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We retrospectively assessed our center's experience with a protocol of low-dose (450 mg once daily) valganciclovir administered for 3-6 months (median 5 months) in a cohort of of 55 cytomegalovirus (CMV) donor-positive (D+) and/or recipient-positive (R+) heart transplant recipients. Although no CMV disease occurred in patients while receiving low-dose valganciclovir, during the 12-month post-transplantation observation period of this study, 4 (22.2%) of the 18 D+/R- patients and 1 (2.7%) of the 37 R+ patients developed symptomatic CMV viremia. Leukopenia was frequent, including neutropenia [absolute neutrophil count (ANC), <1,000 cells/µL] that occurred in 21.8% and severe neutropenia (ANC <500 cells/µL) in 7.3%. Among CMV R+ heart transplant recipients, low-dose valganciclovir appeared to be an effective, less expensive strategy for CMV prophylaxis; however, caution may be necessary among D+/R- recipients.

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OBJECTIVES: We sought to use echocardiography to assess the presentation and potential for recovery of left ventricular (LV) function of patients with fulminant myocarditis compared with those with acute myocarditis. BACKGROUND: The clinical course of patients with myocarditis remains poorly defined. We have previously proposed a classification that provides prognostic information in myocarditis patients. Fulminant myocarditis causes a distinct onset of illness and severe hemodynamic compromise, whereas acute myocarditis has an indistinct presentation, less severe hemodynamic compromise and a greater likelihood of progression to dilated cardiomyopathy. METHODS: Echocardiography was performed at presentation and at six months to test the hypothesis that fulminant (n = 11) or acute (n = 43) myocarditis could be distinguished morphologically. RESULTS: Patients with both fulminant (fractional shortening 19 +/- 4%) and acute myocarditis (17 +/- 7%) had LV systolic dysfunction. Patients with fulminant myocarditis had near normal LV diastolic dimensions (5.3 +/- 0.9 cm) but increased septal thickness (1.2 +/- 0.2 cm) at presentation, while those with acute myocarditis had increased diastolic dimensions (6.1 +/- 0.8 cm, p < 0.01 vs. fulminant) but normal septal thickness (1.0 +/- 0.1 cm, p = 0.01 vs. fulminant). At six months, patients with fulminant myocarditis had dramatic improvement in fractional shortening (30 +/- 8%) compared with no improvement in patients with acute myocarditis (19 +/- 7%, p < 0.01 for interaction between time and type of myocarditis). CONCLUSIONS: Fulminant myocarditis is distinguishable from acute myocarditis by echocardiography. Patients with fulminant myocarditis exhibit a substantial improvement in ventricular function at six months compared with those with acute myocarditis. Echocardiography has value in classifying patients with myocarditis and may provide prognostic information.

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BACKGROUND: Lymphocytic myocarditis causes left ventricular dysfunction that may be persistent or reversible. There are no clinical criteria that predict which patients will recover ventricular function and which cases will progress to dilated cardiomyopathy. We hypothesized that patients with fulminant myocarditis may have a better long-term prognosis than those with acute (nonfulminant) myocarditis. METHODS: We identified 147 patients considered to have myocarditis according to the findings on endomyocardial biopsy and the Dallas histopathological criteria. Fulminant myocarditis was diagnosed on the basis of clinical features at presentation, including the presence of severe hemodynamic compromise, rapid onset of symptoms, and fever. Patients with acute myocarditis did not have these features. The incidence of the end point of this study, death or heart transplantation, was ascertained by contact with the patient or the patient's family or by a search of the National Death Index. The average period of follow-up was 5.6 years. RESULTS: A total of 15 patients met the criteria for fulminant myocarditis, and 132 met the criteria for acute myocarditis. Among the patients with fulminant myocarditis, 93 percent were alive without having received a heart transplant 11 years after biopsy (95 percent confidence interval, 59 to 99 percent), as compared with only 45 percent of those with acute myocarditis (95 percent confidence interval, 30 to 58 percent; P=0.05 by the log-rank test). Fulminant myocarditis was an independent predictor of survival after adjustments were made for age, histopathological findings, and hemodynamic variables. The rate of transplantation-free survival did not differ significantly between the patients considered to have borderline myocarditis and those considered to have active myocarditis according to the Dallas histopathological criteria. CONCLUSIONS: Fulminant myocarditis is a distinct clinical entity with an excellent long-term prognosis. Aggressive hemodynamic support is warranted for patients with this condition.

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Epidemiologic studies suggest that 20-30% of patients diagnosed with symptomatic congestive heart failure (CHF) have intraventricular conduction disorders characterized by a discoordinate contraction pattern and wide QRS. Biventricular pacing is an emerging therapy allowing simultaneous electrical stimulation of the right and left ventricles with the use of an implantable pacing system. The aim of this article is to describe 2 prospective randomized multicenter trials examining the effects of biventricular pacing on functional capacity, quality of life, and hemodynamic status in patients with dilated cardiomyopathy and intraventricular delay. The VIGOR CHF Trial is designed to assess functional and symptomatic improvement in heart failure patients with biventricular pacing and without a concomitant indication for conventional bradycardia pacemaker therapy. To assess for potential placebo effects, patients are randomized to receive either biventricular pacemaker therapy or no pacing therapy for the first 6 weeks, after which both groups receive pacing therapy. The VENTAK CHF trial uses an implantable cardioverter defibrillator system (ICD) designed to provide chronic biventricular pacing therapy in addition to treating ventricular tachyarrhythmias. All patients receive conventional ICD and CHF therapy throughout the study and are randomized in a 2-period crossover design to receive either no pacing or biventricular pacing for 3-month intervals. Patient enrollment in both studies is ongoing, with a closed analysis. The unique designs of these trials provide the opportunity to study this therapy in high-risk patients who have been optimally treated for heart failure.

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To develop a safe, noninvasive, simple, inexpensive, and clinically adaptable method for estimating cardiac output, we evaluated the potential of lung to finger circulation time (LFCT) and buildup time (Tb) of oxygen as measured by pulse oximetry to estimate cardiac output. Significant correlation was found between cardiac output as measured by thermodilution and the inverse of LFCT (R = 0.76, p < 0.001, SEE = 0.9 L/min) as well as the inverse of Tb (R = 0.72, p < 0.001, SEE = 0.9 L/min).

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BACKGROUND: Controversy exists regarding donor and recipient factors that promote the development and progression of coronary artery disease after heart transplantation and the likelihood of coronary artery disease causing death or retransplantation. METHODS: To investigate this issue in a large cohort of patients, we analyzed 5963 postoperative angiograms performed in 2609 of the 3837 patients undergoing heart transplantation at 39 institutions between January 1990 and December 1994. Coronary artery disease was classified as mild, moderate, or severe on the basis of left main involvement, primary vessel stenoses, and branch stenoses. Coronary artery disease was considered severe if left main stenosis was > 70% or 2 or more primary vessels stenoses were > 70% or branch stenoses were > 70% in all 3 systems. RESULTS: By the end of 5 years after heart transplantation, coronary artery disease was present in 42% of the patients, mild in 27%, moderate in 8%, and severe in 7%. Coronary artery disease-related events (death or retransplantation) had an actuarial incidence of 7% at 5 years and occurred in 2 of 3 of the patients with development of angiographically severe coronary artery disease. By multivariable logistic analysis, risk factors for donor coronary artery disease included older donor age (P < .0001) and donor hypertension (P=.0002). By multivariable analysis in the hazard function domain, risk factors identified for the earlier onset of allograft coronary artery disease included older donor age (P < .0001 ), donor male sex (P=.0006), donor hypertension (P=.07), recipient male sex (P=.02), and recipient black race (P=.01). The actuarial incidence of severe coronary artery disease was 9% at 5 years. CONCLUSIONS: Angiographic coronary artery disease is very common after heart transplantation, occurring in approximately 42% of the patients by 5 years. Older donor age, donor hypertension, and male donor or recipient predict earlier onset of angiographic allograft coronary artery disease. Although severe angiographic allograft coronary artery disease occurs in only 7% of the patients at 5 years, its presence is highly predictive of subsequent coronary artery disease-related events or retransplantation.

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Supplemental O2 reduces cardiac output and raises systemic vascular resistance in congestive heart failure. In this study, 100% O2 was given to normal subjects and peak forearm flow was measured. In experiment 1, 100% O2 reduced blood flow and increased resistance after 10 min of forearm ischemia (flow 56.7 +/- 7.9 vs. 47.8 +/- 6.7 ml.min-1.100 ml-1; P < 0.02; vascular resistance 1.7 +/- 0.2 vs. 2.4 +/- 0.4 mmHg.min.100 ml.ml-1; P < 0.03). In experiment 2, lower body negative pressure (LBNP; -30 mmHg) and venous congestion (VC) simulated the high sympathetic tone and edema of congestive heart failure. Postischemic forearm flow and resistance were measured under four conditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100% O2+LBNP+VC. LBNP and VC did not lower peak flow. However, O2 raised minimal resistance (2.3 +/- 0.4 RA; 2.8 +/- 0.5 O2+LBNP+VC, P < 0.04). When O2 alone (experiment 1) was compared with O2+LBNP+VC (experiment 2), no effect of LBNP+VC on peak flow or minimum resistance was noted, although the return rate of flow and resistance toward baseline was increased. O2 reduces peak forearm flow even in the presence of LBNP and VC.

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Hemolytic uremic syndrome (HUS) is a rare, often fatal complication of mitomycin C therapy. It is generally accepted that HUS is, in part, caused by endothelial cell dysfunction. Endothelial cells modulate blood flow, blood pressure, and myointimal proliferation. Endothelial cells synthesize and release products that modulate vascular tone and regulate vascular smooth muscle cell growth. We describe a patient who developed HUS secondary to mitomycin C, resulting in end-stage renal disease and necessitating chronic hemodialysis. Over several months, the patient subsequently developed multisystem organ failure involving the heart, liver, and intestine that was associated with angiographically documented small, distal vessel occlusive disease and ultrasonographically identified coronary artery intimal hyperplasia. We propose that a diffuse ongoing endothelial cell dysfunction (ie, endotheliopathy) is the putative mechanism for this patient's clinical course. To our knowledge, this continuum of HUS presenting as a multisystem, progressive disorder has not been previously reported.

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Implantation of ventricular assist devices (VADs) to support patients awaiting cardiac transplant has become an effective means of assuring that these critically ill patients survive to transplant. The authors undertook a retrospective analysis of 115 consecutive patients listed for cardiac transplant from January 1992 through June 1995. A VAD was implanted in 19 of these patients. Survival was calculated by intent to treat from the time of transplant listing through heart transplant, if it occurred. The analysis demonstrates that the patients who underwent implantation of a VAD as bridge to transplant had survival times similar to those of patients with medical management. These survival statistics demonstrate the utility of VADs as an effective means to bridge critically ill patients until a suitable donor organ becomes available. In addition, as previous studies have suggested for acute results, earlier implementation and better patient selection may lead to improved long-term survival.

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We performed a retrospective review of patients who underwent esophagogastroduodenoscopy after heart transplantation to determine the clinical setting in which upper gastrointestinal cytomegalovirus disease is identified. No gastrointestinal cytomegalovirus disease was found prior to transplant 51 and this period (from transplant 1 to 50) correspond to a time when significantly fewer esophagogastroduodenoscopies included biopsy. Patients in whom cytomegalovirus was identified were more likely to have been CMV seronegative and to have received a heart from a seropositive donor (60% vs 20%, P = 0.029). In addition, patients with cytomegalovirus used aspirin more commonly (90% vs 31%, P = 0.001), and underwent esophagogastroduodenoscopy earlier after transplantation (123d vs 652d, P = 0.029). We conclude that factors that increase the use of esophagogastroduodenoscopy and biopsy in the early transplant period increase the likelihood of identifying cytomegalovirus in gastrointestinal tissue. However, the clinical course and significance of cytomegalovirus identified in the upper gastrointestinal tract in heart transplant patients may be difficult to discern.

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Between September 1992 and April 1995, 19 patients at the authors' institution received pneumatic, pulsatile left ventricular assist devices (LVADs) for bridging to cardiac transplantation. The mean (+/- SD) age of the patients was 51 +/- 14 years (range, 19-64 years). Nine (47%) patients had end-stage idiopathic cardiomyopathy, five (26%) had ischemic cardiomyopathy, and five (26%) other recipients were in cardiogenic shock caused by acute myocardial infarction (AMI). Fifteen (79%) patients were supported with an intraaortic balloon pump or centrifugal LVAD at the time of LVAD insertion (duration, 5.5 +/- 4.1 days). Aprotinin was given to limit bleeding; heparin, followed by warfarin sodium, was used for anticoagulation. A vigorous exercise and nutrition protocol was followed. Cardiac index averaged 2.94 +/- 0.87 L/min/m2 immediately after the implantation procedure. No patient required placement of a right VAD. Average duration of LVAD support was 45 +/- 39 days (range, 3-153 days). Major complications included bleeding requiring reoperation (three patients); cerebrovascular accident (three patients); and severe dysrhythmias requiring direct current cardioversion (four patients). Fourteen (74%) patients underwent transplantation, with one patient still being mechanically supported. All of the patients receiving transplants were discharged from the hospital. Of the individuals who died while supported with the LVAD, 75% were patients with AMI. Timely application of LVADs as part of the interdisciplinary management of end-stage heart disease has generated excellent results for transplant candidates. Right ventricular dysfunction has not necessitated right VAD placement in the authors' experience. Patients with AMI have a higher risk of death while being supported with the device than do more chronically ill recipients.

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The reconstruction of two-dimensional spatial images with 0.5-mm resolution using radiofrequency gradients generated by an NMR coil system rotated about the sample is demonstrated for 23Na. The method retains chemical shift, should be capable of mapping T1 and T2 information, and might offer sensitivity advantages for nuclides with short T2.

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