138 Letters to the Editor July 1981

Amwican HoerI Journal

REFERENCE

1. American Heart Association Committee Report: Recom- mendations for standardization of leads and of specifications for instruments in electrocardiography and vectorcardiogra- phy. Circulation 52:11, 1975.

LACK OF RESPONSE OF SALT TASTE TklRESHOLD AND PREFERFNCE TO DIETARY SODIUM RESTRICTION IN MILD HYPERTEN’SlON*

To the Editor: Patiente with essential hypertension are reported to have a

greater preference for sodium chloride than normotensives.’ Evidence regarding taste thresholds is conflicting.z We undertook to test the hypothesis that a reduction in dietary sodium intake of untreated men with labile blood pressure elevations sufficient to reduce blood pressure would result in an increase in sodium chloride taste threshold and a decrease in preference for salty liquids, Sodium chloride taste threshold and preference of 15 middle-aged white men with labile blood pressure elevations (diastolic blood pressure >90 mm Hg on screening, average blood pressure after four cImic visits 133/87 k SD 13/6 mm Hg) were measured twice before and at least once after a &month interven- tion program aimed at lowering sodium intake to 70 mmol/day, Threshold was measured by presenting patients with a series of 14 unknown NaCl solutions ranging in concentration from 1 to 60 mmol/L and determining the lowest concentrations correctly differentiated from water and recognixed as distinctly salty. Preference was measured by asking patients to rate the taste of sets of six broth and tomato juice solutions with NaCl concentra- tions ranging from 5 to 500 mmol/L. The average of the iowest concentrations to receive the highest rating for broth and juice was tionsidered to be the concentration of preference. Test-retest Spearman’s rank correlation coefficients were 0.82 and 0.91 for threshold and preference (p < 0.061) at baseline; no significant differences between test and retest values were found (F = 0.03, 0.02 respectively). Patients’ sodium excretion fell from 170 * 55 mmol/24 hr before, to 90 * 83 mmol/24 hr after intervention (p < 0.01). Systolic blood pressure fell 4.4 mm Hg (p < 0.2) and diastolic fell 5.7 mm Hg (p c 0.05). However, there was no significant change in NaCl taste threshold (recognition before 20.2 and after 22.5 mmol/L; change 2.3, p < 0.4, 95% confidence limits (CL) & 7.1). Preference decreased from 98.3 to 64.6 mmol/ L; change 33.8, p < 0.1, 95% CL & 40.2. Thus the loss of the craving for salt and enhanced taste acuity following a reduction in intake from high to moderately low levels noted by Jonathan Swift in Gulliver’s Travels and by many medical and nonmedical observers since, does not seem. to be explained by a large change in objectively measured salt taste threshold, although there was a tendency for preference for salty liquids to decrease. Psychologic habituation may be a more likely explanation for these observa- tions than a physiologic change in taste acuity. The effects of extreme degrees of sodium restriction (5 10 mmol/day) sufficient

*Supported by granta from th Graduakz School, University of Minnesota; the Minnesota Medical Foundation; and National Institutes of I-Iealth Research Career Development Award K04HL-l003!E~ (R. F. Gillurn, M.D.).

to produce intravascular volume depletion were not asses& but might be expected to lower salt taste tbreshold and preference similar to diuretics1

Richard F. Gillurn, M.D. Ronald J. Prineas, B.S., M.B., Ph.D.

Paul Anderson, M.D. Joseph Kebede, M.D.

Laboratory of Physiological Hygiene University of Minnesota School of Public Health

Stadium Gate 27 611 Beacon St., SE.

Minneapolis, MN 55455

REFERENCES

I.

2.

Schechter PJ, Horwitz D, Henken RI: Salt preference in patients with untreated and treated essential hypertension. Am J Med Sci 26>320, 1976. Langford HG, Watson RL, Thomas JG: Salt intake, diuret- ics and the treatment of hypertension. Trans Am Clin Climatol Assoc 66~32, 1977.

VEi4TRKXLAR PREW)TlJRk 8EAT LOCALiZATlON IN WI’RAL VALVE PROLAPSE SYNOROME

To the Editor: We read with interest the article by Dr. Lichstein in the

JOURNALI localizing the site of origin of ventricular premature beats (VPBs) in mitral valve prolapse patients. Utilixing the Frank vectorcardiograph (VCG) lead system, he was able to show that the mean QRS vector of spontaneous VPBs was anterior and inferior in direction in 7 of 10 patients and presumably originated from the posterobasal region of the left ventricle.’ In work not cited by Lichstein, we examined the VCG characteristics of VPBs provoked by mechanical catheter stimulation of the inflow and outflow portions of the left and right ventricles during cardiac catheterization.z Thirty patients with diverse etiologic heart problems (valvular, coronary, congenital, and undetermined) were studied. Two cases probably had mitral valve prolapse. The cube lead system was used and maximum QRS vectors of stimulated VPBs were plotted. Basal left ventricular VPBs were consistently oriented in an inferior (33 degrees k 14 degrees frontal plane) and anterior (35 degrees k 33 degrees transverse plane) direction and either slightly to the left or to the right. It would be of interest to correlate the VCG orientation of both spontaneous and stimulated VPBs in patienta with mitral valve prolapse and selected patients with coronary heart disease whose myocardial damage was local&d in the posterobasal regions of the left ventricle.

Michuel D. Klein, M.D. Charles L. Feldman, Sc.D.

Section of Cardiology UniversiQ Hospital

75 E. Newton St. Boston, MA 02118

REFERENCES

1. Lichstein E: Site of origin of ventricular premature beate in patients with mitral valve prolapse. AM HEART J IMh450, 1930.

Volume102 Number I Letters to the Editor 139

2. Klein MD, Feldman C, Clark DL, Flessas AP, Ryan TJ, Peura RA: Vectorial characteristics of ventricular extrasys- toles stimulated during cardiac catheterization. J Electro- cardiol9~103, 1976.

REPLY

To the Editor: I appreciate the intereat that Dm. Klein and Feldman have

shown in my report. I regret that I overlooked their article in my bibliography, since it is a very well done study. I am gratified to see that their resulta concerning ventricular premature beat (VPB) localization are similar to mine. I agree that it would be of clinical interest to correlate orientation of both spontaneous and stimulated VPBs in these patients It is with this type of clinical study that we may determine the mechanism of ventricular irritability in patients with mitral valve prolapse.

Edgar Lichstein, M.D. Mairnonides Medical Center

Division of Cardiology 4802 Tenth Ave.

Brooklyn, NY 11219

MITRAL VALVE PROLAPSE SYNDROME IN ANXIETY NEUROSIS

To the Editor: This communication is in regard to the recent report by

Venkatesh et al. in the JOU~AL.~ Our clinic has a number of patients suffering from the effort syndrome with the typical symptoms outlined in their article. While it is noteworthy that the effort syndrome is associated with increased prevalence of mitral valve prolapse, I am concerned that these patients, who are generally extremely anxious about whether or not they have heart disease, are likely to become even more handicapped by being informed that they have a cardiologic abnormality.

It is my experience that patients with the effort syndrome are referred among specialty clinics for investigations of increasing sophistication since this condition is not well understood. The syndrome can be recognized by hematologic screening, ECG, and chest x-ray. Thyroid function tests. and fasting blood glucose are useful in assuring the patient that she (five of six patients at our hospital are women) does not have a metabolic disease. Echocar- diography will not help me in limiting the number of studies for these troubled patients In my opinion, their anxiety might increase upon detection of mitral valve prolapse, a condition for which there is no substantive therapy. I subscribe to the theory that one of the most important causative features of the effort syndrome is poor selfimage. Too often these patients spend much nonproductive time in comparing their (as they believe) insignif-

icant attainments to those of more talented (again as they believe) siblings or spouse.

Richard D. Forrest Dept. of Internal Medicine

Central Hospital S-961 85 Boden, Sweden

REFERENCE

1. Venkatesh A, Pauls DL, Crowe R, Noyes R, Van Valken- burg C, Martins JB, Kerber RE: Mitral valve prolapse in anxiety neurosis. AM HEART J 100:302, 1980.

REPLY

To the Editor: We believe that all patients with anxiety neurosis or effort

syndrome symptoms should be suspected of having the mitral valve prolapse syndrome. Therefore all patients should have a careful physical examination looking for systolic clicks and murmurs in the supine as well as the standing position. In those patients with murmurs and/or clicks suggestive of mitral valve prolapse, contirmatory evidence by echo may be helpful since (1) subacute bacterial endocarditis prophylaxis is probably indicated and (2) propranolol may be helpful in prolapse patients with chest pain or symptomatic arrhythmias. Patients with anxiety should not have organic abnormalities passed over because of fear that anxiety would be accentuated. Organic disease should always be managed appropriately. If the echo is negative for mitral valve prolapse, the patient with an otherwise benign murmur may be appropriately reassured about the absence of valvular heart disease. Patients who complain of palpitations at rest or excercise should not be reassured until investigation either by resting ECG during symptoms, or during 24-hour Holter ECG or exercise testing with production of symptoms, yields benign sinus tachycardia or premature complexes. The finding of supra- ventricular or ventricular tachycardias does not warrant reassur- ance in the anxious patient but suggests further consideration for drug or surgical therapy.

The use of further testing, therefore, is helpful to confirm symptoms and findings in patients in whom prolapse or arrhyth- mias may occur and for which therapy may prove helpful. Conversely, if testing is not indicative of organic abnormalities, reassurance of the patient and specific treatment for anxiety neurosis can then be based upon data and not an assumption that the symptoms are anxiety related.

Richard E. Kerber, M.D. A. Venkatesh, M.D.

Raymond R. Crowe, M.D. RusseLl Noyes, M.D.

James B. Martins, M.D. Cardiovascular Division

Department of Internal Medicine lJniversi& of Iowa Hospital and Clinics

Iowa City, IA 52242