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Vitamin therapy for infarction
LETTERS TO THE EDITOR
brillation or severe and long-standing idiopathic hypertrophic subaortic stenosis, left atria1 enlargement is puzzling. Obviously, additional studies are necessary to ascertain the sensitivity and specificity of this echocardiographic sign. At this time, the exact mechanism of early systolic closure of the aortic valve in patients with idiopathic hypertrophic subaortic stenosis has not been determined. However, our preliminary results, along with the findings of others, suggest that early aortic valve closure is directly related to the presence of a significant left ventricular outflow tract gradient. Zvonimir Krajcer, MD Leonard W. Pechacek Efrain Garcia, MD, FACC Robert D. Leachman, MD, FACC St. Luke’s Episcopal Hospital Houston, Texas References 1. Glawr J: M&systolic AV clousre in IHSS. Circulation 51: 1172. 1975 2. Roughnor OR, Scfwld RL, Pnsaud JA: Hypertrophic obstructive cardiomyopathy: assessment by echocardiographic and Doppler ultrasound techniques. Br Heal J 37: 917-923.1975 3. Felge”baum H: Echocardiogaphy, second edition. Philadelphia, Lea 8 Febiger. 1976, p 161
VITAMIN THERAPY
Govkr Ww: The effect of experimental coronary artery liitlon o” the cwnryme I and cocarboxylasa content of the myocardium of the dog. Am Heart J 29:364-369.1945 WH, of aI: Metabolic changes in heart muscle dwlng Mkhal 0, Naogk S, GMorlh anoxia. Am J Fhysiol 197:1147-1151, 1959 Cafva E, M6jka A, tiz R. @I al: MltochoMrk I biiical changes and glucose-KCl solution in cardiac infarct. Am J physiol211:71-76. 1966 Dohwtv JE: Tfwrv of mvoowdial infarction and cwonarv Mart disease. In. Braln and tieart infarct (Z&h KJ,- Kauhna”” W. Hossmann KA: Hossrna”” v. ed). Serlln. Springer-Veriag. 1977, p 323-331
FEVER AS A MANIFESTATION OF DISSECTING ANEURYSM OF AORTA
Although the protean clinical manifestations of dissecting aneurysms have been repeatedly emphasized,’ fever is an occasional feature of this disorder that, if not recognized as such, may lead the clinician to an unnecessary and frequently dangerous diagnostic pursuit of illnesses more commonly associated with a febrile response.2,3 We report a case of aortic dissection associated with fever in which surgical intervention was delayed because the patient was initially thought to have bacterial endocarditis. Case Report A 51 year old man was in excellent health until December 1977, when he experienced severe, sharp, anterior chest pain that did not radiate and was associated with marked dyspnea and weakness. These complaints persisted for approximately
FOR INFARCTION
The recent work of NGfiez et al.ls2 has shown that one of the significant biochemical events in experimental myocardial infarction is the loss of pyridine nucleotide, brought about through activation of the enzyme NAD glycohydrolase. Although the mechanism of NAD glycohydrolase activation is unknown, the depletion of NAD+ from the infarcted area,3,4 especially from the mitochondria,5 would explain the decreased ability of the affected tissue to engage in oxidative phosphorylation, the principal source of adenosine triphosphate (ATP) in the heart. As long as NAD+ remains depleted, ATP synthesis will continue to be impaired, even though normal oxygen tension is restored. The reason is that most of the dehydrogenases responsible for oxidation of citric acid cycle intermediates require NAD+ as an essential cofactor. These considerations indicate the desirability of intervening to prevent the undue loss of NAD+ during infarction. This may be achieved through administration of nicotinamide, which inhibits NAD glycohydrolase and is also a biosynthetic precursor of NAD+. It is already known that injection of nicotinamide prior to experimental infarction leads to the preservation of myocardial NAD +.3 Thus, immediate treatment with nicotinamide would appear to be of obvious benefit, although prolonged treatment may be better accomplished with nicotinic acid, which is not as readily converted to excretory products. Nicotinamide and nicotinic acid are not now recognized for their therapeutic value in myocardial infarction.6 However, the cited experimental evidence suggests that clinical trials, at least on a limited scale, would be well merited. Carl Bernofsky, PhD Department of Biochemistry Tulane University School of Medicine New Orleans, Louisiana References 1. NGiazR,Calva
E, Marrch M, el al: NAD glycohydrolase activity in hearts with acute experi~ntal infarctkn. Am J Physiol231:1173-1177. 1976 2. HiiwzR,Cslv~E,afrrmE,~al:Nicotinamidecoennlmesinheartandawoneryblood during myocardial infarction. Am J Physiol 226:73-76. 1974
FfGURE 1. Angiogram demonstrating the long dissection. seen here along tha descending aorta and coursing over the aortic arch.
September 1979
The American Journal of CARDIOLOQY
Volume 44
551
brillation or severe and long-standing idiopathic hypertrophic subaortic stenosis, left atria1 enlargement is puzzling. Obviously, additional studies are necessary to ascertain the sensitivity and specificity of this echocardiographic sign. At this time, the exact mechanism of early systolic closure of the aortic valve in patients with idiopathic hypertrophic subaortic stenosis has not been determined. However, our preliminary results, along with the findings of others, suggest that early aortic valve closure is directly related to the presence of a significant left ventricular outflow tract gradient. Zvonimir Krajcer, MD Leonard W. Pechacek Efrain Garcia, MD, FACC Robert D. Leachman, MD, FACC St. Luke’s Episcopal Hospital Houston, Texas References 1. Glawr J: M&systolic AV clousre in IHSS. Circulation 51: 1172. 1975 2. Roughnor OR, Scfwld RL, Pnsaud JA: Hypertrophic obstructive cardiomyopathy: assessment by echocardiographic and Doppler ultrasound techniques. Br Heal J 37: 917-923.1975 3. Felge”baum H: Echocardiogaphy, second edition. Philadelphia, Lea 8 Febiger. 1976, p 161
VITAMIN THERAPY
Govkr Ww: The effect of experimental coronary artery liitlon o” the cwnryme I and cocarboxylasa content of the myocardium of the dog. Am Heart J 29:364-369.1945 WH, of aI: Metabolic changes in heart muscle dwlng Mkhal 0, Naogk S, GMorlh anoxia. Am J Fhysiol 197:1147-1151, 1959 Cafva E, M6jka A, tiz R. @I al: MltochoMrk I biiical changes and glucose-KCl solution in cardiac infarct. Am J physiol211:71-76. 1966 Dohwtv JE: Tfwrv of mvoowdial infarction and cwonarv Mart disease. In. Braln and tieart infarct (Z&h KJ,- Kauhna”” W. Hossmann KA: Hossrna”” v. ed). Serlln. Springer-Veriag. 1977, p 323-331
FEVER AS A MANIFESTATION OF DISSECTING ANEURYSM OF AORTA
Although the protean clinical manifestations of dissecting aneurysms have been repeatedly emphasized,’ fever is an occasional feature of this disorder that, if not recognized as such, may lead the clinician to an unnecessary and frequently dangerous diagnostic pursuit of illnesses more commonly associated with a febrile response.2,3 We report a case of aortic dissection associated with fever in which surgical intervention was delayed because the patient was initially thought to have bacterial endocarditis. Case Report A 51 year old man was in excellent health until December 1977, when he experienced severe, sharp, anterior chest pain that did not radiate and was associated with marked dyspnea and weakness. These complaints persisted for approximately
FOR INFARCTION
The recent work of NGfiez et al.ls2 has shown that one of the significant biochemical events in experimental myocardial infarction is the loss of pyridine nucleotide, brought about through activation of the enzyme NAD glycohydrolase. Although the mechanism of NAD glycohydrolase activation is unknown, the depletion of NAD+ from the infarcted area,3,4 especially from the mitochondria,5 would explain the decreased ability of the affected tissue to engage in oxidative phosphorylation, the principal source of adenosine triphosphate (ATP) in the heart. As long as NAD+ remains depleted, ATP synthesis will continue to be impaired, even though normal oxygen tension is restored. The reason is that most of the dehydrogenases responsible for oxidation of citric acid cycle intermediates require NAD+ as an essential cofactor. These considerations indicate the desirability of intervening to prevent the undue loss of NAD+ during infarction. This may be achieved through administration of nicotinamide, which inhibits NAD glycohydrolase and is also a biosynthetic precursor of NAD+. It is already known that injection of nicotinamide prior to experimental infarction leads to the preservation of myocardial NAD +.3 Thus, immediate treatment with nicotinamide would appear to be of obvious benefit, although prolonged treatment may be better accomplished with nicotinic acid, which is not as readily converted to excretory products. Nicotinamide and nicotinic acid are not now recognized for their therapeutic value in myocardial infarction.6 However, the cited experimental evidence suggests that clinical trials, at least on a limited scale, would be well merited. Carl Bernofsky, PhD Department of Biochemistry Tulane University School of Medicine New Orleans, Louisiana References 1. NGiazR,Calva
E, Marrch M, el al: NAD glycohydrolase activity in hearts with acute experi~ntal infarctkn. Am J Physiol231:1173-1177. 1976 2. HiiwzR,Cslv~E,afrrmE,~al:Nicotinamidecoennlmesinheartandawoneryblood during myocardial infarction. Am J Physiol 226:73-76. 1974
FfGURE 1. Angiogram demonstrating the long dissection. seen here along tha descending aorta and coursing over the aortic arch.
September 1979
The American Journal of CARDIOLOQY
Volume 44
551