Letters to the Editor
spells, in our opinion. Whereas in the normal, ventilation is controlled with negative feedback (decreasing CO~ and increasing 0~ with increasing ventilation), this is not the case in cyanotic congenital heart disease with diminished pulmonary blood flow? I will not repeat the evidence for paroxysmal hyperpnea except t h a t positive inotropic effects would be totally incapable of explaining these "blue spells" in patients with pulmonary atresia, which account for 20 per cent of these spells. Paroxysma ! hyperpnea, although not a primary event in tachyrhythmias, could nevertheless operate as a central mechanism t h a t would maintain the spells, once begun. Steeg and Hordof have clearly proven t h a t t a c h y r h y t h m i a can initiate the spells, and this contribution is extremely valuable.
Warren G. Guntheroth, M.D. Professor of Pediatrics Head, Division of Pediatric Cardiology School of Medicine Department of Pediatrics University of Washington Seattle, Wash. 98105
REFERENCES Steeg, C. N., and Hordof, A.: The hemodynamic effects of supraventricular tachycardia in ventricular septal defect with pulmonary outflow tract obstruction, AM. HEART J. 90:245, 1975. 2. King, S. B., and Franch, R. H.: Production of increased right-to-left shunting by rapid heart rates in patients with tetralogy of Fallot, Circulation 44:265, 1971. 3. Guntheroth, W. G.: "Tetralogy of Fallot" in Moss and Adams, eds.: Heart disease in infants, children and adolescents, Baltimore, 1968, Williams and Wilkins, p.435. 4. Guntheroth, W. G., Morgan, B. C., and Mullins, G. L.: Physiologic studies of paroxysmal hyperpnea in cyanotic congenital heart disease, Circulation 31:70, 1965. 5. Van Lingen, B., and Whidborne, J.: Oximetry and congenital heart disease with special reference to the effects of voluntary hyperventilation, Circulation 6:740, 1952. 1.
cardiovascular procedure which, perhaps, may be explained by the premedication.
Carl N. Steeg, M.D. Associate Professor, Clinical Pediatrics Director, Pediatric Cardiovascular Laboratory Allan J. Hordof, M.D. Assistant Professor, Pediatrics Department of Pediatrics College of Physicians & Surgeons Columbia University 630 W. 168th St. New York, N. Y. 10032
REFERENCE 1. Guntheroth, W. G.: Tetrology of Fallot in: Heart disease in infants, children and adolescents, Moss, A. J., and Adams, F. H., editors, Baltimore, 1968, Williams & Wilkins, pp. 435-436.
Sudden death in sexual activity To the Editor: Dr. Green 1 has discussed sudden death during coitus in his excellent article which was titled "Sexual activity and the postmyocardial infarction patient." According to him this subject was not so clear and he stated t h a t some factors such as emotion, a big meal, or alcohol can be causative factors in unexpected death. We have studied the electrocardiographic changes during sexual intercourse by utilizing a Holter monitor. In cases with old myocardial infarction or coronary insufficiency ST segment depression with marked tachycardia was observed although these patients did not suffer from any precordial pain or discomfort. However, the same patients suffered from precordial pain during exercise when their electrocardiograms showed less ST segment depression and a lesser degree of tachycardia. We believe t h a t this phenomen is related to the "analgesic effect" of sexual activity (Fig. 1). We would like to state t h a t this "analgesic effect" may play
Reply To the Editor: We appreciate Dr. Guntheroth,s remarks. Technically we agree with Dr. Guntheroth's definition of "spasm" and concur t h a t "increased right ventricular outflow tract obstruction" would have been a better term. It should be stated t h a t the use of "spasm" in this regard appears to be rather protean. Indeed, Dr. Guntheroth employs it without modification i n his discussion of the subject. 1 We did not mean to imply t h a t paroxysmal hyperpnea was the sole etiology, according to Guntheroth, and we have no reason to doubt his explanation for spells, one widely accepted in pediatric cardiologic circles. Dr. G u n t h e r o t h does state, however, t h a t "hyperpnea is the crucial event in these spells," tending, we believe, to detract from initiating episodes such as a tachyarrhythmia.' Our patient showed no clinical or laboratory evidence of either hyperventilation or hyperpnea at any time during the
American Heart Journal
Fig. 1
405
Letters to the Editor
a role in sudden deaths during sexual activity. Patients can easily stop physical activity when they suffer from precordial pain and they can also use nitrates when necessary. But during the course of sexual activity they do not suffer from pain or discomfort because of "sexual analgesia" and therefore they tend to continue the sexual activity, which in turn may result in a new myocardial infarction or sudden death.
Istemi Nalbantgil, M.D. ~)mer Yi$itbaqi, M.D. Bftlent Kiliqcio~lu, M.D. Ege University Medical School Internal Medicine Clinic Izmir, Turkey
the coronary patients. Inability to standardize Holter momtors limits the value of the tracing to rate, rhythm, and conduction pattern analysis with S-T and T-wave changes being interpreted with caution because of distortion in the recording system and changes in the positional activity. 1 Secondly, onset of angina has been correlated with the heart rate • blood pressure product? The individuals described had a faster coita] heart rate compared to the rate at the time exercise pain appeared. Blood pressure recordings might put these data in proper perspective. Therefore. while many conceive of coital death as a pleasant end. I am not convinced that "death in the saddle" would be pain-free.
Andrew W. Green, M.D. State University of New York at Buffalo Department of Medicine 462 Grider St. Buffalo, N.Y. 14215
REFERENCE 1.
Green, A. W.: Sexual activity and the postmyocardial infarction patient, AM. HEART J. 89:246, 1975.
Reply To the Editor: "Sexual analgesia" as proposed by Drs. Nalbantgil and associates certainly may be a contributory factor in coital sudden death. However, the two observations from which the analgesia hypothesis was derived deserve comment. The Holter monitor tracing demonstrating coital S-T depressions was compared to the exercise electrocardiogram of
406
REFERENCES Hinkle, L. E., Meyer, J., Stevens, M., and Carver. S. T.. Tape recordings of the ECG of active men: limitations and advantages of the Holter-Avionics instruments, Circulation 36:752. 1967. 2. NIH Conference: Angina Pectoris: Pathophysiology, evaluation and treatment, Ann. Intern. Med. 75:263, 1971. 1.
March, 1976, Vol. 91, No. 3
spells, in our opinion. Whereas in the normal, ventilation is controlled with negative feedback (decreasing CO~ and increasing 0~ with increasing ventilation), this is not the case in cyanotic congenital heart disease with diminished pulmonary blood flow? I will not repeat the evidence for paroxysmal hyperpnea except t h a t positive inotropic effects would be totally incapable of explaining these "blue spells" in patients with pulmonary atresia, which account for 20 per cent of these spells. Paroxysma ! hyperpnea, although not a primary event in tachyrhythmias, could nevertheless operate as a central mechanism t h a t would maintain the spells, once begun. Steeg and Hordof have clearly proven t h a t t a c h y r h y t h m i a can initiate the spells, and this contribution is extremely valuable.
Warren G. Guntheroth, M.D. Professor of Pediatrics Head, Division of Pediatric Cardiology School of Medicine Department of Pediatrics University of Washington Seattle, Wash. 98105
REFERENCES Steeg, C. N., and Hordof, A.: The hemodynamic effects of supraventricular tachycardia in ventricular septal defect with pulmonary outflow tract obstruction, AM. HEART J. 90:245, 1975. 2. King, S. B., and Franch, R. H.: Production of increased right-to-left shunting by rapid heart rates in patients with tetralogy of Fallot, Circulation 44:265, 1971. 3. Guntheroth, W. G.: "Tetralogy of Fallot" in Moss and Adams, eds.: Heart disease in infants, children and adolescents, Baltimore, 1968, Williams and Wilkins, p.435. 4. Guntheroth, W. G., Morgan, B. C., and Mullins, G. L.: Physiologic studies of paroxysmal hyperpnea in cyanotic congenital heart disease, Circulation 31:70, 1965. 5. Van Lingen, B., and Whidborne, J.: Oximetry and congenital heart disease with special reference to the effects of voluntary hyperventilation, Circulation 6:740, 1952. 1.
cardiovascular procedure which, perhaps, may be explained by the premedication.
Carl N. Steeg, M.D. Associate Professor, Clinical Pediatrics Director, Pediatric Cardiovascular Laboratory Allan J. Hordof, M.D. Assistant Professor, Pediatrics Department of Pediatrics College of Physicians & Surgeons Columbia University 630 W. 168th St. New York, N. Y. 10032
REFERENCE 1. Guntheroth, W. G.: Tetrology of Fallot in: Heart disease in infants, children and adolescents, Moss, A. J., and Adams, F. H., editors, Baltimore, 1968, Williams & Wilkins, pp. 435-436.
Sudden death in sexual activity To the Editor: Dr. Green 1 has discussed sudden death during coitus in his excellent article which was titled "Sexual activity and the postmyocardial infarction patient." According to him this subject was not so clear and he stated t h a t some factors such as emotion, a big meal, or alcohol can be causative factors in unexpected death. We have studied the electrocardiographic changes during sexual intercourse by utilizing a Holter monitor. In cases with old myocardial infarction or coronary insufficiency ST segment depression with marked tachycardia was observed although these patients did not suffer from any precordial pain or discomfort. However, the same patients suffered from precordial pain during exercise when their electrocardiograms showed less ST segment depression and a lesser degree of tachycardia. We believe t h a t this phenomen is related to the "analgesic effect" of sexual activity (Fig. 1). We would like to state t h a t this "analgesic effect" may play
Reply To the Editor: We appreciate Dr. Guntheroth,s remarks. Technically we agree with Dr. Guntheroth's definition of "spasm" and concur t h a t "increased right ventricular outflow tract obstruction" would have been a better term. It should be stated t h a t the use of "spasm" in this regard appears to be rather protean. Indeed, Dr. Guntheroth employs it without modification i n his discussion of the subject. 1 We did not mean to imply t h a t paroxysmal hyperpnea was the sole etiology, according to Guntheroth, and we have no reason to doubt his explanation for spells, one widely accepted in pediatric cardiologic circles. Dr. G u n t h e r o t h does state, however, t h a t "hyperpnea is the crucial event in these spells," tending, we believe, to detract from initiating episodes such as a tachyarrhythmia.' Our patient showed no clinical or laboratory evidence of either hyperventilation or hyperpnea at any time during the
American Heart Journal
Fig. 1
405
Letters to the Editor
a role in sudden deaths during sexual activity. Patients can easily stop physical activity when they suffer from precordial pain and they can also use nitrates when necessary. But during the course of sexual activity they do not suffer from pain or discomfort because of "sexual analgesia" and therefore they tend to continue the sexual activity, which in turn may result in a new myocardial infarction or sudden death.
Istemi Nalbantgil, M.D. ~)mer Yi$itbaqi, M.D. Bftlent Kiliqcio~lu, M.D. Ege University Medical School Internal Medicine Clinic Izmir, Turkey
the coronary patients. Inability to standardize Holter momtors limits the value of the tracing to rate, rhythm, and conduction pattern analysis with S-T and T-wave changes being interpreted with caution because of distortion in the recording system and changes in the positional activity. 1 Secondly, onset of angina has been correlated with the heart rate • blood pressure product? The individuals described had a faster coita] heart rate compared to the rate at the time exercise pain appeared. Blood pressure recordings might put these data in proper perspective. Therefore. while many conceive of coital death as a pleasant end. I am not convinced that "death in the saddle" would be pain-free.
Andrew W. Green, M.D. State University of New York at Buffalo Department of Medicine 462 Grider St. Buffalo, N.Y. 14215
REFERENCE 1.
Green, A. W.: Sexual activity and the postmyocardial infarction patient, AM. HEART J. 89:246, 1975.
Reply To the Editor: "Sexual analgesia" as proposed by Drs. Nalbantgil and associates certainly may be a contributory factor in coital sudden death. However, the two observations from which the analgesia hypothesis was derived deserve comment. The Holter monitor tracing demonstrating coital S-T depressions was compared to the exercise electrocardiogram of
406
REFERENCES Hinkle, L. E., Meyer, J., Stevens, M., and Carver. S. T.. Tape recordings of the ECG of active men: limitations and advantages of the Holter-Avionics instruments, Circulation 36:752. 1967. 2. NIH Conference: Angina Pectoris: Pathophysiology, evaluation and treatment, Ann. Intern. Med. 75:263, 1971. 1.
March, 1976, Vol. 91, No. 3
