Volume 106 Number 2

the legs caused immediate relief of pain. The possible explanation for this phenomenon seems to be the sudden increase in venous return, causing brisk dilatation of the right atrium and ventricle, probably resulting in closer approximation between the myocar- dium and the inflamed pericardium. We have observed this sign in six of eight consecutive patients with acute pericarditis. One patient in whom this sign could not be elicited had a moderate pericardial effusion which probably prevented contact between myocardium and pericardium. The “elevated legs” sign was present in three patients prior to appearance of a friction rub and in four patients prior to demonstrable ECG changes. This sign may be helpful in the early diagnosis of pericarditis without effusion in the absence of a friction rub or ECG changes.

D. Aderka, M.D. J. Pinkhas, M.D.

Department of Medicine “D” Beilinson Medical Center

Petah Tikua 49100 Israel

HYPOPHOSPHATEMIA IN MYOCARDIAL INFARCTION

To the Editor: Although Yaroslavsky et al.’ may be correct in hypothesizing

that the mild decline in serum phosphate levels found in patients with acute myocardial infarction may reflect transcellular shifts to intracellular compartments, there is no evidence that this is limited to cardiac muscle. The stress response may include hyperventilation, which is a potent stimulus for transcellular shifts of phosphorus into skeletal muscle.2 Many respiratory illnesses are associated with a high prevalence of more profound hypophosphatemia than is found with acute myocardial infarc- tion.3 Therefore the mechanism by which serum phosphate decreases in patients with acute myocardial infarction needs to be elucidated, as it may represent a more generalized phenomenon found in hospitalized patients who are anxious, in pain, and are treated with intravenous dextrose.4

Jeffrey Fisher, M.D. Division of Cardiology

The New York Hospital-Cornell Medical Center 525 E. 68th St.

New York, NY 10021

Letters to the Editor 425

REFERENCES

Yaroslavsky A, Blum M, Peer G, Bernheim J, Aviram A: Serum phosphate shift in acute myocardial infarction. AM HEART J 1049384, 1982. Knochel J: The pathophysiology and clinical characteristics of severe hypophosphatemia. Arch Intern Med 137:203, 1977. Fisher J, Magid N, Kallman C, et al: Respiratory illness and hypophosphatemia. Chest 83:504, 1983. Guillou PJ, Morgan DB, Hill GL: Hypophosphatemia: A complication of “innocuous dextrose-saline.” Lancet 2:710, 1976.

REPLY

To the Editor: We agree that the possible phosphate shift is not limited to

myocardial tissue. However, we do not feel that hyperventilation plays a significant role in this phenomenon. The hyperventilation is usually limited to the first day and respiratory alkalosis, if present, is mild and of short duration. The hypophosphatemia, on the other hand, was manifested on the third and fourth days. Moreover, the control group selected by us was similar to the infarct group concerning factors such as pain and anxiety. Intravenous glucose, if given, was provided only as an “open line,” and amounts of glucose actually administered were very small.

Miriam Blum, M.D. Department of Nephrology

Rokach Hospital Tel-Aviv Medical Center, Israel