Criteria for mitral valve prolapse

Criteria for mitral valve prolapse

LETTERS is elevated within the ischemic zone and because catecholamines are released from intraventricular sympathetic nerve terminals, it has been p...

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is elevated within the ischemic zone and because catecholamines are released from intraventricular sympathetic nerve terminals, it has been postulated that acute ischemia might be conducive to the genesis of slow channel-dependent action potentials.5 Indeed, these conditions are somewhat similar to those required in vitro to induce the “slow responses.” On the other hand, other factors such as hypoxia, acidosis and poor energy reserves, which undoubtedly are of importance during ischemia, tend to inhibit the genesis of the slow response.” The analogy between the experimentally induced “slow response” and that which might occur during acute ischemia is limited because, in vitro, the primary alterations that occur are those of the extracell milieu whereas, during acute ischemia, the alterations of this milieu are secondary to alterations of the cell membrane. Thus, although some conditions during ischemia appear favorable to the genesis and maintenance of the “slow response,” other factors may inhibit its development. Nevertheless, if one assumes that slow channel-dependent action potentials are generated in the ischemic zone, and that they are responsible for the delayed and slow activation of that zone, then inhibition of the “slow response” by verapamil should result in a loss of activation of the ischemic zone and, therefore, in further deterioration of co’nduction at that site. On the contrary, verapamil increased the amplitude and decreased the time to onset of the electrogram recorded from the ischemic zone. Conceivably, verapamil might improve conduction by suppressing slow channel-dependent automaticity and restore maximal diastolic potential toward normal, but this is quite speculative. In fact, the conditions induced by acute myocardial ischemia may not be appropriate for the genesis of slow channel-dependent automaticity.7

problem but from the opposite perspective. They presented 12 patients who had angiographic evidence of posterior systolic motion of one or both mitral valve leaflets. Of this group, nine had no systolic click, and eight had echocardiograms that were reported as clearly negative for mitral valve prolapse. They concluded from these results that the clinical and echocardiographic manifestations of mitral valve prolapse lack the sensitivity of the ventricular angiogram. The correlation of the echocardiographic and clinical findings of mitral valve prolapse is not given in this paper. It would also be interesting to know what the frequency of angiographically determined mitral valve prolapse is in a random collection of angiograms from their institution. In conclusion, it appears that the diagnosis of mitral valve prolapse lacks a gold standard. I agree with Smith et al. that before one can brand the echocardiogram as insensitive or alternatively brand the angiogram as nonspecific, more reliable criteria for the diagnosis for valve prolapse need to be established. Jack D. Horton, MD Division of Cardiology Georgetown University Hospital Washington, D. C. References 1. Smith ER, Fraser

DB, Purdy JW, Anderson RN: An&graphic dlaqnosis of mitral valve prolapse: correlation with &hocardiography. Am J Cardiol 40:165-170, 1977 2. Ruwitch JF, Weiss AN, Fleg JL, McKnighl RC, Ludbrook PA: Insensitivity of echocardiography in detecting mitral valve prolapse in older patents with chest pain. Am J Cardiol 40:666-690. 1977

Victor Elharrar, PhD Winston E. Gaum, MD, FACC Douglas P. Zipes, MD, FACC Department of Medicine Indiana University School of Medicine Indianapolis, Indiana


References 1. Smith HJ, Singh BN, Nisbet HD, et al: Effect of verapamil on infarct size following experimental coronary occlusion. Cardwasc Res 9:569-576. 1975 2. Smnh HJ, Goldstein RA, Grmh JM, et al: Selective depression of ischemic myocardium by verapamil (abstr) Am J Cardiol 37: 174. 1976 3. Kuparsmilh J, Shiang H, Litwak RS, et al: Electrophysiologic effects of verapamil in canine myocardiol ischemia (abstr). Am J Cardiol 37:149, 1976 4. Bailey JC. Elharrar V, Zipes DP: Slow channel depotarization:mechanism and control of arrhythmia. Ann Rev Med. in press 5. Cranefield PF: The Conduction of the Cardiac Impulse. Mount Kisco. NY, Futura, 1975 6. Sperelakis N, Schneider JA: A metabolic control mechanism for calcium ion influx that may protect the ventricular mvocardwxl cell. Am J Cardiol 37:1079-1065, 1976 7. WI&IS JR, Cranefield PF: Two levels of resting potential in canine cardiac Purkinje fibers exposed to sodium-free solutions. Circ Res 39:466-474. 1976






An interesting sequence of papers has recently appeared in this Journal. Smith et al.1 reported an angiographic incidence of mitral valve prolapse of 43 percent in 336 consecutive patients undergoing left ventricular angiography. Six of these patients had clinical evidence of the click-murmur syndrome, and all six had echocardiographic evidence of mitral valve prolapse. The high percentage of patients who only had angiographic evidence for mitral valve prolapse led the authors to suggest that posterior bulging of the mitral valve on left ventricular angiography is not specific for mitral valve prolapse. Two months later, Ruwitch et al.? approached the same


October 1978

The American Journal ot CARDIOLOGY


We agree that mitral valve prolapse is indeed a disease “without a gold standard.” At present, the angiographic criteria are possibly no more accurate a reflection of the anatomic abnormality of mitral valve prolapse than are the echocardiographic or, indeed, clinical criteria. The definitive information as yet unavailable is to what extent the angiographic criteria of mitral valve prolapse (or, for that matter, echocardiographic or clinical criteria) correlate with the pathologic findings. Unfortunately, even the pathologic abnormalities themselves are not well defined. Shrivastava et a1.l in a recent excellent review of the pathology of mitral valve prolapse, leave little doubt that there is no clear-cut dividing line between the normal and abnormal mitral valve, on either the microscopic or the macroscopic level. We agree with Smith et al. that posterior billowing of the mitral valve leaflets in systole is not necessarily specific for mitral valve prolapse. The majority of the patients described by Smith et al. had mild (grade I) mitral valve prolapse of a single scallop of the posterior leaflet, presumably the posterolateral scallop in most instances. We chose to exclude such patients in our study, believing that this “abnormality” represented either the normal left ventricular fornix or minimal (insignificant) bulging of the posterolateral scallop. If one excludes these cases from the series of Smith et al., the percentages of angiographic mitral valve prolapse associated with other conditions become substantially smaller and appear less likely to represent normal variation. In our study, we did not deal with the sensitivity of the left ventriculogram relative to either the clinical manifestations or the pathology of mitral valve prolapse. Our goal was simply to select a small number of indisputably abnormal left ventriculograms and to evaluate the echocardiographic sensitivity for mitral valve prolapse in this highly selected group. Util-

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