. 155-182.
American Heart Journal
4.
5.
6.
7. 8.
Fox, S. M., Naughton, J. P., and Gorman, P. A.: Physical activity and cardiovascular health: the exercise prescription, Mod. Concepts. Cardiovasc. Dis. 41:6, 1972. Astrand, P. O., and Rodahl, K.: Textbook of work physiology, New York, 1977, McGraw-Hill Book Company, Inc., chapters 12, 16, and 17. Matthews, D. K., and Fox, E. L.: The physiological basis of physical education and athletics, 2nd ed., Philadelphia, 1976, W. B. Saunders Company, section 4 and chapter 21. Cooper, K. H., et al.: Physical fitness levels vs. selected coronary risk factors, J. A. M. A. 236:166, 1976. Mroczek, W. J.: High school health curricula: A neglected medical resource, AM. HEART J. 92:271, 1976.
Nitroglycerin
ointment
therapy
and
leg edema
To the Editor: Topically applied nitroglycerin ointment has been well demonstrated to have a sustained vasodilatory effect?’ and therefore its use has become fairly commonplace in the chronic therapy of angina pectoris and congestive heart failure. It has also been demonstrated that the major vasodilatory action of nitroglycerin is on the venous circulation,“-’ resulting in a reduction in venous return and left ventricular filling pressure (preload). I have recently observed two cases in which the onset of gross lower extremity edema followed within one week the institution of nitroglycerin ointment therapy. The first case is that of a 57-year-old man who because of chronic severe angina was placed on 2 per cent nitroglycerin ointment 1 inch application every 4 hours one week prior to admission for coronary angiography. Beginning about five days prior to admission, this man, who had never had any previous symptoms of congestive heart failure, began to note the onset of pedal edema for the first time. By the time of admission, his house physicians noted new 3+ edema of his right leg, the source of a saphenous vein for earlier coronary artery bypass grafting, and l-2+ edema of his left leg, and initially felt that he had developed congestive failure. Closer examination, however, revealed no other evidence of right or left heart failure. The edema resolved easily with diuretic therapy. Later therapy with nitroglycerin ointment 1% inches application every 4 hours plus hydrochlorothiazide 50 mg. by mouth every day resulted in no further edema. The second case is that of a 56-year-old man with chronic biventricular failure secondary to diffuse coronary disease with diffuse left ventricular hypokinesis, mitral regurgitation, and an elevated left ventricular end-diastolic pressure of 25, demonstrated by catheterization in 1975. Since that catheterization, he has had several admissions for control of his congestive heart failure, the last being in February, 1977, at which time measurements via a balloon-tipped thermistor catheter revealed a cardiac index (C.I.) of 1.4 and pressures as follows: right ventricle 60/23, pulmonary artery 60134, and mean pulmonary capillary wedge (PCW) 33 mm. Hg. He was initially treated with small doses of intravenous nitroprusside (0.75 pg./Kg./hr.) which resulted within 24 hours in a marked improvement in dyspnea associated with an improvement in his C.I. to 2.3 and PCW to 16. He was then switched to nonparenteral therapy and was eventually discharged on digoxin 0.125, furosemide 120 mg. twice a day, hydralazine 30 mg. four
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272
It is astonishing that Dr. Loeliger and associates build their assertion on this study alone, since only 12 of the patients with single aortic valves had received adequate anticoagulation. Dr. Loeliger and associates state that they very seldom see thromboembolic complications in patients with artificial heart valves. A better documentation of the intensity of the treatment, its antithrombotic effect, and the rate of bleeding complications would, however, be more valid. Finally, their assumption does not take into consideration the role of the platelets for the thrombotic process. While the dominant mechanism for venous thrombosis is plasma coagulation, platelet aggregation is important for the formation of arterial thrombi. Although adequate anticoagulation certainly is of some benefit, it does not affect the reactivity of the platelets. Therefore, arterial thrombosis on prosthetic aortic valves will most probably represent a problem even during very intensive anticoagulant therapy.
Jon Dale Institute for Thrombosis Research Rikshospitalet, Oslo 1 Norway REFERENCES 1.
2. 3.
4.
5.
6.
7.
8.
9.
10. 11.
More
Dale, J.: Arterial thromboembolic complications in patients with Starr-Edwards aortic ball valve prostheses, AM.HEART J. 91:653,1976. Owren, P. A.: Thrombotest: A new method for controlling anticoagulant therapy, Lancet 2:754, 1959. Cleland, J., and Molloy, P. J.: Thrombo-embolic complications of the cloth-covered Starr-Edwards prostheses no. 2300 aortic and no. 6300 mitral, Thorax 28:41, 1973. Friedli, B., Aerichide, N., Grondin, P., and Campeau, L.: Thromboembolic complications of heart valve prostheses, AM. HEART J. 81:702, 1971. Duvoisin, G. E., Wallace, R. B., Ellis, F. H., Andersson, M. W., and McGoon, D. C.: Late results of cardiac-valve replacement, Circulation 37 and 38 (Suppl. 11):75, 1968. Akbarian, M., Austen, W. G., Yurchak, P. M., and Scannell, J. G.: Thromboembolic complications of prosthetic cardiac valves, Circulation 37:826, 1968. Matloff, J. M., Collins, J. J., Sullivan, J. M., Gorlin, R., and Harken, D. E.: Control of thromboembolism from prosthetic heart valves, Ann. Thorac. Surg. 8:133, 1969. Reed, G. E., Claus+ R. H., Tice, D. A., and Acinapura, A. J.: Five-year experience with Magovern aortic prostheses, Circulation 43 and 44 (Suppl. 1):73, 1971. Bjbrk, V. O., Henze, A., and Holmgren, A.: Five years experience with the Bjerk-Shiley tilting disc valve in isolated aortic valvular disease, J. Cardiovasc. Surg. 16:451, 1975. Dale, J., and Myhre, E.: Platelet functions in patients with aortic ball valves, AM. HEART J. 94:359, 1977. Lam-PO-Tang, P. R. L. C., and Potter, L.: Oral anticoagulant therapy and its control: An international survey, Thromb. Diath. Haemorrh. 34:419, 1975.
on high
school
health
curricula
To the Editor: I was relieved to discover that the problem of an inadequate and inappropriate high school health curricula was at last cited by Dr. Mroczek in the AMERICAN HEART JOURNAL." I would lie to add three points to his editorial.
February, 1978,Vol. 95, No. 2
Letters to the Editor My first point is to label high school health textbook material as also being inadequate and inappropriate. If you will observe the contents of most high school (and some college) health texts, you will discover an imbalance in subject matter favoring subjects other than cardiovascular disease and cancer. The one thing that I can remember from my high school health education is the proper procedure for brushing my teeth. Cardiovascular disease was not even mentioned in high school curriculum at this time (early 1960’s). I believe high school health care texts should be joint-authored by the physician, exercise physiologist, and health educator alike. My second point is more specific to my own profession. High school physical education classes are often an unstructured and non-educational experience. Inappropriate curricula is the culprit here as well. Overemphasis on superior athletic performance, body physique, and non-dynamic forms of exercise have been the rule rather than the exception. Cardiovascular endurance types of exercises and recreation should be at least 60 per cent of the emphasis. If secondary school curriculum specialists would just wake up and start reading even a portion of current medical literature relating to exercise physiology, the problem would be partially solved. Finally, my last point is what I believe to be the crux of the problem. The training of health educators at the college level is far out of line. Speaking from my own experiences, some of the nation’s largest and supposedly most prestigious universities are the most misaligned with regard to the training of secondary school health educators. Regardless of how well we improve college-level health education textbooks, we still see the type of professor who remains bolted to a few 40-year-old ideas. I’m speaking specifically about neglecting to teach lifelong cardiovascular endurance exercise habits and how they frequently have a positive effect on CHD-related risk factors. Nearly every significant piece of research that has been published in the last 6 years has been either ignored or is contrary to what is presently taught in many high school physical education classes. There is no excuse for ignorance regarding the proper forms of exercise when you consider the availability of current publications.‘-’ My suggestion is that we re-educate some of the professors who are responsible for instilling (or not instilling) health care information into our secondary health education teachers. One step further-evaluate the chairmen of university health, physical education, and recreation departments.
Ralph L. LaForge, M.&Y. Physiologist Lovelace-Bataan Medical Center Preventive Medicine 5400 Gibson Blvd. SE Albuquerque, N. M. 87108 REFERENCES Committee on Exercise, American Heart Association: Exercise testing and training of apparently healthy individuals, New York, 1972, American Heart Association, pp. l-6, 40. American College of Sports Medicine: Guidelines for graded exercise testing and exercise prescription, Philadelphia, 1975, Lea & Febiger, Publishers, pp. 28-49. Pollock, M.: The quantification of endurance training programs, in Exercise and sport sciences reviews, vol. 1, Wilmore, J., ed., New York, 1973, Academic Press, Inc., pp. 155-182.
American Heart Journal
4.
5.
6.
7. 8.
Fox, S. M., Naughton, J. P., and Gorman, P. A.: Physical activity and cardiovascular health: the exercise prescription, Mod. Concepts. Cardiovasc. Dis. 41:6, 1972. Astrand, P. O., and Rodahl, K.: Textbook of work physiology, New York, 1977, McGraw-Hill Book Company, Inc., chapters 12, 16, and 17. Matthews, D. K., and Fox, E. L.: The physiological basis of physical education and athletics, 2nd ed., Philadelphia, 1976, W. B. Saunders Company, section 4 and chapter 21. Cooper, K. H., et al.: Physical fitness levels vs. selected coronary risk factors, J. A. M. A. 236:166, 1976. Mroczek, W. J.: High school health curricula: A neglected medical resource, AM. HEART J. 92:271, 1976.
Nitroglycerin
ointment
therapy
and
leg edema
To the Editor: Topically applied nitroglycerin ointment has been well demonstrated to have a sustained vasodilatory effect?’ and therefore its use has become fairly commonplace in the chronic therapy of angina pectoris and congestive heart failure. It has also been demonstrated that the major vasodilatory action of nitroglycerin is on the venous circulation,“-’ resulting in a reduction in venous return and left ventricular filling pressure (preload). I have recently observed two cases in which the onset of gross lower extremity edema followed within one week the institution of nitroglycerin ointment therapy. The first case is that of a 57-year-old man who because of chronic severe angina was placed on 2 per cent nitroglycerin ointment 1 inch application every 4 hours one week prior to admission for coronary angiography. Beginning about five days prior to admission, this man, who had never had any previous symptoms of congestive heart failure, began to note the onset of pedal edema for the first time. By the time of admission, his house physicians noted new 3+ edema of his right leg, the source of a saphenous vein for earlier coronary artery bypass grafting, and l-2+ edema of his left leg, and initially felt that he had developed congestive failure. Closer examination, however, revealed no other evidence of right or left heart failure. The edema resolved easily with diuretic therapy. Later therapy with nitroglycerin ointment 1% inches application every 4 hours plus hydrochlorothiazide 50 mg. by mouth every day resulted in no further edema. The second case is that of a 56-year-old man with chronic biventricular failure secondary to diffuse coronary disease with diffuse left ventricular hypokinesis, mitral regurgitation, and an elevated left ventricular end-diastolic pressure of 25, demonstrated by catheterization in 1975. Since that catheterization, he has had several admissions for control of his congestive heart failure, the last being in February, 1977, at which time measurements via a balloon-tipped thermistor catheter revealed a cardiac index (C.I.) of 1.4 and pressures as follows: right ventricle 60/23, pulmonary artery 60134, and mean pulmonary capillary wedge (PCW) 33 mm. Hg. He was initially treated with small doses of intravenous nitroprusside (0.75 pg./Kg./hr.) which resulted within 24 hours in a marked improvement in dyspnea associated with an improvement in his C.I. to 2.3 and PCW to 16. He was then switched to nonparenteral therapy and was eventually discharged on digoxin 0.125, furosemide 120 mg. twice a day, hydralazine 30 mg. four
273