LETTERS

Our experience with stenosis of internal mammary artery grafts is cited in the article. In the entire series, only two pa- tients who were restudied had stenotic graft anastomosis. We doubt that internal mammary artery anastomosis, properly performed, is associated with late anastomotic occlusion. Thus far, 27 patients have had more than one postoperative an- giogram and none had a late stenosis.

In our entire experience through 1976, a total of 1,114 in- ternal mammary artery grafts have been restudied after an average interval of 14 months; the patency rate is 96.2 percent. As stated clearly in the article, the improved survival in the series cannot be attributed solely to the internal mammary artery graft. Better criteria for patient selection, technical improvements, more complete revascularization and a smaller incidence of perioperative infarction are factors that have contributed to the improved results over the years. None- theless, improved patency with the internal mammary artery graft cannot be ignored and may indeed contribute to the fa- vorable evolution of bypass graft operations.

Floyd D. Loop, MD, FACC William C. Sheldon, MD, FACC Department of Thoracic and Cardiovascular Surgery The Cleveland Clinic Foundation Cleveland, Ohio

A-V BLOCK IN PRINZMETAL’S ANGINA

Bharati et al.’ write that transient atrioventricular (A-V) block during attacks of Prinzmetal’s angina has been well docu- mented and that electrocardiograms have suggested an A-V junctional block in all published cases but one, reported by Bodenheimer et al2 In our opinion the exception ought not to be considered so. Indeed, in that case the QRS complex during the A-V block was of the supraventricular type and, in the absence of a His bundle recording, it seems logical to suppose that the block occurred at A-V node.

Actually A-V block, when it is related to anginal attacks as in Prinzmetal’s angina, always occurs at the A-V junction and cannot occur in the distal portion of the conduction system.3 This portion has multiple vascularization provided by both the anterior and the posterior descending arteries so that a widespread disturbance of blood supply is necessary for the onset of an A-V block and the conduction defect never occurs without a concurrent extensive septal myocardial infarction. On the contrary, the block during angina1 attacks always oc- curs at the A-V node because this structure is highly sensitive to ischemia4 and is more vulnerable because it is supplied by a single vessel, the arteria “septi fibrosi.” The arteria arises from the vessel that inferiorly crosses the crux cordis and therefore, in PrinzmetaI’s angina, which is generally associated with active disease of a single coronary artery, A-V block al- most constantly appears when angina affects the inferior wall of the heart. This rule3 that the A-V block in angina1 attacks always occurs at A-V node is not invalidated by the rare cases5 in which the block complicates an angina affecting the anterior wall of the heart. Indeed also in these cases in which an un- common blood supply of A-V node must be supposed, the QRS complex is of the supraventricular type.

Do Bharati et al. agree with our rule? PierFilippo kzzini, MD Francesco Marchi, MD Department of Cardiology Arcispedale Santa Maria Nuova Florence, Italy

References

1. Bharatl S, Dhingra RC, Lev M, et al: Conduction system in a patient with Prinrmetal’s angina and transient atrioventricular block. Am J Cardiol39:120-125. 1977

2. Bodenhelmer M. LIpskI J, Danoao E, et al: Prinzmetal’s variant angina: a clinical and electrocardiogreph~c study. Am Heart J 87:304-313. 1974

3. Dolara A, Fazzlni PF, March1 F. el al: Transient atrioventricular block in variant form of angina pectoris. Acta Cardiol 28~314-322, 1973

4. Siuckey JM, Hofhnan BF: Direct studies of the in situ special&xl conducting system. In. The Soecialised Tissues of ilw Heart. Amsterdam. Elsevier. 1961

5. B&u A, !&gnac A. Bcusga M: The variant form of angina: diagnostic and therapeutic implications. Am Heart J 87:272-278. 1974

REPLY

There is not enough information reported by Bodenheimer and co-workers concerning the patient in question (Patient 2), to draw a strong conclusion regarding site of A-V block. The patient had ventricular tachycardia and one blocked P wave during an episode of Prinzmetal’s angina. Careful scrutiny of the blocked P wave (Fig. 3 of their paper), reveals conducted P waves with a narrow QRS complex before and after the one blocked P wave, with a slight decrease in the P-R interval after the block. This observation is consistent with A-V nodal block. Because of the presence of ventricular arrhythmia, it is also conceivable that the blocked P wave reflected pseudo A-V block secondary to a concealed ventricular ectopic beat.1*2

We agree with Fazzini and Marchi that A-V block compli- cating anginal attacks is usually of A-V nodal origin. However, it is conceivable to us that transient ischemia in the His bundle or trifascicular conduction system, or both, might also produce acute reversible block.3 The latter occurrence might be more likely in patients with preexistent conduction disease and obstructive coronary disease involving several coronary ar- teries, so that the ventricular septum with its overlying spe- cialized conduction system might be supplied by only one coronary vessel. Spasm of this vessel could trigger block at a site other than the A-V node.

Our experience in both electrophysiology and pathology makes us very hesitant about formulating rules. Almost as quickly as we formulate new rules, our co-workers in other laboratories (and sometimes we ourselves) find exceptions.

Kenneth M. Rosen, MD, FACC Saroja Bharati, MD, FACC Ramesh Dhingra, MD, FACC Maurice Lev, MD, FACC

References

Congenital Heart Disease Research and Training Center

Chicago, Illinois

1. Roaw KM, Rahlmloola BH, Bunnar RM: Pseudo A-V block secondary to premature nonpropagated His bundle depolarizations. Circulation 42367-373. 1970

2. Casteflanoa A., Bafale~ B, Yynbwg RJ: Pseudo AV block produced by concealed ex- basystoles arising below the bifurcation of the His bundle. Br Heart J 36:457-461, 1974

3. El-Bhwff N, Bchetlag BJ, Lazzara R. et al: The pathophysiology of tachycardia-de- pendent paroxysmal atrlovmtrkulw block after acute myocardial ischemia. Experimental and clinical observations. Circulatkm 501515-528. 1974

DOBUTAMINE IN ACUTE MYOCARDIAL INFARCTION

There are two possible errors in the report by Gillespie et al.’ on dobutamine in patients with myocardial infarction. The first occurs in the Methods section in which one of the criteria for entering the study is “pulmonary arterial occlusive pres- sure less than 10 mm Hg.” This statement is at odds with the statement in the Results section that the treated patients had a “significant decrease in pulmonary arterial occlusive pres-

March 1978 The Am&an Journal of CARWOLOGY Volume 4 1 821

LETTERS

sure (from 21.5 f 2.7 to 16.7 f 1.6 mm Hg).” These two statements are obviously mutually exclusive. The second is the stated criterion of the “cardiac index less than 2.7 liters/ min per m2.” In the Results the authors report “a significant increase in cardiac output (from 4.9 f 0.37 liters/min. . .) be- fore treatment to 6.0 f 0.38 liters/min. . . .” If the “standard” figure of body surface area of 1.73 m2 is used, then the mean cardiac index before treatment was 2.83 liters/min per m2, which is above the range stated as criterion for admission to the study.

Donald S. Ruffett, MD

References

Department of Medicine Hartford Hospital Hartford, Connecticut

1. Gillasple TA, Ambos HD, Bobel BE. et al: Effects of dobutamine in patients with acute myocardial infarction. Am J Cardiol 39566-594, 1977

REPLY

The values for pulmonary arterial occlusive pressure and cardiac index should indeed have read “10 mm Hg or more” and “2.7 liters/min or more” rather than “less than” those values. We regret the errors in notation.

Thomas A. Gillespie, MD H. Dieter Ambos Burton E. Sobel, MD, FACC Robert Roberts, MD, FACC Cardiovascular Division Department of Internal Medicine Washington University School of Medicine St. Louis. Missouri

OBESITY AND ISCHEMIC HEART DISEASE

The results of Rabkin et al.l leave no doubt that a higher body mass index is significantly associated with development of myocardial infarction, sudden death and coronary insuffi- ciency. However, I find their conclusion that “overweight is a definite risk factor” is not adequately proved by their data.

Definition requires that a risk factor must have a proved causal relation to the disease implied, and it seems to me that this is not fulfilled in the case of obesity and ischemic heart disease. The possibility exists that subjects who start to ex- perience the results of an early and slight coronary athero- sclerosis react with self-restriction with regard to physical activity, without admitting this to themselves. It is more than natural that someone who tires more easily than usual and experiences a slight shortness of breath or other indications that “‘he is not in a good physical shape” will react with a re- duced desire for sports and other physical activities and that this response will result in weight gain. Such a sequence of events has not been excluded by Rabkin et al. and therefore, although I fully accept their findings that a greater incidence of ischemic heart disease is found in obese subjects, I would like to add a word of caution to their conclusion that obesity is a “risk factor” in the development of coronary atheroscle- rosis.

Shlomo Stern, MD, FACC Hebrew University-Hadassah Medical School

and Shaare Zedek Hospital Jerusalem, Israel

1. Rabkla SW, Mathewson FAL, Hsu P: Relation of body weight to development of ischemic heart disease in a cohort of young North American men after a 26 year obsewation period: The Manitoba Study. Am J Cardiol 39:452-458. 1977

REPLY

The requirement for a causal relation is not part of the defi- nition of a risk factor in general usage:

1. “The coronary risk factors are those abnormali- ties-demonstrable in persons free of clinical CHD (coronary heart disease)“-known to be associated with significantly increased risk of developing the dis- ease in subsequent years.“’

2. “An attribute which appears to occur more com- monly among persons with coronary heart disease than control subjects is defined as a risk factor. It is implied in this particular definition that an association between the disease and a risk factor is not necessarily causal.‘12

3. “The risk factor concept in coronary heart disease (CHD) is based on the finding of statistically signifi- cant associations between incidence of CHD and values for the variables in question. Studies performed so far have not shown that any of the risk factors are ac- tually causative.“”

4. “Follow-up studies of persons judged to be free of CHD at entry examination have identified several characteristics associated with increased risk of CHD in future years. Age, arterial blood pressure and serum cholesterol concentration uniformly emerge as impor- tant risk factors.“4

5. “Epidemiological studies have shown a significant relationship between the incidence of CHD and various prospective characteristics commonly termed risk fac- tors.‘15 Finding an association is only one step in the proof of cau-

sation. We hoped that our finding of an association between body weight and ischemic heart disease would stimulate hy- potheses in this field and we are interested to read Stern’s. Although we have no evidence to support or refute his hy- pothesis that early coronary atherosclerosis limits physical activity, which in turn causes an increase in body weight, some comments are in order. The young age of our cohort at entry means that the coronary atherosclerosis would have had to exert its effects when these men were in their 20’s so that they would be overweight at entry. This and the fact that physical inactivity is one of many variables in the equation yielding overweight do not make this hypothesis attractive to us.

S. W. Rabkin, MD, FACC F. A. L. Mathewson, MD, FACC University of Manitoba Department of Medicine (Section Cardiology)

and Social and Preventive Medicine Winnipeg, Manitoba, Canada

References 1. Stemler J: Lectures on Preventive Cardiology. New York, Grune 8 Stranon. 1967, p

748 2. Epstein FHz The epidemiology of coronary heart disease. A review. J Chronic Dis 18:

735-774. 1965 3. Wllhelmeen L, We&l H, Tlbblns 0: Multivariate analysis of risk factors for coronary

hearl disease. Circulation 48:950-956. 1973 4. Keys A, Aravanls C, Blackburn H, et al: Probability of middle aged men developing

coronarv heart disease in five years. Circulation 45:815-628. 1972 5. Brand dJ, R-an RH. Bh& RI, et al: Multivariate prediction of coronary heart

disease in the Western Collaborative Group Study compared to the findings of the Framingham Study. Circulation 53:346-355. 1976

622 March 1976 The American Journal of CARDIDLDDY Volume 41