Letters
to the Editor
the rise in blood pressure following norepinephrine.6 Propranolol, apparently, not only prevents beta arteriolar dilatation but also displaces norepinephrine from beta receptors so that it becomes more concentrated at the alpha sites which cause arteriolar constriction. Although propranolol is commonly used in the treatment of hypertension, where it is thought to be helpful by lowering cardiac output, it increases the blood pressure under certain circumstances. It may precipitate a hypertensive crisis with pheochromocytoma6 by permitting unopposed alpha stimulation. In a diabetic it caused hypoglycemia with a secondary adrenergic response and extreme hypertension’ because alpha stimulation was not balanced by beta stimulation. A similar mechanism has been invoked to explain complete heart block (by vagal reflex) occurring when propranolol and epinephrine were given at the same time.s In addition, peripheral arterial insutllciency has been observed in patients taking propranolol,g giving further evidence of peripheral constriction. Finally, we wish to call attention to the decrease in sodium excretion which has been found with the use of propranolol.” This would tend to increase the blood volume and minimize the effect of peripheral vascular pooling as a factor in orthostatic hypotension. Frank Barth Theodore Lawrence, M. D. Veterans Administration Hospital and The Medical College of Pennsylvania Philadelphia, Pa. 19104
1. Wiggers, C. J.: Physiology in health and disease, 5th ed., Philadelphia, 1949, Lea & Febiger, p. 1124. 2. Wolf& L.: Clinical aspects of paroxysmal heart action, N. Engl. J. Med. 226:640, 1942. 3. Weiseler, A. M., Leonard, J. J., and Warren, J. V.: Effects of posture and a&pine on the cardiac output, J. Clin. Invest. 36:1656, 1957. 4. Epstein, S. E., and Braunwald, E.: Beta-adrenergic receptor blocking drugs, N. Engl. J. Med. 275:1106, 1966. 5. Glover, W. E., and Hutchinson, K. J.: The effect of a beta receptor antagonist (propranolol) on the cardiovascular response to intravenous infusions of noradrenaline in man, J. Physiol. 177:59P, 1965. 6. Prichard, B. N. C., and Ross, E. J.: Use of propranolol in conjunction with alpha receptor blocking drugs in pheochromocvtoma. Am. J. Cardiol. 18:394. 1966. 7. McMurtry, R.-J.: Propranolol, hypoglycemia; and hypertensive crisis, Ann. Intern. Med. 80:669, 1974. 8. Kram, J., et al.: Propranolol, Ann. Intern. Med. 80:282, 1974. 9. Frohlich, E. D., et al.: Peripheral arterial insufficiency, J.A.M.A. 208:2471,1969. 10. Nies, A. S., McNeil, J. S., and Schrier, R. W.: Mechanism of increased sodium reabsorption during propranolol administration, Circulation 44:596, 1971.
RePJY To the Editor: Doctors Barth and Lawrence have appropriately focused an important pharmacologic action of propranolol which may well have played a therapeutic role in the patient we re-
544
ported Indeed, I plead particular sin for our not having discussed this possibility, inasmuch as Doctors Luria, Kaplan, and I actually treated prolonged hypotension with a beta receptor blocking agent in 1964.’ We did discuss peripheral vasoconstrictor properties of beta blockers in that paper, and mentioned the possibility that neurotransmitter substance was displaced from beta to alpha sites in the periphery. In our recent paper, we perhaps did overly emphasize relief of the orthostatic tachycardia as the explanation for the patient’s subjective improvement. While I gladly accept the appropriate chastisement from Doctors Barth and Lawrence, I would like to again emphasize our major message. Namely, propranolol did effectively slow orthostatic tachycardia without adverse side effects Albert J. Miller, M.D. Northwestern Memorial Hospital Wesley Pavilion Superior St. and Fairbanks Ct. Chicago, Ill. 60611 REFERENCE
I.
Luria, M. H., Miller, A. J., and Kaplan, B. M.: Successful therapy of prolonged hypotension with an adrenergic beta-receptor blocking agent, Circulation 29:494, 1964.
lschemic ST segment depression and dyspnea To the Editor: The annotation entitled “Silent angina and coronary bypass surgery” by Dr. Burch in the October, 1974, issue of the JOURNAL(88:530,19741 emphasizes the absence of angina pectoris and chest discomfort, and the presence of dyspnea associated with ST-segment depression after a Master twostep test. This dyspnea manifested upon stress was quickly relieved by rest and sublingual nitroglycerin. Our experience with ambulatory 24-hour Holter recordings confirms the observation that ischemic ST-segment depression may present with the clinical symptom of dyspnea only. An illustrative case, J.M.J., a 57-year-old active male presented completely asymptomatic as a normal participant in a two channel 24-hour Holter recording protocol. Trend analysis revealed seven episodes of ischemic ST-segment depression encompassing a total time of 210 minutes, the most striking of which (Fig. 1) was precipitated by a brisk walk. Patient diary revealed no symptoms, and query of the patient within one hour of completion of the Holter recording ellicited, in retrospect, only the presence of mild dyapnea during the brisk walk. Treadmill testing utilizing the Bruce protocol was performed for 370 seconds reaching a maximal blood pressure of 154/80 mm. Hg and a maximal heart rate of 170 beats per minute with 4.5 mm. of ischemic ST-segment depression before being terminated with exertional hypotension accompanied by dyspnea. The patient denied angina pectoris or chest discomfort. Angiography revealed a 70 to 80 per cent narrowing of the left main coronary artery, 80 to 90 per cent narrowing of the proximal left anterior descending coronary artery, and a normal left ventricular ejection fraction of 58 per cent. Left ventricular end diastolic pressure was normal, and calcification was noted in the left main and proximal left anterior descending coronary arteries.
April,
1975, Vol. 89, No. 4
Letters
Fig 1, Left and Right. 9:21 P.M. a heart rate time sample print-out CBVs) lead.
Two channel Holter recordings. Left trend analysis print-out indicates at approximately (top) of 130 beats per minute and S-T level (bottom) depression of 3 to 4 mm. Rkht, real at 9:21 P.M. confirms 3 to 4 mm. of ischemic ST-segment depression in chest bipolar V,
“Silent” clinical symptoms associated with ST-segment depression,’ angina pectoris,2 or ischemic heart disease3 have received recent attention in the literature. Our observations’ are similar to that reported by Dr. Burch in identifying dyspnea without precordial or angina1 symptoms as being present in patients with concurrent ischemic ST-segment depression which is relieved by rest or sublingual nitroglycerin. Clinicians should be aware of this finding in the management of patients diagnosed or suspected of ischemic heart disease.
Harold L. Kennedy, M.D. Stephen J. Underhill Department of Cardiovascular Services and Clinical Investigations U. S. Public Health Service Hospital Baltimore, Md. REFERENCES 1.
2. 3.
Allen, R., Gettes, L., and Phalan, C.: “Silent” S-T segment depression in patients with angina pectoris, Circulation 63uppl. III)so: 122, 1974. Burch, G. E.: Silent angina and coronary bypass surgery, AM. HEART J. 9&630,1974. Stern, S., and Tzivoni, D.: Early detection of silent
American
Heart Journal
to the Editor
4.
ischaemic heart disease by 24-hour electrocardiographic monitoring of active subjects, Br. Heart J. 36~481, 1974. Kennedy, H. L., Underhill, S. J., Caralis, D., and Warbasse, J. R.: Ischemic ST-segment depression without precordial or angina1 symptoms detected by Holter recordings. (To be submitted)
_.-alerated block
AV-conduction
and complete A-V
To the Editor: The article entitled “Accelerated A-V conduction associated with complete A-V block” by Drs. Krishnaswami and Geraci (AM. HJZART J. 89463, 1974) is interesting. However, the term “accelerated A-V conduction” is a misnomer. Perhaps the authors meant”accelerated A-H conduction.” But even if this was so, an A-H interval of 80sec. does not represent faster-than-normal conduction velocity. The most that can be said is that the A-H interval was at the lower limits of normal. What they did find was that the A-H did not increase during atria1 pacing at increasing rates up to 1301min. This is probably significant although it would have been interesting to see at what rate A-H Wenckebach developed.
to the Editor
the rise in blood pressure following norepinephrine.6 Propranolol, apparently, not only prevents beta arteriolar dilatation but also displaces norepinephrine from beta receptors so that it becomes more concentrated at the alpha sites which cause arteriolar constriction. Although propranolol is commonly used in the treatment of hypertension, where it is thought to be helpful by lowering cardiac output, it increases the blood pressure under certain circumstances. It may precipitate a hypertensive crisis with pheochromocytoma6 by permitting unopposed alpha stimulation. In a diabetic it caused hypoglycemia with a secondary adrenergic response and extreme hypertension’ because alpha stimulation was not balanced by beta stimulation. A similar mechanism has been invoked to explain complete heart block (by vagal reflex) occurring when propranolol and epinephrine were given at the same time.s In addition, peripheral arterial insutllciency has been observed in patients taking propranolol,g giving further evidence of peripheral constriction. Finally, we wish to call attention to the decrease in sodium excretion which has been found with the use of propranolol.” This would tend to increase the blood volume and minimize the effect of peripheral vascular pooling as a factor in orthostatic hypotension. Frank Barth Theodore Lawrence, M. D. Veterans Administration Hospital and The Medical College of Pennsylvania Philadelphia, Pa. 19104
1. Wiggers, C. J.: Physiology in health and disease, 5th ed., Philadelphia, 1949, Lea & Febiger, p. 1124. 2. Wolf& L.: Clinical aspects of paroxysmal heart action, N. Engl. J. Med. 226:640, 1942. 3. Weiseler, A. M., Leonard, J. J., and Warren, J. V.: Effects of posture and a&pine on the cardiac output, J. Clin. Invest. 36:1656, 1957. 4. Epstein, S. E., and Braunwald, E.: Beta-adrenergic receptor blocking drugs, N. Engl. J. Med. 275:1106, 1966. 5. Glover, W. E., and Hutchinson, K. J.: The effect of a beta receptor antagonist (propranolol) on the cardiovascular response to intravenous infusions of noradrenaline in man, J. Physiol. 177:59P, 1965. 6. Prichard, B. N. C., and Ross, E. J.: Use of propranolol in conjunction with alpha receptor blocking drugs in pheochromocvtoma. Am. J. Cardiol. 18:394. 1966. 7. McMurtry, R.-J.: Propranolol, hypoglycemia; and hypertensive crisis, Ann. Intern. Med. 80:669, 1974. 8. Kram, J., et al.: Propranolol, Ann. Intern. Med. 80:282, 1974. 9. Frohlich, E. D., et al.: Peripheral arterial insufficiency, J.A.M.A. 208:2471,1969. 10. Nies, A. S., McNeil, J. S., and Schrier, R. W.: Mechanism of increased sodium reabsorption during propranolol administration, Circulation 44:596, 1971.
RePJY To the Editor: Doctors Barth and Lawrence have appropriately focused an important pharmacologic action of propranolol which may well have played a therapeutic role in the patient we re-
544
ported Indeed, I plead particular sin for our not having discussed this possibility, inasmuch as Doctors Luria, Kaplan, and I actually treated prolonged hypotension with a beta receptor blocking agent in 1964.’ We did discuss peripheral vasoconstrictor properties of beta blockers in that paper, and mentioned the possibility that neurotransmitter substance was displaced from beta to alpha sites in the periphery. In our recent paper, we perhaps did overly emphasize relief of the orthostatic tachycardia as the explanation for the patient’s subjective improvement. While I gladly accept the appropriate chastisement from Doctors Barth and Lawrence, I would like to again emphasize our major message. Namely, propranolol did effectively slow orthostatic tachycardia without adverse side effects Albert J. Miller, M.D. Northwestern Memorial Hospital Wesley Pavilion Superior St. and Fairbanks Ct. Chicago, Ill. 60611 REFERENCE
I.
Luria, M. H., Miller, A. J., and Kaplan, B. M.: Successful therapy of prolonged hypotension with an adrenergic beta-receptor blocking agent, Circulation 29:494, 1964.
lschemic ST segment depression and dyspnea To the Editor: The annotation entitled “Silent angina and coronary bypass surgery” by Dr. Burch in the October, 1974, issue of the JOURNAL(88:530,19741 emphasizes the absence of angina pectoris and chest discomfort, and the presence of dyspnea associated with ST-segment depression after a Master twostep test. This dyspnea manifested upon stress was quickly relieved by rest and sublingual nitroglycerin. Our experience with ambulatory 24-hour Holter recordings confirms the observation that ischemic ST-segment depression may present with the clinical symptom of dyspnea only. An illustrative case, J.M.J., a 57-year-old active male presented completely asymptomatic as a normal participant in a two channel 24-hour Holter recording protocol. Trend analysis revealed seven episodes of ischemic ST-segment depression encompassing a total time of 210 minutes, the most striking of which (Fig. 1) was precipitated by a brisk walk. Patient diary revealed no symptoms, and query of the patient within one hour of completion of the Holter recording ellicited, in retrospect, only the presence of mild dyapnea during the brisk walk. Treadmill testing utilizing the Bruce protocol was performed for 370 seconds reaching a maximal blood pressure of 154/80 mm. Hg and a maximal heart rate of 170 beats per minute with 4.5 mm. of ischemic ST-segment depression before being terminated with exertional hypotension accompanied by dyspnea. The patient denied angina pectoris or chest discomfort. Angiography revealed a 70 to 80 per cent narrowing of the left main coronary artery, 80 to 90 per cent narrowing of the proximal left anterior descending coronary artery, and a normal left ventricular ejection fraction of 58 per cent. Left ventricular end diastolic pressure was normal, and calcification was noted in the left main and proximal left anterior descending coronary arteries.
April,
1975, Vol. 89, No. 4
Letters
Fig 1, Left and Right. 9:21 P.M. a heart rate time sample print-out CBVs) lead.
Two channel Holter recordings. Left trend analysis print-out indicates at approximately (top) of 130 beats per minute and S-T level (bottom) depression of 3 to 4 mm. Rkht, real at 9:21 P.M. confirms 3 to 4 mm. of ischemic ST-segment depression in chest bipolar V,
“Silent” clinical symptoms associated with ST-segment depression,’ angina pectoris,2 or ischemic heart disease3 have received recent attention in the literature. Our observations’ are similar to that reported by Dr. Burch in identifying dyspnea without precordial or angina1 symptoms as being present in patients with concurrent ischemic ST-segment depression which is relieved by rest or sublingual nitroglycerin. Clinicians should be aware of this finding in the management of patients diagnosed or suspected of ischemic heart disease.
Harold L. Kennedy, M.D. Stephen J. Underhill Department of Cardiovascular Services and Clinical Investigations U. S. Public Health Service Hospital Baltimore, Md. REFERENCES 1.
2. 3.
Allen, R., Gettes, L., and Phalan, C.: “Silent” S-T segment depression in patients with angina pectoris, Circulation 63uppl. III)so: 122, 1974. Burch, G. E.: Silent angina and coronary bypass surgery, AM. HEART J. 9&630,1974. Stern, S., and Tzivoni, D.: Early detection of silent
American
Heart Journal
to the Editor
4.
ischaemic heart disease by 24-hour electrocardiographic monitoring of active subjects, Br. Heart J. 36~481, 1974. Kennedy, H. L., Underhill, S. J., Caralis, D., and Warbasse, J. R.: Ischemic ST-segment depression without precordial or angina1 symptoms detected by Holter recordings. (To be submitted)
_.-alerated block
AV-conduction
and complete A-V
To the Editor: The article entitled “Accelerated A-V conduction associated with complete A-V block” by Drs. Krishnaswami and Geraci (AM. HJZART J. 89463, 1974) is interesting. However, the term “accelerated A-V conduction” is a misnomer. Perhaps the authors meant”accelerated A-H conduction.” But even if this was so, an A-H interval of 80sec. does not represent faster-than-normal conduction velocity. The most that can be said is that the A-H interval was at the lower limits of normal. What they did find was that the A-H did not increase during atria1 pacing at increasing rates up to 1301min. This is probably significant although it would have been interesting to see at what rate A-H Wenckebach developed.
