Myocardial bridge associated with pacing-induced coronary spasm

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1994

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3. End-diastolic and end-systolic (shaded area) contours in the left anterior oblique projection. A, Immediately after PTCA the contraction pattern showsseverehypokinesisof the interventricular septum. B, Before hospital dischargemyocardial dynamics are normalized. Fig.

In our case,prolonged chest pain, pathologic elevation of cardiac enzymes,and R wave reduction supported the diagnosisof myocardial infarction. However, myocardial necrosiswas not responsiblefor the development of a new Q wave; indeed, the abnormal Q wave rapidly disappeared after PTCA restored coronary bloow flow. Transient pathologic Q waves have been describedin ischemicheart disease,1-4 but not in acute myocardial infarction. Some believe that transient Q waves are due to an intraventricular conduction disturbance: while others link the phenomenon to an electrical death of ischemic cells without actual anatomic death.* Whatever the genesisof transient Q waves may be, our report strongly suggeststhat new Q wavesduring evolving myocardial infarction may reverse, in the beginning, if coronary reperfusion is obtained. Other findings demonstrate that PTCA reduced tissue damage:(1) ECG showedonly temporary abnormalities of T waves and slight loss of R waves amplitude; (2) left ventriculography was normal on discharge; (3) exercise test wasnegative and the patient remainedasymptomatic. In comparison with thrombolytic therapy,6 PTCA offers the advantage of a rapid resolution of both coronary occlusion and residual stenosis.Our report demonstrates that PTCA can be a first-line therapy in evolving myocardial infarction due to subocclusive coronary stenosis, although its usein the presenceof total coronary occlusion does not seemjustified at this time. REFERENCES

Hdat R, Chiche P: Transient abnormal Q waves in the course of ischemic heart disease. Chest 65:140, 1974. 2. Bateman T, Gray R, Maddahi J, Rozanski A, Raymond M, Berman D: Transient appearance of Q waves in coronary disease during exercise electrocardiography: Consideration of mechanisms and clinical importance. AM HEART J 104:182, 1982. 3. Rubin IL, Gross H, Vigliano EM: Transient abnormal Q waves during coronary insufficiency. AM HEART J 71:254, 1.

1966.

4. Meller J, Conde CA, Donoso E, Dack S: Transient Q waves in Prinzmetal’s angina. Am J Cardiol35:691, 1975. 5. Gambetta M, Childers R: Rate-dependent right precordial Q waves: “Septal focal block.” Am J Cardiol32:196, 1973. 6. Rentrop P, Blanke H, Karsch KR, Kaiser H: Selective intracoronary thrombolysis in acute myocardial infarction and unstable angina pectoris. Circulation 63:307, 1981.

Myocardial bridge associated with pacing-induced coronary spasm Maleah Grover, M.D., and G. B. John Mancini, M.D. San Diego, Calif.

The coronary arteries and their major branches usually course on the surface of the heart in the subepicardial tissue. Occasionally, a portion of the artery may be embedded in muscle, a condition termed myocardial bridging. The angiographic appearance of myocardial bridges has been well described, but the hemodynamic significance of myocardial bridging remains controversial.‘-” Although it has been suggestedthat myocardial bridges may be associatedwith coronary artery spasm, this associationhas not previously been definitively demonstrated. We describea patient with myocardial bridging of the left anterior descendingartery (LAD) who demonstrated spasmin, and distal to the area of the myocardial bridge, as well as in a diagonal artery. Moreover, this spasmwasreproducibly induced by rapid atrial pacing. From the Department of Medicine, Division of Cardiology, University of California, San Diego. Reprint requests: G. B. John Mancini, M.D., Divisionof Cardiology (lllA), VA Medical Center, 2215 Fuller Rd., Ann Arbor, MI 48105.

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Fig. 1. A, End-diastolic frame of the left anterior coronary artery taken in the 60-degreeleft anterior oblique, 30-degreecaudocranialprojection. B, End-systolic frame demonstratesmarked systolic narrowing due to a large myocardial bridge, These frames were obtained with the patient in a control, pain-free state.

The patient is a 56-year-old man with a 3-year history of chestpressurewhich usually occurred at rest. The discomfort wassometimesassociatedwith dizziness, diaphoresis, nausea,and left arm radiation, but wasusually relieved by nitroglycerin (NTG). On several of many admissionsfor prolonged chest pain his creatine phosphokinaseand MB fraction were mildly elevated. During two of these admissions his ECG showed ST segment flattening in the anterior precordial leads that subsequently normalized. His medications at the time of referral were isosorbide dinitrate, 80 mg orally every 8 hours, nifedipine, 20 mg orally every 8 hours, and metoprolol, 100 mg orally every 12 hours. The ECG and echocardiogramwere normal. A thallium exercise tolerance test was suboptimal because the patient only exercisedfor 4 minutes and did not have symptoms. The thallium distribution scintigram immediately after exercisewas normal. A supine bicycle exercise test documented a normal increase in the radionuclide ejection fraction, but the left ventricular size increased and tardokinesisof the inferoapical myocardium wasseen. No chest pain occurred. A first cardiac catheterization demonstrated myocardial bridging of the LAD after the seconddiagonal artery (Fig. 1). Becausethe hemodynamic significance of the bridge wasunclear, the patient wasreferred for further investigation while all medications were withheld. During the second catheterization a stable baseline heart rate was maintained by right atria1 pacing at 77 bpm. Duplicate coronary sinus and systemic arterial blood sampleswere taken to measurebaselinelactate extraction. A 30-degree right anterior oblique (RAO) left ventriculogram wasthen obtained at the same heart rate. Ten minutes after the ventriculogram, the right atrium was paced in a stepwise fashion to a maximal rate of 160 bpm for 5 minutes. This induced the patient’s typical chest pain, during which repeat blood sampleswere drawn for lactate determination. A repeat 30-degree RAO left ventriculogram was

Fig. 2. Left coronary arteriogram obtained soon after rapid atria1 pacing while chest pain was still severe. The open arrow showsthe original area of myocardial bridging which now demonstratesspasm.Solid areas point to other areasof severespasm.In contrast to Fig. 1, these narrowings showedno phasicvariation in severity throughout the cardiac cycle.

obtained immediately post pacing. This showedthat the end-diastolic volume enlarged slightly from 79 to 99 ml and the end-systolic volume rose from 17 to 30 ml. The ejection fraction fell from 0.79 to 0.70 and anteroapical

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December, 1984 Heart Journal

Fig. 3. A and B represent the end-diastolic and end-systolic frames of the left coronary arteriogram obtained during rapid atrial pacing at a rate of 160 bpm, which induced chest pain. In contrast to Fig. 1, cyclical variation in the stenosisis absentand is in keeping with spasmat the area of myocardial bridging. Other areas of snasmwere not demonstrated at this time, possibly due to prior administration of nitroglycerin.

hypokinesis was noted. Coronary sinus lactate measurements showedan initial extraction (25%) which changed to lactate production (-9%). No definite ECG changes were noted during this period. After the ventriculogram and during continued chest pain, a left coronary arteriogram demonstrated severe narrowing of approximately 80% to 90% at the previous area of myocardial bridging (Fig. 2). This narrowing showed no cyclical variation throughout the cardiac cycle and wasfelt to be compatible with spasm.In addition, severespasmof a diagonal artery and three severefocal areasof spasmin the distal segment of the LAD were seen. The patient’s chest pain resolved after intracoronary administration of 0.3 mg NTG. The subsequentarteriogram showed resolution of spasm and typical systolic narrowing remained in the area of myocardial bridging. The administration of NTG did not accentuate the systolic narrowing. In view of the severity of spasm,ergonovine was not administered; however, rapid atrial pacing was repeated to a rate of 160 bpm. This again induced chest discomfort but no ECG changes.A repeat arteriogram at this time showedseverenarrowing in the area of myocardial bridging with no cyclical variation in severity. This wasagain felt to be consistent with pacing-induced spasm (Fig. 3). Diffuse spasmas initially seen (Fig. 2) was not induced. This may have been due to the prior administration of NTG. Angelini et a1.3have recently reviewed the comparative anatomy, clinical features, and possible pathogenetic mechanismsof myocardial bridges. They concluded that patients with equal degreesof systolic narrowing do not exhibit any common clinical or laboratory patterns. In addition, they felt that the available literature does not provide conclusive evidence that myocardial bridges induce ischemia, particularly in view of the fact that systolic narrowing can affect only 5% to 30% of total coronary blood flow, the remaining portion being diastolic.

It has beensuggestedthat systolic compressionmay cause impairment of diastolic flow if “recoil” of the area is sluggish and not yet complete during early diastole.5 Alternatively, Krawczyk et al6 have postulated systolic vascular closure with incomplete reopening distal to the bridged area that might account for impaired diastolic coronary flow. It is not clear how frequently these mechanisms may be involved in the genesis of chest pain syndromesin patients with myocardial bridges.Although abnormal vasospasmat the site of the myocardial bridge hasbeen suspected,4clear documentation of this phenomenon has not been shown. Angelini et a1.3reported that efforts to induce spasmwith ergonovinewere unsuccessful in their patient population and the degree of systolic narrowing was unchangedor decreasedby this challenge. In addition, they noted similar angiographic findings when the affected artery wasfilmed during atria1pacing at 150 bpm and no instancesof spasmwere reported. The current casereport demonstrates several unusual features. First of all, reproducible coronary spasmat the site of myocardial bridging was demonstrated. Furthermore, this was in association with chest pain, lactate production, and deterioration in global and regional ventricular function. Although the spasmwasnot confined to the area of bridging in this patient, the reproducible spasmwas seen only in that area. The second unusual feature is that the spasmwas induced by rapid atrial pacing. Tada et a1.7reported one other patient with pacing-induced vasospasmof the LAD coronary artery. Although they also found an associatedincreasein coronary sinusthromboxane Bz, a vasoconstrictor, the role of such substancesin mediating significant vasoconstriction in responseto atria1 pacing remains controversial.* This casedemonstratesthat an aggressivesurgical approach in responseto the finding of a myocardial bridge in patients with chest pain syndromes should be replaced by an aggressivediagnostic approach that might uncover unique

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pathogenetic mechanisms.Objective evidence of iachemia-related symptomsin conjunction with either metabolic and/or functional markers of ischemiamust be obtained before any therapy is justified for these patients, because the condition may well be benign in the majority of cases.3*g Finally, associatedcoronary spasm,although rare, should be ruled out. Ergonovine challenge and atria1 pacing may be useful in this regard. REFERENCES

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3. 4.

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Greenspan M, Iskandrian AS, Catherwood E, Kimbris D, Bemis CE, Segal BL: Myocardial bridging of the left anterior descending artery: Evaluation using thallium-201 myocardial scintigraphy. Cathet Cardiovasc Diagn 6:173, 1980. Noble J, Bourassa MG, Petitclerc R, Dyrda I: Myocardial bridging and milking effect of the left anterior descending coronary artery: Normal variant or obstruction? Am J Cardiol 37:993, 1976. Angelini P, Trivellato M, Donis J, Leachman RD: Myocardial bridges: A review. Prog Cardiovasc Dis 26:75, 1983. Froment R, Normand J, Amiel L: Angine de poitrine de type Prinzmetal. Coronaries permeable mais spasme de l’interventriculaire anterieure en tours de crise. Arch Ma1 Coeur 667~755, 1973. Hill RC Chitwood WR, Bashore TM, Sink JD, Cox JL, Wechsler AS: Coronary flow and regional function before and after supraarterial myotomy for myocardial bridging. Ann Thorac Surg 31:176, 1980. Krawczyk JA, Dashkoff N, Mays A, Klocke FJ: Reduced coronary flow in a canine model of “muscle bridge” with inflow occlusion extending into diastole: Possible role of downstream vascular closure. Trans Assoc Am Physicians 93:100, 1980. Tada M, Kuzuya T, Inoue M, Kodama K, Mishima M, Yamada M, Inui M, Abe H: Elevation of thromboxane B, levels in patients with classic and variant angina pectoris. Circulation 64:1107, 1981. Martin JL, Wilson JR, Burch JW, Untereker WJ, Kaskey W, Ferraro N, Hirshfeld JW Jr: Effect of atria1 pacing on intracoronary thromboxane production in coronary artery disease. J Am Co11 Cardiol 1:1194, 1983. Kramer JR, Kitazume H, Proudfit WL, Sones FM Jr: Clinical significance of isolated coronary bridges: Benign and frequent condition involving the left anterior descending artery. AM HEART J 103:283, 1982.

with an acute myocardial infarction and biventricular congestive heart failure. Two episodesof marked tachypnea shortly after admission led to performance of a perfusion lung scan. This study was interpreted as compatible with high probability of pulmonary embolization. Although pulmonary embolismwasnot proven, the perfusion scan and the presenceof biventricular failure were felt to make anticoagulation the appropriate decision,and heparin sodiumwasadministered by continuous infusion. On the seventh day of heparin therapy the platelet count was200,000mm3.On the ninth day the patient developed acute arterial insufficiency in the right leg. Embolization from a left ventricular mural thrombus was suspected. The partial thromboplastin time, previously in the therapeutic range, was found to be normal. The patient underwent exploration of the right iliac and femoral arteries, which revealed organized thrombus with new clot formation distally. A thrombectomy wasperformed and heparin was continued. On the first postoperative day (tenth day of heparin therapy), the platelet count was found to be 38,000 mm3. In the laboratory, the patient’s platelets aggregated in the presence of heparin; there was no spontaneous platelet aggregation. Control platelets did not aggregate with heparin. A diagnosis of heparinassociated thrombocytopenia resulting in a localized thrombotic disorder wasmade. Heparin was discontinued but the patient progressivelydeteriorated and died on the secondpostoperative day. Heparin-associatedthrombocytopenia is often first recognized at the time of a new or recurrent thromboembolic event in a patient receiving heparin,‘B2and thromboembolism rather than bleedinghasbeenresponsiblefor many of the reported fatalities. The onset is usually after a meanof 5 days of treatment, but may be shorter in patients with prior exposure to the drug. The syndrome has been described with continuous infusion, intermittent bolus, and subcutaneous “mini” heparin. Thrombocytopenia may be mild and clinically insignificant and may resolve though the drug is continued, or it may be severe and associated with fatal complications. Heparin-dependent platelet aggregatingactivity can be isolated from the IgG fraction

Heparin-related thrombosis myocardial infarction

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Katherine A. Hawkins, M.D., and Myles J. Schwartz, M.D. New York, N.Y.

From the Department College of Physicians

1543

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Center,

M.D., St. Luke%-Roosevelt York, NY 10025.

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lead to thrombocytopenia as well as to thrombosia4 In a number of casesthe syndrome has been accompaniedor preceded by increasing heparin requirementa An increasein heparin dosein an attempt to correct “inadequate anticoagulation” or to treat the recurrent thromboembolism would be contraindicated. Once the diagnosisof heparin-associatedthrombocytopenia is made, most authorities recommend discontinuation of heparin becauseof the potential thrombotic and hemorrhagic complications. Substitution of oral anticoag-

ulants or dextran has been used for patients who must remain anticoagulated. Steroid therapy is not useful. Patients have been switched from one type of heparin to