Volume 117 Number
Brief Communications
6
stable, 30 hours after the onset of symptoms, the patient suddenly developed complete heart block and ventricular asystole. After cardiopulmonary resuscitation and transvenous pacemaker placement, sinus rhythm was eventually restored. Repeat angiography was unchanged from his previous study except that there was enhanced flow (TIM1 grade 3) in the LAD. After the cardiac arrest, his bifascicular block returned and was present until the fifth hospitalization day, when normal conduction reappeared. An electrophysiologic study was performed on the fourteenth day of hospitalization. The patient had AH and HV intervals of 100 and 65 msec in normal sinus rhythm, respectively. No infra-Hisian block was noted with premature electrical stimulation of the atrium with one extrastimulus in paced or sinus rhythm or with atria1 decremental pacing. Two premature atria1 stimuli revealed inducible bifascicular block with subsequent infra-Hisian block with more premature stimuli. The prognostic significance of this latter finding is not known. A permanent transvenous dual-chamber pacemaker was implanted and the patient subsequently had an uneventful recovery. Repeat cardiac catheterization on the twentieth hospital day revealed a left ventricular ejection fraction of 21% , significant mitral regurgitation, and a 20% stenosis of the LAD at the angioplasty site. The patient was admitted 6 months later in congestive heart failure and while improving he became pacemaker-dependent. He died suddenly in electromechanical dissociation 24 hours later. This case illustrates two important points. Reperfusion therapy may be able to reverse conduction disturbances in the absence of significant myocardial salvage. However, despite reperfusion, new bifascicular block complicating an AM1 may suddenly deteriorate to high-grade atrioventricular block, even when it is transient and associated with an open infarct-related artery. Animal and human studies have shown that early reperfusion can lead to significant myocardial salvage.4 Whether reperfusion can ameliorate the incidence and prognosis of conduction disturbances after an MI is not known. This was suggested by the Second International Study of Infarct Survival (ISIS-2) trial,5 in that streptokinase significantly reduced the incidence of cardiac arrest (including nonventricular fibrillation deaths) when compared to placebo. Canine experiment@ have demonstrated that conduction in the subendocardium outlasts that in the subepicardium during ischemia, despite the fact that infarction progresses through the myocardium in the opposite direction. Possible explanations for the observed resiliency of conduction tissue include superior glycolytic metabolism, exposure to the salutary effects of cavity blood, and electrotonic interactions within Purkinje fibers. Our case report raises several important questions. Does reperfusion alter the incidence and prognostic significance of conduction disturbances after an MI? If so, is this due only to His-Purkinje fiber salvage or is myocardial salvage also required? Will reperfusion alter the current indications for prophylactic temporary and permanent pacing in AMI? The answer to some of these questions awaits completion of an analysis of a large cohort of patients with
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conduction disturbances and successful reperfusion. Until more information is available, patients with bifascicular block complicating an AM1 should have prophylactic temporary pacing irrespective of the success of reperfusion therapy. REFERENCES 1.
2.
3.
4. 5.
6.
Klein RC, Zakauddin V, Mason DT. Intraventricular conduction defects in acute myocardial infarction: incidence, prognosis and therapy. AM HEART J 1984,108:1007-13. DeGuzman M, Rahimtoola SH. What is the role of pacemakers in patients with coronary artery disease and conduction abnormalities? In: Rahimtoola SH, ed. Current controversies in coronary heart disease. Philadelphia: FA Davis Co, 1983:191-2(X. Hindman MC, Wagner GS, JaRo M, Atkins JM, Scheinman MM, DeSanctis RW, Hutter AH, Yeatman L, Rubenfire M, Pujura C, Rubin M, Morris JJ. The clinical significance of bundle branch block complicating acute myocardial infarction. 2. Indications for temporary and permanent pacemaker insertion. Circulation 1978;58:689-99. Sheehan FH. Determinants of improved left ventricular function after thrombolytic therapy in acute myocardial infarction. J Am Co11 Cardiol 1987;9:937-44. ISIS-2 Collaborative Group. Randomized trial of intravenous streptokinase, oral aspirin, both or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988;2:349-60. Gilmour RF, Zipes DP. Different electrophysiological responses of canine endocardium and epicardium to combined hyperkalemia, hypoxia and acidosis. Circ Res 1980; 46814-25.
“Pseudo-critical” aortic stenosis during pregnancy: Role for Doppler assessment of aortic valve area Stephen T. Hustead, DO, Annette Quick MD, Harry R. Gibbs, MD, Caroline A. Werner, MD, and Dev Maulik, MD, PhD. Kansas City, MO. There remains a paucity of literature concerning pregnancy complicated by aortic stenosis. However, a recent review’ of the relatively few reported cases suggests a very significant maternal mortality rate (exceeding 17 % ) and a perinatal mortality rate of over 31% . With the advent of newer, noninvasive imaging techniques such as twodimensional echocardiography, the diagnosis of congenital heart disease has been markedly simplified. Doppler echocardiography has virtually eliminated the need for cardiac catheterization in many patients, and has been shown to be quite accurate at estimating instantaneous peak and mean valve gradients.2s3 However, in the presence of high flow states or left ventricular volume overFrom the Gynecology Medicine.
Departments (Perinatology),
of Medicine University
Reprint requests: Stephen T. Hustead, City School of Medicine, 2411 Holmes
(Cardiology), and of Missouri-Kansas DO, University Ave., Kansas
Obstetrics and City School of
of Missouri-Kansas City, MO 64108.
June 1989
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Brief Communications
load, aortic valve peak flow velocities used to calculate valve gradients can overestimate the severity of aortic stenosis.4 An index of left ventricular function can be particularly helpful at these times. Several noninvasive methods to calculate aortic valve area that use Dopplerderived indices of left ventricular function have been described.*a5 Presently the hemodynamics of pregnancy remain incompletely defined. Plasma volume increases by nearly 50% during pregnancy, and is reflected by an increase in both right and left ventricular end-diastolic volumes. Cardiac output (CO) begins to rise early, increasing by 30% to 40% at 20 weeks, related to both an increase in heart rate (HR) and stroke volume (SV).‘js7The following case demonstrates how continuous-wave Doppler echocardiography might overestimate the severity of aortic stenosis if indices of left ventricular function are ignored. In addition, the safe and uneventful spontaneous vaginal delivery in the left lateral decubitus position is described. A 17-year-old primigravida was originally referred from an outside clinic for continued prenatal care and evaluation at 36 weeks of gestation. On initial obstetrical examination, a harsh systolic ejection murmur, and associated suprasternal thrill were present. An outpatient M-mode and two-dimensional echocardiogram demonstrated marked concentric left ventricular wall thickening, normal chamber sizes, excellent left ventricular (LV) contraction, and a doming, bicuspid aortic valve. She was referred immediately for cardiac evaluation. She had been aware of a heart murmur since early childhood, but had never had a formal cardiac evaluation. Before pregnancy she had been free of symptoms, even while participating as a high school cheerleader. She now admitted only to being more easily fatigued, but remained otherwise asymptomatic. On physical examination her blood pressure was 140/100 mm Hg in both arms while sitting. The carotid pulses were diminished, the cardiac apex was sustained, and a suprasternal thrill was noted to palpation. On auscultation an ejection click was heard along the left sternal border, followed by a harsh grade 4 late peaking systolic ejection murmur. The second heart sound was single. The electrocardiogram (ECG) met voltage criteria for left ventricular hypertrophy (LVH). A Doppler echocardiogram was obtained. Peak aortic valve flow slightly exceeded 5.2 m/set, in the absence of aortic insufficiency. With the use of the simplified Bernoulli equation (P = 4V2), the estimated instantaneous peak aortic valve gradient was 108 mm Hg. Even when corrected for an increased left ventricular outflow tract (LVOT) velocity of 1.4 m/set, the peak instantaneous gradient remained markedly increased at 100 mm Hg (P = 4(VZhlAx- VzLvoT).However, the Doppler-estimated aortic valve area was 1.8 cm2 using the continuity equation. Estimates of right heart pressures were unobtainable in the absence of Doppler evidence of tricuspid or pulmonary insufficiency. In view of excellent underlying LV systolic function and the absence of symptoms, no intervention was recommended other than close observation. Unfortunately, the
American
Heart Journal
patient failed to return for any scheduled appointments, but arrived at 39 weeks of gestation in active labor. A repeat two-dimensional echocardiogram showed continued hyperdynamic LV contractility, with persistent Doppler evidence of greatly increased aortic valve flow. The maximum transaortic valve velocity was 5.3 m/set, with an LVOT velocity of 1.4 m/set, yielding an estimated corrected instantaneous peak valve gradient of 104 mm Hg. The patient was transferred immediatedly to the cardiac catheterization laboratory for placement of a flow-directed, balloon-tipped, right heart catheter. Right heart pressures were all normal, and the pulmonary capillary wedge pressure (PCWP) mean was 8 mm Hg. Fetal monitoring was continuous throughout labor and delivery, and at no time was fetal distress noted. Labor proceeded in the left lateral decubitus position. In order to avoid potential hypotension and subsequent cardiovascular collapse, crystalloid, in the form of 0.9% normal saline, was administered to maintain a PCWP mean of 8 to 12 mm Hg. The CO obtained by thermodilution at multiple times throughout labor remained stable at 14.0 to 15.0 L/ min/m2, yeilding an increased cardiac index (CI) of 7.0 to 7.5 L/min/m2. Aortic valve area was again estimated at 1.8 cm2 by the continuity equation, and at 1.6 cm* using the modified Gorlin formula.4,5 The mother remained hemodynamically stable throughout labor, and delivered a viable male infant in the left lateral decubitus position 8 hours after being hospitalized. Doppler echocardiograms of aortic valve flow at each stage of labor, immediately after delivery, and 30 minutes following delivery failed to demonstrate any significant change in peak velocity. She refused any subsequent evaluations, and left the hospital against medical advice soon after delivery. Fortunately, pregnancy complicated by significant or critical aortic stenosis remains uncommon. However, limited reports are not encouraging with regard to maternal safety and fetal salvage.’ Surgical correction is recommended prior to considering pregnancy in women with severe aortic stenosis.6s’ Continuous wave Doppler has been shown to be an accurate, noninvasive technique for evaluating the severity of aortic stenosis in most patients.2,” Generally, an instantaneous peak gradient exceeding 75 to 80 mm Hg in the presence of normal or depressed CO reflects severe aortic stenosis. However, the pressure gradient across a narrowing is highly dependent on Aow, and flow in turn is directly affected by loading conditions, or by ventricular performance. The presence of high flow states, as seen with combined aortic stenosis and aortic insufficiency, can result in exaggerated peak flow velocities, yielding estimated valve gradients that when used alone will grossly overestimate the severity of aortic stenosis.4 This might be termed “pseudo-critical” aortic stenosis. Pregnancy is characterized by hemodynamic changes that result in a high flow state that could also result in an overestimation of valve obstruction. In order to account for the effect of flow, a determination of aortic valve area is necessary. In the past, this required cardiac catheterization. Recently, accurately estimated valve areas have been obtained noninvasively with the use
Volume 117 Number 6
of Doppler values and the continuity equation.’ In our patient, the estimates of aortic valve area were similar whether derived from the continuity equation or from the simplified Gorlin equation5 using the invasively obtained cardiac output and Doppler-derived valve velocity, and these estimates were consistent with significant, but not critical aortic stenosis. Unfortunately, we were unable to compare these values with those classically obtained by cardiac catheterization. To our knowledge, there has been only one previous report* in which continuous-wave Doppler was used to monitor the course of a pregnancy complicated by aortic stenosis. At various intervals, peak instantaneous valve gradients were obtained in a young woman with a deteriorating aortic valve prosthesis. Aortic valve area was unreported. The authors rightfully cautioned misinterpretation of Doppler-derived estimates of valve gradients in view of known pregnancy-related hemodynamic changes. However, estimates of aortic valve area, which take into account the effect of flow, should be valid. We await the establishment of normal Doppler values for pregnancy and further investigation in associated pathologic states is needed. In spite of these limitations, Doppler-derived data obtained in the overall noninvasive evaluation of this patient played a vital role in outlining the appropriate peripartum management. The preferred method of delivery in these patients remains controversial. The major objective is to avoid volume depletion and hypotension, which can lead to catastrophic hemodynamic collapse. This can be precipitated by peripartum blood loss, supine vena caval obstruction, anesthetic-related vasodilatation, and even myocardial infarction..1~6~7In view of this patient’s persistent excellent LV systolic function, Doppler estimates of noncritical aortic stenosis, and normal right heart and PCWPs, we elected to allow her to undergo labor and to deliver entirely in the left lateral decubitus position with continuous fetal and right heart pressure monitoring. In conclusion, we describe the safe and uneventful labor and delivery of an otherwise healthy young woman with congenital aortic valve stenosis. The degree of stenosis was originally considered critical when only peak aortic valve velocity and estimated gradient were considered. However, the Doppler-derived estimates of aortic valve area, which should take into account the hyperdynamic flow state known to exist during pregnancy, were not consistent with critical valve stenosis. Doppler values reflecting LV function can assist in differentiating critical from “pseudo-critical” aortic stenosis. REFERENCES
1. Arias F, Pineda J. Aortic stenosis and pregnancy. J Reprod Med 1978;20:229. 2. Hatle L. Noninvasive assessment and differentiation of left ventricular outflow obstruction with Doppler ultrasound, Circulation 1981;64:380. 3. Currie PJ, *Seward JB, Reeder GS, Vlietstra RE, Bresnahan DR, Bresnahan JF, Smith HC, Hagler DJ, Tajik AJ. Continuous wave Doppler echocardiographicassessmentof severity of aortic stenosis: a simultaneous Doppler-catheter correlative study in 100 adult patients. Circulation 1985;71:1162.
Brief Communications
4.
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Otto CM, Pearlman AS, ComessKA, Reamer RP, Janko CL, Huntsman LL. Determination of the stenotic aortic valve area in adults using Doppler echocardiography. J Am Co11
Cardiol 19&X7:509. Teirstein P, Yeager M, Yolk PG, Popp RL. Doppler echocardiographic measurement of aortic valve area in aortic stenosin: an&cation of the Gorlin formula. J Am ___ -a noninvasive . ~.. Co11 Cardiol 1986;8:i659. 6. Sullivan JM, Ramanathan KB. Management of medical problems in pregnancy-severe cardiac disease. N Engl J Med 1985;313:304. 7. Clark SL. Labor and delivery in the patient with structural cardiac disease. Clin Perinatol 1986;13:695. RH, Wyner J, Cohen S, Ueland K. 8. Rose BI, Holbrook Efficacy of Doppler echocardiography in the evaluation of aortic stenosis during pregnancy. Obstet Gynecol 1987; 69:431. 5.
Cardiac hydatid cyst with clinical features resembling subaortic stenosis Giovanni Russo, MD, Corrado Tamburino, MD, Salvatore CuscunB, MD, Giuseppe Arcidiacono, MD, Rosario Foti, MD, Domenico R. Grimaldi, MD, Valeria Calvi, MD, Salvatore Felis, and
Giuseppe Giuffrida, MD. Catania, Italy Cardiac involvement in hydatid disease is rare, occurring in less than 2% of cases.’ The most common site of involvement is the left ventricle, although involvement of the right ventricle and right atrium has also been reported.2 We report a case in which a large cyst located in the interventricular septum was indicative of clinical subaortic stenosis. The patient, a 50-year-old man, had been treated surgically at 20 years of age for a right pulmonary hydatid cyst and at age 38 years for a cyst in the left lobe of the liver. When he was 42 years of age, clinical and echocardiographic findings accidentally revealed obstructive hypertrophic cardiomyopathy, and he was treated with beta blockers (propanolol, 40 mg 3 times day). He was hospitalized because of a 2-month history of fatigue, dizziness, and dyspnea after slight physical exertion. At the time of admission the patient was in good clinical condition. The apical precordial impulse was displaced laterally (at the fifth intercostal
space, 2 cm externally
to the left midclav-
icular line and was forceful and enlarged. A presystolic apical impulse was present. No systolic thrill was palpable on the precordial area. The first heart sound was normal and the second heart sound was normally split. A 3/6 crescendo-decrescendo, blowing, systolic murmur was heard between the apex and the left sternal border of the third intercostal space. lt began well after the first heart sound and radiated to the axillae. No diastolic murmur was heard. From the Istituto di Cardiologia, Cattedra di Cardiochirurgia, tituto di Clinica Medica II, UniversitL di Cat&a. Reprint requests: Giovanni Russo, MD, Via S. Nico16,322-95045, anco (CT), Italy.
and the IsMisterbi-