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The Risk of Adverse Events Associated With Atropine Administration During Dobutamine Stress Echocardiography in Cardiac Transplant Patients: A 28-Year Single-Center Experience
Background
Although dobutamine stress echocardiography (DSE) is performed in heart transplant patients, the safety profile of atropine administration in DSE in this setting is unclear.
Methods and Results
We identified heart transplant patients who received atropine during DSE from January 1984 to August 2011 at our institution and compared them with a propensity-scored matched control group of heart transplant patients who underwent DSE without atropine. Adverse events were defined as significant arrhythmias (sinus arrest, Mobitz type II heart block, complete heart block, ventricular tachycardia, or ventricular fibrillation), hypotension requiring hospitalization, syncope or presyncope, myocardial infarction, and death. Forty-five heart transplant patients (median age 62 years, 82% male) received 0.2–1 mg atropine during DSE. Of these, 1 patient (2.2%) developed temporary complete heart block. No adverse events were identified in the control group of 154 patients who received dobutamine without atropine.
Conclusions
Our findings suggest that complete heart block can occur infrequently with the administration of atropine in heart transplant patients undergoing DSE. Therefore, patients should be appropriately monitored for these adverse events during and after DSE
Ease of noninvasive measurement of cardiac output coupled with peak VO<sub>2</sub> determination at rest and during exercise in patients with heart failure
Peak cardiac power output, measured noninvasively, is a powerful predictor of outcome in chronic heart failure
Preoperative Assessment of High-Risk Candidates to Predict Survival After Heart Transplantation
Circulating T-Cell Subsets, Monocytes, and Natural Killer Cells in Peripartum Cardiomyopathy: Results From the Multicenter IPAC Study
•Immune cell subsets were examined in healthy postpartum and peripartum cardiomyopathy (PPCM) women.•In the early postpartum, PPCM women had lower NK and higher CD3+CD4–CD8–CD38+ T cell levels.•Levels largely normalized by 6 months postpartum.
The aim of this work was to evaluate the hypothesis that the distribution of circulating immune cell subsets, or their activation state, is significantly different between peripartum cardiomyopathy (PPCM) and healthy postpartum (HP) women.
PPCM is a major cause of maternal morbidity and mortality, and an immune-mediated etiology has been hypothesized. Cellular immunity, altered in pregnancy and the peripartum period, has been proposed to play a role in PPCM pathogenesis.
The Investigation of Pregnancy-Associated Cardiomyopathy (IPAC) study enrolled 100 women presenting with a left ventricular ejection fraction of <0.45 within 2 months of delivery. Peripheral T-cell subsets, natural killer (NK) cells, and cellular activation markers were assessed by flow cytometry in PPCM women early (<6 wk), 2 months, and 6 months postpartum and compared with those of HP women and women with non–pregnancy-associated recent-onset cardiomyopathy (ROCM).
Entry NK cell levels (CD3–CD56+CD16+; reported as % of CD3– cells) were significantly (P < .0003) reduced in PPCM (6.6 ± 4.9% of CD3– cells) compared to HP (11.9 ± 5%). Of T-cell subtypes, CD3+CD4–CD8–CD38+ cells differed significantly (P < .004) between PPCM (24.5 ± 12.5% of CD3+CD4–CD8– cells) and HP (12.5 ± 6.4%). PPCM patients demonstrated a rapid recovery of NK and CD3+CD4–CD8–CD38+ cell levels. However, black women had a delayed recovery of NK cells. A similar reduction of NK cells was observed in women with ROCM.
Compared with HP control women, early postpartum PPCM women show significantly reduced NK cells, and higher CD3+CD4–CD8–CD38+ cells, which both normalize over time postpartum. The mechanistic role of NK cells and “double negative” (CD4–CD8–) T regulatory cells in PPCM requires further investigation