Spontaneous resumption of sinus rhythm after prolonged AF

Letters

Mitral

valve

prolapse

syndrome

To the Editor: In the March, 1979, issue of AMERICAN HEART JOURNAL there appeared several interesting articles about the mitral valve prolapse syndrome. In the study by Udoshi and associates, (97:303, 1979), the authors made some interesting observations regarding time relations between systolic murmur and echocardiographic mitral prolapse. Although the study was not primarily designed to evaluate the acoustic characteristics of the rnitral valve prolapse syndrome, I should like to make some comments regarding tlhese characteristics. In typical cases the murmur associated with mitral valve prolapse is meso- to telesystolic, and there is correlation with the timing of prolapse on echocardiography. On the other hand, there are cases of mitral valve prolapse where we can register only early systolic murmurs, but now they do not correspond with the timing of prolapse determined by echocardiography. Of six patients with protosystolic murmur, described in the article by IJdoshi and colleagues, five had late systolic prolapse and one had holosystolic prolapse. In those patients with early systolic murmur and late systolic prolapse there need not be any causal relationship between the mitral valve prolapse and the murmur. The latter may represent coincidental murmur of different genesis, for instance an innocent murmur. In such cases the mitral valve prolapse in reality is silent. Perhaps the rnitral valve prolapse syndrome only rarely or never causes early systolic murmurs. , There are some practical implications of this presumption. Subjects with systolic murmur which is related to the mitral valve prolapse generally have a less favorable prognosis regarding progression of mitral regurgitation or the risk of developing infective endocarditis, when we compare them with those patients who have only an isolated systolic click. Hence, in subjects with the mitral valve prolapse syndrome and protosystolic murmur with or without an associated systolic click, the mere existence of the murmur perhaps does not influence the prognosis. Dr. &rko Mauri6 Institute for Health Protection Cardiovascular Department B. Kidr&a 52a, 51000 RGeka Yugoslavia

Spontaneous resumption after prolonged AF

of sinus

rhythm

To the Editor: In the Case Report of spontaneous resumption of sinus rhythm in an elderly patient after 13 years of permanent atria1 fibrillation, Dr. Chevalier (AM. HEART J. 98:361, 1979) describes a case showing an interesting and a rare event. We had a similar experience with two patients (R.I. Med. J. 325: 297, June, 1977) who, on recent follow-up visits, have been noted to maintain normal sinus rhythm. As noted also by Dr. Chevalier, we believe that Holzmann’s theory offers the best explanation for this phenomenon. We postulated the following. Atria1 fibrillation is usually explained on the basis of two mechanisms-i.e., the unifocal theory and the reentry phe-

American

Heart

Journal

to the Editor

nomenon (or the circus movement). It is possible that progressive fibrotic changes taking place in the atria may abolish atria1 fibrillation. In the case of unifocal theory, the triggering focus may be eradicated as it gets incorporated into the fibrotic process. In the case of the reentry phenomenon, it is possible that the fibrotic process interrupts the reentry pathway and terminates atria1 fibrillation. In any case, it is necessary that the sinus node be capable of taking over once atria1 fibrillation ceases. If this was not the case sinus arrest would result on cessation of atria1 fibrillation, as was seen in the case described by Fleeve and colleagues (AM. HEART J. SO: 127,1975). Thus the change from chronic atria1 fibrillation to spontaneous sinus rhythm probably represents worsening of the conduction system. A bdul Hakim Khan, M.D. Brown University Division of Cardiology The Memorial Hospital Pawtucket, RI 02860

Adsorption

of MTlG

To the Editor: We agree with Cacace and associates’ that adsorption of nitroglycerin to glass containers does not create many problems; our own results concerning this item are consistent with their findings. However, the clinical importance is doubtful when you don’t know how much NTG is retained in the infusion system. Therefore we conducted an infusion set adsorption study. NTG solutions were prepared from an ethanolic stock solution, containing 1% W./W. of NTG, by diluting with distilled water to a concentration of 5 mg./ml. The solution was filtered through an 0.2 micron filter and after discarding the first 50 ml. (we found up to 25% decrease of NTG after filtering the lirst portion), was filled into 5 ml. glass ampules. After sealing, the ampules were heated for 30 minutes at 105” (Branje and Berghuis’). Five milliliters NTG was added to 500 ml. of normal saline in a glass bottle and a polyvinyl chloride (PVC) infusion system was connected. Flow rate was kept constant with an Ivac 531 flow controller. Flow rates used were 0.25, 0.50, 0.75, and 1.00 ml./minute (equivalent to 12.5,25,37.5 and 50 micrograms per minute, respectively). Samples were retained at zero, 30, 60, SO, 120, 180, 240, 300, ,and 360 minutes and were immediately assayed by means of the kinetic method of Yap and coworkers.3 At the same time, samples drawn from the glass container were assayed; this concentration did not change during the experiment. The results are summarized in Table I. The loss of NTG turns out to be flow-dependent; after a rapid decrease a gradua.1 increase is subsequently seen which perhaps results in a plateau after six hours. For the fastest flow rate this seems to be at 90% of the original concentration, whereas it is only 60% for the lowest. Most reports concerning the use of NTG infusions don’t mention the type off infusion set they use. Our results indicate that this omission is not justified. Much time is spent on determining stability of intravenous fluids in bottles or bags,

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