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The etiology of arteriosclerosis
Volume Number
84 4
Letters to the Editor
heart rate, pericardial chamber size, or shape to provide the conditions we propose to be necessary in most cases of electrical alternans. The case Dr. Spodick cites from his 1968 article showed electrical alternans with a small pericardial volume. It is intriguing to note that this case also showed adhesions around the great vessels in the basal portions of the pericardium which would shorten the radius of the pendulum and therefore probably decrease the volume needed to provide the motion we associate with electrical alternans. Fig. 3 of the quoted 1962 article shows the cardiogram of a patient with atria1 fibrillation, but we would not agree that it demonstrates “strict 2:l Obviously there are unanswered quesalternation.” tions in pericardial tamponade and we hope that this discussion stimulates continued investigations into these problems. The use of cardiac echography in such cases should help confirm or deny our hypotheses. The demonstration of electrical alternans in the absence of the oscillatory motion displayed in our article would certainly make us revise our conclusions. We will look forward to continued personal discussions with Dr. Spodick in order to draw on his vast experience in this topic. Bruce
The
W. Usher,
etiology
M.D., Major (MC) USAR Brooke General Hospital Fort Sam Houston, Texas Richard L. PO@. M.D. Assistant Professor of Medicine Stanford University Stanford, Calg.
of arteriosclerosis
To the Editor: The annotation “The etiology of arteriosclerosis-a thought” which appeared in the March, 1972, issue of the AMERICAN HEART JOURNAL (83:434, 1972) is a refreshingly new approach for the clarification of the arteriosclerotic process. Dr. Burch daringly brings back to focus the possibility of a more fundamental pathogenetic process of endothelial cell injury and death as an initial step in atherogenesis and subsequent deposition of lipids and calcium. In view of recent knowledge of cell membranes’s2 and the active transport of electrolytes and water requiring expendit;re of energy in the form of ATP. Dr. Burch does not have to struerrle -to look for a virus particle under each atherosclerotic patch. The mere interference with optimum supply and utilization of the ATP and ATPase enzyme system of the membranes will interfere with the sodiumpotassium pump, thus allowing sodium and calcium to accumulate intracellularly, water to passively follow, and potassium to leak out-thus causing swelling of the cells. If the process reaches a point of no return, cell injury will terminate in cell death, thus providing the nidus for the deposition of lipids and calcium. Most, if not all of the factors associated with coronary disease can interfere through different metabolic ways with the sodium and potassium pump, causing cell swelling. Also, a derangement of intraand extracellular ionic balance can
575
explain better the absolute increase of coronary disease in the younger age group in highly competitive societies through stress and endocrine hypersecretion. The patchy nature and the erratic patterns of arteriosclerotic plaques suggest that all these contributing factors (including possibly virus infections) at one time, or several of the factors at different times, cause the initial damage through one common final pathway-interference with the sodium-potassium pump, cell swelling, and eventual death. This concept of pathogenesis of the disease is not new. Leaf,3 in an editorial in the American Journal of Medicine, suggests cell swelling and death as the initial process in vessel disease. However, up to now more superficial and dramatic approaches to the over-all coronary problem have unfortunately been given priority (venous bypass graft, artificial pumps, heart transplantation, etc.) and have captured the imagination of the researchers and diverted vital research money to very questionable solutions. Hopefully, with the present available knowledge, research will be directed toward cell swelling and death as an initial triggering mechanism. If the above pathogenetic concept is verified, coronary atherosclerosis may become a preventable disease. Sarko M. Tilkiaz, N.D. Granada Medical Arts Center 10660 White Oak Ave. Granada Hills, Calif. 913-W REFERENCES Bittar, E. E., editor: Membranes and ion transport, Vols. 1-3, New 7iork, 1970-71, John Wiley & Sons, Inc. Richter, G. W., and Scarpelli, D. G.: Cell membranes, biological and pathological aspects, Baltimore, 1971, The Williams & Wilkins Company. Leaf, A.: Regulation of intracellular fluid volume and disease, Am. J. Med. 49:291, 1970.
Fascicular blocks vs. left ventricular hypertrophy To the Editor: When is a cat not a cat? The answer to this is whenever a cat is a lion or a tiger or any other member of the cat family other than the common house cat. Dr. Ray Pryo;, in his very excellent editorial entitled “Fascicular blocks and the bilateral bundle branch block syndrome” which appeared in the April issue of thd AMERICAN HEART-JOURNAL (83: 441. 1972). , has an examole of what he calls “anterior fascicular block” in F’ig. 1. To my eye this is a classical electrocardiographic example of left ventricular hypertrophy in a 30-year-old man with aortic regurgitation. It is now becoming very popular to call every electrocardiographic phenomenon that has a left axis deviation either left anterior fasciculnr block, left anterior hemiblock, or the like. \I’e can therefore rephrase my original question about the cats by asking “When is a left anterior fascicular block not
84 4
Letters to the Editor
heart rate, pericardial chamber size, or shape to provide the conditions we propose to be necessary in most cases of electrical alternans. The case Dr. Spodick cites from his 1968 article showed electrical alternans with a small pericardial volume. It is intriguing to note that this case also showed adhesions around the great vessels in the basal portions of the pericardium which would shorten the radius of the pendulum and therefore probably decrease the volume needed to provide the motion we associate with electrical alternans. Fig. 3 of the quoted 1962 article shows the cardiogram of a patient with atria1 fibrillation, but we would not agree that it demonstrates “strict 2:l Obviously there are unanswered quesalternation.” tions in pericardial tamponade and we hope that this discussion stimulates continued investigations into these problems. The use of cardiac echography in such cases should help confirm or deny our hypotheses. The demonstration of electrical alternans in the absence of the oscillatory motion displayed in our article would certainly make us revise our conclusions. We will look forward to continued personal discussions with Dr. Spodick in order to draw on his vast experience in this topic. Bruce
The
W. Usher,
etiology
M.D., Major (MC) USAR Brooke General Hospital Fort Sam Houston, Texas Richard L. PO@. M.D. Assistant Professor of Medicine Stanford University Stanford, Calg.
of arteriosclerosis
To the Editor: The annotation “The etiology of arteriosclerosis-a thought” which appeared in the March, 1972, issue of the AMERICAN HEART JOURNAL (83:434, 1972) is a refreshingly new approach for the clarification of the arteriosclerotic process. Dr. Burch daringly brings back to focus the possibility of a more fundamental pathogenetic process of endothelial cell injury and death as an initial step in atherogenesis and subsequent deposition of lipids and calcium. In view of recent knowledge of cell membranes’s2 and the active transport of electrolytes and water requiring expendit;re of energy in the form of ATP. Dr. Burch does not have to struerrle -to look for a virus particle under each atherosclerotic patch. The mere interference with optimum supply and utilization of the ATP and ATPase enzyme system of the membranes will interfere with the sodiumpotassium pump, thus allowing sodium and calcium to accumulate intracellularly, water to passively follow, and potassium to leak out-thus causing swelling of the cells. If the process reaches a point of no return, cell injury will terminate in cell death, thus providing the nidus for the deposition of lipids and calcium. Most, if not all of the factors associated with coronary disease can interfere through different metabolic ways with the sodium and potassium pump, causing cell swelling. Also, a derangement of intraand extracellular ionic balance can
575
explain better the absolute increase of coronary disease in the younger age group in highly competitive societies through stress and endocrine hypersecretion. The patchy nature and the erratic patterns of arteriosclerotic plaques suggest that all these contributing factors (including possibly virus infections) at one time, or several of the factors at different times, cause the initial damage through one common final pathway-interference with the sodium-potassium pump, cell swelling, and eventual death. This concept of pathogenesis of the disease is not new. Leaf,3 in an editorial in the American Journal of Medicine, suggests cell swelling and death as the initial process in vessel disease. However, up to now more superficial and dramatic approaches to the over-all coronary problem have unfortunately been given priority (venous bypass graft, artificial pumps, heart transplantation, etc.) and have captured the imagination of the researchers and diverted vital research money to very questionable solutions. Hopefully, with the present available knowledge, research will be directed toward cell swelling and death as an initial triggering mechanism. If the above pathogenetic concept is verified, coronary atherosclerosis may become a preventable disease. Sarko M. Tilkiaz, N.D. Granada Medical Arts Center 10660 White Oak Ave. Granada Hills, Calif. 913-W REFERENCES Bittar, E. E., editor: Membranes and ion transport, Vols. 1-3, New 7iork, 1970-71, John Wiley & Sons, Inc. Richter, G. W., and Scarpelli, D. G.: Cell membranes, biological and pathological aspects, Baltimore, 1971, The Williams & Wilkins Company. Leaf, A.: Regulation of intracellular fluid volume and disease, Am. J. Med. 49:291, 1970.
Fascicular blocks vs. left ventricular hypertrophy To the Editor: When is a cat not a cat? The answer to this is whenever a cat is a lion or a tiger or any other member of the cat family other than the common house cat. Dr. Ray Pryo;, in his very excellent editorial entitled “Fascicular blocks and the bilateral bundle branch block syndrome” which appeared in the April issue of thd AMERICAN HEART-JOURNAL (83: 441. 1972). , has an examole of what he calls “anterior fascicular block” in F’ig. 1. To my eye this is a classical electrocardiographic example of left ventricular hypertrophy in a 30-year-old man with aortic regurgitation. It is now becoming very popular to call every electrocardiographic phenomenon that has a left axis deviation either left anterior fasciculnr block, left anterior hemiblock, or the like. \I’e can therefore rephrase my original question about the cats by asking “When is a left anterior fascicular block not