Unusually High Pacemaker Threshold in Severe Myxedema

changes are much less frequent. Thus, experimental, autopsy, and coronary angiographic data suggest that substantial cardiac injury may be a consequence of cardiac irradiation. The mantle technique by which our patient was treated protected the apex of his heart with lead shields, but the remainder of the heart was within.the radiation field. It is suggested that radiation-induced injury was a provocation of the myocardial infarction that our patient suffered when he was 33 years old, six years after treatment for Hodgkin's disease. H this is so, it would be worthwhile to consider modification of the mantle technique of administering radiation to provide better protection of the coronary vessels while not reducing the effect of the radiation on neoplastic disease. 12

REFERENCES 1 Cohn KE, Stewart JR, Fajardo LF, et al: Heart disease following radiation. Medicine 46:281-296, 1967 2 Huff H, Sanders EM: Coronary artery occlusion after radiation. N Engl J Med 286:780, 1972. 3 Tracy GP, Dou~ EB, Johnson LW, et al: Radiationinduced coronary artery disease. JAMA 228:1660-1664, 1974 4 Pearson HES: Incidental dangers of x-ray therapy. Lancet 1:222-22.3, 1958

5 Dollinger MR, Lavine DM. Foye LV Jr: Myocardial infarction due to postirradiation fibrosis of the coronary arteries. JAMA 195:316-319, 1966 6 Rubin E, Camara J, Grayzel DM, et al: Radiation induced cardiac fibrosis. Am J Med 34:71-75, 1963 7 Prentice RTW: Myocardial infarction following radiation. Lancet 2:388, 1965 8 Feher J: Myocardial infarction following radiation. Lancet 2:643-644, 1965 9 Kirkpatriclc JB: Pathogenesis ·of foam cell lesions in ir.radiated arteries. Am J Pathol50:291-309, 1967 10 Fajardo LF, Stewart JR: Experimental radio-induced heart disease: 1. Light microscopic studies. Am J Patbol 59:299-316, 1970 11 Fajardo LF, Stewart JR, Cohn KE: Morphology of radiation-induced heart disease. Arch Pathol 86:512-519, 1968 12. Fajardo LF, Stewart JR: Coronary artery disease after radiation. N Engl J Med 286:1265-12.66, 1972.

Unusually High Pacemaker Threshold in Severe Myxedema* Decrease with Thyroid Hormone Therapy Debal BIJIU, M.D., tmd Kanu Chattertee, M.B.

In a patient with myxedema and complete heart block, an usually high pacemaker threshold was observed lnltlaDy during transvenons rlgbt ventricular endocardial pacing. The paceQJ.aker threshold padually decnMed with thyroid replacement therapy, 111111estlna that the lack of thyroid hormone In some patients mflbt 1ncrea1e the pacemaker threshold. •From the Department of Medicine and the Cardiology Division, University of California, San Francisco. .

CHEST, 70: 5, NOVEMBER, 1976

A

lthough minor changes in pacemaker threshold · might occur due to various causes, including electrolytic disturbance and catecholamine in£usion,1 - 8 a marked increase in pacemaker threshold in the absence of right ventricular perforation, electrode displacement, or breakage is uncommon. We report the case of a patient with severe myxedema and complete heart block, in whom an unusually high pacemaker threshold was observed uiitially, which gradually decreased coincident with thyroid replacement tho/8PY·

CAsE fu:roRT " A 78-year-old white man was admitted with at least a sixmonth history of repeated blacJcout spells and was found to have extreme bradycardia, with a pulse rate of 35 beats per minute. The patient's history and the findings from clinical examination were consistent with myxedema and complete atrioventricular blocJc. An electrocardiogram revealed complete atriovenbicular blocJc with bilateral bundle-branch block (Fig 1). Since the patient had classic symptoms of Stokes-Adams syndrome and profound . bradycardia, a temporary transvenous pacemakeT was inserted through the right subclavian vein and was positioned in the apex of the right ventricle. A unipolar electrogram recorded from the distal electrode demonstrated the characteristic pattern of a right ventricular intracardiac electrogram with very small amplitude of the P wave and large QRS complexes.4 The right ventricular endocardial potential was 9 mv (Fig 2) which was within range. II The right venbicular electrogram also showed good contact with the endocardium, as evidenced from the magnitude of ST-segment elevation, which exceeded 4 mv; however, ventricular capture could not be obtained below a current of 8 ma. Several different positions near the apex and outflow tract were explored in an attempt to achieve a lower pacing threshold; however, in each position, ventricular capture could only be obtained with a pacing threshold of 8 ma or more. The position of the catheter was verified by a lateral chest x-ray film and also by measuring the right ventricular endocardial potential and the ST-segment elevation due to endoCardial cpntact, which on each occasion were about 9 mv and 4 mv, respectively. It was believed that such a high pacemaker threshold may be related to myxedema, and it may decrease with thyroxine therapy. The patient's serum electrolytic levels, particularly the serum potassium level, were within DOI'Dlal limits at the time of .fusertion of the temporary transvenous pacemaker. Laboratory study at this time confirmed the diagnosis of myxedema (thyroxine iodine lT4] level, 0.5,.g/100 ml; thyrotropin lTSH] level, 90 MU/ml by radioimmunoassay). On the seventh day of hospitalization, after initiation of thyroxine therapy, the patient's pacemaker threshold decreased from 8 ma to 2.5 ma. Because of the persistence of complete abioventricular blocJc, a permanent pacing system was installed on the 12th day- of hospitalization. The pacing threshold at the time of permanent pacemaker insertion was 0.8 ma. DISCUSSION

A very high initial pacemaker threshold during transvenous endocardial pacing is uncommon in the absence of malposition of the electrode, electrode breakage, a displaced electrode, or perforation of the right ventricle.

UNUSUALLY HIGH PACEMAKER THRESHOLD 671

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F'IcUIIE 1. Standard 12-Jead ECG showing complete atrioventricular block and bilateral bundlebranch block (June 10, 1975) .

The pacemaker threshold may be high when the tip of the pacing electrode is not in contact with right ventricular endocardium. In the present case, despite the fact that the pacing catheter was carefully positioned several times in different areas of the right ventricular endocardium, including the right ventricular apex, the threshold was consistently 8 rna or higher. In each electrode position, there was a good contact between the electrode and the right ventricular endocardium, as indicated by significant ST-segment elevation as recorded in the right ventricular endocardial potential. Although with such magnitude of ST-segment elevation, a relatively low pacemaker threshold is expected, the threshold was consistently 8 rna or higher in the present case. It appears, therefore, that technical problems such as malposition of the pacing electrode or lack of contact of the electrode with the right ventricular endocardium cannot be incriminated in this patient as the cause of the unusually high pacemaker threshold. Drugs such as procaine amide hydrochloride, quini-

dine, or propranolol or an electrolytic imbalance like hyperkalemia' is known to increase the pacemaker threshold. The patient reported here was not receiving any such drugs, and his serum potassium level was normal at the time of insertion of the intravenous pacing system. It is likely, therefore, that severe myxedema was contributing to the high pacing threshold in this case. This likelihood is further supported by the fact that the pacing threshold gradually decreased from 8 to 0.8 rna as the thyroid replacement therapy was continued. Usually, tl)e pacing threshold gradually increases and exceeds the initial threshold by two to three times the initial value in two to three weeks, before reaching a plateau; 2 however, in the present case the threshold decreased. instead of the usual increase, after the initial insertion of the intravenous pacing system. These findings strongly suggest that a lack of thyroid hormone may in some patients markedly increase the pacemaker threshold, which may decrease with thyroid replacement therapy.

F'IcUIIE 2. Right ventricular unipolar endocardial potential recorded from distal electrode. Amplitude of QRS complexes is 9 mv, and magnitude of ST-segment elevation is 4 mv.

878 BASU, CHATTERJEE

CHEST, 70: 5, NOVEMBER, 1976

REFERENCES 1 Preston TA, Judge RD: Alteration of pacemaker threshold by dmg and physiologic factors. Ann NY Acad Sci 167: 686, 1969 2 Sowton E, Barr 1: Physiological changes in threshold. Ann NY Acad Sci 167:679, 1969 3 Kubler W, Sowton E: Influence of beta blockade on myocardial threshold in patients with pacemakers. Lancet 2:67,1970 4 Chatterjee K, Sutton R, Layton CA, et al: The cavity electrocardiogram in 'emergency artifical pacing. Postgrad Med J 43:713, 1969 5 Chatterjee K, Harris A, Davies C, et al: The fall of endocardial potentials following acute myocardial infarction. Lancet 1: 1308, 1970 6 Surawicz B, Shlebus H, Reeves JT, et al: Increase of ventricular excitability threshold by hyperpotassemia. JAMA 191:1049, 1965

Retroclavicular Route for Electrode Placement in Endocardial Pacemakers* F. Gosalbez, M.D.; ]. Cofitio, M.D.; A. Lkwente, M.D.; and F. A. de Linef'a, M.D. 00 In order to avoid skin erosion and electrode infection In

endOcardial pacemakers placed through the external jugular vein, we direct the wires from their point of entry into the vessel to the pacing unit placed in the pectoral region by dissecting a retroclavkular tunnel. This can be done under general or local anesthesia, and so far we bave not seen any injuries to the subclavian vein. In this way the entire pathway of the cables is deep enough so tbat they caunot be palpated through the sldn, and the dangers of exposure through erosion are minimized.

P

ermanent endocardial pacing is performed using as an entrance point for the electrodes either the cephalic or the jugular vein. The former can, on occasion, be too small or frngile to be used. Furman and ass~ ciates1 • 2 have reported an incidence of 27 percent in their series of patients in which the situation arose. On the other hand, the external jugular vein is very constant, easy to dissect, and large enough to allow passage of the electrodes without difficulty. Usually from the point of entry into the vein to the pocket created for the pacing unit in the pectoral zone, the electrodes are directed subcutaneously over the clavicle. In our experience, erosion through the skin and subsequent infection occur in this situation, either over the clavicle or in the loop left in the neck. Reports of this complication are found in mariy series of patients. 3 - 5

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FIGURE 1. ·P athway of cables beneath clavicle (atTOW). 1, First rib; and 2, second rib.

the clavicle, next to the subclavius muscle, which allows· passage of a dissecting instrument. Usually, QPly small veins of no significance are encouhtered, and the subclavian ve~ is removed enough to assure safety ( Fig 1 ) . In our last 30 procedures for placement of permanent endocardial pacemakers, we have tunneled this space from below and above, using the incisions made for positioning of the unit and for isolation of the vein (Fig 2). Dissection must be kept next to the periosteum, and the subclavian vein is not visualized. The cables are then pulled through from the neck to the chest with the help of a surgical instrument or after insertion into a small chest tube placed for that purpose. If the pocket is developed subcutaneously, the fibers of the greater pectoral muscle must be separated next to the clavicle. We prefer to place the pulse generator in a submuscular position, but this can be painful when the entire procedure is done under local anesthesia. We have not seen any significant bleeding at the time of surgery or hematoma formation after surgery. Chest x-ray films have not disclosed mediastinal widening or pneumothorax. As additional protection against skin erosion, the vein used for electrode placement is tied and cut cephalad to the point of entry of the electrodes. The cables then drop behind the clavicle. So that they may be recovered if repositioning is needed, they are loosely sutured to the posterior periosteum, or a heavy siDe tie is placed around them and through neck

METHOD

In trying to prevent this problem, we found in the autopsy room that there is a space behind the posterior periosteum of

From the Department of Thoracic Surgery, Hospital General de Asturias, Oviedo, Spain. Chief of Service, Department of Thoracic Surgery. Reprint requests: Df'. Gosalbez, Deparlment qf Thoracic Suf'gef'!l, Hospital Genet'al de &tunas, Oviedo, Spain 0

00

CHEST, 70: 5, NOVEMBER, 1976

FIGURE 2. Dissecting instrument has been placed underneath clavicle to neck, in order to grasp electrodes and pull them through.

RETROCLAYICUlAR ROUTE FOR ELECTRODE PLACEMENT 879