Impact of a Transplantation Critical Care Model on Short-Term Outcomes Following Liver Transplantation in High Acuity Patients: A Single-Center Experience.

BACKGROUND: Orthotopic liver transplantation (OLT) is the definitive treatment for end-stage liver disease (ESLD). Patients with high acuity ESLD are frequently denied life-saving OLT by transplant centers due to reported inferior outcomes. We sought to analyze the impact of a specialized transplant critical care model (TCCM) on patient access to OLT and survival outcomes in high acuity patients. METHODS: From January 2009 to December 2016, 122 adults were wait-listed at our transplant center with laboratory Model for ESLD ≥35 or Status I. Outcomes in Era I (prior to TCCM) were compared to Era II (TCCM established October 1, 2012). RESULTS: Era II (TCCM) led to a significant increase in patients' access to OLT. Frequency and need to seek OLT at another center dropped 4-fold in Era II. Compared to Era I, the majority of patients in Era II required intensive care unit management (22% vs 83%, P < .01) and renal replacement therapy (11% vs 70%, P < .01) prior to OLT. Despite a higher acuity of illness in Era II, 1-year patient survival was comparable (89% Era I, 80% Era II, P = .35). CONCLUSION: Implementation of a specialized TCCM expanded OLT access to high acuity patients, reduced the need to seek higher level of care elsewhere, and achieved excellent short-term post-transplant survival outcomes.

Outcomes in patients who are hepatitis B surface antigen-positive before transplantation: an analysis and study using the joint ISHLT/UNOS thoracic registry.

BACKGROUND: Hepatitis B surface antigenemia (HBsAg) has been considered at least a relative contraindication for heart transplantation, yet patients have undergone liver transplantation for hepatitis B-induced chronic liver disease, albeit with poorer results than for other liver diseases. The impact of asymptomatic hepatitis B infection on heart transplant outcome is not known. METHODS: To examine this question, we queried the Joint International Society for Heart and Lung Transplantation/United Network of Organ Sharing Thoracic Registry for all patients undergoing heart transplantation who had been identified as positive for HBsAg before transplantation. We then sent a 4-question data instrument to the centers responsible for the identified patients. Seventy-eight patients were identified. Of the 78 data forms sent, 53 forms were returned with the requested data. Of the 53 data forms returned, the centers incorrectly identified 23 patients as positive for HBsAg, resulting in 30 patients who were confirmed as HBsAg positive and who served as the final cohort for this analysis. RESULTS: The cohort included 24 males and 6 females, with a mean age of 46 +/- 16 years (range 0 to 68 years). Eleven patients had coronary artery disease, 14 had dilated cardiomyopathy, and 5 patients had a variety of other cardiac diseases. Of those tested at most recent follow-up, 20 of 25 patients continued to be positive for HBsAg, whereas 7 of 21 patients studied had converted and were hepatitis B serum antibody-positive. Approximately 37% of the patients had evidence of active hepatic inflammation or cirrhosis. We found a statistically significant correlation between positivity for hepatitis C antibodies and clinical liver disease (p = 0.0105). No difference in survival could be demonstrated between the study cohort and a reference heart transplant cohort, yet 5 of the 9 deaths were considered to be related to hepatitis B. CONCLUSIONS: These data demonstrate that clinical liver disease is common post-transplantation in HBsAg+ patients who presumably have no overt liver disease at the time of transplantation. Despite the inability to show a survival difference in this cohort, the fact that the majority of deaths were related to hepatitis B should suggest caution in accepting HBsAg+ patients for cardiac transplantation.

Acute smoking increases ST depression in humans during general anesthesia.

UNLABELLED: We tested the hypothesis that acute smoking is associated with ST segment depression during general anesthesia in patients without ischemic heart disease. The carbon monoxide (CO) concentration in expired gas and hemodynamic data was measured during general anesthesia for noncardiac or nonperipheral vascular surgery in patients without symptoms or evidence of ischemic heart disease. Increased expired CO concentrations are indicators of recent smoking. Logistic regression analysis identified significant predictors of ST segment depression > or = 1 mm. Both rate pressure product (odds ratio 1.20 for each increase of 1000, 95% confidence interval = 1.04-1.41, P = 0.007) and expired CO concentration (odds ratio 1.05 for each part per million increase, 95% confidence interval = 1.03-1.08, P = 0.001) were significant predictors of ST segment depression when considered simultaneously. Males demonstrated a lower probability of having an episode of ST depression (odds ratio = 0.16, P = 0.01), but this did not change the relationship between rate pressure product and CO as predictors of ST depression. Approximately 25% of chronically smoking patients smoked on the morning of surgery despite instructions not to smoke. IMPLICATIONS: Patients under age 65 without symptoms of ischemic heart disease who smoked shortly before surgery had more episodes of rate pressure product-related ST segment depression than nonsmokers, prior smokers, or chronic smokers who did not smoke before surgery. Females were at greater risk of ST depression than males.

Periaortic hematoma formation leading to aortic valve failure. A complication of homograft placement for second valve surgery.

The aortic homograft has become the replacement valve of choice in the treatment of complicated endocarditis involving native and prosthetic aortic valves. Complications are rare, typically involving chronic leaflet degeneration causing valvular insufficiency or rarely chronic calcific stenosis. We present a case in which functional stenosis of the homograft valve was caused by compression and distortion by blood transmitted directly from the left ventricle into a space between the homograft and an external cavity formed by a Dacron wrap. The latter had been placed to help control suture-line bleeding. This case presentation demonstrates an unusual cause of homograft failure and suggests that wrapping of a homograft conduit by native aorta or an external Dacron wrap is not a substitute for meticulous surgical technique to assure a hemostatic suture line.

Chronic therapy for congestive heart failure with benazepril HCl, a new angiotensin converting enzyme inhibitor.

Benazepril HCl is an orally effective angiotensin converting enzyme (ACE) inhibitor previously shown to have significant acute hemodynamic benefits in patients with congestive heart failure. In this study, 21 patients with New York Heart Association Class III or IV congestive heart failure were treated with 2 to 15 mg of benazepril HCl as a single daily oral dose for 28 days to determine the clinical and hemodynamic value of chronic therapy. Each patient underwent clinical evaluation during the 28-day period, as well as invasive hemodynamic studies on the first two and last two days of the trial. Plasma ACE activity and aldosterone levels fell significantly and renin levels rose after therapy. Benazepril HCl produced significant (p less than 0.01) reductions in arterial pressure and systemic vascular resistance, with corresponding increases in cardiac output and decreases in pulmonary artery wedge pressure. Responses after 28 days of therapy were equivalent to those after the initial doses. Clinical effects included reduced rest, exertional and paroxysmal nocturnal dyspnea, as well as reduced peripheral edema. Only one patient developed symptomatic orthostatic hypotension. Thus, benazepril HCl, given once daily, is an effective and well tolerated oral agent for the chronic treatment of advanced congestive heart failure.

A multicenter study of the safety and efficacy of benazepril hydrochloride, a long-acting angiotensin-converting enzyme inhibitor, in patients with chronic congestive heart failure.

Benazepril hydrochloride is a nonsulfhydryl, long-acting angiotensin-converting enzyme inhibitor that is orally effective. This study was designed to determine the acute hemodynamic effects of this agent in patients with chronic congestive heart failure. Twenty-six patients with New York Heart Association class III or IV congestive heart failure and left ventricular ejection fractions less than 35%, cardiac indexes less than 2.1 L/min/m2, and pulmonary artery wedge pressures greater than 12 mm Hg were given 2 or 5 mg benazepril hydrochloride. All does produced significant (p less than 0.05) increases in cardiac output (26.7% to 31.6% above control) and heart rate (5.4% to 11.2% above control) and decreases in systemic (27.1% to 32.0% below control) and pulmonary (34.8% to 55.5% below control) vascular resistances, mean pulmonary (25.3% to 30.3% below control) and systemic (13.4% to 18.5% below control) arterial pressures, and pulmonary artery wedge pressure (46.9% to 51.1% below control). Twenty-four hours after an initial dose, systemic vascular resistance and pulmonary artery wedge pressures remained below control levels. Angiotensin-converting enzyme activity fell by 67.8% +/- 6.4%, with a 15.8% +/- 7.6% decline in aldosterone levels. Thus benazepril hydrochloride is an effective angiotensin-converting enzyme inhibitor that produces hemodynamic effects that persist for 24 hours after a single oral dose.

Antihypertensive effects of pinacidil in patients with and without indomethacin pretreatment.

To determine the potential role of prostaglandins in mediating the hypotensive action of the new antihypertensive agent pinacidil, we measured the blood pressure, regional blood flow and neurohumoral responses to pinacidil in thirteen hypertensive patients randomly assigned to receive pretreatment with either indomethacin (75 mg) or placebo. After baseline measurements had been obtained, each patient received an oral dose of pinacidil to which he had previously demonstrated a therapeutic response. The doses of pinacidil administered between the two groups did not differ. Serial measurements of blood pressure and heart rate over two hours revealed no attenuation of the hypotensive effect of pinacidil in the indomethacin-pretreated patients (-12.7 +/- 4.1 mm Hg) compared to the placebo group (-9.3 +/- 3.2 mm Hg). While significant vasodilation was not observed in the forearm, renal vasodilation occurred and was not different between the two groups. Pinacidil had no effect on glomerular filtration rate. Neither did pinacidil significantly increase plasma catecholamines or renin activity. The results indicate that prostaglandins probably do not play a major role in the vasodilator action of pinacidil, and that therapeutic doses of the drug have a differential effect on regional blood flows that result in hypotension, but not significant neurohumoral stimulation, in patients with mild to moderate hypertension.

Hemodynamic and regional blood flow response to milrinone in patients with severe congestive heart failure: a dose-ranging study.

This study was undertaken to assess the hemodynamic efficacy, changes in regional blood flow, and safety of milrinone over a range of intravenous bolus injections (12.5 to 125 micrograms/kg), a continuous 18-hour infusion (0.2 to 0.7 microgram/kg/min), and following oral administration. All eighteen patients with New York Heart Association class III or IV congestive heart failure demonstrated hemodynamic improvement following intravenous bolus therapy. Dose-related increases in cardiac index occurred, ranging from a 12 +/- 6% increase following a 12.5 micrograms/kg bolus to a 37 +/- 10% increase after 75 micrograms/kg. Pulmonary wedge pressure fell 17 +/- 5% following 12.5 micrograms/kg and 28 +/- 9% following 75 micrograms/kg. Little change was apparent during the continuous infusion except for a late increase in cardiac index, but similar changes occurred in response to a single oral dose. Forearm blood flow increased significantly after 3 hours in the two higher infusion groups, but there was no consistent change in hepatic blood flow. We conclude that hemodynamic parameters and forearm blood flow are improved in patients with severe congestive heart failure following intravenous and short-term oral milrinone therapy.

Indomethacin attenuates the hypotensive action of hydralazine.

To determine whether indomethacin affects the vasodilator action of hydralazine in man, we studied nine healthy human subjects in a crossover, double-blind, randomized trial. Subjects received either oral indomethacin (200 mg) or placebo, after which they received two 0.15 mg/kg doses of intravenous hydralazine given 30 minutes apart. During the placebo phase there was a prompt hypotensive response after the first dose of hydralazine, with concomitant increases in heart rate, renal blood flow, and plasma norepinephrine and epinephrine levels but no consistent changes in forearm blood flow or vascular resistance. In contrast, the hypotensive response in the indomethacin phase occurred only after the second dose of hydralazine, and the magnitude of change in blood pressure was less than that in the placebo phase. The effects of hydralazine on heart rate, renal blood flow, limb blood flow, and plasma catecholamine levels were not affected by indomethacin. These results suggest that prostaglandins do play a role in the medication of the vasodilator effects of hydralazine, because its hypotensive effect was attenuated by indomethacin. However, this interaction must occur in vascular beds other than the limb or renal circulations, where no effect of indomethacin was observed.