Prognostic significance of ischemic electrocardiographic changes with regadenoson stress myocardial perfusion imaging.

BACKGROUND: In patients undergoing regadenoson SPECT myocardial perfusion imaging (MPI), the prognostic value of ischemic ST-segment depression (ST↓) and the optimal ST↓ threshold have not been studied. METHODS: A retrospective cohort study of consecutive patients referred for regadenoson stress MPI was conducted. Patients with uninterpretable ECG were excluded. Two diagnostic thresholds of horizontal or downsloping ST↓ were studied, ≥ 0.5 mm and ≥ 1.0 mm. The primary endpoint was the composite major adverse cardiac events (MACE) of cardiac death, myocardial infarction, or coronary revascularization. RESULTS: Among 8615 subjects (mean age 62 ± 13 years; 55% women), 89 (1.0%) had ST↓ ≥ 1.0 mm and 133 (1.5%) had ST↓ ≥ 0.5 mm. Regadenoson-induced ST↓ was more common in women (P < .001). Mean follow-up was 2.5 ± 2.2 years. After multivariate adjustment, ST↓ ≥ 1.0 mm was associated with a non-significant increase in MACE risk (P = .069), irrespective to whether MPI was abnormal (P = .162) or normal (P = .214). Ischemic ST↓ ≥ 0.5 mm was independently associated with MACE in the entire cohort (HR 2.14; CI 1.38-3.32; P = .001), whether MPI is normal (HR 2.07; CI 1.07-4.04; P = .032) or abnormal (HR 2.24; CI 1.23-4.00; P = .007), after adjusting for clinical and imaging covariates. An ST↓ threshold of ≥ 0.5 mm provided greater incremental prognostic value beyond clinical and imaging parameters (Δχ2 = 12.78; P < .001) than ≥ 1.0 mm threshold (Δχ2 = 3.72; P = .093). CONCLUSION: Regadenoson-induced ischemic ST↓ is more common in women and it provides a modest independent prognostic value beyond MPI and clinical parameters. ST↓ ≥ 0.5 mm is a better threshold than ≥ 1.0 mm to define ECG evidence for regadenoson-induced myocardial ischemia.

Prognostic implications of diastolic dysfunction in patients with acute pulmonary embolism.

BACKGROUND: A history of congestive heart failure has been used to determine the prognosis in patients with acute pulmonary embolism. Diastolic dysfunction is responsible for the half of congestive heart failure but has not been understood well. METHODS: A total of 205 patients were reported admitted with acute pulmonary embolism from January 2009 to July 2011. We excluded hemodynamically unstable patients who received thrombolytics or underwent thromboembolectomy. We included hemodynamically stable patients who underwent echocardiogram within 72 hours of diagnosis. We reviewed medical records of 107 patients to investigate whether diastolic dysfunction increases in-hospital mortality or adverse clinical outcomes. RESULTS: Out of 107 patients, 10 patients died during hospitalization with in-hospital mortality rate of 9.3%. Among 84 patients without diastolic dysfunction as assessed by echocardiogram, six patients died with in-hospital mortality rate of 7.1%. Meanwhile, among 23 patients with diastolic dysfunction, four patients died with in-hospital mortality rate of 17.4%. The multivariable adjusted odds ratio was calculated as 2.71, with 95% confidence interval of 0.59 - 12.44. CONCLUSIONS: For hemodynamically stable patients with acute pulmonary embolism, diastolic dysfunction as assessed by echocardiogram could increase in-hospital mortality 2.71 fold, although this was not statistically significant. Further study with a large patient population is needed to determine the statistically significant implications of diastolic dysfunction in patients with acute pulmonary embolism.