Mycotic pseudoaneurysm of the ascending aorta after heart transplantation: case report.

Mycotic pseudoaneurysm of the ascending aorta is a rare but potentially life-threatening complication after orthotopic heart transplantation. We present a case of a 53-year-old man who developed a mycotic pseudoaneurysm of the ascending aorta after orthotopic heart transplantation. The pseudoaneurysm was surgically resected and the ascending aorta was replaced with allograft. The Gram stain and multiple cultures of the pseudoaneurysm wall revealed that the causative microorganism was coagulase-negative Staphylococcus. To the best of our knowledge, this is the first case report that describes mycotic pseudoaneurysm owing to coagulase-negative Staphylococcus infection after heart transplantation. Although S aureus and Pseudomonas aeruginosa are common pathogens in previously published literatures describing mycotic pseudoaneurysms in heart transplant recipients, coagulase-negative Staphylococcus is aslo an important and virulent pathogen that can cause mycotic aortic pseudoaneurysm in immunosuppressed patients. Once diagnosed, aggressive surgical treatment with prudent operative strategy, appropriate postoperative antibiotic therapy and close follow-up by radiographic study are mandatory in managing patients with this potentially fatal condition.

Echocardiography, nuclear scintigraphy, and stress testing in the emergency department evaluation of acute coronary syndrome.

There are between 3 and 5 million visits to EDs each year for complaints of chest pain. Of these, about one half of the patients have a noncardiac cause for their chest pain. Of the remainder, about 30% to 50% have significant coronary disease. It is quite clear that patients who are at high risk for a coronary event should be admitted to the hospital. For the low-to-moderate risk patients, the decision to admit or discharge the patient from the ED is not quite so easy. The emergency physician has to decide which tests can be helpful in the decision-making process, this can be undertaken in conjunction with a consultative cardiologist. It can be argued that if a patient does not have a normal test result whichever that evaluatory test is), then the patient should be admitted for further work-up and evaluation. The easiest test to perform in the ED setting is an echocardiogram. The images can be sent by telecommunication to a qualified echocardiogram reader for interpretation. This also has a reasonable NPV, although not necessarily as good as some of the other modalities available, unless interpreted in light of cardiac enzyme test results. If the index of suspicion is still high, then a stress echocardiogram can be considered. This has an excellent NPV and can be easily performed in [table: see text] most patients. This should not be undertaken in the face of an evolving MI, and patients should be observed for at least 8 hours after their initial presentation to the ED prior to undergoing a provocative test. Nuclear scintigraphy, another modality available for cardiac risk stratification, can be a logistical nightmare. The nuclear isotopes are strictly regulated by the Nuclear Regulatory Commission. The emergency physician may inject the isotopes, provided that he or she has undergone the necessary radiation training. Also, the patient must be removed from the ED to a radioisotope-approved area for the duration of the scan. One of the most difficult questions left open after review of all these analytical modalities is the duration of time these test results remain valid; when does an individual patient need to be reevaluated as to their specific pretest probability? The answer to this question lies in the presenting clinical scenario. If the patient presents with a similar inciting trigger for his or her symptoms, and the cardiac risk profile has not changed appreciably, then the previous study (whether a provocative stress test or even a cardiac catheterization) probably can be reliably counted. If the patient's risk profile has changed or the symptoms are new or more intense, the physician is compelled to pursue this encounter as a new, acute event. This can be true even in the setting of a previous cardiac catheterization that showed nonobstructive coronary disease, because plaque rupture can be acute and unpredictable. Ultimately, optimal care calls for each institution to develop a specific approach, in conjunction with their consultative cardiologist or critical care specialist, to enhance patient care, safety, and diagnostic outcome, while maintaining cost efficiency.

Early fungal endocarditis in homograft recipients.

Retrospective analysis of 200 homograft valve recipients at our institution revealed two cases of fungal endocarditis. Pathogenesis appears to be related to either recipient seeding in one elderly immunocompromised patient or a previously contaminated donor valve implanted in an otherwise healthy recipient. Therefore, our experience underscores the need for both meticulous prevention of fungal infection preoperatively in the recipient and elimination of previously contaminated homograft valves from the donor pool.

Donor-specific HLA antibodies after transplantation are associated with deterioration in cardiac function.

Although there is increasing evidence that mismatched donor HLA antigens are associated with a lowering of survival of human cardiac allografts, the effect of antibodies that bind those antigens is less clear. The existence of lymphocytotoxic antibodies prior to cardiac transplantation has been associated with a poor outcome in the majority of reports of relevant studies, as has their appearance post-transplantation. But how such antibodies, especially those with HLA specificity, cause poor outcomes has been poorly understood. The purpose of this study was to investigate the effect of anti-HLA antibodies appearing in the circulation after human orthotopic heart transplantation. Such antibodies were identified by a standard microlymphocytotoxicity technique using panels of frozen lymphocytes from normal donors who had been tissue typed. Of 74 patients transplanted over a 12-month period, 4 (5.4%) developed alloantibodies specific for mismatched donor HLA antigens. The first patient developed antibodies to HLA-A23 and B44 together with poor ventricular function and vascular rejection requiring retransplantation within 4 months. The other patients (3) developed antibodies specific for HLA-DQ antigens and experienced variable numbers of episodes of cellular rejection with no evidence of vascular rejection on endomyocardial biopsy. Two of these three patients died (8 and 11 months post-transplant) after three and six rejection episodes, respectively. The one surviving patient had seven rejection episodes and continues to have poor ventricular function 18 months post-transplant. We conclude that alloantibodies specific for mismatched donor HLA antigens may have a deleterious effect on the outcome of the human cardiac allograft and should be monitored closely post-transplant. Furthermore, such antibodies may mediate effects on the transplanted heart which are not detectable in specimens obtained by endomyocardial biopsy.

Functional and morphologic adaptation of undersized donor hearts after heart transplantation.

OBJECTIVES: This study analyzes our experience with transplantation of small donor hearts in a subgroup of moribund patients who could not be bridged to transplantation with mechanical assist devices. BACKGROUND: The major problem facing transplant programs in the United States is the lack of donor heart availability. One method of expanding the donor pool may be to liberalize the criteria for an acceptable donor heart. METHODS: We analyzed the growth and adaptation of 14 undersized and 14 conventionally sized donor hearts over a period of 10 weeks after heart transplantation. The left ventricular systolic and diastolic diameters, septal and posterior wall thicknesses, left ventricular mass calculated by the Penn convention and left ventricular ejection fraction were obtained by M-mode and two-dimensional echocardiography and documented by a single reader in blinded manner. Echocardiographic measurements were obtained before implantation and at 5 and 10 weeks after orthotopic heart transplantation. RESULTS: The mean (+/- SD) donor/recipient weight ratios were 0.53 +/- 0.06 for undersized hearts and 0.98 +/- 0.05 for normal-sized hearts. All 28 patients received similar immunosuppressive regimens, including intravenous steroids, cyclosporine and azathioprine. The length of hospital stay after transplantation did not vary significantly between the two groups. All the patients had at least one rejection episode during the 10-week study period. There was a tendency toward higher pulmonary pressures in undersized hearts, which was not statistically significant. Heart rate was significantly higher for undersized hearts, due in part to the use of theophylline or terbutaline to maintain tachycardia. There was a significant increase in left ventricular systolic and diastolic dimensions in undersized hearts compared with conventionally sized hearts. Undersized hearts increased in left ventricular mass over the 10-week period, whereas the conventionally sized donor hearts did not change between 5 and 10 weeks. CONCLUSIONS: In undersized hearts the increase in left ventricular mass and internal dimensions, with preservation of the posterior/septal wall thickness ratio, suggests that the left ventricle adapts to the larger recipient circulation early after transplantation. Despite denervation and a mismatched load, undersized transplanted hearts adapt appropriately to their new hemodynamic milieu.

Postpartum multivessel coronary dissection.

A 29-year-old woman had an acute myocardial infarction 5 days after giving birth. Serial coronary angiography showed multiple progressive coronary artery dissections, which eventually involved both the right and left coronary trees. Persistent cardiogenic shock necessitated emergent orthotopic heart transplantation. Examination of the cardiectomy specimen confirmed the presence of multiple myocardial infarctions, coronary artery dissection, and fibromuscular dysplasia of the coronary arteries. Fibromuscular dysplasia combined with changes in the arterial ground substance and hormonal milieu attributable to pregnancy or parturition are proposed as possible causes of coronary artery dissection in this case.

The treatment of cluster headache with repetitive intravenous dihydroergotamine.

We reviewed our experience with 54 cluster headache patients (23 episodic, 31 chronic) admitted to our headache center 64 tines over the past five years and treated with repetitive intravenous dihydroergotamine (IV DHE). DHE therapy was initiated on admission and prophylactic medication regimens were started or adjusted. All 54 patients had complete relief of their cluster headache, usually within two days. Most (82.8%) had no side effects. The average length of hospitalization was 6.7 days. At the three month followup, 92.9% of the episodic cluster patients were headache-free and 7.1% had a 50-74% improvement; at six months, all were headache-free. Of the chronic cluster patients, 44.4% were headache-free at three months and 52.8% had at least 50% improvement. At six months, 75% were headache-free and 22.2% were at least 75% improved, probably as a result of continued prophylactic medication. Repetitive IV DHE safely, rapidly, and effectively controls cluster headache.