LETTERS

diabetics despite the control of the blood sugar level. Possibly Somatostatin, a naturally occurring growth hormone,g recurrent hypoglycemia, or some unknown factors might be incriminated. “(.j) Genetics: Most agree that genetics play a major role in the arteriosclerotic process. Now that genetic engineering seems possible, major research into the relationship of genetics and heart disease is vitally needed.” We would hope that Dr. Blackburn would see this not as “sniping” and not just as “an all-pervasive dream,” but as a simple necessity, and that he would join those of us who, like Dr. Whereat, are looking toward new vistas. EliotCorday, MD, FACC Stephen

R. Corday,

MD

Cedars-Sinai

Medical Center

Los Angeles,

California

References 1. Corday E. Corday SR: Prevention of heart disease by control of risk factors: the time 2. 3. 4. 5. 6.

7. 6. 9.

has cane to face the facts. Am J Cardiol 35330-333. 1975 The Coronary Drug Project Research Group: The coronary drug project. JAMA 226: 652-657, 1973 The Coronary Drug Project Research Group: Clofibrate and niacin in coronary artery disease. JAMA 231:360-361, 1975 Immunological start to atherosclerosis? Lancet 1:206. 1975 Whlttlngham S, Mackay IR: Autoimmune mechanisms in human vascular disease. Lancet 21423, 1974 Meller J. Conde CA, Depplsch LM, et al: Myocardial infarction due to coronary atherosclerosis in three young adults with systemic lupus eryihematosus. Am J Cardiol 55309-314. 1975 Haust MD, More RH, Movat HZ: The role Of smooth muscle cells in the fibrcgenesis of arteriosclerosis. Am J Pathol 37:377-369. 1960 Spaet TH: Optimism in the control of atherosclerosis. N Engl J Med 291:576-577, 1974 Lundbaek K: Diabetic angiopathy. Mod Concepts Cardiovasc Dis 43:103-107. 1974

onstrated by coronary angiography. In paired samples at rest the arterial lactate was 8.50 mg/IOO ml and coronary sinus lactate 8.65 mg/lOO ml, indicating myocardial lactate production (extraction -2 percent). After the administration of atropine the arterial lactate was 7.05 mg/lOO ml and the coronary sinus lactate 6.50 mg/lOO ml, indicating lactate extraction (extraction +8 percent). Case 2: A 45 year old woman with atypical chest pain had a normal electrocardiogram at rest and on effort sufficient to produce a heart rate of 160 beats/min. Coronary angiography was not performed, but she was not considered to have ischemic heart disease. Resting arterial lactate was 5.50 mg/lOO ml and coronary sinus lactate 5.20 mg/lOO ml, (extraction + 5 percent). After administration of atropine (0.6 mg), arterial lactate was 5.70 mg/lOO ml and coronary sinus lactate 4.85 mg/lOO ml (extraction + 15 percent). Although it is difficult to suggest a mechanism for a possible effect of atropine in increasing myocardial lactate extraction in normal and diseased hearts, we believe that this possibility exists, and that the common practice of administrating atropine before or during pacing would be better replaced by the insertion of a separate pacing catheter into the right ventricle if block occurs. G. L. Jennings, MRCP P. H. Kidner, MRCP Department

of Cardiology

St. Mary’s Hospital London, England Reference

IDENTIFYING

PROPRANOLOL

1. Boudoulas H, Cobb TC, Lelghton RF, ei al: Myocardial lactate production in patients with angina-like chest pain and angiographically normal coronary arteries and left ventricle. Am J Cardiol 34:501-505. 1974

USERS

As physicians and cardiologists we are sensitive to the very important hemodynamic effects that are accomplished with propranolol. Unfortunately, the patient is not always fully aware of the extent to which this drug may mask various physiologic stresses to the cardiovascular system. Moreover, as a result of accident or acute illness he may be unable to communicate the fact that he is under the influence of this drug. I therefore urge all my patients to carry a card or some other form of identification indicating that they are receiving this drug. I recommend that other physicians follow a similar program with their patients. Morton A. Goldmann, Skokie.

MYOCARDIAL

LACTATE CORONARY

MD, FACC

Illinois

IN PATIENTS

WITH

NORMAL

ARTERIES-l

Boudoulas et al.’ in their article on myocardial lactate production in patients with angiographically normal coronary arteries have provided useful information on a difficult group of patients. However, we suggest that the use of atropine in some patients in their study, those in whom Wenckebach conduction developed, might have affected myocardial lactate production, which could obscure pacing-induced changes. We have studied two patients who had sampling catheters placed in the coronary sinus and left ventricle. Samples were taken from both the left ventricle and coronary sinus for analysis of lactate, before and after the intravenous administration of atropine (0.6 mg). Case 1: A 51 year old man with angina at rest and a left ventricular aneurysm, had severe three vessel disease dem-

REPLY

Drs. Jennings and Kidner, on the basis of findings in only two patients, suggest that atropine given intravenously may affect myocardial lactate production. However, one cannot be sure that they had stable arterial lactate levels throughout their sampling period as we required of our patients. Many of our patients who did not produce lactate received atropine without any noticeable effect on lactate extracti0n.l In addition, lactate extraction seemingly improved in their patients, which would be the opposite response to that observed in our patients who produced lactate with pacing. Concerning their argument for right ventricular pacing in order to avoid administering atropine, our experience in the study groups of patients was different. Right ventricular pacing was performed in four of our patients but a decrease in left ventricular pressure, due to loss of atria1 systole and dysenergy of contraction, made the induction of chest pain more difficult despite the fast heart rates. Harisios Boudoulas,

MD, FACC

Division of Cardiology Ohio State University Columbus,

MYOCARDIAL

LACTATE

IN PATIENTS

CORONARY

Hospitals

Ohio

WITH

NORMAL

ARTERIES-II

Boudoulas et al.’ reported a midsystolic click in three, and a mid-systolic murmur in one patient in the group produc-

March 4, 1976

The American

Journal

of CARDIOLOGY

Volume

37

453

Letter: Identifying propranolol users.

LETTERS diabetics despite the control of the blood sugar level. Possibly Somatostatin, a naturally occurring growth hormone,g recurrent hypoglycemia,...
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