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Mitral anular calcification and idiopathic hypertrophic subaortic stenosis
LETTERS TO THE EDITOR
REPLY
We totally agree that every effort should be made not ta cross a Bjork-Shiley valve through its smaller opening. On the basis of our experience, howevei, we believe that the retrograde approach is safe and effective if the transseptal technique is contraindicated or unavailable. We would attach the following suggestions regarding technique: Smaller catheters are much less likely to interfere with valve function or to dislodge the valve disc. We have always: measured hemodynamic variables and performed angiography, with ihe use of no.‘5 French catheters. Secondly, the entrance into the left ventricle should be made through the larger valv’e opening of the Bjork-Shiley prosthesis. Steven Wolfson, MD, FACC Cardiology Associates of New Haven New Haven, Connecticut
cent had calcific aortic valve disease and 40 percent had left atrid enlargement. Therefore when mitral anular calcification is demonstrated the most common coexistent abnormality is calcific aprtic valve disease or left atria1 enlargement, or both, as hag been described before. The incidence of idiopathic hypertrpphic subaortic stenosis if; small and seems well within that acceptable for patients referred for noninvasive evaluation’ of a murmur or cardiac symptoms, or both. Therefore, although mitral anular ctilcification is frequently noted in patients greater than 55 years of age with idiopathic hypertrophic subaortic stenosis the converse is not true. The prevalence of idiopathic hypertrophic subaortic stenosis in patients greater than 55 years of age with mitral anular calcification seems to be no greater than in the gerieral population. Thfrefore it is inappropriate to pursue aggressivelv the diagnosis of idiopathic hypertrophic Subaortic stenosis in a// patients with mitral ariular calcification unless other clinical or diagnostic information specifically suggests that such further procedures are warranted. Kenneth M. Kessler, MD, FACC Abdur Rahim, MD Non-Invasive Laboratory Mount Sinai Medical Center Miami Beach, Florida
MITRAL ANULAR CALCIFICATION AND IDIOPATHIC HYPERTROPHIC SUBAORTlC STENOSIS
Kronzon and Glassman’ have demonstrated an increased prevalence of mitral anular calcification in their p&i&&s with idiopathic hypertrbphic’ subaortic stenosis, especialljr in subjects greater than 55 years of age. However, they conclude (last line of their abstract) th$ calcification of the mitral valve anulus “dempnstration should raise the suspicion‘of ass6ciated idiopathic hypertrophic subaortic &e&is.” This conclusion cannot be properly derived from the data presented, ilr that it requires knowledge‘@ the incidence of idiopathic hype;trophic subaortic stenosis in patients demonstrating such calcification. To explore these questions in our patient population we first reexamined 28 randomly chosen, technically complete echocardiographic studies in patients greater than 55 years of&e with idiopathic hypertrophic- subaortic stenosis (defined as asymmetric septal hypertrophy and restin’g systolic anterior motion of the mitral valve). Three of these 28 patients were male; none of the 3 phowed calcification of the mitral anulus and 1 hadcalcific aortic valve disease. Of the 25 worhen, 8 had mitral anular calcification and 8 had calcific aofiic valve disease (only 2 of these patients had both findings ‘sitiultaneously). Thus, in OUTpopulation of 28 patients, with a mea’n age of 71 years and a standard deviation qf 7 years, there wtls a 29 percent incidence rat& of calcification of the mitral valve anulus and a 32 tiercent incidence iate of calcific aortic valve disease.‘The prevalence of mitral anular calcification in our laboratory in age-matched patients iti 30 percent-in women and 6 percent in men. Therefore in our patient pdpuhtion mitral anular calcification is a frequent finding, but its prevalence in patients with idiopathic hypertrophik subaortic steriosis is no different from that in our geneial (age-matched) population. To explore the question in reverse, that is, the incidence of idiopathic hypertrophic subaortic stenosis in patidntll’with mitral anular calcification, we reviewed 75 randumly chosen, complete echocardiographic recoids of patients greater than 55 years of age with definite mitral anular calcification as defined by Kronzon and Glassman. Of 21 men, none had evidence of idiopathic hypertrophic subaortic stenosis, 13 had calcific aortic valve’ disease and 11 had left atrial enlargement. Of the 54 women 2 had idiopathic hypertrophic,subaortic stenosis (as defined before), 34 had calcific aortic valve diiease and 19 had left atria1 enlargement. In our overall group with a mean age of 77 years (standard deviation 7 years), 2.7 peicent had idiopathic hypertrophic subaortic stenosis, 63 per-
-ember
1. K~UIZOII I, Ch8smm E: Mitral ring calcification in idiopathic hyperirophic subaortic stenosis. Am J Cardiol 4260-66. 1978
REPLY
It is evident that both groups find a high incidence of mitral anular calcification in older patients with idiopathic hypertrophic subaortic’stenosis. The major point of contention is whether this is an unusually high rate of coexistence or is secondary to an intrinsically elevated frequency of mitral anular calcification in all patients of&thisage group. Obviously, the basis of selection of patients for &hocardiographic study may influgnce the rate of fending mitral anular calcification. Kessler and Rahime indicated the prevalence of mitral anular calcification in’their laboratory in age-matched patients is 30 percent in women and 6 percent in meh. However, they give no details concerning types of patients who undergo echocardiographic stud& at their institution. The incidence of mitral anular calcification in ou? own-age-matched control subjects reported in the article is considerably lower. Possibly the discrepancy in our interpretation of these results is based ’ upon this djvergence of findings. In their group of patients with demonstrated mitral anular calcification, the mean age of 77 years was considerably higher than that in ours, which was only 64 years. Perhaps, in this population, the incidence of mitral anular calcification does iise precipitously with advancing age and may help to explain the disparate findings. Because 63 percent of their patients with mitral anular calcification had calcific aortic valve disease one might conclude that there is a high rate of coexistence of these two findings. This would be of interest if confirmed, but obviously requires further investigation. A nonexhaustive review of our own files does not support this hypothesis. We have observed:as is commonly recognized, calcification of the anterior mitral leaflet in association with calcific aortic stenosis. Although careful fluorosc!,py and echocardiogrephic analysis should separate thjs finding from mitral anular calcification it may be a source of confusion. Kessler and Rahime also mentionbd that calcific aortic stenosis was present in . . . . . assoclatlon with ldlopathlc hypertrophic subaort~c stenohi>
1979
The Amarkan Journal of CARDIDLDGY
Volume 44
579
REPLY
We totally agree that every effort should be made not ta cross a Bjork-Shiley valve through its smaller opening. On the basis of our experience, howevei, we believe that the retrograde approach is safe and effective if the transseptal technique is contraindicated or unavailable. We would attach the following suggestions regarding technique: Smaller catheters are much less likely to interfere with valve function or to dislodge the valve disc. We have always: measured hemodynamic variables and performed angiography, with ihe use of no.‘5 French catheters. Secondly, the entrance into the left ventricle should be made through the larger valv’e opening of the Bjork-Shiley prosthesis. Steven Wolfson, MD, FACC Cardiology Associates of New Haven New Haven, Connecticut
cent had calcific aortic valve disease and 40 percent had left atrid enlargement. Therefore when mitral anular calcification is demonstrated the most common coexistent abnormality is calcific aprtic valve disease or left atria1 enlargement, or both, as hag been described before. The incidence of idiopathic hypertrpphic subaortic stenosis if; small and seems well within that acceptable for patients referred for noninvasive evaluation’ of a murmur or cardiac symptoms, or both. Therefore, although mitral anular ctilcification is frequently noted in patients greater than 55 years of age with idiopathic hypertrophic subaortic stenosis the converse is not true. The prevalence of idiopathic hypertrophic subaortic stenosis in patients greater than 55 years of age with mitral anular calcification seems to be no greater than in the gerieral population. Thfrefore it is inappropriate to pursue aggressivelv the diagnosis of idiopathic hypertrophic Subaortic stenosis in a// patients with mitral ariular calcification unless other clinical or diagnostic information specifically suggests that such further procedures are warranted. Kenneth M. Kessler, MD, FACC Abdur Rahim, MD Non-Invasive Laboratory Mount Sinai Medical Center Miami Beach, Florida
MITRAL ANULAR CALCIFICATION AND IDIOPATHIC HYPERTROPHIC SUBAORTlC STENOSIS
Kronzon and Glassman’ have demonstrated an increased prevalence of mitral anular calcification in their p&i&&s with idiopathic hypertrbphic’ subaortic stenosis, especialljr in subjects greater than 55 years of age. However, they conclude (last line of their abstract) th$ calcification of the mitral valve anulus “dempnstration should raise the suspicion‘of ass6ciated idiopathic hypertrophic subaortic &e&is.” This conclusion cannot be properly derived from the data presented, ilr that it requires knowledge‘@ the incidence of idiopathic hype;trophic subaortic stenosis in patients demonstrating such calcification. To explore these questions in our patient population we first reexamined 28 randomly chosen, technically complete echocardiographic studies in patients greater than 55 years of&e with idiopathic hypertrophic- subaortic stenosis (defined as asymmetric septal hypertrophy and restin’g systolic anterior motion of the mitral valve). Three of these 28 patients were male; none of the 3 phowed calcification of the mitral anulus and 1 hadcalcific aortic valve disease. Of the 25 worhen, 8 had mitral anular calcification and 8 had calcific aofiic valve disease (only 2 of these patients had both findings ‘sitiultaneously). Thus, in OUTpopulation of 28 patients, with a mea’n age of 71 years and a standard deviation qf 7 years, there wtls a 29 percent incidence rat& of calcification of the mitral valve anulus and a 32 tiercent incidence iate of calcific aortic valve disease.‘The prevalence of mitral anular calcification in our laboratory in age-matched patients iti 30 percent-in women and 6 percent in men. Therefore in our patient pdpuhtion mitral anular calcification is a frequent finding, but its prevalence in patients with idiopathic hypertrophik subaortic steriosis is no different from that in our geneial (age-matched) population. To explore the question in reverse, that is, the incidence of idiopathic hypertrophic subaortic stenosis in patidntll’with mitral anular calcification, we reviewed 75 randumly chosen, complete echocardiographic recoids of patients greater than 55 years of age with definite mitral anular calcification as defined by Kronzon and Glassman. Of 21 men, none had evidence of idiopathic hypertrophic subaortic stenosis, 13 had calcific aortic valve’ disease and 11 had left atrial enlargement. Of the 54 women 2 had idiopathic hypertrophic,subaortic stenosis (as defined before), 34 had calcific aortic valve diiease and 19 had left atria1 enlargement. In our overall group with a mean age of 77 years (standard deviation 7 years), 2.7 peicent had idiopathic hypertrophic subaortic stenosis, 63 per-
-ember
1. K~UIZOII I, Ch8smm E: Mitral ring calcification in idiopathic hyperirophic subaortic stenosis. Am J Cardiol 4260-66. 1978
REPLY
It is evident that both groups find a high incidence of mitral anular calcification in older patients with idiopathic hypertrophic subaortic’stenosis. The major point of contention is whether this is an unusually high rate of coexistence or is secondary to an intrinsically elevated frequency of mitral anular calcification in all patients of&thisage group. Obviously, the basis of selection of patients for &hocardiographic study may influgnce the rate of fending mitral anular calcification. Kessler and Rahime indicated the prevalence of mitral anular calcification in’their laboratory in age-matched patients is 30 percent in women and 6 percent in meh. However, they give no details concerning types of patients who undergo echocardiographic stud& at their institution. The incidence of mitral anular calcification in ou? own-age-matched control subjects reported in the article is considerably lower. Possibly the discrepancy in our interpretation of these results is based ’ upon this djvergence of findings. In their group of patients with demonstrated mitral anular calcification, the mean age of 77 years was considerably higher than that in ours, which was only 64 years. Perhaps, in this population, the incidence of mitral anular calcification does iise precipitously with advancing age and may help to explain the disparate findings. Because 63 percent of their patients with mitral anular calcification had calcific aortic valve disease one might conclude that there is a high rate of coexistence of these two findings. This would be of interest if confirmed, but obviously requires further investigation. A nonexhaustive review of our own files does not support this hypothesis. We have observed:as is commonly recognized, calcification of the anterior mitral leaflet in association with calcific aortic stenosis. Although careful fluorosc!,py and echocardiogrephic analysis should separate thjs finding from mitral anular calcification it may be a source of confusion. Kessler and Rahime also mentionbd that calcific aortic stenosis was present in . . . . . assoclatlon with ldlopathlc hypertrophic subaort~c stenohi>
1979
The Amarkan Journal of CARDIDLDGY
Volume 44
579