Search

We report a case of an 81-year-old man with bacterial myocarditis presenting with elevated troponins and sepsis, who succumbed due to a ruptured ventricle. The infecting organism was found to be methicillin-resistant Staphylococcus aureus. Bacterial myocarditis is a rare occurrence when independent of infective endocarditis. Generally, this is a complication of bacteremia that is discovered post-mortem. Rarely, as in our patient, it causes significant necrosis of the myocardium leading to rupture of a ventricle. As with viral myocarditis, this disease can present with signs and symptoms of acute myocardial infarction, complicating the diagnosis. Much of the available data on bacterial myocarditis was collected before the development of many modern diagnostic tests and before antibiotics. Accordingly, the appropriate workup, diagnosis and treatment remain unclear. Our patient represents the first reported case of ventricular rupture due to methicillin-resistant S. aureus-associated bacterial myocarditis., (Copyright 2008 S. Karger AG, Basel.)

Infectious myocarditis can be caused by a variety of agents, with enteroviruses being the most common. Myocarditis due to enteric bacteria is rare. We present pathological documentation of a rare case of a Campylobacter jejuni bowel infection leading to rapidly fatal myocarditis.

We present the case of a 40 year-old man with biventricular nonvalvular vegetations presenting with acute onset of unilateral hearing loss and headache as a result of septic emboli. The medical literature involving the rare diagnosis of mural vegetation is reviewed and unusual features of this case are discussed.

Reported here is a 39-year-old man with Wegener's granulomatosis who had died due to endocarditis during his follow up. The concomitance of these two pathologies is discussed in the light of the pertinent literature.

Scedosporium apiospermum, the asexual state of Pseudallescheria boydii, is increasingly recognized as an opportunistic pathogen. We report a case of prosthetic valve endocarditis caused by this organism that developed in a patient following cardiac surgery.

Postpartum cardiomyopathy is rare form of cardiac failure, with the potential for cardiac function to recover to normal. When medical therapy fails to control symptoms or haemodynamic stability, circulatory support with a ventricular assist device may be considered as a bridge to cardiac transplantation. We describe 2 patients with severe postpartum cardiomyopathy, in whom cardiac function recovered sufficiently during mechanical circulatory assistance to enable device explantation. Bacteremia during device support was treated with chronic suppressive antibiotics, yet after cannula explantation and ventricular repair, residual infection led to destruction of the primary repair, with formation of a left ventricular pseudoaneurysm. This is a complication of device support not previously reported. Surgery was necessary to repair the infected ventricular cannula site. Both patients recovered; however one patient developed recurrent cardiomyopathy 4 months later.

This report describes a patient with a rupture of the noncoronary sinus of Valsalva caused by erosion of its wall by a large right atrial vegetation not attached to the tricuspid valve without aortic valve involvement. The rupture site was located right posterior to the tricuspid septal leaflet and communicated both with the right atrium and the right ventricular inflow tract, resulting in a significant left-to-right shunt leading to severe right heart failure and shock. The diagnosis was made by transthoracic and transesophageal echocardiography. To our knowledge no similar case has been reported in the literature.

Clostridial myonecrosis or gas gangrene occurs most frequently in contaminated wounds following trauma or surgery. It is caused by a wide variety of Clostridium species, the most common being Clostridium perfringens. Spontaneous, non-traumatic clostridial myonecrosis is uncommon and is usually associated with gastrointestinal and haematological malignancy, diabetes mellitus and peripheral vascular disease. The case of a previously healthy 16-year-old boy with acute onset of gastrointestinal symptoms, who died of bacterial sepsis without apparent preceding trauma, is presented here. Clostridium fallax was identified as the most probable causative agent. As far as is known, this is the first report of fatal sepsis in humans due to C. fallax, which has been described only rarely as a cause of gas oedema in animals.

Myocardial dysfunction is believed to be a central part of septic multiorgan manifestations. The aim of the present study was to assess whether E. coli sepsis in an in vivo model would induce a dysfunction in the relationship between mechanical work and energy consumption in the left ventricle (LV). Accordingly, we measured hemodynamics, left ventricular pressure-volume area (PVA), and myocardial oxygen consumption (MVo2) in deeply anesthetized pigs. Eight pigs received 2.0 +/- 0.5 x 10(9) E. coli bacteria intravenously, and seven served as controls. Compared with baseline and the control group, no alternations were observed in LV diastolic function or indices of contractility in the septic group. The MVo2-PVA relationship was highly linear in both groups (all r2 = 0.96-0.99). At 5 h, the y-axis intercept of the MVo2-PVA relationship (nonmechanical MVo2) had increased in the sepsis group by 70% compared with baseline (P = 0.004) and by 60% compared with the control group (P = 0.003). Contractile efficiency (the inverse of the MVo2-PVA slope) remained unchanged over time and between groups. The study demonstrates a profound increase in nonmechanical oxygen consumption during E. coli sepsis in the LV.

Immunosuppression can allow organisms that are not usually pathogenetic to cause disease; under such circumstances, Aspergillus species frequently form large masses of fungal elements. We describe the case of a 12-year-old girl with hematologic remission of leukemia. She had a left ventricular pedunculated mass that was detected by echocardiographic study; at surgery, the presence of Aspergillus terreus was confirmed.

Hydatid cyst in the heart is rare, occurring in about 3% of human echinococcosis. A 21-year-old woman was admitted to hospital with a third degree atrioventricular block. Echocardiography showed a cystic mass with a diameter of 2.5 cm within the interventricular septum. Serologic testing for Echinococcus was clearly positive, and hence cardiac surgery was planned. Sterilization of the cystic cavity was achieved by injecting formaldehyde solution in the cavity before cystectomy. Definitive pacemaker implantation was necessary before discharge. Cardiac hydatid cysts constitute an indication for surgery which is necessary to prevent potentially lethal complications such as cystic rupture with embolic phenomena and anaphylactic shock.

Scedosporium apiospermum, the asexual state of Pseudallescheria boydii, is increasingly recognized as an opportunistic pathogen. We report a case of native valve endocarditis due to this organism that developed in an elderly patient following a prolonged hospitalization. Literature on endocarditis caused by S. apiospermum and P. boydii is reviewed., (Copyright 2002 The British Infection Society.)

This article describes an unusual case of endocarditis in a 73-year-old man with a permanent pacemaker. Echocardiography revealed vegetations in the right ventricle below the tricuspid valve only, and he required open heart surgery for removal of the pacemaker system. This case demonstrates the potentially protracted course of infective endocarditis many years after pacemaker insertion. It also emphasizes the importance of echocardiography in diagnosing right ventricular vegetations; and the need for total replacement of the endocardial pacing system whenever it becomes infected.

A 63-year-old man with salmonella endocarditis of a ventricular aneurysm is presented. The patient had a documented apical aneurysm with mural thrombus and left ventricular dysfunction following a previous myocardial infarction. His condition was unresponsive to maximal medical therapy and was cured by surgery. A review of the English-language literature revealed that only two other published cases of nonvalvular salmonella endocarditis resulted in patient survival. This report underscores the importance of suspecting a cardiovascular origin in cases of salmonella bacteremia to avoid delay in diagnosis and surgical intervention in this deadly condition.

Postmortem blood cultures were obtained by separate puncture of the right and left side of the heart during autopsy of 18 patients with solid cancer and 26 patients with non-neoplastic diseases. Concordant isolates were obtained from the right and left side in six patients (14%, 95% confidence limits: 5-28%). Growth was unilateral in 7 patients and cardiac aspirates were sterile in 31 patients (70%, 95% CL: 55-83%). One patient had been treated for Staphylococcus aureus bacteraemia and eight patients had negative premortem blood cultures. Separate culture of blood from the right and left side of the heart may add to the information gained by postmortem blood culture.

Purpose: To demonstrate ophthalmic findings of bacterial endocarditis in a patient with a cardiac structural anomaly and to illustrate the potential usefulness of transesophageal echocardiography in the examination of such patients., Methods: We examined a patient with bacteremia who had white-centered retinal hemorrhages. Complete clinical, laboratory, and echocardiographic evaluations were performed., Results: Streptococcal bacteremia was proven and, by using transesophageal echocardiography, a ventricular false chorda was demonstrated., Conclusions: Patients with white-centered retinal hemorrhages should undergo thorough systemic examinations. In this unusual case of such hemorrhages caused by bacteremia in a patient with a ventricular false chorda, modern, high-resolution transesophageal echocardiography played an important role in confirming the diagnosis.

A 31-year-old patient without past history of cardiac disease presented with an atypical form of Streptococcus milleri endocarditis. The disease progressed in an unusually aggressive manner, with abscess formation in the apex of the left ventricular cavity. The cardiac valves functioned normally and were not affected by the disease.

A case of infective endocarditis caused by Acinetobacter haemolyticus affecting and interventricular patch is reported. The patient, a 21-year-old man with a Fallot's tetralogy who had undergone cardiovascular surgery several years before, received imipenem and gentamicin for 6 and 4 weeks respectively and showed a good response without needing surgical treatment. Endocarditis by Acinetobacter species is very unusual and, to our knowledge, this is the first reported case of infective endocarditis caused by A. haemolyticus. As the clinical characteristics and the response to antibiotics appear to be similar to those reported for infective endocarditis by Acinetobacter lwoffi, prosthetic infective endocarditis by A. haemolyticus is apparently not always an indication for surgical treatment.

The effects of beta-adrenergic agonists on pHi were studied on single ventricular myocytes isolated from adult rat heart and loaded with the acetoxymethyl ester (AM) form of the pH indicator SNARF-1. In modified Krebs' solution containing 20 mmol/L HEPES and 4.4 mmol/L HCO3-, isoproterenol (1 mumol/L) caused a significant decrease of steady-state pHi from 7.20 +/- 0.02 to 7.13 +/- 0.02 (mean +/- SEM) within 2 minutes. This acidification, which was also observed in myocytes that were preloaded with the Ca2+ chelator BAPTA and superfused with nominally Ca(2+)-free solution, was blocked by propranolol as well as by the specific beta 1-antagonist CGP 20712 A but not by the beta 2-antagonist ICI 118,551. Forskolin (10 mumol/L) induced a similar reversible decrease of pHi (average decrease, 0.11 +/- 0.02 pH unit). Furthermore, adenosine (100 mumol/L) substantially attenuated the isoproterenol-induced decrease of pHi. The effect of isoproterenol was not prevented by inhibitors of the Na(+)-H+ antiport, amiloride (1 mmol/L) and 2-N,N-hexamethylene amiloride (20 mumol/L). On the other hand, blockers of Cl- transport mechanisms, DIDS (200 mumol/L) and probenecid (100 mumol/L), inhibited this acidification, Isoproterenol also failed to induce a decrease of steady-state pHi in myocytes incubated in Cl(-)-free medium. Rather, the initial rate of rise of pHi observed on removal of external Cl- ions was significantly increased in the presence of isoproterenol or dibutyryl cAMP. Because the alkalinization induced by removal of Cl- ions is mainly due to reversal of the Cl(-)-HCO3- exchanger, the augmentation of this initial rate of pHi rise directly points to a beta-adrenergic stimulation of the exchanger. Furthermore, the pHi recovery following NH4Cl exposure was accelerated by isoproterenol in the presence of probenecid, indicating that the Na(+)-HCO3- cotransport and/or the Na(+)-H+ antiport also could be activated.(ABSTRACT TRUNCATED AT 250 WORDS)

The vagus nerve exerts a profound influence on the heart, regulating the heart rate and rhythm. An extensive vagal innervation of the cardiac ventricles and the central origin and extent of this innervation was demonstrated by transynaptic transport of pseudorabies virus with a virulent and two attenuated pseudorabies viral strains. The neurons that innervate the ventricles are numerous, and their distribution within the nucleus ambiguus and dorsal motor nucleus of the vagus is similar to that of neurons innervating other cardiac targets, such as the sino-atrial node. These data provide a neuroanatomical correlate to the physiological influence of the vagus nerve on ventricular function.

Bacterial infection (Salmonella enteritidis) of left ventricular true and false aneurysm in a 62-year-old man was followed by septic saddle embolus. The septic saddle embolus was removed and the aneurysm was later resected with coronary bypass grafting. The patient is alive with satisfactory function over 5 years postoperatively.

An unusual case of staphylococcal endocarditis with a vegetation attached to the left ventricular myocardium is described. No valvular vegetations are present. The diagnosis was made by transesophageal echocardiography. The patient had no chronic debilitating disease, nor was she immunosuppressed.

Two hundred fifteen patients infected with human immunodeficiency virus (HIV) participated in a prospective longitudinal study of HIV-related heart disease. Evaluation included signal-averaged electrocardiography and echocardiography. Fifteen patients underwent endomyocardial biopsy, 5 had cardiovascular symptoms and 10 did not. Cardiac myocytes or dendritic cells were prepared by individual cell microdissection to sort them from other cell types such as interstitial cells or circulating blood elements. HIV proviral sequences were amplified in samples of 15 to 20 cells of each type by multiplex, nested, polymerase chain reaction and hybridized to 32P-labeled probes specific for regions within the gag and pol genes of HIV-1. The results showed the presence of HIV sequences in myocytes of 2 of 5 patients with cardiac symptoms and in 6 of 10 without. Thus, symptomatic HIV cardiomyopathy did not appear to be a direct consequence of the virus on myocardial cells. In dendritic cells, HIV sequences were detected in 5 of 5 patients with cardiac symptoms and in 8 of 10 with apparently normal ventricular function. Furthermore, dendritic cells were somewhat more numerous in the myocardium of symptomatic than asymptomatic patients. Our studies are the first to directly detect the HIV genome in purified cardiac myocytes from patients with and without cardiac dysfunction. Our findings do not support a direct role of the virus in myocardial dysfunction. However, the results do suggest that the interstitial dendritic cells may be involved in some manner in the development of cardiac dysfunction observed in HIV-infected patients.

In 30 patients with congestive cardiomyopathy, right ventricular biopsies were performed. The biopsy material was investigated by virological and morphological methods. In all cases it was impossible to isolate viruses from the right ventricular myocardium, corresponding to the lack of infiltrative changes as shown by morphology. Results point against a direct causative role of viruses in the genesis of congestive cardiomyopathy.

The myocardiu m of a young patient who had clinically established cardiomyopathy and suspected Coxsackie virus B4 infection was studied. Coxsackie B4 viral antigen was found in the ventricular and atrial myocardium by specific immunofluorescent antibody staining. Histologic examination revealed varying degrees of myocardial damage. Interstitial fibrosis and edema, swelling and deterioration of hypertrophic muscle fibers, connective tissue proliferation, stasis of small coronary blood vessels, atrophy of myocardial fibers with pyknosis of nuclei, and lytic deterioration were observed. Electron microscopic examination showed portions of the Z bands to be either widened or displaced into the sarcomere. Adjacent cell membranes in the region of the intercalated disc in the myocardium of both the ventricle and the atrium were separated, forming large gaps. Morphologic changes were most pronounced in the atrium adjacent to the mitral valve, in which the mitochondria were grossly swollen, and large vesicles were present in the sarcoplasm. The pathologic changes found in the myocardium of all chambers of the heart apparently were due to Coxsackie B4 viral infection.

Sinoatrial node, perinodular working myocardium of the right atrium and subendocardial muscle fibers of the left ventricle of 8 persons who died suddenly at the age of 23-69 years were studied ultrastructurally. In 1% of working cardiomyocytes, in 2 out of 5 cases of sudden cardiac death, viruses were detected. Myofibrils were destroyed in the damaged myocytes but the contact zones with undamaged myocytes remained intact. Rod-like bacteria were observed in the interstitium of the subendocardial myocardium of the left ventricle in one case. Destructive changes of the mitochondria, myofibrils and intercalated discs were found in the myocytes adjacent to bacteria. Viruses and bacteria were absent in 3 control cases. The possible role of viruses and bacteria in the development of sudden cardiac death is discussed.

Medical-surgical treatment of antibiotic refractory endocarditis requires determination of the site of infection, which is not always possible with conventional cardiac catheterization. The cases of two patients with right-sided endocarditis who survived after combined medical-surgical therapy are presented. One had persistent Pseudomonas aeruginosa bacteremia and three possible sites of infection. Multiple quantitative blood cultures proximal and distal to each suspected site indicated the pulmonary valve alone was infected. The second had sustained bacteremia with three enteric organisms and no apparent valvular abnormality. Quantitative cultures excluded the abdomen as the continuing source of bacteremia and suggested the tricuspid valve was infected. This was confirmed by a second catheterization using multiple cultures in conjuction with dye dilution studies, intracardiac phonocardiography, and angiography. These bacteriologic and cardiologic techniques may be especially useful in detecting right-sided endocarditis and may also be helpful in detecting concomitant infection of both sides of the heart.

Evidence of chronic Coxiella burneti infection of the heart, a disease previously considered peculiar to patients with valvular heart-disease, was found in a patient during routine serological tests before resection of a ventricular aneurysm and also by isolation of the rickettsia from the resected tissue. The patient had no symptoms or signs of Q-fever endocarditis and none of the laboratory evidence usually associated with it.

Endocarditis was induced in the rabbit by the placement of a polyethylene catheter in the right heart. The catheter was filled with stable L-phase variants of Staphylococcus aureus to determine if the variant form would colonize the damaged endocardium and produce further tissue injury similar to that produced by the vegetative bacterial phase. No L-phase variants were recovered from cultures of blood or vegetations, although pure cultures of L-phase variants were obtained from all catheters, including one in place for 70 days. The vegetations were grossly similar in control animals with sterile media in the catheters and animals with catheters containing L-phase variants, although polymorphonuclear leukocytes and eosinophils were more frequently found in vegetations from animals inoculated with L-phase variants. Endocarditis was also induced in animals with vegetative S. aureus and then treated with penicillin G. Blood cultures in hypertonic media often grew vegetative S. aureus when there was no growth in routine media, but no L-phase variants were detected. Vegetative S. aureus, but not wall-defective variants, were isolated from vegetations of all treated animals.