Physician-directed heart failure transitional care program: a retrospective case review.

BACKGROUND: Despite a variety of national efforts to improve transitions of care for patients at risk for rehospitalization, 30-day rehospitalization rates for patients with heart failure have remained largely unchanged. METHODS: This is a retrospective review of 73 patients enrolled in our hospital-based, physican-directed Heart Failure Transitional Care Program (HFTCP). This study evaluated the 30- and 90- day readmission rates before and after enrollment in the program. The Transitionalist's services focused on bedside consultation prior to hospital discharge, follow-up home visits within 72 hours of discharge, frequent follow-up phone calls, disease-specific education, outpatient intravenous diuretic therapy, and around-the-clock telephone access to the Transitionalist. RESULTS: The pre-enrollment 30-day readmission rates for acute decompensated heart failure (ADHF) and all-cause readmission was 26.0% and 28.8%, respectively, while the post-enrollment rates for ADHF and all-cause readmission were 4.1% (P < 0.001) and 8.2% (P = 0.002), respectively. The pre-enrollment 90-day all-cause and ADHF readmission rates were 69.8%, and 58.9% respectively, while the post-enrollment rates for all-cause and ADHF were 27.3% (P < 0.001) and 16.4% (P < 0.001) respectively. CONCLUSIONS: Our physician-implemented HFTCP reduced rehospitalization risk for patients enrolled in the program. This program may serve as a model to assist other hospital systems to reduce readmission rates of patients with HF.

Direct Telephonic Communication in a Heart Failure Transitional Care Program: An observational study.

BACKGROUND: This study investigated the trend of phone calls in the Banner Good Samaritan Medical Center (BGSMC) Heart Failure Transitional Care Program (HFTCP). The primary goal of the HFTCP is to reduce 30-Day readmissions for heart failure patients by using a multi-pronged approach. METHODS: This study included 104 patients in the HFTCP discharged over a 51-week period who had around-the-clock telephone access to the Transitionalist. Cellular phone records were reviewed. This study evaluated the length and timing of calls. RESULTS: A total of 4398 telephone calls were recorded of which 39% were inbound and 61% were outbound. This averaged to 86 calls per week. During the "Weekday Daytime" period, Eighty-five percent of the totals calls were made. There were 229 calls during the "Weekday Nights" period with 1.5 inbound calls per week. The "Total Weekend" calls were 10.2% of the total calls which equated to a weekly average of 8.8. CONCLUSIONS: Our experience is that direct, physician-patient telephone contact is feasible with a panel of around 100 HF patients for one provider. If the proper financial reimbursements are provided, physicians may be apt to participate in similar transitional care programs. Likewise, third party payers will benefit from the reduction in unnecessary emergency room visits and hospitalizations.

Cyclic strain upregulates VEGF and attenuates proliferation of vascular smooth muscle cells.

OBJECTIVE: Vascular smooth muscle cell (VSMC) hypertrophy and proliferation occur in response to strain-induced local and systemic inflammatory cytokines and growth factors which may contribute to hypertension, atherosclerosis, and restenosis. We hypothesize VSMC strain, modeling normotensive arterial pressure waveforms in vitro, results in attenuated proliferative and increased hypertrophic responses 48 hrs post-strain. METHODS: Using Flexcell Bioflex Systems we determined the morphological, hyperplastic and hypertrophic responses of non-strained and biomechanically strained cultured rat A7R5 VSMC. We measured secretion of nitric oxide, key cytokine/growth factors and intracellular mediators involved in VSMC proliferation via fluorescence spectroscopy and protein microarrays. We also investigated the potential roles of VEGF on VSMC strain-induced proliferation. RESULTS: Protein microarrays revealed significant increases in VEGF secretion in response to 18 hours mechanical strain, a result that ELISA data corroborated. Apoptosis-inducing nitric oxide (NO) levels also increased 43% 48 hrs post-strain. Non-strained cells incubated with exogenous VEGF did not reproduce the antimitogenic effect. However, anti-VEGF reversed the antimitogenic effect of mechanical strain. Antibody microarrays of strained VSMC lysates revealed MEK1, MEK2, phospo-MEK1T385, T291, T298, phospho-Erk1/2T202+Y204/T185+T187, and PKC isoforms expression were universally increased, suggesting a proliferative/inflammatory signaling state. Conversely, VSMC strain decreased expression levels of Cdk1, Cdk2, Cdk4, and Cdk6 by 25-50% suggesting a partially inhibited proliferative signaling cascade. CONCLUSIONS: Subjecting VSMC to cyclic biomechanical strain in vitro promotes cell hypertrophy while attenuating cellular proliferation. We also report an upregulation of MEK and ERK activation suggestive of a proliferative phenotype. Hhowever, the proliferative response appears to be aborogated by enhanced antimitogenic cytokine VEGF, NO secretion and downregulation of Cdk expression. Although exogenous VEGF alone is not sufficient to promote the quiescent VSMC phenotype, we provide evidence suggesting that strain is a necessary component to induce VSMC response to the antimitogenic effects of VEGF. Taken together these data indicate that VEGF plays a critical role in mechanical strain-induced VSMC proliferation and vessel wall remodeling. Whether VEGF and/or NO inhibit signaling distal to Erk 1/2 is currently under investigation.

Mitigation of coagulation by removing clotting factors part 1: in vitro feasibility study.

Heparin is associated with adverse effects in some patients during extracorporeal circulation. A potential alternate anticoagulation strategy explored in this investigation involved mitigation of coagulation by removing clotting factors from blood by adsorption on a protamine-immobilized Sepharose matrix (PSM). Human or porcine plasmas treated with PSM in vitro were tested for clotting factors I (fibrinogen), II (prothrombin), VIII, and X, and proteins C and S, and for prothrombin time (PT), activated partial thromboplastin time (APTT), and total protein concentration. Bovine blood treated with PSM was also perfused through a hollow-fiber cartridge to assess thrombogenic potential in a shear flow system. PT increased with increasing protamine-Sepharose-to-plasma ratios and with increasing mixing time. When the PT and APTT of treated plasma were prolonged three to six times the baseline, Factors II and X were significantly removed (>90%), Factors I and VIII were partly removed (<35%), and total protein concentration remained >80% of the initial value. When blood depleted of clotting factors was perfused through hollow-fiber cartridges without an anticoagulant, cartridge patency was prolonged compared with cartridges perfused with untreated blood. This investigation demonstrated that inhibition of blood coagulation by removal of key clotting proteins is feasible.

Mitigation of coagulation by removing clotting factors part 2: heparin-free extracorporeal circulation in a porcine model.

A subpopulation of patients would benefit from an anticoagulation strategy during extracorporeal circulation (ECC) that does not involve systemic administration of heparin and protamine. Inhibition of coagulation by adsorption of plasma clotting factors using protamine immobilized on a Sepharose matrix (PSM) has been explored. This investigation extends previous in vitro studies and demonstrates the feasibility of heparin-free ECC. In a porcine ex vivo circuit, plasma was separated from blood via plasmapheresis, passed through a column containing PSM beads, and returned to the animal. Hemodialyzers and stents were placed in the circuit before, during, and after ECC and examined for device thrombosis. After 90 minutes, prothrombin time (PT) was prolonged >10 times the baseline, and blood clotting Factors I, II, VIII, and X were decreased significantly (>90%); this state was maintained for 2.5 hours without detectable adverse consequences. After cessation of ECC, PT approached normal levels within 60 minutes. Examination of hemodialyzers and coronary stents placed in the circuit revealed that the removal of clotting factors significantly reduced device thrombosis and that transfusion of homologous blood ( approximately 10% V/V) resulted in immediate restoration of hemostasis. It is possible to remove clotting factors from circulating blood to allow extracorporeal circulation of blood without the use of heparin.