New primary pulmonary hypertension registry

FORUM-LETTERS

TO THE EDITOR

BUNDLEBRANCHBLOCKAFTERCORONARY BYPASS SURGERY To the Editor: We read with great interest the paper by O’Connell et al. entitled “Transient Bundle Branch Block Following Use of Hypothermic Cardioplegia in Coronary Artery Bypass Surgery” published in the January, 1982, issue of the JOURNAL.’ In March, 1981, we reported a similar phenomenon in the articles “Perioperative Complete Right Bundle Branch Block After Aorto-Coronary Bypass surgery.“* Our study encompassed 322 patients who underwent aorta-coronary bypass operation between 1975 and 1978. The myocardial preservation was done with hypothermic cardioplegia after the method of Bleese et al.’ The first postoperative ECG taken into consideration was that recorded 15 hours after the operation. In 18 patients (5.6%), complete right bundle branch block (CRBBB) was observed perioperatively, without evidence of perioperative myocardial infarction. Left bundle branch block (LBBB) was not observed. We compared these 18 patients with perioperative CRBBB to the remaining 304 patients without CRBBB. We found that three factors favored the appearance of perioperative CRBBB after aorta-coronary bypass operation: (1) the preoperative existence of inferior myocardial infarction, (2) the preoperative existence of three-vessel coronary disease, and (3) prolonged aortic cross-clamping time at operation. In 10 of the patients, perioperative CRBBB was irreversible. Postoperative angiographic studies revealed no relationship between bundle branch block development and graft occlusion. C. Bantea,

M.D.

infarction. Most important, the first ECG obtained after aortocoronary bypass surgery was taken 15 hours postoperatively, a time when 82% of our patients with bundle branch block had returned to normal. Their patient population was different also. Sixteen out of eighteen, or 89%, of their patients with bundle branch block had a prior myocardial infarction (MI) and 78% had an inferior wall MI, while only one in our bundle branch block group had a prior infarction; however, the degree of three-vessel disease (84% vs 89% ) was similar. It is interesting that Bantea’s figure of a 5.6% incidence of bundle branch block after aortocoronary bypass surgery correlates with a 6% incidence of permanent bundle branch block seen after the first day of surgery in our cardioplegic group and the 6% incidence of bundle branch block in our control group using core hypothermia and ventricular fibrillation. Satinsky et al.“, using the same techniques as our control group, found a 4% incidence of bundle branch block. The mechanism of transient and fixed postoperative bundle branch block may involve scar tissue and arteriosclerotic change as well as ischemic time during surgery as Bantea et al. suggest. However, we believe that the 34% incidence of bundle branch block in our series, accompanied with a prolonged QT, interval using the method of cold potassium cardioplegia, reflects the effects of hypothermia on the conduction system or localized high concentrations of potassium and is largely a temporary and benign phenomenon.

Loyola

Department of Cardiovascular Surgery University Hospital Hamburg-Eppendorf Martinistrasse 52, D-2000 Hamburg 20 West Germany

University

Diane E. Wallis, M.D. John B. O’Connell, M.D. Stritch School of Medicine 2160 South First Ave. Maywood, IL 60153

REFERENCES REFERENCES

1. O’Connell BJ, Wallis D, Johnson AS, Pifarre R, Gunnar MR: Transient bundle branch block following use of hypothermic cardioplegia in coronary artery bypass surgery: High incidence without perioperative myocardial infarction. AM HEART J 103:85, 1982. 2. Bantea C, Bleese N, Kalmar P, Krebber H-J, Riidiger W, Rodewald G: Perioperativ entstandener kompletter Rechtsschenkelblock nach aorta-coronarer Bypass-Chirurgie. Herz 6:123, 1981. 3. Bleese N, Doring V, Kalmar P, Pokar H, Polonius M-J, Steiner D, Rodewald G: Intraoperative myocardial protection by cardioplegia in hypothermia. J Thorac Cardiovasc Surg 75:405, 1978.

1. Bantea C, Bleese N, Kalmar P, Krebber H-J, Riidiger W, Rodewald G: Perionerativ entstandener komnletter Rechtsschenkelblock nach aortocoronarer Bypass-dhirurgie. Hem 6:123, 1981. 2. O’Connell JB, Wallis DE, Johnson SA, Pifarre R, Gunnar RM: Transient bundle branch block following use of hypothermic cardioplegia in coronary artery bypass surgery: High incidence without perioperative myocardial infarction. AM HEART JOURNAL 103:85, 1982. 3. Satinsky JD, Collins JJ Jr, Dalen JE: Conduction defects after cardiac surgery. Circulation 50(supp111):170, 1974.

NEW PRIUARY PULMONARY HYPERTENSION REGISTRY REPLY To the Editor:

We enjoyed reviewing the paper by C. Bantea et al.’ and agree with them that perioperative bundle branch block does not necessarily equate with postoperative myocardial infarction. It is difficult, however, to compare their data with ours.1 There are significant differences in methodology. The aortic cross-clamp time in their study was much longer. The cardioplegic solutions were different in that they had smaller concentration of potassium chloride. Cardiac arrest was induced by procaine and magnesium aspartate, while arrest was induced in our series by the cold potassium cardioplegic solution. We excluded those patients with left ventricular hypertrophy, previous conduction disturbances including fascicular block, and Q waves suggestive of a prior 1114

To the Editor:

The National Heart, Lung and Blood Institute, through its Division of Lung Diseases, is establishing a patient registry to obtain and evaluate data on primary pulmonary hypertension. Physicians are being asked to refer patients to the 35 medical centers participating in the 3-year program. The purpose of the registry is to obtain and analyze data on the etiology, history, pathogenesis, diagnosis, and treatment of the disorder with the hope of developing new and effective strategies for early diagnosis and treatment. Patients eligible for entry into the registry include children older than 1 year of age and adults who have pulmonary hypertension of unknown origin. It is hoped that at least 150 patients can be entered on the registry each year. Physicians who currently are treating patients with primary pulmonary hyper-

Volume Number

104 5. Part 1

Letters

tension and who would like additional information or the name of the nearest cooperating clinical contact Dr. Carol Vreim, Chief, Interstitial Branch, DLD, National Heart, Lung and Blood Bethesda, MD 20205; phone (3(X)496-7034.

to the Editor

1115

on the registry center should Lung Diseases Institute, NIH,

Larry E. Blaser Chief, Research Reporting Section Public Inquiries and Reports Branch National Institutes of Health National Heart, Lung and Blood Institute Bethesda,

MD 20205

ECG CHANGES IN EARLY STAGE OF MAGNESIUM DEFICIENCY 7’0 the Editor: Since magnesium is essential to the body, a deficiency generally manifests itself biochemically and clinically, although diagnosis is often difficult because of its atypical clinical presentation. Magnesium deficiency is not at all a rarity and occurs in many disease states such as diabetic coma, alcoholic cirrhosis of the liver, heart failure, malabsorption syndromes, polyuric stage of tubular necrosis, acute pancreatitis, postoperative states (especially after operations of the gastrointestinal tract), primary aldosteronism, and hypoparathyroidism. Calcitonin promotes magnesium shift into osseous tissues, and growth hormone facilitates shifts of ‘J ECG changes associated with magmagnesium intracellularly. nesium deficiency have not been clearly defined. Serum and 24-hour urinary magnesium determinations are the only reliable means of diagnosis. Atomic absorption spectroscopy cannot at present replace the rather unreliable chemical method of detecting magnesium deficiency. In an attempt to find a simple and practical method for the diagnosis of magnesium deficiency, we analyzed the ECGs of nine patients with magnesium deficiency. The diagnostic criteria were based on serum magnesium values below 2.5 mEq/L and/or 24-hour urinary magnesium values lower than 4.0 mEq as determined by atomic absorption spectroscopy. Four patients with cholangitis and one each with cholecystitis, pulmonary and intestinal tuberculosis, pulmonary emphysema with infection, bacillary dysentery, and acute myocardial infarction were observed to have magnesium deficiency. When magnesium sulfate was used in an attempt to relax the biliary tract smooth muscle, a marked improvement in lethargy and gastrointestinal symptoms were noted in the case of cholangitis, suggesting an underlying magnesium deficiency in biliary tract diseases. The apparent high frequency of cholangitis in the present series is the result of a special search for magnesium deficiency in gallbladder abnormalities. Serum and urinary magnesium were determined in the other patients after ECG abnormalities suggestive of magnesium deficiency, inferred from the patients with cholangitis, were noted. Serum magnesium values in eight cases ranged from 1.16 to 3.0 mEq/L (normal 2.5 to 3.0 mEq/L). Twenty-four-hour urinary magnesium levels in five patients were determined by the same spectroscopic method and ranged from 1.1 to 3.6 mEq (normal 4 to 10 mEq/L). In the three patients whose serum values were 2.7 to 3.0 mEq/L, urinary magnesium values were all below normal, suggesting that urinary magnesium determination is the more sensitive diagnostic indicator. Abnormal ECG findings were limited to the T wave and could be categorized as follow: (1) Increase in amplitude and/or broad-

Fig. 1. A, ECGs recorded from leads V, and V, in case 1 showing broad T waves. Blood magnesium 3.0 mEq/L; urine magnesium 3.0 mEq/24 hr. 6, ECG recorded from lead V, in case 8 showing broad, tall T waves. Blood magnesium 2.0 mEqk. C, ECGs recorded from leads V, and V, in case 3 showing spinous T waves. Blood magnesium 2.7 mEq/L; urine magnesium 3.6 mEq/24 hr. Calibration 1 mV = 10 mm.

Fig. 2. A, ECGs recorded from leads II and V, in case 7 showing bifid T waves with first peak higher than second. 6, ECG recorded from V, in case 5 showing T waves with two peaks of equal height. Blood magnesium 2.0 mEq/L; urine magnesium 1.1 mEq/24 hr. C and D, ECGs recorded from leads V, and V, showing bifid T waves with second peak higher than first. Blood magnesium 2.5 mEq/L. Calibration 1 mV = 10 mm.

ening of its base were found in the ECGs of four patients. In three of the four, the ECGs had a spinous appearance and one showed increases in amplitude and duration (Fig. 1). (2) In four patients T waves were bifid (Fig. 2). QT prolongation was not noted and the presence of U waves was ruled out by Lepeschkin’s method of differentiating T and U waves.) The T wave was flattened and inverted in one case (Fig. 3). A correlation between bifid waves (so-called cloven T) and the lowest serum and urinary magnesium values was noted. In all cases, 20 ml of 25% magnesium sulfate was given intravenously in a single dose and repeated when