Search

OBJECTIVES The study sought to investigate the association between soluble growth stimulation expressed gene 2 (sST2) Level and adverse outcomes in acute heart failure (HF).BACKGROUND Several studies have demonstrated the prognostic utility of sST2 Levels in HF.METHODS sST2 levels were measured in sequential baseline and follow-up (48 to 72 h and 30 days) plasma samples from 858 acute HF subjects enrolled in the ASCEND-HF (Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure) trial biomarker substudy and were related to in-hospital and post-discharge clinical outcomes.RESULTS Higher sST2 levels were associated with increased death risk at 180 days (baseline hazard ratio [FIR]: 2.21; follow-up HR: 2.64; both p 60 ng/ml) sST2 Levels at follow-up had higher 180-day death rates than those with lower follow-up sST2 Levels (adjusted HR: 2.91, p = 0.004). Neither baseline nor follow-up sST2 levels were associated with dyspnea improvement. Changes in sST2 from baseline were less in the nesiritide versus placebo group at follow-up, but were similar at 30 days.CONCLUSIONS Elevated levels of sST2 were associated with an increased risk of adverse clinical events in acute HF, but prognostic value of baseline sST2 diminished after adjusting for clinical covariates and aminoterminal pro-B-type natriuretic peptide. In those with elevated baseline sST2 Levels, persistently elevated sST2 levels at follow-up were associated with increased mortality risk. In addition, nesiritide did not demonstrate an incremental impact on sST2 Levels over standard therapy. (C) 2016 by the American College of Cardiology Foundation.

Background Timing of initial treatment for acute decompensated heart failure (ADHF) varies across hospitals and its impact on outcomes remains poorly defined. We examined the association between time to first intravenous (IV) heart failure (HF) therapy and patient outcomes. Methods Using the ADHERE-EM linked to Medicare claims data, we identified patients ≥65 years old who were hospitalized for ADHF and received IV HF therapy during index admission. Cox proportional hazard model was used to assess the association of time to treatment with a composite of 30-day all-cause mortality or re-admission. Generalized linear mixed models were used to examine the association of time to treatment with in-hospital all-cause mortality, index hospitalization length of stay, and total days alive and out-of-hospital at 30 days. Results Of 6,971 patients, the median time to first IV HF therapy was 2.3-hours (interquartile range 1.1, 4.4). The cumulative incidence of 30-day all-cause mortality or readmission was 27.4%. After adjusting for covariates, time to treatment was not associated with increased risk of composite 30-day all-cause mortality or re-admission (HR 1.00; 95% CI 1.00-1.00; P = .221). However, every hour delay in treatment was associated with a modest increased risk of in-hospital mortality (adjusted OR 1.01; 95% CI 1.00-1.02; P = .001) and an approximately 1.4-hour increase in index admission length of stay ( P Conclusion Among older patients presenting with ADHF, delay in initiating IV HF therapy was associated with modestly higher risk for in-hospital mortality and longer length of stay, but was not associated with 30-day outcomes.

Background Patients hospitalized with heart failure (HF) have elevated B-type natriuretic peptide (BNP) levels and increased risk for thromboembolic events. Associations between BNP level and thromboembolic events in patients with HF without atrial fibrillation (AF) are not well studied. Methods We linked data from the ADHERE registry for 2003 through 2006 with Medicare claims to identify patients ≥65 years who were hospitalized with HF, did not have AF, and did not receive warfarin at discharge. We estimated rates of all-cause mortality, thromboembolic events, myocardial infarction (MI), and stroke using Kaplan-Meier methods and the cumulative incidence function. We used Cox models to assess associations between log BNP level and each outcome after adjustment for potential confounders. Results The study population included 11,679 patients from 146 sites. Patients in the highest quartile of BNP level were older and more often male and African American. They had higher rates of coronary artery disease, renal insufficiency, and peripheral vascular disease and lower rates of diabetes mellitus and chronic obstructive pulmonary disease. After multivariable adjustment, each 30% increase in BNP level was associated with increased risks of death (hazard ratio 1.07, 95% CI 1.05-1.08) and MI (1.07, 1.04-1.10) but not thromboembolism or stroke. Conclusion Higher BNP level upon admission with HF among older patients without AF was associated with increased risks of MI and mortality; however, higher BNP level was not associated with subsequent thromboembolism or stroke.

The aim of this study was to evaluate the mode of death and hospitalizations in advanced heart failure (HF) patients with renal dysfunction and to examine the rate of concordance between events reported by the clinical events committee and site investigators (using case report forms) in the Second Follow-Up Serial Infusions of Nesiritide (FUSION II) trial. Little is known about the cause of death and hospitalization in patients with advanced HF. FUSION II was a randomized, double-blind, placebo-controlled trial evaluating outpatient nesiritide infusions versus placebo, with 911 patients with advanced HF (New York Heart Association class III or IV) and renal dysfunction enrolled. There were 151 deaths and 1,041 hospitalizations at 24 weeks. The clinical events committee classified events as cardiac, renal, cardiorenal, other or noncardiovascular, or unknown. Kappa statistics and McNemar tests were used to assess agreement (overall and by individual modes of death and hospitalization indications). In conclusion, the most common cause of death or hospitalization was cardiac related, with 70% of deaths and 60% of hospitalizations due to cardiac causes. There was 74% agreement (26% disagreement) on cardiac cause of death (κ = 0.40, McNemar p = 0.001) and 75% agreement (25% disagreement) between the investigators and the clinical events committee on cardiac classification for hospitalization (κ = 0.49, McNemar p

Objectives We undertook this analysis to determine whether there is a relationship between the time to measurement of immunoreactive B-type natriuretic peptide (iBNP) and early intervention for acutely decompensated heart failure (ADHF) and whether these variables are associated with morbidity and mortality in ADHF patients. Background Although natriuretic peptides (NPs) can aid emergency department (ED) physicians in the diagnosis of ADHF, the relationship between the time to measurement of NP levels and time to treatment is not clear. In addition, the impact of time to treatment on clinical outcomes has not been demonstrated. Methods Patients from ADHERE (Acute Decompensated Heart Failure National Registry) who were admitted to the ED and who received intravenous diuretics were included. Recordings of iBNP levels and the timing of intravenous diuretic therapy were documented. Patients were divided by quartiles of time to treatment and iBNP levels, creating 16 categories. Results In 58,465 ADHF episodes from 209 hospitals, patients with the longest average time to iBNP draw also had the longest time to treatment. Mean ED time increased with increased time-to-treatment quartiles. Rales on initial examination were associated with early recognition of HF and earlier institution of therapy. The later the treatment took place, the fewer patients were asymptomatic at the time of hospital discharge. Within the time-to-treatment quartiles, mortality increased with increasing iBNP. Treatment delay was independently, but modestly, associated with increased in-hospital mortality with a risk-adjusted odds ratio 1.021, 95% confidence interval 1.010 to 1.033, and p Conclusions In the ED setting, delayed measurement of iBNP levels and delay in treatment for ADHF were strongly associated. These delays were linked with modestly increased in-hospital mortality, independent of other prognostic variables. The adverse impact of delay was most notable in patients with greater iBNP levels (Registry for Acute Decompensated Heart Failure Patients; NCT00366639).

Background An improved understanding of the characteristics, treatment, and outcome of patients with “Stage D” heart failure (HF) may improve patient outcomes. We conducted an analysis of the ADHERE LM to enhance this understanding. Methods ADHERE LM is a multicenter registry designed specifically to prospectively collect observational data on chronic Stage D HF. The findings were analyzed and compared to data from ADHERE CM, a multicenter registry designed to prospectively collect data on the entire spectrum of acute decompensated HF. Descriptive statistics and Kaplan-Meier analysis were used to evaluate data from all 1433 patients in ADHERE LM. Results Compared to patients with acute decompensated HF, patients with chronic Stage D HF tended to be younger (69.6 vs 72.8 years), males (65% vs 49%), with hyperlipidemia/dyslipidemia (65% vs 41%), and with coronary artery disease (73% vs 57%). In Stage D patients, use of intravenous diuretics (73%) and vasoactive agents (84%) was common. Kaplan-Meier–estimated 1-year survival was 71.9% (95% CI 69.3%-74.5%) and estimated 1-year freedom from hospitalization or death was 32.9% (95% CI 30.2%-35.6%). Conclusions Patients with Stage D HF are frequently males with dyslipidemia and coronary artery disease. Morbidity and mortality are high. Therapeutic decisions based on studies in HF patients with different characteristics may not be applicable; additional research is needed to determine optimal therapeutic regimens for these patients.

OBJECTIVESWe sought to test the hypothesis that plasma volume (PV) expansion in heart transplant recipients (HTRs) is caused by failure to reflexively suppress the renin-angiotensin-aldosterone (RAA) axis.BACKGROUNDExtracellular fluid volume expansion occurs in clinically stable HTRs who become hypertensive. We have previously demonstrated that the RAA axis is not reflexively suppressed by a hypervolemic stimulus in HTRs.METHODSPlasma volume and fluid regulatory hormones were measured in eight HTRs (57 ± 6 years old) both before and after treatment with captopril (225 mg/day). Antihypertensive and diuretic agents were discontinued 10 days before. The HTRs were admitted to the Clinical Research Center (CRC), and, after three days of a constant diet containing 87 mEq/day of Na+, PV was measured by using the modified Evans blue dye dilution technique. After approximately four months (16 ± 5 weeks), the same HTRs again discontinued all antihypertensive and diuretic agents; they were progressed to a captopril dose of 75 mg three times per day over 14 days, and the CRC protocol was repeated.RESULTSCaptopril pharmacologically suppressed (p < 0.05) supine rest levels of angiotensin II (−65%) and aldosterone (−75%). The reductions in vasopressin and atrial natriuretic peptide levels after captopril did not reach statistical significance. The PV, normalized for body weight (ml/kg), was significantly reduced by 12% when the HTRs received captopril.CONCLUSIONSExtracellular fluid volume is expanded (12%) in clinically stable HTRs who become hypertensive. Pharmacologic suppression of the RAA axis with high-dose captopril (225 mg/day) returned HTRs to a normovolemic state. These findings indicate that fluid retention is partly engendered by a failure to reflexively suppress the RAA axis when HTRs become hypervolemic.

R research interest has focused on the effects of heparin on allograft survival. In addition to anticoagulant properties, heparin has immunosuppressive effects and inhibitory effects on smooth muscle cell proliferation.1 Animal studies1–4 have shown that low doses of heparin devoid of anticoagulant activity extend the survival of skin allografts as well as heterotopic and xenographic cardiac allografts. The addition of low molecular weight heparin (LMWH) to cyclosporine immunosuppression reduced the frequency and severity of accelerated graft coronary disease and the extent of acute parenchymal rejection in a rat model of heterotopic heart transplantation.5 Because endothelial dysfunction has been proposed as a surrogate end point for the subsequent development of cardiac allograft vasculopathy,6 we undertook a pilot study to evaluate the effect of LMWH in addition to enhanced antirejection therapy on endothelium-dependent vasomotor responses in acute cardiac allograft rejection. • • • Thirteen orthotopic heart transplant recipients who had International Society for Heart and Lung Transplant grade III or IV acute allograft rejection7 confirmed by endomyocardial biopsy between July 1, 1995, and March 1, 1997, were screened for this randomized, parallel-design pilot study comparing the effects of standard therapy and LMWH with standard therapy alone on endothelium-dependent vasomotor responses. Exclusion criteria included age ,18 years, angiographically significant coronary stenosis (.50% luminal diameter narrowing), hemodynamically compromising rejection with systolic blood pressure ,90 mm Hg and/or cardiac index ,2.0 L/min/m, a major contraindication to anticoagulation such as life-threatening bleed in the previous 6 months, platelet count ,50,000 or prior allergic reaction to heparin. One patient was excluded from the study because of early hemodynamic complications from the rejection episode. Three patients refused consent. The remaining 9 patients with acute cellular allograft rejection underwent cardiac catheterization and vasomotor function testing within 18 hours of the histologic diagnosis of rejection, before initiation of any antirejection therapy. After vasomotor function testing, patients were randomized into 2 groups. All patients received enhanced immunosuppression with intravenous methylprednisolone 1,000 mg/day for 3 days. Four patients in group 1 received LMWH (Enoxaparin, Rhone-Poulenc Rorer, Collegeville, Pennsylvania) 2 mg/kg/day in 2 divided subcutaneous doses for 3 days in addition to methylprednisolone. Five patients in group 2 were treated with methylprednisolone alone. At the time of the next endomyocardial biopsy (10 6 3 days), all but 1 patient underwent repeat vasomotor function assessment. All study patients had received 3-drug (prednisone, cyclosporine, and azathioprine) immunosuppression with therapeutic drug levels and 1 in each group had received diltiazem for hypertension before the acute episode. All vasoactive medications were discontinued $12 hours before the study procedure. After coronary angiography from the femoral approach, all patients received 5,000 U of unfractionated heparin intravenously. Using an 8Fr wide lumen guiding catheter, a steerable 0.014-inch, 12-MHz Doppler guidewire (Flowire, Cardiometrics, Inc., Mountainview, California) and a 3.2Fr, 30-MHz intravascular ultrasound catheter (IVUS; Cardiovascular Imaging Systems, Inc., Sunnyvale, California) were positioned in the middle left anterior descending artery for simultaneous assessment of vascular structure and function in relation to coronary blood flow. Use of these 2 systems together has been previously reported.8,9 The Doppler transducer at the tip of the Flowire was positioned 5 to 10 mm distal to the tip of the imaging transducer to avoid interference with Doppler velocity signals caused by the IVUS catheter. Identical catheter positions on serial studies were confirmed by reference to branch vessels in 2 views. Simultaneous IVUS and Doppler recordings were made during intracoronary infusions of adenosine 16 mg, acetylcholine 60 mg, and nitroglycerin 200 mg as boluses. Time was allowed for coronary blood flow (CBF) and luminal diameter to return to baseline before administration of each agent. Doppler and IVUS signals were recorded on 1/2-inch videotape for off-line analysis. The interventional cardiologists that performed these studies were not blinded. Quantitative measurements of average peak velocity were made and CBF reserve was defined as the ratio of hyperemic to resting baseline average peak velocities. Vessel cross-sectional area was measured directly by tracing the lumen-wall interface from a single diastolic frame using the Cardiovascular ImagFrom the University of Florida College of Medicine, Division of Cardiovascular Medicine, Gainesville, Florida. This research was supported in part by the American College of Cardiology/Merck Research Fellowship Award, Bethesda, Maryland; the American Heart Association, St. Petersburg, Florida; Florida Affiliate Research Fellowship Award, and the Bracco Diagnostics/Society for Cardiac Angiography and Interventions Research Fellowship Award, Breckenridge, Colorado; and a grant from Rhone-Poulenc Rorer, Collegeville, Pennsylvania. Dr. Mills’ address is: Division of Cardiology, The Cleveland Clinic, 9500 Euclid Avenue, Cleveland, Ohio 44195. Manuscript received September 13, 1999; revised manuscript received and accepted January 7, 2000.

OBJECTIVES The goal of this study was to further define the role of nesiritide (human b-type natriuretic peptide) in the therapy of decompensated heart failure (HF) by assessing the hemodynamic effects of three doses (0.015, 0.03 and 0.06 μg/kg/min) administered by continuous intravenous (IV) infusion over 24 h as compared with placebo. BACKGROUND Previous studies have shown beneficial hemodynamic, neurohormonal and renal effects of bolus dose and 6-h infusion administration of nesiritide in HF patients. Longer term safety and efficacy have not been studied. METHODS This randomized, double-blind, placebo-controlled multicenter trial enrolled subjects with symptomatic HF and systolic dysfunction (left ventricular ejection fraction ≤35%). Central hemodynamics were assessed at baseline, during a 24-h IV infusion and for 4 h postinfusion. RESULTS One hundred three subjects with New York Heart Association class II (6%), III (61%) or IV (33%) HF were enrolled. Nesiritide produced significant reductions in pulmonary wedge pressure (27% to 39% decrease by 6 h), mean right atrial pressure and systemic vascular resistance, along with significant increases in cardiac index and stroke volume index, with no significant effect on heart rate. Beneficial effects were evident at 1 h and were sustained throughout the 24-h infusion. CONCLUSIONS The rapid and sustained beneficial hemodynamic effects of nesiritide observed in this study support its use as a first-line IV therapy for patients with symptomatic decompensated HF.

“Human beings, who are almost unique in having the ability to learn from the experience of others, are also remarkable for their apparent disinclination to do so.” Douglas Adams, Last Chance to See ([1][1]) Learning to interpret immunoreactive B-type natriuretic peptide (iBNP) levels in heart

The mechanisms responsible for immediate adjustments in cardiac output at onset of exercise, in the absence of neural drive, are not well defined in heart transplant (HT) recipients. Seven male HT recipients (mean ± SD 57 ± 6 years) and 7 age-matched sedentary normal control subjects (mean age 57 ± 5 years) performed constant load cycle exercise at 40% of peak power output (Watts). Cardiac output and plasma norepinephrine were determined at rest and every 30 seconds during the first 5 minutes of exercise and at minutes 6, 8, and 10. All subjects were admitted to the General Clinical Research Center for determination of plasma volume. After 3 days of equilibration to a controlled and standardized diet, plasma volume was measured using a modified Evans Blue Dye (T-1824) dilution technique. Heart rate at rest was higher in the HT group (105 ± 12 vs 74 ± 6 beats/min), but during submaximum exercise, heart rates in the control group increased more rapidly (p ≤0.05) and to a greater magnitude (54 ± 7% vs 17 ± 4% above rest). Stroke volume at rest was lower in HT recipients (45 ± 4 vs 68 ± 9 ml) but was significantly augmented immediately after onset of exercise (30 seconds) and the relative increase was greater than controls at peak exercise (61% vs 38% greater than baseline). Cardiac output at rest was within the normal range in both groups (4.58 ± 0.27 vs 4.94 ± 0.40 L/min). Relative increases in cardiac output were similar (p ≥0.05) for the HT (106 ± 12%) and control groups (97 ± 10%). Plasma norepinephrine did not become significantly greater than resting values until approximately 4 minutes after onset of exercise in both groups. Blood volume, normalized for body weight, was 12% greater in the HT group. Thus, HT recipients with expanded blood volume (12%) augment stroke volume immediately after the onset of exercise. Plasma norepinephrine levels contribute negligibly to the rapid adjustment in cardiac output. Rather, we speculate that abrupt on-transit increases in stroke volume are due to augmented venous return, secondary to expanded blood volume.

Objectives.We attempted to demonstrate that theophylline, an adenosine receptor antagonist, can reverse bradyarrhythmias after orthotopic heart transplantation.Background.Sinus node dysfunction, primarily sinus bradycardia, frequently occurs after orthotopic heart transplantation and may lead to permanent pacemaker implantation. Endogenous adenosine has been implicated as a cause of such posttransplantation bradyarrhythmia.Methods.Twenty-nine transplant recipients (group 1) were given theophylline after bradyarrhythmias developed after transplantation. Data in these patients were compared with those in a control group of 18 patients without bradyarrhythmias (group 2) who were not given theophylline.Results.The mean heart rate in group 1 increased from 62 ± 7 to 89 ± 10 beats/min after administration of theophylline (p < 0.0001); the mean heart rate in group 2 was 88 ± 12 beats/min. Patients in group 1 required more days of temporary atrial pacing (3.5 ± 1 vs. 1.5 ± 3, p < 0.04) before the administration of theophylline than did patients in group 2. The length of hospital stay after transplantation did not differ significantly between groups 1 and 2 (17 ± 7.5 vs. 20 ± 16 days, p = NS). Age, gender, underlying disease, preoperative use of amiodarone, graft ischemia time or the incidence of moderate to severe rejection were not different between patient groups.Conclusions.The use of theophylline for posttransplantation bradyarrhythmias increased heart rate and facilitated the withdrawal of chronotropic support. We conclude that theophylline offers effective and specific therapy for heart transplant patients with early bradyarrhythmias, reducing the need for implantation of a permanent pacemaker.

The recent wave of enthusiasm for including inflammation as one of the primary pathophysiologic processes in cardiovascular disease has substantial merit [(1)][1]. Arterial inflammation is central to plaque progression and plaque rupture. Among clinical markers of inflammation, C-reactive protein (

These observations show that in a given patient with stable angina, the coronary artery is capable of a broad spectrum of responses to acetylcholine and nitroglycerin. These findings refute the notion that the endothelial functional response is a generalized “all-or-nothing” phenomenon.

Coronary artery dissection is an infrequent but serious complication of coronary angioplasty that can lead to periprocedural vessel occlusion, emergency bypass surgery, myocardial infarction or death. Recently, a perfusion balloon catheter was developed that permits passive perfusion of blood through the central lumen of the catheter. It enables prolonged balloon inflations to be performed and has been used to provide distal blood flow after coronary occlusion. To evaluate the effectiveness of the perfusion balloon catheter in patients with major coronary dissections, 36 consecutive patients treated with the perfusion balloon catheter were compared with 46 consecutive patients treated before its availability. The 2 groups were similar in terms of clinical, angiographic and initial procedural characteristics. Use of the perfusion balloon catheter permitted a significantly longer inflation than standard balloon inflation (average 18 +/- 5 min). Angiographic success was significantly greater with the perfusion balloon catheter (84 vs 62% for conventional therapy), whereas complications were markedly reduced (48 vs 78%). With the perfusion balloon catheter there were fewer deaths (2 vs 6%), myocardial infarctions (14 vs 40%) and emergency bypass operations (11 vs 25%). The findings of this retrospective comparison demonstrate that the perfusion balloon catheter is effective for the management of major dissections after coronary angioplasty. The use of the perfusion balloon catheter should be considered when a major coronary dissection occurs and when emergency bypass surgery is contemplated.

QT dispersion has been cited as a measure of nonuniform myocardial repolarization and a predictor of sudden cardiac death. We describe 38 patients who underwent atrioventricular nodal ablation, 3 of whom had an increase in measured QT dispersion and experienced potentially fatal, pulseless, polymorphic ventricular tachycardia after the procedure.

We present the case of a patient with left ventricular pseudoaneurysm following acute myocardial infarction. Survival for 2 years following diagnosis, despite the large size of the aneurysm, and subsequent management with cardiac transplantation represent unusual and interesting aspects of this complication of myocardial infarction.

In conclusion, CSR that occurs during sleep in patients with severe CHF is eliminated by HT.

For 300 years, from the time of William Harvey and Stephan Hales ([1][1]) until Braunwald, Ross, and Sonnenblick ([2][2]), physicians and investigators focused their attention on the pumping function of the heart with great success. During the past 50 years, however, a steadily growing body of

Acute coronary syndrome (ACS) patients benefit from dual antiplatelet therapy (DAPT), and most patients with atrial fibrillation (AF) merit anticoagulation stroke prophylaxis (AcP). Real world reporting of overall antithrombotic therapy among patients with ACS + AF is limited. We describe

It is unclear what factors determine the use of anticoagulants among patients presenting with acute coronary syndrome (ACS), in which the use of single (SAPT) or dual (DAPT) antiplatelet therapy is required. We retrospectively evaluated clinical factors associated with in-hospital and post

Most patients hospitalized with acute decompensated heart failure (ADHF) present through the emergency department (ED). Prior studies suggest that ED treatment delay may be associated with an increased risk of in-hospital mortality; however, the association with 30-day mortality and re-admission

The prognostic significance of transient hypotension during hospitalization for acute decompensated heart failure (ADHF) is uncertain. We evaluated factors associated with hypotension and its relationship with 30-day (30d) outcomes in the ASCEND-HF trial (which randomized patients without baseline

In this issue of the Journal, Ardehali et al describe heir experience with endomyocardial biopsy in 845 atients, a subset of the 1230 patients who underwent ndomyocardial biopsy at Johns Hopkins during the 15 ears between December 1982 and December 1997. he authors have an impressive clinical database from hich to draw, and from which we all may learn. For practicing clinicians, this study will again raise he question, “Whom should I refer for biopsy?” To ffer an answer to this question, we would like to first eview some basic facts about the technical aspects of ndomyocardial biopsy, then take a critical look at oth previous data and the Hopkins experience. Then, e will attempt to put the data into the format of a ayesian analysis to look at the clinical value added rom biopsy data. Sakakibara and Konno described transvenous endoyocardial biopsy in the early 1960s. Over the ensung 40 years, the equipment and technique have volved to the point where satisfactory tissue samples an be safely obtained in over 90% of diagnostic atempts and even more often in transplanted hearts. onetheless, technical problems still exist, including: 1) small sample size, (2) heterogenous distribution of issue pathology in many cardiac diseases, leading to nherent sampling errors, (3) subjective pathological nterpretation of the microscopic findings, and (4) unnown true-positive/false-positive and true-negative/ alse-negative rates for biopsy findings in most disases. Given these issues, our comments are based on the ssumption that patients who might be considered for iagnostic endomyocardial biopsy will be referred to a enter with experience in safely performing biopsies, nd in handling, preparing, and interpreting the biopsy amples. Looking at the data from Hopkins, 131 patients fell nto the categories “infiltrative, drug-related, connec

Two female patients with carcinoid heart disease, ages 56 and 32 years, underwent pulmonic valve resection surgery and tricuspid valve replacement with a porcine bioprosthesis. Preoperatively, both patients were in function class 4 with severe right-side congestive failure and signs of tricuspid regurgitation and pulmonic stenosis. Both underwent surgery for porcine tricuspid valve replacement (33 and 31 mm valves) and pulmonic valve resection. Postoperatively, both patients had only minimal symptoms, including trace ankle edema and soft pulmonic murmurs, despite persistence of the systemic symptoms of carcinoid syndrome. Pre- and postoperative catheterization data documented hemodynamic improvements. One patient eventually died of hepatic failure due to metastatic disease. At autopsy, her bioprosthesis was free of carcinoid valvular changes.