Pericardial Friction Research Articles

Age-stratified patterns in clinical presentation, treatment and outcomes in acute pericarditis: a retrospective cohort study

BackgroundThere are limited data on acute pericarditis according to different age groups. The aim of this study is to investigate the role of age-related features in clinical characteristics, management, and...

Occurrence and predictors of severe arrhythmia in patients with myocarditis

Abstract Funding Acknowledgements Type of funding sources: None. Background/Introduction Patients with myocarditis are at risk for severe, life-threatening arrhythmia. However, predictors to identify high-risk patients are lacking. Purpose We investigated the occurrence and potential risk factors of severe arrhythmia in myocarditis patients. Methods 212 myocarditis patients that were hospitalized for arrhythmia monitoring at a tertiary university hospital were retrospectively enrolled. Non-sustained ventricular tachycardia (VT), sustained VT, ventricular fibrillation or cardiac arrest were considered as severe arrhythmia. We used a stepwise logistic regression model to investigate potential predictors. These included age, sex, clinical presentation (chest pain, palpitations, dyspnea, syncope, cardiac murmur, edema, pericardial friction, arrhythmia at presentation, Killip-class), comorbidities (hypertension, diabetes, coronary heart disease), imaging parameters (left ventricular ejection fraction [LVEF], pericardial effusion, edema and LGE on MRI), ECG variables (PQ depression, ST elevation, ST depression) and maximum levels of blood biomarkers (CRP, leukocytes, Troponin T, CK-MB). Results Mean age was 40.8 years, 73.1% were male and mean LVEF was 52.9%. During the hospital stay, 40 (18.9%) patients experienced severe arrhythmia: 33 (15.6%) non-sustained VT, 9 (4.2%) sustained VT, 1 (0.5%) ventricular fibrillation and 3 (1.4%) cardiac arrests (arrhythmia not mutually exclusive). Most arrhythmia occurred in the first 72h of monitoring (Figure). Significant predictors selected by the stepwise model (OR [95% CI]) for severe arrhythmia were LVEF (per 1% increase 0.95 [0.92; 0.99], p=0.005), syncope at presentation (7.9 [1.5; 40.4], p=0.01), any arrhythmia at first presentation (6.5 [1.3; 32.7], p=0.02) and CK-MB (per 10-unit increase 1.2 [1.1; 1.3], p=0.001). Conclusion(s) Myocarditis patients with low LVEF, presenting with arrhythmia and syncope and with increased CK-MB are at increased risk for severe arrhythmia and should be closely monitored. Further studies are needed to define, if patients without these risk factors might be safely discharged early.

Noninfectious pericarditis: management challenges for cardiologists.

The aim of this review is to deal with management challenges related to diagnosis and therapy of noninfectious pericarditis. In the European countries in which a low prevalence of tuberculosis is noted, determining the etiology of pericarditis is essentially aimed at the exclusion of the most common causes, which may require a specific therapy and are associated with an increased risk of complications: systemic autoimmune or autoinflammatory diseases, postcardiac injury syndrome (5%-20%), neoplastic pericardial involvement (5%-10%), tuberculosis (about 5%), and rarely purulent pericarditis in less than 5% of cases. In developing countries that report a high prevalence of tuberculosis, this condition is the most common cause of pericardial diseases. The diagnosis is based on clinical criteria (pericarditis‑related chest pain and pericardial rubs) complemented by laboratory (elevated levels of C‑reactive protein) and imaging findings (electrocardiography, echocardiography, and other imaging modalities to provide evidence of pericardial inflammation in doubtful cases). Poor prognostic predictors (high fever >38 °C, subacute course, large pericardial effusion, cardiac tamponade, and lack of response to empiric anti‑inflammatory therapies) identify high‑risk patients who should be admitted to the hospital in order to determine disease etiology and receive appropriate treatment. The mainstay of medical therapy of noninfectious pericarditis is based on nonsteroidal anti‑inflammatory drugs and colchicine, with possible adjunct of corticosteroids at low‑to‑moderate doses in unresponsive patients. Additional therapies, particularly with anakinra, have been implemented for those who develop corticosteroid dependence and are colchicine‑resistant. Disease recurrence is the most common and troublesome complication of pericarditis, whereas the risk of developing constrictive pericarditis is related to the etiology and not to the number of recurrences.

Clinical management and therapy of idiopathic recurrent pericarditis

Recurrent pericarditis is defined when pericarditic chest pain reappears after a symptom-free period of at least 4 to 6 weeks and after completion of full-dose anti-inflammatory therapy. Idiopathic pericarditis is the commonest etiology. The diagnosis of idiopathic cases is essentially an exclusion diagnosis, supported by a typical clinical course. The diagnosis is based on the association of typical symptoms and signs: mainly pericarditic chest pain plus pericardial rubs or electrocardiographic alterations or pericardial effusion. The optimal regimen for recurrences includes combination of non-steroidal anti-inflammatory agents, colchicine, and corticosteroids. In the resistant forms, immunotherapy (azathioprine, intravenous immunoglobulins, and particularly anakinra) has shown to be effective. The long term outcome of idiopathic recurrent pericarditis is good, with no evolution towards constrictive form.

Diagnosis and treatment of pericarditis

### Learning objectives 1. Review the definitions, classification and aetiology of pericarditis. 2. Describe the clinical presentation, diagnostic criteria and work-up, laboratory and imaging findings of pericarditis. 3. Review and...

Spontaneous isolated pericardial tamponade associated with warfarin.

To the Editor, An 83-year-old female patient was admitted to the emergency department with progressive dyspnea and orthopnea for 3 days. She was discharged with warfarin therapy (5 mg per day) due to pulmonary embolism 5 months previously. On admission she was orthopneic and tachypneic. Her arterial blood pressure was 90/60 mmHg and heart rate was 115/min with sinus rhythm. On cardiac auscultation, S1 and S2 intensity were decreased, and pathologic murmur and pericardial friction were not observed. Other physical examination findings were unremarkable. An increased cardio-thoracic ratio was revealed on chest X-ray (Figure 1a). Decreased QRS voltage and sinus tachycardia was evaluated on electrocardiogram. The internalised normalised ratio (INR) level was 8.6 and the prothrombin time was 70 seconds. Haemoglobin was determined to be 11.1 g/dL. The other laboratory findings were normal. An emergency thoracic computed tomography (CT) scan was performed to exclude recurrent pulmonary embolism, and surprisingly showed a massive pericardial effusion (Figure 1b). However, echocardiography revealed severe pericardial effusion that was compressing the right ventricle. Therefore, vitamin K and fresh frozen plasma infusion were administered promptly. As a result, the INR was decreased to 1.4 and 800 mL haemorrhagic fluid was drained percutaneously (P/S) with the apical approach. The patient’s blood pressure, orthopnoea and dyspnoea improved dramatically. There was no other source of bleeding except haemopericardium. Consequently, the cardiac tamponade in our patient, secondary to haemopericardium, was considered to be the result of the incorrect dosage of Warfarin. On control echocardiography, there was no recurrence of pericardial fluid and the patient was discharged on the 5th day. FIG. 1. a, b. Increased cardio-thoracic ratio due to pericardial effusion on chest X-ray (a). CT scan of chest showing large pericardial effusion (see arrow) (b) Cardiac tamponade is a life-threatening emergency condition. It is an acute type of pericardial effusion in which fluid accumulates in the intrapericardial space. This creates a mechanical pressure in the cardiac chambers which disrupts cardiac filling. (1). The common causes of pericardial effusion resulting in tamponade are pericarditis, malignancy, acute myocardial infarction, congestive heart failure, collagen vascular diseases, end stage renal disease, viral and bacterial infections (1). Cardiac tamponade secondary to haemopericardium is rarely seen and occurs with traumatic and non-traumatic causes. Non-traumatic causes are less common and associated with a number of conditions such as malignancy, infection, uraemia or coagulopathy (2). Today, warfarin sodium is still the most commonly used agent for anticoagulant therapy. The risk of spontaneous bleeding in patients using warfarin is less than 10%, whereas the risk of bleeding into the pericardial space is less than 1% (3). Echocardiography, which is the diagnostic test of choice, evaluates the haemodynamic consequences and guides transcutaneous drainage; CT is useful for further workup. These methods are superior to echocardiography for anatomical information, characterisation of the effusion, and providing information about the adjacent structures (2). The primary treatment of pericardial tamponade is pericardiocentesis.. Echocardiography-guided pericardiocentesis has been shown to be a safe and effective method which can be performed at the patient’s bedside (4). Isolated haemopericardium and cardiac tamponade secondary to warfarin are seen very rare. Haemorrhagic cardiac tamponade should be excluded in patients on warfarin with unexplained hypotension and excessive anticoagulation. Close monitoring of INR level is very important in the management of patients, especially in the elderly receiving warfarin treatment (5).

Case 1/2014 - Syncope Due to Cardiogenic Shock in a 25-year-old Male Patient

The patient was a twenty-five-year-old male individual, who suddenly started feeling faint and malaise at fainted on February 18th, 2009. He was taken to the medical emergency service of the local hospital by family members approximately one hour after symptom onset. The patient was previously healthy and asymptomatic. There was no history of hypertension, diabetes, dyslipidemia, heart disease or use of illegal drugs. At physical examination the patient had lowered level of consciousness, 60/50 mmHg blood pressure, heart rate (HR) of 150 beats per minute (bpm), no palpable pulses in the upper limbs and symmetrical pulses in the lower limbs. Several tests were performed on the day of hospital admission. The electrocardiogram (ECG) showed sinus tachycardia, with a HR of 150 bpm, PR interval of 120 ms, QRS duration of 80 ms (Figure 1). Chest radiography showed cardiomegaly, mediastinal enlargement and clear pulmonary fields (Figure 2). The transthoracic echocardiography showed dissection of the ascending aorta with cardiac tamponade (compression of the right atrium). Figure 1 Resting electrocardiogram showing sinus tachycardia. Figure 2 Chest radiography showing cardiomegaly, mediastinal enlargement and clear pulmonary fields. Laboratory assessment showed hemoglobin of 14.2 g/dL, hematocrit 42.9%, leukocytes 12,400/mm3 (78% neutrophils, 2% eosinophils, 14% lymphocytes and 6% monocytes), platelets 202.000/mm3, urea 30.5 mg/dL, creatinine 1.2 mg/dL, potassium 3.8 mEq / L, sodium 146 mEq/L, glucose 132 mg/dL, alkaline phosphatase 46 IU/L, gamma-glutamyl transpeptidase 37 IU/L, aspartate aminotransferase 21 IU/L and alanine aminotransferase 34 IU/L. Due to the patient's clinical instability, tracheal intubation for ventilatory support was required, as well as volemic expansion with 0.9% saline solution and a vasoactive drug (norepinephrine) to elevate blood pressure. After volume expansion and noradrenaline administration, blood pressure increased to 126/40 mmHg, with a heart rate of 135 bpm, and due to the severity of the clinical picture, his transfer to the Emergency Department of Instituto do Coracao (InCor) was requested in the same evening. Upon admission to InCor on February 19, 2009, the patient was sedated, assisted by mechanical ventilation and with pallor (++/6). The cardiorespiratory examination, showed a heart rate of 110 bpm, blood pressure 110/70 mmHg, normal pulmonary auscultation; however, cardiac auscultation showed muffled heart sounds (no accessory heart sounds, murmurs or pericardial friction rubs were identified). Abdominal examination was normal and there were no arterial pulses in the upper limbs, with bilateral cyanosis in the fingers. The arterial pulses were palpable and symmetrical in the lower limbs. The laboratory assessment performed on February 19, 2009 showed: hemoglobin of 17.1 g / dL, hematocrit 54%, 26,900/mm 3 leukocytes (1% rods, 84% segmented neutrophils, 7% lymphocytes and 8% monocytes), 107.000/mm 3 platelets, urea 39 mg/dL, creatinine 2.6 mg/dL (glomerular filtration, 32 mL/min/1.73m2), sodium 134 mEq/L, potassium 4.9 mEq/L, lactate 33 mg/dL, prothrombin time (International Normalized Index, INR) of 3.8 and activated partial thromboplastin time ratio of 1.53. Arterial blood gas analysis showed a pH of 7.22, partial pressure of Carbon Dioxide (pCO2) of 32.9 mmHg, partial pressure of oxygen (pO2) of 206 mm Hg, O2 saturation of 99.9%, bicarbonate 13 mEq/L and excess of base (-) of 13.7 mEq/L. The ECG was suggestive of electrical alternans (Figure 3). Figure 3 Resting electrocardiogram showing electrical alternans. Transesophageal echocardiography showed left ventricular hypertrophy with normal systolic function and a 62-mm aneurysmal dilation in the ascending aorta with the dissection lamina starting 1.7 cm from the valve. The dissection extended up after the aortic arch and affected the innominate artery, the left common carotid artery and the left subclavian artery. Severe aortic valve regurgitation and large pericardial effusion were also observed, with signs of right ventricular restriction to diastolic inflow. Surgical treatment of the aortic dissection was indicated; however, the patient had bradycardia in the perioperative period, followed by asystole unresponsive to resuscitation maneuvers and died.

Good Prognosis for Pericarditis With and Without Myocardial Involvement

Background— The natural history of myopericarditis/perimyocarditis is poorly known, and recently published studies have presented contrasting data on their outcomes. The aim of the present article is to assess the prognosis of myopericarditis/perimyocarditis in a multicenter, prospective cohort study. Methods and Results— A total of 486 patients (median age, 39 years; range, 18–83 years; 300 men) with acute pericarditis or a myopericardial inflammatory syndrome (myopericarditis/perimyocarditis; 85% idiopathic, 11% connective tissue disease or inflammatory bowel disease, 5% infective) were prospectively evaluated from January 2007 to December 2011. The diagnosis of acute pericarditis was based on the presence of 2 of 4 clinical criteria (chest pain, pericardial rubs, widespread ST-segment elevation or PR depression, and new or worsening pericardial effusion). Myopericardial inflammatory involvement was suspected with atypical ECG changes for pericarditis, arrhythmias, and cardiac troponin elevation or new or worsening ventricular dysfunction on echocardiography and confirmed by cardiac magnetic resonance. After a median follow-up of 36 months, normalization of left ventricular function was achieved in >90% of patients with myopericarditis/perimyocarditis. No deaths were recorded, as well as evolution to heart failure or symptomatic left ventricular dysfunction. Recurrences (mainly as recurrent pericarditis) were the most common complication during follow-up and were recorded more frequently in patients with acute pericarditis (32%) than in those with myopericarditis (11%) or perimyocarditis (12%; P <0.001). Troponin elevation was not associated with an increase in complications. Conclusions— The outcome of myopericardial inflammatory syndromes is good. Unlike acute coronary syndromes, troponin elevation is not a negative prognostic marker in this setting.

Clinical presentation and long-term follow-up of perimyocarditis

The natural history of perimyocarditis (PMY) is not yet completely known. We aimed to analyse the clinical laboratory data of PMY at diagnosis and during follow-up, in order to assess the natural history and prognostic stratification of the disease (including different aetiology). We enrolled 62 consecutive patients (men 79%, aged 38 ± 18 years) with PMY (84% idiopathic, 8% autoimmune, 8% infective) from August 2002 to July 2010. The diagnosis has been made according to clinical and laboratory data (significant increase of troponin I in all patients). After at least 1 year (mean follow-up: 1635 ± 298 days), 59 patients (95%) had available data. Chest pain was present in 59 patients (95%), flu-like syndrome in 36 (58%) and pericardial rubs in 15 (24%). None of the patients showed heart failure at presentation. At admission, eight patients (13%) presented mild-moderate left ventricular systolic dysfunction, 13 (22%) showed wall motion abnormalities, and 10 (17%) showed mild pericardial effusion. At 1 year no patients died, developed heart failure or showed abnormal echocardiogram. NSAIDs were the first choice therapy in 61 (98%) patients with clinical resolution in 58 (95%) of them. Seven patients (12%) experienced intermittent recurrences without development of constrictive pericarditis or heart failure. This study underlines the benign mid- to long-term outcome of PMY regardless of clinical laboratory characteristics at presentation, different aetiology and possibility of relapses; minimizing the role of endomyocardial biopsy in these specific patients.

Diagnostic Yield of Extensive Infectious Panel Testing in Acute Pericarditis: Fanne RA, Banai S, Chorin U, et al. Cardiology 2011;119:134–9.

This retrospective cohort study from Israel examined the diagnostic yield of the standard infectious panel, characteristics of myocardial involvement, and the utility of investigating myocardial involvement in patients with viral or idiopathic pericarditis. All consecutive patients with a diagnosis of acute pericarditis or myopericarditis admitted to the Cardiology Department from an urban area (> 500,000) from March 2005 through March 2008 were enrolled. Acute pericarditis was defined as pericarditic typical chest pain, pericardial friction rubs, new widespread ST elevation or PR depression, and new or worsening pericardial effusion.

Abstract 285: Acute Myocardial Infarction Following Free-Fall Trauma in a 21-Year-Old Male Patient

A 21-year-old man who was sleeping was fallen from the higher deck of a double-deck bed. 10 minutes after free fall, he experienced chest pain and then took a nonsteroidal antiinflammatory medication, however, which did not relieve the pain. The pain continued to increase, and prompting him to seek medical attention. 6 hours after the trauma, he was admitted to the emergency room of our hospital. Although the accident just caused mild subcutaneous hemorrhage, he felt severe chest pain, headache and left hand pain. He has 4 year's history of cigarette smoking, no history of diabetes mellitus, hypertension, hyperlipidemia coronary artery disease. On admission, physical examination showed blood pressure of 120/80 mm Hg and regular pulse at 100 beat per minute. X ray revealed no bone fracture around the chest. Cardiac examination showed regular heart rhythm without murmurs and pericardial rubs. Electrocardiogram (ECG) performed on admission demonstrated Q wave and 1mm ST segment elevation in leads V1 to V5. Laboratory test results are as follows: serum creatine phosphokinase MB 89.8 U/L, Troponin I 120 ng/ml. Due to the persistent injury pattern on the ECG, the patient underwent emergency cardiac catheterization following the administration of aspirin, Clopidogrel and Atorvastatin etc. CAG showed an acute thrombus induced 99% occlusion in Left Anterior Descending artery and no serious atherosclerotic disease was seen in the remaining coronary arteries. Then, the thrombus has been taken out with a Thrombus Aspiration Catheter. Afterwards, CAG showed the occlusion has been relieved and considering his age, we didn’t implant any artificial stent in the left anterior descending artery. After procedure, the patient felt good and discharged

Electrocardiographic abnormalities caused by acute pancreatitis

A 51-year-old man presented with severe acute upper abdominal pain and elevated serum levels of pancreatic enzymes due to acute pancreatitis associated with alcohol consumption. On admission, his heart rate was 60 beats per min, blood pressure was 90/65 mmHg, and temperature was 37.1°C. There were no signs of right-sided heart failure. The heart sounds were normal, no murmurs, and no pericardial friction rubs were heard. The electrocardiogram (ECG) on admission (Fig. 1) demonstrated sinus rhythm, normal axis, normal conduction and generalised aspecific ST-segment abnormalities. The ST-segment abnormalities were not limited to a specific coronary territory. Serum electrolytes and cardiac markers were normal. Transthoracic echocardiography demonstrated a normal left ventricular function, without valvular abnormalities or pericardial effusion. Coronary angiography was normal. The patient received general supportive care including fluid administration and pain control. After 4 days the electrocardiogram had substantially improved (Fig. 2). Fig. 1 Twelve-lead electrocardiogram on admission demonstrating generalised ST–T abnormalities caused by acute pancreatitis Fig. 2 Twelve-lead electrocardiogram after 4 days demonstrating few residual ST–T abnormalities Previous studies have described the association between pancreatitis and ECG abnormalities; up to 50% of patients hospitalised for acute pancreatitis have non-specific ST–T changes, diffuse T-wave inversions or ST-segment elevation [1, 2]. Transient wall motion abnormalities may also be present in patients with acute pancreatitis in the absence of coronary artery disease [1]. Potential pathophysiological mechanisms are circulating proteolytic enzymes, a vagally mediated reflex or systemic inflammatory response [1–4].

Triage and management of pericardial effusion

Pericardial effusion may be detected as an incidental finding during echocardiography or following a diagnostic imaging study for a symptomatic patient. When a pericardial effusion is detected the first step is to assess its size, hemodynamic importance, and possible associated diseases. The more common causes of pericardial effusions include infections (viral, bacterial, especially tuberculosis), cancer, connective tissue diseases, pericardial injury syndromes, metabolic causes (i.e. hypothyroidism), myopericardial and aortic diseases. The relative frequency of different causes depends on the local epidemiology, the hospital setting and the diagnostic protocol that has been adopted. Many cases still remain idiopathic in developed countries, whereas tuberculosis is the dominant cause in developing countries. Specific testing should be performed according to clinical suspicion. The presence of elevated inflammatory markers and other criteria (chest pain, pericardial rubs, ECG changes) suggest pericarditis and management should be directed accordingly. Treatment should be targeted at the etiology as much as possible. Nevertheless, when diagnosis is still unclear, or idiopathic and inflammatory markers are elevated, empiric anti-inflammatory therapy may be worthwhile. A true isolated effusion may not require a specific treatment if the patient is asymptomatic, but large ones have a theoretical risk of progression to cardiac tamponade (up to one-third) if subacute with signs of right-sided collapse, and especially chronic (>3 months). Pericardiocentesis alone may be curative for large effusions but recurrences are also common and pericardiectomy or less invasive options (i.e. pericardial window) should be considered whenever fluid re-accumulates (especially with tamponade), becomes loculated, or biopsy material is required.

71-Year-Old Man With Chronic Kidney Failure and Sudden Change of Mental Status

71-year-old man was admitted to the hospital for al- tered mental status. His wife reported that the patient had become progressively confused and had been having visual hallucinations, seeing people and animals that were not really there. These symptoms started about 2 weeks before admission as intermittent episodes. She could not identify any triggering events or temporal pattern for these episodes. In the past 2 days, the patient's symptoms had become more persistent. She added that he had become in- creasingly forgetful in the past year but had had no prob- lem performing simple tasks or taking care of himself. This type of confusion had never occurred previously. The patient had a 12-year history of type 2 diabetes, had undergone coronary artery bypass 3 years previously, had symptomatic peripheral vascular insufficiency, and had stage V chronic kidney disease primarily due to diabetic nephropathy. For the past 10 months, he had been undergo- ing hemodialysis 3 times weekly for 3.5 hours each time via a left arm arteriovenous fistula. He had last undergone dialysis 3 days previously and was due for his scheduled dialysis on the day of admission. Two months before admission, the patient developed critical lower limb ischemia and a nonhealing left foot ul- cer. Multiple vascular interventions failed to restore suffi- cient limb blood flow; a month later, the patient underwent a transmetatarsal amputation. Postoperatively, he devel- oped surgical wound infection, necessitating repeated de- bridement and intravenous vancomycin administration. The patient's medications included stable doses of as- pirin, atenolol, atorvastatin, calcium acetate, insulin, gaba-

Heart sounds and murmurs

The University of Dundee's human Heart Sounds and Murmurs website (www.dundee.ac.uk/medther/Cardiology/hsmur.html) is ideal for a basic introduction or a quick refresher of heart sounds and murmurs. It includes audio files of examples of S3, S4, gallop rhythm, aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation, pulmonary stenosis, atrial fibrillation, and pericardial rubs. Each sound is accompanied by a brief description of the physiology behind it, where to hear it, and what else might be found on examination. For more detail about auscultation findings visit Blaufuss Multimedia (www.blaufuss.org). Each …

Echocardiography

Echocardiography is the pivotal diagnostic modality for assessing the clinical significance of a heart murmur in horses. The echocardiographic examination can be used to identify the etiology of a heart murmur, determine the severity of the underlying disease that is present, and assess its potential impact on the horse’s performance and life expectancy. The echocardiographic examination is also the cornerstone of the diagnosis of endocarditis, pericarditis, and myocardial dysfunction in horses. An echocardiographic examination is indicated in horses with loud systolic murmurs, holodiastolic murmurs, continuous murmurs, muffled heart sounds, pericardial friction rubs, and in horses with exercise intolerance or poor performance.

Index of suspicion.

Index of suspicion.

Myiasis Due to Hypoderma lineatum Infection Mimicking the Hypereosinophilic Syndrome

Myiasis Due to Hypoderma lineatum Infection Mimicking the Hypereosinophilic Syndrome

Frequency of Pericardial Friction Rub (“Pericarditis”) After Direct Percutaneous Transluminal Coronary Angioplasty in Q-Wave Acute Myocardial Infarction

The clinical significance of infarct-associated pericarditis was examined in 201 consecutive patients with acute Q-wave myocardial infarction with successful direct percutaneous transluminal angioplasty. A pericardial rub was a reliable clinical sign of extensive myocardial damage in patients with direct angioplasty.

Late Failure of Surgical Treatment for Bioprosthetic Valve Endocarditis Due to Candida tropicalis

Late treatment failures may occur after surgical treatment of endocarditis due to Candida species [1,2] and Pseudomonas spe­ cies [3]; this finding suggests that cure should not be assumed until long-term follow-up has been completed. Failures occurring from 9 months [1] to 7 years [2] after surgical treatment have been reported for intravenous drug users, and such failures have occurred after 6 months in patients who did not use intravenous drugs [1]. We report a case of Candida tropicalis endocarditis in a patient who was not an intravenous drug user; this patient had a probable relapse 44 months after surgery. A 50-year-old man with chronic rheumatic valvular disease un­ derwent aortic valvuloplasty and mitral valve replacement with a bovine pericardial bioprosthesis. Routine culture of the implanted prosthesis was sterile. After the operation, mild aortic insufficiency was noted; fever, pericardial and pleural friction rubs, and atrial fibrillation ensued. The diagnosis ofpostpericardiotomy syndrome was made, and treatment with indomethacin (150 mg daily) was initiated. The patient defervesced and was discharged. The fever relapsed after therapy with indomethacin was discon­ tinued, and the patient was readmitted to the hospital 73 days after discharge (81 days after surgery). On physical examination, aortic insufficiency and splenomegaly were observed. Findings on an echocardiogram were suggestive of vegetations on the prosthesis. After blood for cultures was drawn, therapy with penicillin and streptomycin was started; however, seven of eight sets of blood cultures later yielded C. tropicalis. Antibiotic therapy was changed to that with amphotericin B, and the patient underwent surgery 2 days later. At surgery, rupture of the bioprosthesis and vegetations on the atrial surface of the leaflets were detected; however, there was no involvement ofthe mitral annulus, and aortic valve insuffi­ ciency without endocarditis was noted. The bioprosthesis and the valve were replaced with two bovine pericardial prostheses. Cul­ ture of the excised prosthesis yielded Candida species, although culture of the aortic valve was sterile. Histologic examination of sections of the prosthesis revealed numerous hyphae and spores compatible with a Candida species. A total dose of 2.1 g ofampho­ tericin B (50 mg/d) was administered over 6 weeks. The patient was discharged on the 59th postoperative day, and no evidence of metastatic infection was detected on follow-up.