Ventricular Arrhythmias following Mitral Valve Replacement

Ventricular Arrhythmias following Mitral Valve Replacement* Control with Intra-aortic Balloon Counterpulsation E. H. Williams, M.D.; 00 G. F. 0. Tyers, M.D.;t S. L. Carter, M.D.; and D. R. Williams

Two patients with severe left ventricular failure (New York Heart Association's class 4) secondary to acute mitral insufficiency underwent mitral valve replacement after their condition had been stabilized by intra-ao'rtic balloon counterpulsation. The need for hemodynamic support declined rapidly foUowing valve replacement in both cases, but when the frequency of balloon counterpulsation was reduced, the immediate onset of lifethreatening arrhythmias was noted. The resumption of 1:1 intra-aortic balloon counterpulsation always immediately abolished the arrhythmia. The dependency upon counterpulsation for arrhythmia suppression gradually diminished, and after a week the intra-aortic balloon was

removed from the second patient, who subsequently made a complete recovery. The intra-aortic balloon was removed from the first patient four days after surgery and one day after its antiarrhythmic effect had been noted. Twenty-four hours later, this patient succumbed to a ventricular tachycardia which terminated in ventricular fibriUation. When no surgically correctable lesion is present, prolonged use of the intra-aortic balloon is recommended for all patients who develop ventricular or low nodal arrhythmias in response to decreasing the frequency of counterpulsation. As in our second patient, this will on occasion save a very high-risk patient.

Coronary artery bypass grafts have been successfully used to control intractable ventricular arrhythmias.1·3 Preoperative and postoperative intraaortic balloon counterpulsation has proven a very useful adjunct in these cases for the control of ectopic ventricular and nodal activity. 3 Recently, two patients with acute mitral insufficiency were encountered who required intra-aortic balloon counterpulsation prior to surgery for severe failure. Cardiac function improved rapidly in both patients following emergency mitral valve replacement so that the original indication for the counterpulsation was no longer present by the second or third postoperative day. However, when the frequency of counterpulsation was reduced from 1:1 to 1:4 or 1:8, potentially lethal arrhythmias developed which were immediately eliminated in both patients by increasing the frequency of counterpulsation.

another hospital with severe epigastric and left shoulder pain, progressive shortness of breath, and diaphoresis. Initially the electrocardiogram showed poor R-wave progression and STsegment depression in leads Vt through V~ . The patient developed congestive heart failure with bilateral pleural effusions, pulmonary edema, and cardiomegaly. Therapy with digoxin and diuretics failed to improve the patient's condition, and he was transferred to the Milton S. Hershey Medical Center, Hershey, Pa, 17 days after his myocardial infarction. When seen immediately after transfer, the patient was confused, in moderate respiratory distress with a respiratory rate of 32, a regular pulse of 120 beats per minute, a blood pressure of 100/60 mm Hg, and grade 2 hypertensive retinopathy. Prominent v waves were noted in the patient's distended neck veins while he reclined at 45• . There were bilateral rales and dullness at the left lung base. Examination of the heart revealed a left sternal heave, a grade 2/6 holosystolic murmur at the apex radiating to the axilla, and a prominent S4 gallop. The liver edge was 3 em below the right costal margin and tender to palpation, and there was 2+ pedal edema. The ECG now revealed ST -segment elevation in leads 1 and a VL with reciprocal depressions in the precordial leads. There were multiple ventricular and atrial ectopic beats. Serum electrolyte levels were within normal limits. The chest radiograph showed cardiomegaly and congestive failure . Arterial blood gas analyses while breathing room air revealed arterial oxygen pressure ( Pa02) of 61 mm Hg, arterial carbon dioxide tension ( PaCO~) of 37 mm Hg, and pH of 7.51. Cardiac catheterization revealed severe mitral regurgitation, left ventricular end-diastolic pressure of 20 mm Hg, total occlusion of the right coronary artery, tight stenosis of the circumflex branch of the left coronary artery, and a cardiac index of 1.2 L / min/ sq M. Twenty-three days after his myocardial infarction and following the insertion of an intra-

CASE REPORT CASE

1

A 60-year-old man with a 25-year history of hypertension and a two-year history of angina pectoris was admitted to °From the Department of Surgery, Division of Cardiathoracic Surgery, the Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pa. 0 0 Instructor. t Associate Professor. Manuscript received April!; revision accepted May 20. Reprint requests: Dr. Tyers, Milton S. Hershey Medical Center, Hershe y, Pennsylvania 17033

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VENTRICULAR ARRHYTHMIAS AnER MITRAL VALVE REPLACEMENT 641

+

tl

1!!• • I . ' aortic balloon for counterpulsation, the patient underwent mitral valve replacement with a No. 4 Starr-Edwards Silasticball valve prosthesis. The stenotic coronary vessels were not grafted because of a dense fibrinous pericarditis which obliterated all epicardial landmarks. After surgery the patient initially did well hemodynamically and after three days no longer required balloon assistance to maintain an adequate systemic pressure and cardiac and urinary output~. However, he continued to have series of ventricular arrhythmias whenever the frequency of intra-aortic balloon counterpulsation was reduced. These arrhythmias were completely abolished by 1: 1 augmentation ( Fig 1 ) . By the fourth postoperative day the patient no longer had continuous ventricular arrhythmias when the rate of counterpulsation was reduced to 1:8, and the intra-aortic balloon was removed on the fifth postoperative day. On the sixth day following valve replacement, the patient suddenly developed ventricular tachycardia which terminated in ventricular fibrillation. Attempts at resuscitation were unsuccessful. Postmortem examination revealed a massive left ventricular infarction of approximately a month's duration that spared only the interventricular septum ( Fig 2) . CASE

2

A 58-year-old man was admitted to the Milton S. Hershey Medical Center complaining of chest pain, dyspnea, and lightheadedness. By history the patient had longstanding hypertension, atherosclerotic cardiovascular disease, and adult-onset diabetes mellitus. Atrial fibrillation had been present for several years. Medications included digoxin, quinidine, and chlorpropamide ( Diabinese) . The patient appeared pale, chronically ill, and at least ten years older than his stated age. His temperature was 38.6•C ( 10l.S•F) rectally, his blood pressure was 110/70 mm Hg, and his pulse was 120 and erratically irregular. There were grade 2 hypertensive changes in his fundi, and his neck veins remained distended when he was elevated to 45•. Rales were present bilaterally. There was a grade 3/6, blowing, apical systolic murmur radiating up the left sternal border and into the left axilla, an increased St, and a loud s~ gallop. The liver was three fingerbreadths below the right costal margin, and the spleen was enlarged and easily palpable. Splinter hemorrhages and an Osler's node were detected. There was bilateral lower-extremity venous stasis with left ankle edema. An ECG showed atrial fibrillation with ST -segment depres-

642 WILLIAMS ET AL

FIGURE l. Electrocardiogram following mitral valve replacement in case l. A (top) . Without intra-aortic balloon counterpulsation, patient immediately developed ventricular bigeminy. B (bottom) . Simultaneous with onset of 1 : 1counterpulsation, ventricular premature contractions totally ceased. Ventricular arrhythmias always immediately appeared whenever counterpulsation was discontinued during first 72 hours after surgery. sion in leads V~ through V6· Chest radiography revealed pulmonary edema. The results of arterial blood gas analyses with the patient breathing room air were a pH of 7.47, PaCO~ of 26 mm Hg, and PaO~ of 60 mm Hg. The hematocrit reading was 28 percent. Prior to initiating antibiotic therapy, cultures of the blood and the Osler's node were obtained, which subsequently grew out a group D Streptococcus. The patient was placed on ampicillin therapy, 1 gm intravenously every four hours, which provided a bactericidal effect in a 1: 16 serum dilution. Therapy was continued for one month. During this time, the patient remained in congestive failure, complicated by multiple ventricular ectopic beats and runs of ventricular tachycardia. Cardiac catheterizaton performed following the completion of antibiotic therapy revealed severe eccentric mitral insufficiency with a peak pulmonary artery pressure of 120 mm Hg and a cardiac index of 1.9 L/min/sq M. A decision was made to replace the patient's mitral valve six weeks following admission to the hospital. An intra-aortic balloon was inserted, 1: 1 augmentation was begun, and the following morning the patient was taken to the operating room. The posterior leaflet of the mitral valve was flail secondary to the rupture of several chordae, and a 3.5 X 1.5-cm brownish mass which adhered to it subsequently proved to still be infected with group D Streptococcus. The mitral valve was replaced with a No. 4 Starr-Edwards Silastic-ball valve prosthesis.

FIGURE 2. Cross section of heart from case 1 showing marked thinning of whole free wall of left ventricle. LAD, Left anterior descending coronary artery.

CHEST, 68: 5, NOVEMBER, 1975

I

I I

FIGURE 3. Simultaneous rcc and radial-pulse pressure traces from ca~e 2. A (top) . Without intra-aortic balloon counterpulsation, nodal bigeminy immediately ensued. B (bottom). As soon as counterpul~ation was resumed, arrhythmia was abolished. As in case 1, this correlation was consistently and immediately demonstrated for several days following mitral valve replacement.

After surgery the patient only briefly required intra-aortic balloon counterpulsation to maintain a satisfactory pressure and cardiac output, but he had frequent nodal and ventricular premature heats when balloon counterpulsation was not being used. When he was augmented 1:1, these ectopic beats ceased ( Fig 3). Because of our prior experience, the balloon was not removed until over a week after valve replacement and several days after the disappearance of the close relationship between decreased frequency of counterpulsation and the appearance of arrhythmia~ . The patient subsequently made an uncomplicated recovery and continues to do well. DISCUSSION

Intra-aortic balloon counterpulsation might be expected to decrease left ventricular irritability by augmenting coronary flow to the ischemic myocardium, while decreasing left ventricular work. 4 •5 Intra-aortic balloon counterpulsation has decreased ventricular irritability in patients with intractable arrhythmias after anterolateral infarction 3 and has also been used in these cases as adjuvant therapy for arrhythmia control prior to coronary artery bypass grafting. 3 \Ve consider the effectiveness of counterpulsation in this latter situation to be of prognostic value, since those patients who respond to intra-

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aortic balloon pumping with a decrease in irritability can be expected to have their arrhythmias controlled by aortocoronary bypass surgery. Both methods of treatment improve blood flow to the ischemic myocardium. The subject of this report is the abolition by counterpulsation of postoperative arrhythmias in two patients after mitral valve replacement. In both cases, the intra-aortic balloon had been inserted prior to surgery because of chronic congestive failure, low cardiac output, and poor ventricular function secondary to acute mitral insufficiency. The need for hemodynamic support had ended by the third postoperative day, the patients continuing to have good blood pressure, cardiac output, and renal function when the frequency of balloon assist was reduced from 1:1 to 1:8. However, in both cases on multiple occasions, termination of l: I assist with the balloon was immediately followed by the onset of life-threatening arrhythmias. In the first case, this effect became much less pronounced after 24 hours, and the balloon was removed. On the next day the patient died following an episode of ventricular tachycardia which terminated in ventricular fibrillation. The second patient also became much less dependent on the balloon assistance device for arrhythmia control approximately 24 hours after it was demonstrated that he no longer needed hemodynamic support. In spite of this, balloon counterpulsation was continued for several additional days until he was essentially arrhythmia-free when off counterpulsation. The balloon was then removed, and the patient made a complete recovery. The first patient had documented coronary artery disease, although this did not appear to involve the left anterior descending system, the focus of his arrhythmias. His mitral regurgitation was a sequela of a massive acute myocardial infarction. The arrhythmias in the second patient may have been due to myocardial ischemia secondary to low cardiac output or subclinical coronary artery disease, but the possibility of small mycotic coronary emboli cannot be ruled out. His mitral regurgitation was a sequela of bacterial endocarditis. Whatever the basic pathology, the common underlying etiology of the arrhythmia in each patient was undoubtedly an ischemic myocardial focus, which was alleviated by intra-aortic balloon counterpulsation, even though hemodynamic stability no longer required assistance. Extended postoperative intra-aortic counterpulsation is recommended as a saving procedure for any patient who demonstrates a marked increase in the incidence of ventricular or low nodal arrhythmias when the frequency of counterpulsation is reduced, and in whom a surgically correctable basis for the arrhythmia is not present.

VENTRICULAR ARRHYTHMIAS AFTER MITRAL VALVE REPLACEMENT 643

REFERENCES

Eckt>r RH. \lullens CB, Grammer JC, et al: Control of intractable n·ntricular tachycardia by coronary revascularizatiou . Circulation 44:666-670, 1971 2 Lambert CJ. Adam M, Geisler GF, et al: Emergency myocardial re,·a~cularization for impending infarctions and arrhythmias. J Thorac Cardiovasc Surg 62:552-528, 1971 3 Mundth ED. Buckley ~1], DeSanctis RW, et al: Surgical

treatment of ventricular irritability. J Thorac Cardiovasc Surg 66:913-951, 1973 4 Braunwall E, Covell JW, Moroko PR, et al : Effects of drugs and of counterpulsation on myocardial oxygen consumption : Observations on the ischemic heart. Circulation 40 ( suppl 4) :220-230, 1969 5 Braunwald E , llloroko PR: Intra-aortic balloon counterpulsation : An assessment. Ann Intern llled 76:659-661, 1971

The First Literary Agent As H. G. Wells became a man of letters, he acquired a man of business. The idea of a "literary agent" was a new one-it seems that the phrase was coined by the first of them, A. P. Watt, but soon after Watt, a small lively Scotsman named James Brand Pinker set up in the same line. On 13 January 1896, just as he started his new venture, Pinker wrote Wells saying "my friend, Marriott Watson, has written to you of my enterprise. He thought you might place your affairs in my hands." Wells became one of Pinker's first clients. Pinker made a reputation as a successful agent as fast as some of the young men on his

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list made a name for themselves as authors-and for that reason. He had the knack of picking winners which made winners come to him. Oscar Wilde brought him The Ballad of Reading Gaol. Stephen Crane sought him out when he arrived in London. Through Wells he later added James and Bennett to his list, and it was his support that kept Conrad going in the years before his books began to yield a living income. Mackenzie, Nand Mackenzie, J: HG Wells, New York, Simon & Schuster, 1973

CHEST, 68: 5, NOVEMBER, 1975