Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay: insights from a coronary sinus sampling study.

OBJECTIVES: The purpose of this study was to assess whether: 1) very small increases in troponin T, measured by a new highly sensitive cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis; and 2) serial changes can discriminate ischemia from other causes of cardiac troponin T (cTnT) release. BACKGROUND: A new hs-cTnT assay offers greater sensitivity than current assays. METHODS: Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple time points during and after incremental rapid atrial pacing. cTnT was quantified using both a standard and a pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing. RESULTS: cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 min after termination of rapid atrial pacing (p < 0.0001), changes that were mirrored at 180 min in peripheral blood (5.1 to 11.8 pg/ml, p < 0.0001). Although peripheral cTnT concentrations tended to be higher at 180 min following pacing for patients with CAD and lactate elution (n = 7) when compared with those without either marker (n = 5) (25.0 pg/ml vs. 10.2 pg/ml, p = 0.10), relative (1.7-fold vs. 5.2-fold) and absolute (6.8 pg/ml vs. 8.8 pg/ml, p = 0.50) changes were not different between groups. CONCLUSIONS: Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive CAD. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.

The effect of acute hypoxemia on coronary arterial dimensions in patients with coronary artery disease.

OBJECTIVES: To assess the influence of acute hypoxemia on the dimensions of diseased and nondiseased coronary arterial segments in humans. METHODS: In 18 subjects (age 53 +/- 8 years) with known or suspected coronary artery disease, quantitative coronary angiography was performed before and after being randomly assigned to breathing (1) an inspired oxygen concentration (fraction of inspired oxygen, FIO2) of 21% (room air, RA) for 20 min (n = 4, controls) or (2) an FIO2 of 15 and 10% for 10 min each (corresponding to altitudes of 2,500 and 5,500 m, respectively; n = 14). RESULTS: In the control subjects, no hemodynamic, oximetric or angiographic variable changed. In the 14 study subjects, the arterial partial pressure of oxygen averaged 85 +/- 13 mm Hg on RA, 65 +/- 15 mm Hg on 15% FIO2 and 44 +/- 13 mm Hg on 10% FIO2. Average arterial segment diameter was 2.52 +/- 0.63 mm on RA, 2.55 +/- 0.62 mm on 15% FIO2 (not significant vs. RA) and 2.66 +/- 0.66 mm on 10% FIO2 (p < 0.001 vs. RA). The increase in coronary arterial diameter with 10% FIO2 occurred only in normal segments (2.74 +/- 0.64 vs. 2.97 +/- 0.64 mm; p < 0.001), but not in diseased segments (2.34 +/- 0.57 vs. 2.38 +/- 0.55 mm; not significant). CONCLUSIONS: In humans, severe hypoxemia induces vasodilation of angiographically normal coronary arterial segments, whereas it causes no change in diseased segments.

Inaccuracies of oximetry in identifying the location of intracardiac left-to-right shunts in adults.

Although oximetric analysis of blood from the right heart chambers is the most commonly used method for assessing the presence of intracardiac left-to-right shunting, it sometimes provides misleading information because a patient with a left-to-right shunt in only 1 location sometimes manifests a significant oxygen step-up (1) in >1 chamber or (2) in a chamber other than that in which the shunt is actually located. This study was performed (1) to assess the frequency with which oximetric data provide such misleading results and (2) to determine which variables (if any) may contribute to the occurrence of such erroneous oximetric results. Accordingly, we analyzed oximetric data from 168 patients (61 men, 107 women, 14 to 76 years of age) with a proved left-to-right shunt at only 1 site and oximetric evidence of significant oxygen step-up. Using the criteria of Dexter et al (J Clin Invest 1947;26:554-560), Antman et al (Am J Cardiol 1980;46:265-271), or Pirwitz et al (Am Heart J 1997;133:413-417) for a significant oxygen step-up, 34%, 42%, and 35% of subjects, respectively, manifested a significant step-up in >1 chamber or a step-up only in an incorrect chamber. Compared with those with a step-up in the correct chamber only, those with a step-up in >1 chamber had larger Qp/Qs ratios (mean +/- SD, 2.7 +/- 1.2 vs 3.5 +/- 1.8, respectively, p <0.001), whereas subjects with a step-up only in an incorrect chamber had smaller Qp/Qs ratios than those with a step-up in the correct chamber (2.2 +/- 0.9 vs 2.8 +/- 1.3, respectively, p <0.001). In conclusion, in adult subjects with left-to-right intracardiac shunting in only 1 location, carefully obtained oximetric data often provide erroneous information.

Predictors of coronary artery disease in patients with left bundle branch block undergoing coronary angiography.

Patients with left bundle branch block (LBBB) and concomitant coronary artery disease (CAD) have a worse prognosis than those with LBBB without CAD. In addition, subjects with CAD and concomitant LBBB have a higher cardiovascular mortality than those with a similar extent of CAD but without LBBB. Because the presence of LBBB makes the noninvasive identification of CAD problematic, patients with LBBB often are referred for coronary angiography to assess the presence and severity of CAD. To determine the clinical and demographic variables that might help identify those with CAD, we analyzed data from 336 consecutive patients with LBBB referred for coronary angiography. Of the 336, 54% had CAD. In conclusion, those with CAD were likely to be older, Caucasian, and men; they were more likely to have angina pectoris, myocardial infarction, and diabetes mellitus; and they were more likely to have a left ventricular ejection fraction <0.50. In contrast, patients with heart failure were less likely to have CAD.