LETTERS TO THE EDITOR

The platelet has been postulated to be important not only in initiating thrombosis b u t also in forming early plaque-like lesions. T h a t platelets might be involved in the genesis of atherosclerosis is not a new idea. Rokitansky suggested it well over 100 years ago. In 1947, Duguid demonstrated microthrombi in various stages of development in the aorta of autopsy patients and postulated that these thrombi may be the forerunner of atherosclerosis. Of significance, was Duguid's demonstration 2 t h a t endothelial cells could grow over mural thrombi and result in a smooth endothelial lining of the lumen. Experimentally, Spaet et al. 3 have shown t h a t mechanical injury to the rabbit aorta is followed by adhesion of platelets to endothelial surfaces. Harker et al. 4 have shown t h a t vascular endothelial damage occurs in baboons injected With homocystine. These lesions are the precursors to progressive muscular and endothelial changes which are indistinguishable from human atherosclerotic lesions. Prior t r e a t m e n t with platelet deaggregating agents will prevent these changes from occurring. 4 Homocystinuria, characterized by accelerated atherosclerosis, has been shown to be associated with decreased platelet survival, indicating increased consumption. Recently, it has been shown ~ that the accelerated development of atherosclerosis in the coronary arteries of heart transplant patients can be slowed by t r e a t m e n t with dipyridamole, although a causative role for these agents was not directly established. Abnormal platelet function, as d e t e r m i n e d b y decreased survival and increased aggregation, has been measured in some patients with coronary artery disease. 6,7 Agents such as aspirin, dipyridamole, warfarin sodium and sulfinpyrazone are being studied for their ability to prevent thrombosis in patients with arteriosclerotic cardiovascular disease. However, there are no clear-cut data that any one agent or combination of agents will prevent, in a statistically significant fashion, future coronary events. Are there human subjects with congenital coagulation disorders who can be used to study platelet function in the prevention of atherosclerotic heart disease? Hemophiliac patients die with coronary artery disease, s These patients have a deficiency of factor VIII, b u t without abnormalities of platelet-vessel wall interaction. However, patients with von Willebrand's disease (occurring in both male and female subjects) not only have deficiencies in factor VIII but also have abnormalities in platelet-vessel wall interaction. Thus, these patients with this life-long hereditary disorder may welt be an ideal model for study. Unfortunately, autopsy material and cardiac catheterization data on patients with van Willebrand's disease are scant. Preliminary reports indicate t h a t in pigs with von Willebrand's disease (pig), there may be a reduced incidence of atherosclerosis. 9 Because one would not choose to use invasive techniques in these patients for the diagnosis of atherosclerotic heart disease, one should rely heavily on data obtained from noninvasive procedures as well as prospective follow-up data. Pooled d a t a on these patients might shed light on the in vivo role of platelets in the development of atherosclerotic heart disease. John A. Ambrose, MD Louis M. Aledort, MD The Department of Medicine and the Division of Cardiology The Mount Sinai School of Medicine of the City University of New York New York, New York References 1. Stehbens WE: Role of hemodynamics in the pathogenesis of atherosclerosis. Prog Cardiovaso Dis 18:89-103, 1975 2. Ouguid JB: Pathogenesisof atherosclerosis. Lancet 2:925-927, 1949 3. Spaet TB, Gaynor E, Stemerman MB: Thrombosis, atherosclerosis and endothelium. Am Heart J 87:661-667, 1974

668

November 4, 1976

The American Journal of CARDIOLOGY

4. Harker LA, Slichter SJ, Scolt CR, et al: Homocystinemia--vascular injury and ar[erial thromhi, N Engl J Med 291:537-543, 1974 5. Rider AK, Copeland JA, Hunt SA, et ah Status of cardiac transplantation, 1975. Circulation 52c531-539, 1975 6. Steele PP, Welly HS, Davies H, et al: Platelet function studies in coronaryartery disease. Circulation 48:1194-1200, 1973 7. Haft Jl: Platelets, coronary a~ery disease and stress. In, Thrombosis, Platelets Anticoagulation and Acetyl Salicylic Acid (Donoso E, Haft JI, ed). New York, Stratton Intercontinental Medical Book, 1976, p 97-109 8. Aledort LM: Death in hemophilia. F.D.A. Proceedings of a Workshop on Hemophilia, 1976. In press 9. Bowie EJW, et al: Resistance to the development of spo.taneous atherosclerosis in pigs with von Willebrand's disease (ahstr). Program, Vth Congress of the International Society on Thrombosis and Haemostosis, Paris, France, July, 1975, p 322

INTRAAORTIC BALLOON PUMPING IN ACUTE MYOCARDIAL INFARCTION

We are from a 160-bed community hospital with active outpatient, emergency and intensive care unit services. We have a significant number of patients with acute myocardial infarction, some of whom have cardiogenic shock followed by the usual 80 to 90 percent mortality rate despite t r e a t m e n t with all medical means. Recently, we have been urged to transport such patients to larger facilities for intraaortic balloon pumping, with the suggestion that this may allow surgical intervention and significantly improve survival rates. Naturally, much controversy h a s arisen pro and con, and we would very much appreciate comments on whether, indeed, all, s o m e or n o n e of patients with acute myocardial infarction and cardiogenic shock should be so managed. Are there hard d a t a to indicate that this procedure improves survival over t h a t of "intensive" medical management in this s e l e c t e d g r o u p (patients with acute myocardial infarction and cardiogenic shock treated in accord with myocardial infarction research unit standards)? Martin F. Stein, Jr., MD Frank B. Flood, MD St. Joseph's Hospital Yonkers, New York REPLY

The writers pose a pertinent and timely question, the answer to which cannot be given with absolute certainty. Despite the attractive rationale of the intraaortic balloon pump, detailed clinical experience with its use in cardiogenic shock has been relatively sparse. This is because the incidence of shock after acute myocardial infarction is relatively small; in m y institution it is considerably smaller than t h a t cited in previous reports. Whereas a 10 to 15 percent incidence rate of cardiogenic shock in hospitalized patients with acute myocardial infarction is commonly quoted, our studies have shown a much lower rate. Shock developed in only 28 of 663 (4.2 percent) consecutive patients a d m i t t e d to the coronary care unit of Mount Sinai Hospital, New York in an 18 month interval. 1 We have attributed this lower rate to probable prevention of shock by p r o m p t and more effective t r e a t m e n t of congestive heart failure, arrhythmias, fluid deficits and metabolic abnormalities than was the practice before the coronary care unit era. Although it has not been proved, it is probable t h a t considerable progress is already being made in this regard in shock prophylaxis. Nevertheless, we are left with a residuum of patients with extensive acute and old myocardial damage whose shock state is generally refractory to all treatment. Our data indicate that it is unlikely that pump support and surgery will be effective in large numbers of these patients. If one assumes a reasonable "cutoff" age beyond which there should be reluctance to consider a patient for t e m p o r a r y circulatory support, angiography and surgery, only half of our patients with shock (2.4 percent of those with acute myocardial infarction) were less Volume 38

Intraaortic balloon pumping in acute myocardial infarction.

LETTERS TO THE EDITOR The platelet has been postulated to be important not only in initiating thrombosis b u t also in forming early plaque-like lesi...
150KB Sizes 0 Downloads 0 Views