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To clarify the etiology of elevations in plasma MB creatine kinase (CK) in patients after cardiac catheterization, we studied 32 consecutive patients undergoing cardiac catheterization and coronary arteriography. Total CK and MB CK were within the normal range in all patients prior to catheterization. Total CK activity rose from a mean of 61.46 +/- 33.8 IU/1 (SD) to 141 +/- 105 in the first sample after catheterization (p less than .005) and 121.6 +/- 92.4 in the second catheterization sample (p less than .0005). The MB CK activity also rose from a mean of 3.2 +/- 1.6 IU/1 prior to catheterization to a maximum value of 5.0 +/- 2.9. The mean increase in MB CK, though statistically significant (p less than .005), was only 1.8 IU/1. Only one patient's value for MB CK rose to outside of the normal range (greater than 12) likely due to cardiac injury. Thus, our data document that marked elevations in MB CK after cardiac catheterization are unusual. They likely represent cardiac muscle injury rather than MB CK released due to skeletal muscle injury induced by the catheterization itself.

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E nhanced AAIR7DDDR pacing (atrial-based Managed Ventricular Pacing [MVP]) is a novel pacing mode that facilitates intrinsic conduction whenever possible to mitigate the deleterious effects of prolonged duration right ventricular (RV) electric stimulation on left ventricular contractility. The following case illustrates uncommon ECG and hemodynamic consequences of this algorithm in a patient with marked atrioventricular (AV) conduction delay. Brief Case DescriptionA 58-year-old man with a history of acute myeloid leukemia, subsequent bone marrow transplantation, nonablated paroxysmal atrial flutter, and tachy-brady syndrome underwent implantation of a Medtronic Adapta ADDR01 permanent dual-chamber pacemaker (Medtronic Inc., Minneapolis, Minn.) for symptomatic junctional bradycardia with leads positioned in the right atrial (RA) appendage and RV apex. After implantation, flecainide 100 mg twice daily was added to extended-release diltiazem 240 mg daily with a resultant absence of arrhythmia on serial pacemaker telemetry interrogations. His pacemaker was programmed with enhanced AAIR7DDDR pacing enabled at a lower rate limit of 60 bpm. A routine ECG obtained 1 month later (Figure 1) demonstrated atrial pacing and capture in the terminal portion of the preceding T wave with pronounced 1°AV block. Closer scrutiny of the tracing reveals 2 separate atrial depolarization waves. Repolarization abnormalities and QT interval prolongation were attributed to the effects of intermittent RV pacing and the concomitant administration of flecainide, fluoxetine, sulfamethoxazole-trimethoprim, and azithromycin. Two-dimensional echocardiography at that time demonstrated biatrial and RV enlargement with normal left ventricular and RV regional and global function.Figure 2 displays the temporal relationship between the RA and left atrial (LA) depolarization in leads V 1 through V 3 . The right atrial pacemaker stimulus artifact is followed by immediate RA capture. A second atrial deflection with opposite polarity representing LA depolarization is noted Ϸ200 ms after RA activation and is followed 240 milliseconds later by an intrinsically conducted narrow QRS complex. Figure 3 displays contemporaneous transtricuspid and mitral continuous-wave Doppler velocity-time integrals aligned using the atrial pacemaker stimulus artifact. The top panel demonstrates merging of the transtricuspid valve rapid inflow (E wave) velocity-time integral with the RA A wave. The initiation of RA contraction is coincident with RA pacing, and anterograde flow across the transtricuspid valve continues into early ventricular systole. The stimulus-to-QRS interval is Ϸ400 milliseconds. The bottom panel depicts the transmitral valve inflow velocity-time integral. A nearly normal temporal relationship (minimal fusion) of the E and A waves is demonstrated. Baseline artifact and low-amplitude signals hamper definitive identification of the P-wave onset on the ECG rhythm strips displayed; however, the LA A-wave-to-QRS interval is Ϸ185 milliseconds. The paced cycle leng...