The influence of clopidogrel on ischemia diagnosed by myocardial perfusion stress testing.

BACKGROUND: Clopidogrel is a platelet adenosine receptor antagonist which can influence coronary vascular tone and thus can potentially interfere with myocardial perfusion imaging. We investigated whether clopidogrel can hamper the diagnosis of ischemia in patients undergoing myocardial perfusion testing. METHODS: Data from a database of 6349 myocardial perfusion stress tests were analyzed. Using a propensity analysis, patients who were taking clopidogrel were compared with patients not taking clopidogrel for the presence of reversible perfusion defects on myocardial single-photon emission computed tomography scans. RESULTS: Of the 6349 tests, the stress technique was adenosine in 2713 patients and exercise in 3636. At the time of the stress test, 277 (4.3%) of the patients were taking clopidogrel. The odds ratio (OR) for patients taking clopidogrel to have a reversible perfusion defect was 2.75 (95% confidence interval [CI] 2.09-3.62; P < .01). After adjusting for the propensity to take clopidogrel, the OR was 1.06 (CI 0.76-1.49; P = .73) for patients undergoing adenosine stress tests and 1.60 (CI 0.85-3.00; P = .14) for patients undergoing exercise stress tests. CONCLUSIONS: We found no evidence that the use of clopidogrel decreases the likelihood of ischemia on adenosine or exercise stress myocardial perfusion scans.

Left ventricular ejection fraction and left ventricular end-diastolic volume in patients with diastolic dysfunction.

Diastolic dysfunction can be diagnosed on equilibrium radionuclide angiocardiography (ERNA) by a low peak filling rate (PFR) in the setting of a normal left ventricular ejection fraction (LVEF). The authors evaluated the relationship between diastolic dysfunction, LVEF, and end-diastolic volume (EDV). A total of 408 predominantly asymptomatic patients with an LVEF ≥50% by ERNA were studied. LVEF of patients with a low PFR was compared with the LVEF of patients with a normal PFR. Correlation analyses to evaluate the association between PFR and EDV were also performed. The LVEF of patients with a low PFR was lower than the LVEF of patients with normal PFR (59±7 vs 63%±7%; P<.01). There was no correlation between EDV and PFR (r=-0.04; P=.32). The results did not change when the EDV indices were used. In patients who had repeat scans, there was no correlation between the change in EDV and the change in PFR (r=0.16; P=.2). In asymptomatic patients undergoing ERNA who have normal systolic function, a low PFR can be associated with a lower LVEF, but it is not associated with changes in EDV. This suggests that diastolic dysfunction is associated with mild systolic dysfunction.

A 24-hour comparison of serum growth hormone concentrations in patients with heart failure versus healthy controls.

STUDY OBJECTIVE: To compare endogenous serum growth hormone concentrations over a 24-hour period in patients with chronic heart failure (CHF) and matched controls. DESIGN: Prospective, 24-hour, endogenous concentration comparison. SETTING: Hospital research center. PATIENTS: Eight evaluable patients with nonischemic dilated cardiomyopathy and 10 healthy control subjects, matched for age and sex. INTERVENTION: Over a 24-hour period, blood was drawn from the study participants every 20 minutes for determination of growth hormone. MEASUREMENTS AND MAIN RESULTS: For each patient, the area under the concentration-time curve from time 0-24 hours (AUC0-24), maximum concentration (Cmax), and minimum concentration (Cnadir) of growth hormone were determined. The AUC0-24 and Cmax were 74% (p < 0.05) and 62% (p < 0.05) lower in patients with CHF than in controls, respectively. The Cnadir for all participants was 0 microg/L. Variability in growth hormone concentrations over the 24 hours was considerable for all study participants. CONCLUSIONS: Growth hormone concentrations are suppressed over a 24-hour period in patients with CHF versus healthy controls. Variability in levels throughout the day suggests that a single point evaluation cannot be used to determine deficiency or abundance of growth hormone.