A Common Link Between Unstable Angina Pectoris and Acute Myocardial Infarction

Ambrose et ali have suggested that un- stable angina pectoris, non-Q-wave acute mvocardial infarction (AMI) and O-wave AhI are linked by the common presence of unstable coronary lesions-their type II eccentric lesion-in all 3. This concent is similar to a proposal that we made in 1983.* Snecificallv. we nronosed that in- tracoronary thrombi could& intermittent- ly obstruct coronary arteries causing un- stable angina, non-Q-wave or Q-wave AMI-depending on the duration of ob- struction, availability of collateral circu- lation and status of factors determining oxygen demand.

Ambrose et al noted relatively few in- tracoronary thrombi angiographically and suggested that others may be too lib- eral in diagnosing these. We saw intracor- onary thrombi in over half of unstable an- gina patients catheterized within 24 hours of their most recent angina at rest and in 28% of those in whom angiography was performed within 1 to 14 days.3 Our pa- tients did not receive heparin before angi- ography. In contrast, Ambrose’s unstable angina and non-Q-wave AM1 patients were catheterized at an unspecified inter- val following their most recent pain at rest, and one-third received heparin be- fore angiography. We have previously demonstrated rapid disappearance of in- tracoronary thrombi in patients given heparin4 Moreover, angioscopic study has shown a very high incidence of intra- coronary thrombi in unstable angina pa- tients, even when these were not visual- ized angiographically.5

Thus while we agree with Ambrose et al that there is indeed a common link be- tween the 3 unstable ischemic syndromes, we believe that they have insufficiently emphasized the role of intracoronary thrombosis, perhaps because their study was not appropriately designed to detect it.

Steven G. Meister, MD Nelson M. Wolf, MD

Philadelphia, Pennsylvania 14 April 1988

1. Ambrose JA, Hjemdahl-Monsen CE, Boni- car S, Gorlin R, Fuster V. Angiographic dem- onstration of a common link between unstable angina pectoris and non-&-wave acute myocar- dial infarction Am .I Cardiol 1988;61:244- ̂ >-

* Letters (from the United States) concerning a particular article in the Journal must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 dou- ble-spaced typewritten pages. Two copies must be submitted.

2. Mandelkorn JB, Wolf NM, Singh S, Shechter JA, Kersh RI, Rodgers DM, Work- man MB, Bentivoglio LG, LaPorte SM, Meis- ter SG. Intracoronary thrombus in nontrans- mural myocardial infarction and in unstable angina pectoris. Am J Cardiol 1983;52:1-6. 3. Capone G, Wolf NM, Meyer B, Meister SG. Frequency of intracoronary filling defects by angiography in angina pectoris at rest. Am J Cardiol 1985;56:403-406. 4. Wolf NM, Hartman D, Shechter JA, Sokil AB, Capone G, Meister SG. Effect of heparin on intracoronary thrombi in unstable ischemic syndromes (abstr). JACC 1986;7:107A. 5. Forrester JS, Litvack F, Grundfest W, Hick- ey A. A perspective of coronary disease seen through the arteries of living man. Circulation 1987:75:505-513.

REPLY: I believe the comments of Meister and Wolf reflect some confusion on their part concerning intracoronary thrombus formation in unstable angina. The inci- dence of intracoronary thrombus varies widely. Clearly some of these differences are methodologic in that the definition of thrombus is based solely on visual assess- ment and there is no standard definition for intracoronary thrombus, especially when the ischemia-related artery is pat- ent. What 1 investigator describes as in- tracoronary thrombus another might clas- sify as a complex plaque. While complex plaques probably contain thrombus, it is unclear if that thrombus has the same sig- nificance as a “filling defect” distal to or within the lesion. Other important factors that probably influence the incidence of filling defects in unstable angina include the use of heparin before angiography and whether or not the patient has been stabi- lized on medical therapy. These latter fac- tors were alluded to in the article ques- tioned by Meister and Wolf. Therefore, I have no doubt that intracoronary throm- bus is important in unstable angina. While I rarely see distal defects in this syndrome, the identification of complex lesions identifies thrombus in most cases.

John A. Ambrose, we New York, New York

16 May 1988

Mitral Valve Prolapse Is Not a New Disease Entity

I enjoyed reading the 2 recent articles bv Woolevi** concerning the historv of mi- tral valve prolapse (GVP). As Wooley and Boudoulas rightly pointed out,“dur- ing the present century in this country rheumatic heart disease and coronary ar- tery disease are examples of changing prevalence, whereas MVP exemplifies changing recognition.“’ Contrary to a re- cent editorial,3 MVP is not a new disease. In my editorial on MVP, which was pub-

lished over 12 years ago,4 I commented on the evolution of our understanding of the then “hot” topic and cited a story I heard in my medical school days. A professor of medicine always gave the same questions every year in the final examination. When asked by his puzzled peers and students as to why he never changed the questions, the professor’s answer was that, although his questions were the same, the answers he received varied from year to year. This variability of explanation of an identical phenomenon certainly is true for our un- derstanding of MVP, especially regarding its worldwide prevalence.5

Although Griffith6 suggested in 1892 that an apical mid-to-late systolic mur- mur might be due to mitral regurgitation, little further attention was paid to it in the ensuing 50 years. This is because such au- thorities as Gallavardin, McKusick and Leatham all maintained that the midsys- tolic click or late systolic murmur, or both, were mostly extracardiac in origin4 The phenomenon of “hero worship” led Carmichael to conclude that “over time we will find that the mitral prolapse is something new under the sun,” 3 He based his conclusion on his deep faith in all his “medical heroes,” e.g., Kerns, McGuire, Snraaue and White. who anuarentlv did not make this diagnosis and “could not have overlooked this now ubiquitous clini- cal entitv.“3 To this list of “medical he- roes” I should now add Lewis A. Connor, who did not call MVP extracardiac as the other heroes did but merely considered it “accidental and insignificant.“’ Cardiolo- gy, as is medicine in general, is a “pendu- lum that swings perpetually reflecting the progress of medical knowledge and the change of scientific reasoning.“4 MVP is no exception.

Tsung 0. Cheng, MD

Washington, DC 2 May 1988

1. Wooley CF, Boudoulas H. From irritable heart to mitral valve prolapse: World War I- The U.S. experience and the prevalence of api- cal systolic murmurs and mitral regurgitation in drafted men comuared with nresent dav mi- tral valve prolapse Studies. Am-J Cardioli988; 61:X95-899. 2. Wooley CF. Lewis A. Connor, MD (1867- 1950), and lessons learned from examining four million young men in World War I. Am J Cardiol 1988;61:900-903. 3. Carmichael DB. Reflections on medical he- roes and mitral prolapse. Can J Cardiol 1987;3:261-262. 4. Cheng TO. The click-murmur syndrome. A medical pendulum and a unifying concept. Chest 197670.569-572. 5. Cheng TO, Barlow JB. Mitral valve pro- lapse. Its prevalence around the world. Angiol- ogy, in press. 6. Griffith JPC. Midsystolic and late-systolic mitral murmurs. Am J MedSci 1892;104:285- 294.

660 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 62