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Fig. 2. Second two-dimensional echocardiogram 13 days later showing complete disappearance of thrombus.

REFERENCES

1. Butman SM. Rapid resolution of a massive left ventricular thrombus by usual systemic anticoagulation. AM HEARTJ

1991;122:864-6.

2. Kyrle KA, Korninger C, Gossinger H, Glogar D, Lechner K, Niessner H, Pabinger I. Prevention of arterial and pulmonary embolism by oral anticoagulants in patients with dilated cardiomyopathy. Thromb Haemost 1985;54:521-3. 3. Halperin JL, Petersen P. Thrombosis in the cardiac chambers: ventricular dysfunction and atria1 fibrillation. In: Fuster V, Verstraete M, eds. Thrombosis in cardiovascular disorders. Philadelphia: WB Saunders, 1992;165-87. 4l8141828

AMBULATORY BLOOD PRESSURE AND POSTPRANDIAL HYPOTENSION To the Editor:

The recent introduction of a noninvasive ambulatory blood pressure (BP) monitoring technique has provided a great deal of information concerning changes in BP along with various types of physical behavior. Changes in BP in relation to ingestion of meals is representative of them. Patients with autonomic dysfunction

Letters to the Editor

1669

often become hypotensive after eating (postprandial hypotension [PPH]), and this PPH usually lasts for 2 or 3 hours. Therefore noninvasive ambulatory BP monitoring is convenient for detecting a BP reduction after meals. Inasmuch as the frequency of PPH has yet to be determined, we monitored the circadian pattern of BP with special reference to prandial behavior. The purpose of this report was to introduce our experience in treating PPH with caffeine and a somatostatin analogue. Ambulatory BP was monitored in 100 clinically healthy volunteers (55 subjects aged 21 to 40 years; 45 subjects aged 41 to 60 years), 50 patients with hypertension (aged 41 to 60 years), 22 patients with diabetes (aged 47 to 74 years), and 15 patients with Parkinson’s disease (aged 45 to 75 years). Measurements of systolic and diastolic BP and heart rate (HR) were obtained at 15-minute intervals over 48 hours with an ambulatory monitor (ABPM-630, Colin Medical Instruments Inc., Komaki, Japan). This instrument provides both oscillometric and auscultatory measurements. The accuracy of this device has been validated previously.‘-” It is small (16.5 x 3.6 X 8.9 cm), lightweight (830 gm), and nearly silent; hence it is less sleep disturbing. Carbon dioxide cartridges are required to inflate the cuff. Data and events (four event markers are provided by the instrument) are recorded in a solid-state memory, which holds more than 600 sets of data and can be connected to an analyzer (AS-loo) for transfer of data to a personal computer for analysis. PPH was defined in this study as a decrease in systolic BP of more than 20 mm Hg within 3 hours after a meal was eaten. When PPH was observed at least once among the six meal times during the 48hour monitoring period, those subjects were defined as having PPH. In the patients selectively found to have PPH, it was confirmed by a 75 gm oral glucose tolerance test (OGTT). That is, all medication was withheld for 1 day before the study, and there was no oral intake of fluid after midnight. BP and HR were monitored every 5 minutes for at least 3 hours after oral administration of 75 gm of glucose in 225 ml of water. Blood samples were drawn for analysis of glucose and insulin levels at 0, 30, 60, and 120 minutes after the oral administration of glucose. Blood glucose and plasma insulin levels were measured by the Glu-DH method and radioimmunoassay, respectively. In three patients with Parkinson’s disease who had PPH, 250 mg of caffeine was administered orally with 100 ml of water 30 minutes before the 75 gm OGTT. In one of the three patients with Parkinson’s disease, the effect of somatostatin on PPH was also examined. A low dose of a long-acting somatostatin analogue @MS-201-995, 0.4 pg/kg, Sandoz, Inc., East Hanover, N.J.) was administered subcutaneously 30 minutes before the same 75 gm OGTT. An example of a 48-hour BP profile in a patient with PPH is shown in Fig. 1. PPH appears repeatedly after meals are eaten. It should be noted that PPH was observed even in clinically healthy subjects-that is, in 8 of 55 subjects (14.5%) aged 21 to 40 years and 13 of 45 (28.9%) aged 41 to 60 years. Among subjects with hypertension or diabetes, PPH was observed in 18 of 50 (36.0:;) and in 6 of 22 (27.2%), respectively. PPH was most frequently observed in patients with Parkinson’s disease-10 of 15 (66.7 7;). The postprandial decrease in systolic BP in these patients was more than 30 mm Hg and lasted several hours. One patient with Parkinson’s disease, in whom PPH was confirmed by the 75 gm OGTT, had a decrease in systolic BP up to 60 mm Hg, which lasted for more than 3 hours (Fig. 2). Diastolic BP also decreased along with systolic BP, but the HR did not change significantly. In three patients with such marked PPH, the effect of caffeine was examined. As a result, PPH improved in all of them but was not completely resolved (Fig. 2, Lower panel). PPH was prevented in a patient with Parkinson’s disease not only by pretreatment with caffeine (Fig. 3, Middle panel) but also with a low dose of a long-

1670

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to the Editor

4merican

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BP-related phenomenon that occurs most often in patients with Parkinson’s disease. In recent years, noninvasive ambulatory BP monitoring has been used frequently. Results of this study show that this technique is one of the most convenient methods for detecting PPH. The precise mechanism of PPH is as yet unknown, but previous studies have yielded quite a few findings relating to the origin of PPH. It is generally recognized that PPH is caused by inadequate

glucose (759)

a

5

acting somatostatin analogue (Fig. 3, Right panel). In contrast to the incomplete improvement with caffeine, PPH was completely prevented by somatostatin, along with suppression of t,he increase in plasma insulin levels after ingestion of a meal. Overall this report shows that PPH is not uncommon even in young (14.5’; ) and middle-aged (28.9”, ) subjects and confirmed that it is an age- and

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gestion. Food ingestion increases splanchnic blood flow and gastrointestinal fluid secretion. Such redistribution of fluid volume compromises cardiac filling, decreases cardiac output, and leads to systemic hypotension. Certain substances such as caffeine, indomethacin, somatostatin, insulin. IA-threo-XGdihydroxyphenylserine, and vasopressin have been implicated in PPH. Onrot et a1.j have stressed the importance of caffeine in blockmg the effects of adenosine-mediated splanchnic vasodilatation. Hoeldtke et al? have reported that low doses of somatostatin analogue prevent PPH. The physiologic basis for the therapeutic effect of somatostatin is unclear, but it is known to be an agent that inhibits gastrointestinal hormone secretion. Results of the stud,v by Hoeldtke

Fig. 2. PPH confirmed by 75 gm OGTT. Upper panel, Decrease in systolic BP up to 60 mm Hg in patient with Parkinson’s disease. Lower panel, Marked improvement in PPH with pretreatment with caffeine.

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Fig. 3. Another example of PPH. Left panel, PPH along with increasesin blood glucoseand plasmainsulin levels. PPH improves after pretreatment with caffeine (middle panel) and is completely prevented by somatostatin (right panel). Note that somatostatinnot only suppressesPPH but alsoincreasesglucose and insulin levels.

et al.5 showed that insulin secretion was inhibited after administration of somatostatin analogue. Our observation also showed a definite suppression of the increase in plasma insulin levels after a meal was eaten when somatostatin analogue prevented PPH. It is worth mentioning that PPH was prevented in the same patient not only with caffeine but also with somatostatin. This is the first report to provide evidence that PPH is produced by multiple factors. It is well known that patients with autonomic neuropathy may exhibit increased sensitivity to the pressor effects of a variety of drugs including norepinephrine, tyramine, and vasopressin. Therefore it is possible that multiple factors are involved in the pathophysiologic mechanism of PPH. Shigeko Nakajima, MD Kuniaki Otsuka, MD Takashi Yamanaka, MD Keigi Omori, MD Yutaka Kubo, MD Takamichi Toyoshima, MD Yoshihiko Watanabe, MD Haruo Watanabe, MD Department of Medicine I Tokyo Women’s Medical College Daini Hospital Nishiogu 2-l-10, Arakama-ku Tokyo 116, Japan REFERENCES 1. White WB, Lund-Johansen P, McCabe EJ. Clinical evaluation of the Colin ABPM 630 at rest and during exercise: an ambu-

latory blood pressure monitor with gas-powered cuff inflation. J Hypertens 1989;7:477-83. 2. Otsuka K, Cornelissen G, Watanabe H, Hunt SC, Halberg F. Time-varying limits for single blood pressures and heart rates of group-synchronized healthy women Heart Vessels 1991; 6:107-11. 3. Kuwajima I, Suzuki Y, Shimosawa T, Otsuka K. Kawamura H, Kuramoto K. Effect of nifedipine tablets on ambulatory blood pressure in patients aged 65 years with systemic hypertension. Am J Cardiol 1991:68:1351-6. 4. &rot J, Goldberg MR, Biaggioni I, Hollister AS, Kincaid D, Robertson D. Hemodynamic and humoral effects of caffeine in autonomic failure. Therapeutic implications for postprandial hypotension. N Engl J Med 1985;313:549-54. 4l8141829

QT INTERVAL AFTER MYOCARDIAL INFARCTION To the Editor: We point out the following corrections in our recently published article: Peaks of QT, lengthening in Halter recordings as a marker of life-threatening arrhythmias in post-myocardial infarction patients (AM HEART J 1992;124:234). In Table I the statistical significance for group I in columns 2 (QT, ~460) and 3 (QT, 2480) should be deleted, and the significant difference between groups I and II for group I in column 4 (QTc ~500) should be p < 0.02. In Table II the percentage of group III patients in column 2 (QT, ~460) should be 1.6%; the percentage of group II patients should