Effects of an enhanced secondary prevention program for patients with heart disease: a prospective randomized trial.

BACKGROUND: Secondary prevention medications in cardiac patients improve outcomes. However, prescription rates for these drugs and long-term adherence are suboptimal. OBJECTIVE: To determine whether an enhanced secondary prevention program improves outcomes. METHODS: Hospitalized patients with indications for secondary prevention medications were randomly assigned to either usual care or an intervention arm, in which an intensive program was used to optimize prescription rates and long-term adherence. Follow-up was 19 months. RESULTS: A total of 2643 patients were randomly assigned in the study; 1342 patients were assigned to usual care and 1301 patients were assigned to the intervention arm. Prescription rates were near optimal except for lipid-lowering medications. Rehospitalization rates per 100 patients were 136.2 and 132.6 over 19 months in the usual care and intervention groups, respectively (P=0.59). Total days in hospital per patient were similar (10.9 days in the usual care group versus 10.2 days in the intervention group; P not significant). Crude mortality was 6.2% and 5.5% in the usual care and intervention groups, respectively, with no significant difference (P=0.15) in overall survival. Post hoc analysis suggested that after the study team became experienced, days in hospital per patient were reduced by the program (11.1+/-0.91 and 8.9+/-0.61 in the usual care and intervention groups, respectively; P<0.05). CONCLUSIONS: The intervention program failed to improve outcomes in the present study. One explanation for these results is the near optimal physician compliance with guidelines in both groups. It is also possible that a substantial learning curve for the staff was involved, as suggested by the reduction in total days in hospital in the intervention patients during the second part of the study.

Comparative effects of nitroglycerin on intestinal vascular capacitance and conductance.

BACKGROUND: Nitroglycerin (NTG) dilates capacitance veins and resistance arterioles, but its relative effects on veins and arterioles are not known. OBJECTIVES: To compare NTG-induced changes in capacitance and conductance. ANIMALS AND METHODS: Aortic, left ventricular and portal venous (P(port)) pressures, portal flow and relative changes in intestinal blood volume (IBV) ((99m)technetium blood-pool scintigraphy) were measured in seven isoflurane-anesthetized, splenectomized dogs. Changes in intestinal vascular capacitance and conductance (mean portal flow/[mean aortic pressure - mean P(port)]) were determined when NTG was continuously administered (0.8 to 150 microg/kg/min) into a jugular vein. Pressure-volume (ie, P(port)-IBV) curves were defined by impeding portal flow, and capacitance was defined as the IBV at P(port)=7.5 mmHg. RESULTS: At lower doses, NTG increased capacitance without increasing conductance, but conductance increased considerably with little further increase in capacitance at higher doses. Dose-response analysis revealed that the half-maximum capacitance effect was achieved at an NTG infusion rate of 3.5 microg/kg/min, whereas a rate of 35 microg/kg/min was required for the half-maximum conductance effect. CONCLUSIONS: At lower doses, NTG dilates capacitance vessels primarily, and that effect approaches its maximum before significant dilation of conductance vessels is manifest. However, at higher doses, the increase in conductance is substantial with little additional effect on capacitance.

Effects of acute volume loading and hemorrhage on intestinal vascular capacitance: a mechanism whereby capacitance modulates cardiac output.

BACKGROUND: Changes in intestinal vascular capacitance during acute volume loading and hemorrhage have not been described. OBJECTIVES: To determine the effects of volume loading and hemorrhage on the intestinal vascular pressure-volume relationship and cardiac output. PATIENTS AND METHODS: In 11 alpha-chloralose-anesthetized dogs, a pneumatic portal venous constrictor and catheter were positioned to increase and measure portal venous pressure (Ppv), respectively. Relative changes in intestinal blood volume (IBV) were determined by blood-pool scintigraphy and expressed as the percentage change from control values (taken as 100%). Ppv-IBV relationships were constructed by graded portal vein constriction. RESULTS: IBV and cardiac output increased by 60 6% and 178 48%, respectively, and Ppv increased from 5.8 0.9 mmHg to 13.2 1.8 mmHg after initial volume loading (40 mL/kg of an isotonic glucose-saline solution over 7 min). IBV gradually decreased and reached near-control values after 75 min. In seven dogs, hemorrhage (sufficient to decrease mean aortic pressure by 56 4%) decreased IBV and cardiac output to 88 4% and 52 3% of control values, respectively, and Ppv decreased to 3.2 0.8 mmHg. CONCLUSIONS: A sigmoid function curve defined the relationship between cardiac output and IBV. Cardiac output remained constant over a wide range (between approximately 95% and 135% of control IBV). Outside this range, insufficient dilation or constriction resulted in a marked increase or decrease in venous pressures and cardiac output. These data indicate that vasculature capacitance modulates cardiac output during acute volume loading and hemorrhage, thereby maintaining cardiac output relatively constant over a wide range of total vascular blood volume.

A multicenter disease management program for hospitalized patients with heart failure.

BACKGROUND: Despite the availability of proven therapies, outcomes in patients with heart failure (HF) remain poor. In this 2-stage, multicenter trial, we evaluated the effect of a disease management program on clinical and economic outcomes in patients with HF. METHODS AND RESULTS: In Stage 1, a pharmacist or nurse assessed each patient and made recommendations to the physician to add or adjust angiotensin-converting enzyme (ACE) inhibitors and other HF medications. Before discharge (Stage 2), patients were randomized to a patient support program (PSP) (education about HF, self-monitoring, adherence aids, newsletters, telephone hotline, and follow-up at 2 weeks, then monthly for 6 months after discharge) or usual care. In Stage 1 (766 patients) ACE inhibitor use increased from 58% on admission to 83% at discharge (P < .0001), and the daily dose (in enalapril equivalents) increased from 11.3 +/- 8.8 mg to 14.5 +/- 8.8 mg (P < .0001). In Stage 2 (276 patients) there was no difference in ACE inhibitor adherence, but a reduction in cardiovascular-related emergency room visits (49 versus 20, P = .030), hospitalization days (812 versus 341, P = .003), and cost of care (2,531 Canadian dollars less per patient) in favor of the PSP. CONCLUSION: Simple interventions can improve ACE inhibitor use and patient outcomes.