LETTERS TO THE EDITOR
belief that the chest discomfort originated in altered hemodynamic loads buffeting a myocardium underperfused because of extensive and fixed coronary arterial stenosis. However, the theory of vasospasm, even when one brings on the stage the deus ex machina of autoregulatory feedback modulated by as yet undefined substances, leaves much unexplained. Why do some patients with extensive coronary artery disease never experience angina, while others with lesser involvement are severely disabled? The balancing between vasoconstrictor and vasodilator metabolites may indeed be true. But there is a need to identify these substances precisely as well as to define their specific triggers. Current investigative work promises early clarification of the many factors that may be responsible for angina pectoris. But we need not limit ourselves to one outlook. For example, it is conceivable that transient platelet aggregates may induce vascular narrowing. In this context, the recent report by Folb and co-workers2 is highly relevant. They demonstrated a cyclic reduction in coronary arterial flow to near zero in a vessel with fixed narrowing. The alterations in flow were due to platelet aggregations and disaggregations. Earlier, Jorgensen and associates3 found that intracoronary injection of adenosine diphosphate in swine caused profound myocardial ischemic lesions that were preventable by prior induction of thrombocytopenia. It is now evident that platelets may release powerful vasoconstrictors like thromboxane As, while vascular endothelium liberates another prostaglandin, prostacyclin, that disaggregates platelets and relaxes arterial smooth muscle. These important findings, I believe, still require the interplay of neural and neurohumoral factors if we are to account for the diverse clinical aspects of angina pectoris. In this context, it is significant that psychologic or physical stresses that release catecholamines into the circulation induce platelet aggregation in coronary arteries with ensuing myocardial lesions.4 The syndrome so eloquently described by Heberden 2 centuries ago at last may yield the secret of its mechanisms. Bernard Lown, MD, FACC Department of Nutrition Harvard University School of Public Health Boston, Massachusetts References
1. Kwfw
CS, Reenlk WH: Angina pectoris: a syndrome caused by anoxemia of the myocardium. Arch Intern Med 41:769-807. 1929 2. Fofts JD, Crowelf ES, Rowe CO: Platelet aggegatlon in partially obstructed vessels and its elimination with asoirln. Circulation 54~385. 1976 3. Jor9e~.n L, Rowell HC; Hovb 1, 01 ab Adeno&ne diphoaphate-induced platelet aaruaoation and mvocardttl infarction in swine. Lab Invest 17:816. 1967 4. li% Jr, Fan1 K: St&s and induction of Intravascular platelet aggr&tion in the heart. Circulation 48:164. 1973
SEPTAL PERFORATOR COMPRESSION IN IDIOPATHIC HYPERTROPHIC SUBAORTIC STENOSIS
We have analyzed 500 consecutive coronary arteriograms for the presence of septal perforator compression,l and our results are somewhat different from those of Pichard et a1.2 Like the latter, we found septal perforator compression in all 17 patients with idiopathic cardiomyopathy with idiopathic hypertrophic subaortic stenosis included in our series. However, we also observed this phenomenon in 4 of 10 patients with hypertrophic cardiomyopathy without obstruction, 11 of 18 patients with severe aortic stenosis (peak systolic gradient more than 70 mm Hg) (Fig. 1) and 3 of 17 patients with
526
September 1979
The American Journal ti CARDIOLOGY
FIGURE 1. Septal perforator compression in a patient with severe aortic valve stenosis. Upper frame, sy$tole. LOWH frame. diastole. Note that the septal perforators that are visible during diastole (lower frame. arrow) disappear during systole.
mild or moderate aortic stenosis (peak systolic gradient less than 70 mm Hg). In addition, septal perforation compression was present in 4 of 17 patients with myocardial bridge and in 4 of 40 patients with subtotal occlusion (more than 95 percent stenosis) of the proximal left anterior descending coronary artery. It was not present in any of the 58 patients with a normal heart and normal coronary arteries, 4 patients with marked pulmonary hypertension (pulmonary arterial pressure at systemic levels) or 419 patients with other heart disease, including coronary artery disease, rheumatic heart disease, congenital heart disease, myocardial disease and cardiac tumors. Septal perforator compression is thus seen not only in patients with idiopathic hypertrophic subaortic stenosis and cardiomyopathy, as suggested by the data of Pichard et al.,2+3 but in those with a variety of cardiac conditions including aortic stenosis, myocardial bridge and critical stenosis of the left anterior descending coronary artery. These observations and the absence of septal perforation compression in patients with right ventricular pressure at systemic levels, in whom intramyocardial pressure would be similar across the septum, argue against the theory that the abnormal septal anatomy of idiopathic hypertrophic subaortic stenosis is the sole cause of this phenomenon. It appears that a decrease of the intraluminal septal perforator pressure due to an obstruction at the subaortic, aortic valve or coronary arterial level pre-
Volume 42
LETTERS TO THE EDITOR
disposes to this phenomenon, which may be further facilitated by the abnormal septal anatomy of idiopathic hypertrophic subaortic stenosis or other conditions affecting the intraventricular septum. John B. Kostis. MD, FACC Abel E. Moreyra, MD College of Medicine and Dentistry of New Jersey Rutgers Medical School Piscataway, New Jersey References 1. K&k
JB, Maeyra AE, MaWam Ii, at ak “Se+ squwue.” A cOrCWY srterloqaphlc Congress of Cardbvascular Surgery. Athens. Greece. June 1977. p 115 2. Plchwd AD. Meller J, Takhholz LE, at al: Septal perforator compression (narrowing) in ldlooathic hvoertrouic subaortic stenosis. Am J Cardial 40~310-314. 1977 3. PlchGd A, J, ieichMlz L, et ab Ssptal perforator compress& in idiopathic hypwtrophic wbaortlc stenosis: a pathwphysiologii maker (absti). Circulation 54: Suppl ll:ll-105. 1976 clue to the diegnosls of IHSS (abst?). Proc Intsmaticnal
Finally, their discussion of the mechanism of the postextrasystolic beat phenomenon in cavity-obliterating ventricles (impaired ventricular filling leading to less postextrasystolic diastolic stretch and maximal or near maximal ejection fraction during sinus rhythm minimizing any inotropic enhancement that may follow the premature complex), leads me to the opposite conclusion, that is, that the postextrasystolic beat phenomenon should not occur. Still, it does occur; thus, there is something wrong in the logic of the explanation; perhaps, there is good diastolic filling after a premature complex, after all. Reviewing the echocardiograms might show some premature ventricular complexes occurring while the left ventricular cavity was being visualized. The recently described noninvasive technique for evaluating postextrasystolic potentiation with echocardiography should be of help on this point.
M&f
J. E. Val-Mejias, MD Division of Cardiology Saint Louis University School of Medicine
Saint Louis, Missouri REPLY
References
After receiving the letter from Kostis and Moreyra, I went to their cardiac laboratory and personally reviewed examples of their cases of aortic stenosis and coronary disease with septal perforator compression. Their patients did manifest septal perforator compression although it was by no means as prominent as the phenomenon seen in idiopathic hypertrophic subaortic stenosis. All of their patients with aortic stenosis and septal compression had marked left ventricular hypertrophy in addition to hypercontractility with a contraction pattern identical to that seen in idiopathic hypertrophic subaortic stenosis. This has not been our experience. In the last 40 consecutive cases of aortic stenosis, we have not seen septal perforator compression. We do have one patient in our earlier series with aortic stenosis and minimal septal perforator compression. This discordance appears most interesting. We hope that future research will explain the underlying mechanism of the visual phenomenon of septal perforator compression. August0 Pichard, MD
Ralznr AE, Chahlno RI; lahlmorl 1, et al: Clinical correlates of left ventricular cavity obliteration. Am J Cardlol 40~303-309. 1977 2. Cohn PF. An9off QH, 2011 PM, et ab A new. nonlnvasive technique fw inducing postextrasystolic potentiatlon during echocardiography. Circulation 56599-604. 1977
The Mount Sinai Hospital New York, New York
CLINICAL
CORRELATES OF LEFT VENTRICULAR CAVITY OBLITERATION
The article by Raizner et al.’ would have benefited by the addition of a master table describing each individual patient. It is now impossible to trace any individual patient, and some points are not clear. For example, what were the characteristics of the patients who presented systolic anterior motion, and did these patients happen to be the ones who also had mitral regurgitation? Which patients showed mitral valve prolapse-the ones with asymmetric septal hypertrophy or the ones without it? Also, the text states that nine patients had the Brockenbrough phenomenon, but I could trace only seven. Probably the missing two belonged to the group of patients that did not have satisfactory echocardiograms, but I would have liked to know their hemodynamic status. In addition, it would have been interesting to know the response of the left ventricular end-diastolic pressure to angiographic stress and what the carotid or aortic tracings looked like. Did patients with cavity obliteration and no asymmetric septal hypertrophy also have bisferiens pulses?
1.
REPLY
The manuscript as originally submitted did contain a master table; however, this was changed to a summary table at the suggestion of reviewers who believed, appropriately, that the master table was somewhat tedious. Nevertheless, I think we can clarify some specific points of information. 1. Of the three patients with systolic anterior motion of the anterior leaflet of the mitral valve, two had resting intraventricular pressure gradients (one of whom also had a transvalve aortic stenosis gradient) and all three had symmetric septal hypertrophy (septum to posterior wall ratio less than 1.3). Mitral regurgitation was not observed in these three patients. 2. Among the patients with angiographic mitral valve prolapse, echocardiographic data in four revealed symmetric (three) and asymmetric (one) septal hypertrophy. In patients with cavity obliteration, the mitral valve apparatus, although normal, may be disproportionately large for the obliterated cavity, resulting in mitral prolapse. 3. The Brockenbrough, or postextrasystolic beat, phenomenon was seen in nine patients. As Val-Mejias points out, echocardiographic data were not available in two patients. These two patients had no intraventricular pressure gradient, and their findings further reinforce the suggestion that cavity obliteration in itself, without obstructive phenomena, might have important hemodynamic significance. 4. Left ventricular end-diastolic pressure after angiography ranged from 7 to 30 mmHg (mean 18.6 f 1.5 mm Hg). Thirteen of the 24 patients manifested an abnormally elevated (greater than 18 mm Hg) postangiographic left ventricular end-diastolic pressure. 5. We did not systematically record external carotid pulse tracings; hence we do not have data ralative to the incidence of this finding. Clearly, many fascinating clinical correlations may be made in a study of this sort. It would be impossible to discuss all such correlations in a readable paper. We hope we have provided some of the specific information requested.
September 1979
The American Journal of CARMOLOGY
Volume 42
527
belief that the chest discomfort originated in altered hemodynamic loads buffeting a myocardium underperfused because of extensive and fixed coronary arterial stenosis. However, the theory of vasospasm, even when one brings on the stage the deus ex machina of autoregulatory feedback modulated by as yet undefined substances, leaves much unexplained. Why do some patients with extensive coronary artery disease never experience angina, while others with lesser involvement are severely disabled? The balancing between vasoconstrictor and vasodilator metabolites may indeed be true. But there is a need to identify these substances precisely as well as to define their specific triggers. Current investigative work promises early clarification of the many factors that may be responsible for angina pectoris. But we need not limit ourselves to one outlook. For example, it is conceivable that transient platelet aggregates may induce vascular narrowing. In this context, the recent report by Folb and co-workers2 is highly relevant. They demonstrated a cyclic reduction in coronary arterial flow to near zero in a vessel with fixed narrowing. The alterations in flow were due to platelet aggregations and disaggregations. Earlier, Jorgensen and associates3 found that intracoronary injection of adenosine diphosphate in swine caused profound myocardial ischemic lesions that were preventable by prior induction of thrombocytopenia. It is now evident that platelets may release powerful vasoconstrictors like thromboxane As, while vascular endothelium liberates another prostaglandin, prostacyclin, that disaggregates platelets and relaxes arterial smooth muscle. These important findings, I believe, still require the interplay of neural and neurohumoral factors if we are to account for the diverse clinical aspects of angina pectoris. In this context, it is significant that psychologic or physical stresses that release catecholamines into the circulation induce platelet aggregation in coronary arteries with ensuing myocardial lesions.4 The syndrome so eloquently described by Heberden 2 centuries ago at last may yield the secret of its mechanisms. Bernard Lown, MD, FACC Department of Nutrition Harvard University School of Public Health Boston, Massachusetts References
1. Kwfw
CS, Reenlk WH: Angina pectoris: a syndrome caused by anoxemia of the myocardium. Arch Intern Med 41:769-807. 1929 2. Fofts JD, Crowelf ES, Rowe CO: Platelet aggegatlon in partially obstructed vessels and its elimination with asoirln. Circulation 54~385. 1976 3. Jor9e~.n L, Rowell HC; Hovb 1, 01 ab Adeno&ne diphoaphate-induced platelet aaruaoation and mvocardttl infarction in swine. Lab Invest 17:816. 1967 4. li% Jr, Fan1 K: St&s and induction of Intravascular platelet aggr&tion in the heart. Circulation 48:164. 1973
SEPTAL PERFORATOR COMPRESSION IN IDIOPATHIC HYPERTROPHIC SUBAORTIC STENOSIS
We have analyzed 500 consecutive coronary arteriograms for the presence of septal perforator compression,l and our results are somewhat different from those of Pichard et a1.2 Like the latter, we found septal perforator compression in all 17 patients with idiopathic cardiomyopathy with idiopathic hypertrophic subaortic stenosis included in our series. However, we also observed this phenomenon in 4 of 10 patients with hypertrophic cardiomyopathy without obstruction, 11 of 18 patients with severe aortic stenosis (peak systolic gradient more than 70 mm Hg) (Fig. 1) and 3 of 17 patients with
526
September 1979
The American Journal ti CARDIOLOGY
FIGURE 1. Septal perforator compression in a patient with severe aortic valve stenosis. Upper frame, sy$tole. LOWH frame. diastole. Note that the septal perforators that are visible during diastole (lower frame. arrow) disappear during systole.
mild or moderate aortic stenosis (peak systolic gradient less than 70 mm Hg). In addition, septal perforation compression was present in 4 of 17 patients with myocardial bridge and in 4 of 40 patients with subtotal occlusion (more than 95 percent stenosis) of the proximal left anterior descending coronary artery. It was not present in any of the 58 patients with a normal heart and normal coronary arteries, 4 patients with marked pulmonary hypertension (pulmonary arterial pressure at systemic levels) or 419 patients with other heart disease, including coronary artery disease, rheumatic heart disease, congenital heart disease, myocardial disease and cardiac tumors. Septal perforator compression is thus seen not only in patients with idiopathic hypertrophic subaortic stenosis and cardiomyopathy, as suggested by the data of Pichard et al.,2+3 but in those with a variety of cardiac conditions including aortic stenosis, myocardial bridge and critical stenosis of the left anterior descending coronary artery. These observations and the absence of septal perforation compression in patients with right ventricular pressure at systemic levels, in whom intramyocardial pressure would be similar across the septum, argue against the theory that the abnormal septal anatomy of idiopathic hypertrophic subaortic stenosis is the sole cause of this phenomenon. It appears that a decrease of the intraluminal septal perforator pressure due to an obstruction at the subaortic, aortic valve or coronary arterial level pre-
Volume 42
LETTERS TO THE EDITOR
disposes to this phenomenon, which may be further facilitated by the abnormal septal anatomy of idiopathic hypertrophic subaortic stenosis or other conditions affecting the intraventricular septum. John B. Kostis. MD, FACC Abel E. Moreyra, MD College of Medicine and Dentistry of New Jersey Rutgers Medical School Piscataway, New Jersey References 1. K&k
JB, Maeyra AE, MaWam Ii, at ak “Se+ squwue.” A cOrCWY srterloqaphlc Congress of Cardbvascular Surgery. Athens. Greece. June 1977. p 115 2. Plchwd AD. Meller J, Takhholz LE, at al: Septal perforator compression (narrowing) in ldlooathic hvoertrouic subaortic stenosis. Am J Cardial 40~310-314. 1977 3. PlchGd A, J, ieichMlz L, et ab Ssptal perforator compress& in idiopathic hypwtrophic wbaortlc stenosis: a pathwphysiologii maker (absti). Circulation 54: Suppl ll:ll-105. 1976 clue to the diegnosls of IHSS (abst?). Proc Intsmaticnal
Finally, their discussion of the mechanism of the postextrasystolic beat phenomenon in cavity-obliterating ventricles (impaired ventricular filling leading to less postextrasystolic diastolic stretch and maximal or near maximal ejection fraction during sinus rhythm minimizing any inotropic enhancement that may follow the premature complex), leads me to the opposite conclusion, that is, that the postextrasystolic beat phenomenon should not occur. Still, it does occur; thus, there is something wrong in the logic of the explanation; perhaps, there is good diastolic filling after a premature complex, after all. Reviewing the echocardiograms might show some premature ventricular complexes occurring while the left ventricular cavity was being visualized. The recently described noninvasive technique for evaluating postextrasystolic potentiation with echocardiography should be of help on this point.
M&f
J. E. Val-Mejias, MD Division of Cardiology Saint Louis University School of Medicine
Saint Louis, Missouri REPLY
References
After receiving the letter from Kostis and Moreyra, I went to their cardiac laboratory and personally reviewed examples of their cases of aortic stenosis and coronary disease with septal perforator compression. Their patients did manifest septal perforator compression although it was by no means as prominent as the phenomenon seen in idiopathic hypertrophic subaortic stenosis. All of their patients with aortic stenosis and septal compression had marked left ventricular hypertrophy in addition to hypercontractility with a contraction pattern identical to that seen in idiopathic hypertrophic subaortic stenosis. This has not been our experience. In the last 40 consecutive cases of aortic stenosis, we have not seen septal perforator compression. We do have one patient in our earlier series with aortic stenosis and minimal septal perforator compression. This discordance appears most interesting. We hope that future research will explain the underlying mechanism of the visual phenomenon of septal perforator compression. August0 Pichard, MD
Ralznr AE, Chahlno RI; lahlmorl 1, et al: Clinical correlates of left ventricular cavity obliteration. Am J Cardlol 40~303-309. 1977 2. Cohn PF. An9off QH, 2011 PM, et ab A new. nonlnvasive technique fw inducing postextrasystolic potentiatlon during echocardiography. Circulation 56599-604. 1977
The Mount Sinai Hospital New York, New York
CLINICAL
CORRELATES OF LEFT VENTRICULAR CAVITY OBLITERATION
The article by Raizner et al.’ would have benefited by the addition of a master table describing each individual patient. It is now impossible to trace any individual patient, and some points are not clear. For example, what were the characteristics of the patients who presented systolic anterior motion, and did these patients happen to be the ones who also had mitral regurgitation? Which patients showed mitral valve prolapse-the ones with asymmetric septal hypertrophy or the ones without it? Also, the text states that nine patients had the Brockenbrough phenomenon, but I could trace only seven. Probably the missing two belonged to the group of patients that did not have satisfactory echocardiograms, but I would have liked to know their hemodynamic status. In addition, it would have been interesting to know the response of the left ventricular end-diastolic pressure to angiographic stress and what the carotid or aortic tracings looked like. Did patients with cavity obliteration and no asymmetric septal hypertrophy also have bisferiens pulses?
1.
REPLY
The manuscript as originally submitted did contain a master table; however, this was changed to a summary table at the suggestion of reviewers who believed, appropriately, that the master table was somewhat tedious. Nevertheless, I think we can clarify some specific points of information. 1. Of the three patients with systolic anterior motion of the anterior leaflet of the mitral valve, two had resting intraventricular pressure gradients (one of whom also had a transvalve aortic stenosis gradient) and all three had symmetric septal hypertrophy (septum to posterior wall ratio less than 1.3). Mitral regurgitation was not observed in these three patients. 2. Among the patients with angiographic mitral valve prolapse, echocardiographic data in four revealed symmetric (three) and asymmetric (one) septal hypertrophy. In patients with cavity obliteration, the mitral valve apparatus, although normal, may be disproportionately large for the obliterated cavity, resulting in mitral prolapse. 3. The Brockenbrough, or postextrasystolic beat, phenomenon was seen in nine patients. As Val-Mejias points out, echocardiographic data were not available in two patients. These two patients had no intraventricular pressure gradient, and their findings further reinforce the suggestion that cavity obliteration in itself, without obstructive phenomena, might have important hemodynamic significance. 4. Left ventricular end-diastolic pressure after angiography ranged from 7 to 30 mmHg (mean 18.6 f 1.5 mm Hg). Thirteen of the 24 patients manifested an abnormally elevated (greater than 18 mm Hg) postangiographic left ventricular end-diastolic pressure. 5. We did not systematically record external carotid pulse tracings; hence we do not have data ralative to the incidence of this finding. Clearly, many fascinating clinical correlations may be made in a study of this sort. It would be impossible to discuss all such correlations in a readable paper. We hope we have provided some of the specific information requested.
September 1979
The American Journal of CARMOLOGY
Volume 42
527
