Unplanned Readmissions After Acute Myocardial Infarction: 1-Year Trajectory Following Discharge From a Safety Net Hospital.

BACKGROUND: Financial penalties rendered by the Centers for Medicare and Medicaid Services have brought about new challenges for safety net hospitals that serve a vulnerable patient population with risk factors associated with high readmission rates. Our goal was to determine the 1-year trajectory of unplanned readmissions in post-myocardial infarction (MI) patients, and to identify factors associated with readmission. METHODS: A total of 261 acute MI patients admitted from April 2015 to April 2016 were evaluated in a multidisciplinary cardiology clinic within 10 days of hospital discharge and baseline characteristics and medical comorbidities were collected. Readmission and mortality data were obtained at 1 year through chart review and telephone follow-up. RESULTS: At 1 year, there were 90 (34%) unplanned readmissions of which half were for noncardiac diagnoses. Of these, 69 patients (77%) were readmitted once, 16 (18%) were readmitted twice, 2 (2%) were readmitted 3 times, and 3 (3%) were readmitted 4 times over the subsequent year. Cardiac causes of 1-year readmission included recurrent MI in 23 (9%) and decompensated heart failure in 18 (7%) patients. Depressed left ventricular systolic function (hazard ratio, 2.23; 95% confidence interval, 2.00-2.44; P = 0.0003) and diabetes mellitus (hazard ratio, 1.60; 95% confidence interval, 1.38-1.82; P = 0.029) were associated with a significantly higher risk of readmission at 1 year. CONCLUSION: Following acute MI, patients are readmitted for cardiac and noncardiac diagnoses well beyond the 30-day mark. This is likely a function of the vulnerability of the patient population rather than a reflection of the medical care provided. More frequent surveillance may attenuate this problem.

The cooperative roles of the dopamine receptors, D1R and D5R, on the regulation of renal sodium transport.

Determining the individual roles of the two dopamine D1-like receptors (D1R and D5R) on sodium transport in the human renal proximal tubule has been complicated by their structural and functional similarity. Here we used a novel D5R-selective antagonist (LE-PM436) and D1R- or D5R-specific gene silencing to determine second messenger coupling pathways and heterologous receptor interaction between the two receptors. D1R and D5R colocalize in renal proximal tubule cells and physically interact, as determined by co-immunoprecipitation and fluorescent resonance energy transfer microscopy. Stimulation of renal proximal tubule cells with fenoldopam (D1R/D5R agonist) led to both adenylyl cyclase and phospholipase C (PLC) activation using real-time fluorescent resonance energy transfer biosensors ICUE3 and CYPHR, respectively. Fenoldopam increased cAMP accumulation and PLC activity and inhibited both NHE3 and NaKATPase activities. LE-PM436 and D5R siRNA blocked the fenoldopam-stimulated PLC pathway but not cAMP accumulation, whereas D1R siRNA blocked both fenoldopam-stimulated cAMP accumulation and PLC signaling. Either D1R or D5R siRNA, or LE-PM436 blocked the fenoldopam-dependent inhibition of sodium transport. Further studies using the cAMP-selective D1R/D5R agonist SKF83822 and PLC-selective D1R/D5R agonist SKF83959 confirmed the cooperative influence of the two pathways on sodium transport. Thus, D1R and D5R interact in the inhibition of NHE3 and NaKATPase activity, the D1R primarily by cAMP, whereas the D1R/D5R heteromer modulates the D1R effect through a PLC pathway.