Anda di halaman 1dari 5

Normalization of Complete Left Bundle Branch Block Unmasking Acute Inferoposterolateral Myocardial Infarction

Case Report Alon Yarkoni, Lisa Emmans, Robert E. Halligan Jr., Frank Cardello, Kenneth B. Desser
Banner Good Samaritan Regional Medical Center/Veterans Affairs Medical Center Cardiology Fellowship Program, 1111 E. McDowell St, Phoenix, AZ 85006. ______________________________________________________________________________________

Abstract :Left bundle branch block aberration on an electrocardiogram typically occurs in patients with preexisting organic heart disease and confers a worse long term prognosis. Functinal bundle branch block may normalize through a variety of different mechanisms. We present a case of transient normalization of LBBB during an acute inferoposterior myocardial infarct secondary to a proposed rate related phenomenon.

Background Left bundle branch block (LBBB) is a clinically significant finding on the electrocardiogram (ECG). Occurring more frequently with increasing age, it is most frequently associated with underlying organic heart disease including hypertension and coronary artery disease and may portend progressive conduction system disease, possible ventricular dysynchrony and potential resultant worsening of left ventricular function. The Framingham study found one half of patients with new LBBB died within 10 years, with prognosis being influenced by coexisting heart disease1. In the setting of acute myocardial infarction (MI), development of new LBBB meets ACC/AHA guideline criteria for reperfusion therapies2. Normalization of a wide QRS complex in a patient with preexisting QRS prolongation is an important, though much less frequently seen phenomenon. Proposed mechanisms for this finding include loss of transseptal concealed conduction, loss of preexcitation, gap phenomenon, supernormality, equal conduction delay in both bundle branches and change in heart rate. We present a case in which transient normalization of left bundle branch block occurred in the setting of an acute inferoposterolateral wall myocardial infarct with subsequent return of LBBB morphology after reperfusion therapy. Case Report A 53 year old male with history of hypertension and dyslipidemia was admitted to the general medicine service with complaints of fever, flank pain and dysuria. Urinalysis showed pyuria and urine culture grew pan-sensitive E. coli. Intravenous ciprofloxacin was initiated for presumed pyelonephritis. His admission ECG showed a sinus rhythm with an occasional premature ventricular complex and LBBB (Figure1).

On hospital day two the patient developed the acute onset of mid-sternal, non-radiating chest pressure of 8/10 intensity associated with nausea, vomiting, diaphoresis and shortness of breath. Physical exam revealed a diaphoretic male with a blood pressure of 111/49, pulse 63 and an S4 gallop. An ECG obtained during chest pressure demonstrated sinus rhythm at 53 BPM, QRS 78ms, 2-3 mm ST segment elevation in inferior and lateral leads with ST segment depression in leads V1-3 (Figure 2).

Sublingual nitroglycerin, aspirin, beta-blocker and heparin improved pain to 5/10 with persistent ECG changes. The patient then received thrombolytic therapy with tenecteplase. An uneventful hospital course ensued with peak troponin levels of 20.35.

Left heart catheterization showed mild coronary artery disease with suggestion of an ulcerated plaque in the dominant left circumflex coronary artery and mildly reduced LV function. Repeat ECGs demonstrated a return to baseline LBBB pattern with QRS 120ms which persisted through follow-up 14 months later (Figure 3).

Discussion This patient had a well-documented LBBB pattern both prior to and well after an inferoposterolateral myocardial infarction. His MI was thought to be due either to plaque rupture or vasospasm. Following thrombolytic therapy, the QRS interval temporarily normalized in duration with loss of a LBBB pattern and the appearance of diagnostic ST segment elevation. Several mechanisms may cause the sudden transition from wide to narrow QRS complex conduction (Table 1). Acceleration- and deceleration-dependent bundle branch block is a well known phenomenon which can cause BBBs to appear and disappear depending on cycle length. In our patient, who demonstrated prolonged periods of normal QRS complex duration, rather than isolated complexes or short runs of normalization. The rhythm strip (Figure 4) demonstrates progressive narrowing of the QRS duration with infinitesimal lengthening of the R-R interval, highly suggestive of a rate related process mediated by increased vagal tone and beta blockade administered during the acute MI. Acceleration dependent bundle branch block appears to occur more commonly in the left bundle system and often in the presence of preexisting heart disease. Intermitent bundle branch block typically occurs at heart rates in the tachycardic range (though can be found in the range of normal sinus rates) and is not predictive of development of permanent bundle branch block. The unusual mechanism for a bundle branch block disappearing at

slow heart rates is a critical conduction issue related to prolongation of phase III of the bundle branch action potential. This fatigue at more rapid rates may also be associated with the disappearance of concealed trans-septal conduction3.

An alternative explanation may be that we are seeing introduction of a right bundle branch block (RBBB), rather than resolution of a LBBB. Injured myocardium will produce adenosine monophosphate as adenine nucleotides are degraded under conditions in which ATP utilization exceeds capacity to resynthesize. In fact, reduction in the supply-to-demand ratio for oxygen is the primary determinant of adenosine formation4,5. Adenosine (formed through dephosphorylation) acts as a potent vasodilator, serving to increase local perfusion. Injection of adenosine into septal arteries has also been shown to cause right bundle branch block6. Such events could potentially cause slowing of conduction in the contralateral bundle (right) and resultant normalization of the QRS duration, producing temporary normalization of conduction through both ventricles and normalization of the QRS complex. It has been shown that the refractory period of the right bundle branch is longer at slower heart rates and that of the left bundle branch is longer at faster rates7. If such prolongation was to produce a RBBB in conjunction with chronic LBBB, equalization of delay would produce a temporary normalization of the QRS complex. Under these conditions it is assumed that there is no true block in the left bundle but rather a slowing of conduction. TABLE 1. Mechanisms to Convert Wide QRS Complex to Narrow QRS ______________________________________________________________________ Changes in heart rate Increase rate (deceleration-dependent block) Decrease rate (acceleration-dependent block) Peel back refractoriness (transseptal concealed conduction) Rate-dependent progressive shortening of bundle branch refractoriness Gap phenomenon Supernormality Loss of preexcitation PVC ipsilateral to bundle branch block Equal conduction delay in both bundle branches ______________________________________________________________________
Adapted from Prystowsky EN, Klein GJ. Cardiac Arrhythmias: An Integrated Approach for the Clinician. McGraw-Hill 1994; Table 3-2.

Bibliography 1. Schneider JF, Thomas HE Jr; Kreger BE, McNamara PM, Kannel WB. Newly acquired left bundle-branch block: the Framingham study. Ann Intern Med 1979 Mar;90(3):303-10. 2. Antman et al. ACC/AHA guidelines for the management of patients with st-elevation myocardial infarction. Circulation 2004;110(9):e82. 3. Prystowsky EN, Klein GJ. Cardiac Arrhythmias: An Integrated Approach for the Clinician. McGraw-Hill 1994; 64-9. 4. Sparks HV Jr, Bardenheuer H. Regulation of adenosine formation by the heart. Circ Res 1969;58:193. 5. Bardenheuer H, Schrader J. Supply-to-demand ratio for oxygen determines formation of adenosine by the heart. Am J Physiol 1986;250:H-173. 6. James TN, Bear ES, Frink RJ, Urthaler F. Pharmacologic production of atrioventricular block with and without intitial bundle branch block. J of Pharm and Exper Ther 1971;179(2):338-45. 7. Chilson DA et al. Functonal bundle branch block: Discordant response of right and left bundle braches to changes in heart rate. Am J Cardiol 1984;545:313.