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A case of dental infection with spread to the mediastinum causing pericarditis and cardiac tamponade is described. The clinical course of the disease, the investigations undertaken and the treatment given are outlined.
A 59-year-old man was diagnosed as having constrictive pericarditis 17 months after a typical hydralazine-induced autoimmune syndrome. This late complication of hydralazine has been reported only once. Ten years later the patient was found to have anti-neutrophil cytoplasmic antibodies directed against myeloperoxidase.
The purpose of this investigation was to test whether morphine (morphinum hydrochloricum) applied to the receptive field of the thoracic visceral afferent fibres modifies their activity. Experiments were performed on chloralose-anaesthetised cats, paralysed and artificially ventilated, in a state of pericarditis that was induced by intrapericardial injection of lambda-carrageenan and kaolin. Resulting acute inflammation was proven histopathologically and documented electrocardiographically. Single afferent fibres with receptive fields in thoracic viscera were dissected from thoracic sympathetic chain (19 fibres), as well as the vagus nerve (9 fibres). All tested fibres transmitted sensory information from the low-threshold mechanoreceptors. As a final result, it was found that morphine (0.001-1.0 mg/ml) when applied locally activates, depending on the dose, afferent fibres as follows: 12 sympathetic afferents (out of 12 tested), and 7 vagal afferents (out of 9 tested). In examining the specificity of morphine action, the preliminary local application of naloxone (1.0 mg/ml) just before morphine, blocked all excitatory responses. The excitatory response was present whether the receptive field was located in the inflammatory area, or outside it, in group III or IV fibres.
To test the hypothesis that induced atrial flutter evolves from a transitional rhythm, the onset of 99 episodes of induced atrial flutter (mean cycle length 135 +/- 18 ms) lasting greater than 5 min in 40 dogs with sterile pericarditis was first characterized. In 85 (86%) of the 99 episodes, atrial flutter was preceded by a brief period (mean 1.4 +/- 0.9 s, range 0.4 to 42) of atrial fibrillation. Then, in 11 open chest studies, atrial electrograms were recorded simultaneously from 95 pairs of right atrial electrodes during the onset of 18 episodes of induced atrial flutter (mean cycle length 136 +/- 16 ms). Atrial flutter was induced by a train of eight paced atrial beats, followed by one or two premature atrial beats (7 episodes) or rapid atrial pacing (11 episodes). A short period of atrial fibrillation (mean cycle length 110 +/- 7 ms) induced by atrial pacing activated the right atrium through wave fronts, which produced a localized area of slow conduction. Then unidirectional conduction block of the wave front occurred for one beat in all or a portion of the area of slow conduction. This permitted the unblocked wave front to turn around an area of functional block and return through the area of slow conduction that had developed the unidirectional conduction block, thereby initiating the reentrant circuit. The location of the unidirectional block relative to the direction of the circulating wave fronts determined whether the circus movement was clockwise or counterclockwise. The area of slow conduction and unidirectional conduction block occurred where the wave front crossed perpendicular to the orientation of the atrial muscle fibers, suggesting a role for anisotropic conduction. These areas included the high right atrial portion of the sulcus terminalis (10 episodes), the low right atrial portion of the sulcus terminalis (4 episodes) and the pectinate muscle region (4 episodes). It is concluded that the development of a localized area of slow conduction in the right atrium followed by unidirectional conduction block in this area produced during a short period of atrial fibrillation or rapid atrial pacing is necessary for atrial flutter to occur in this model.
OBJECTIVES: We tested the hypothesis that double potentials recorded during atrial flutter in a functionally determined reentrant circuit reflect activation of the reentrant wave front around an area of functional conduction block. BACKGROUND: The center of the atrial flutter reentrant circuit in the sterile pericarditis canine model is characterized by double potentials. METHODS: We studied 11 episodes of atrial flutter in eight dogs during interruption of atrial flutter while pacing the atria. A multielectrode mapping system was used to record simultaneously from 190 electrodes on the right atrium (location of reentry). RESULTS: Interruption of atrial flutter occurred when the orthodromic wave front from the pacing impulse blocked in an area of slow conduction in the reentrant circuit. The response of the double potential with interruption of atrial flutter depended on the location of the recording site relative to this area of block. Two types of response were seen. When the double potential was recorded orthodromically distal to this area of block, interruption of atrial flutter was associated with disappearance of the second deflection, and continued pacing after interruption of atrial flutter was not associated with reappearance of the second potential. When the double potential was recorded at a site orthodromically proximal to the area of block, interruption of atrial flutter was not associated with disappearance of the second potential, and when rapid atrial pacing was continued, the double potential remained despite disappearance of the atrial flutter reentrant circuit. CONCLUSIONS: Double potentials represent functional conduction block in the center of the reentrant circuit, with each deflection of the double potential reflecting activation on either side of the area of functional block. The data also demonstrate that double potentials are not limited to a reentrant circuit, as they were recorded on either side of an area of block in the absence of such a circuit.
OBJECTIVES: This study sought to determine whether temporary epicardial wire electrodes can be used safely and effectively to defibrillate the atria with low energy shocks in the absence of anesthesia. BACKGROUND: Atrial fibrillation after open heart surgery is a significant clinical problem. METHODS: Twelve dogs with sterile pericarditis were studied. In the first group (6 dogs, bilateral thoracotomy group), a wire electrode, insulated except for the distal 6 cm, was placed on the epicardial free wall of each atrium. Each end of the bare wire was then sutured to the parietal pericardium. In the second group (6 dogs, median sternotomy group), the wire electrodes were kept in place by a double loop of Prolene placed around the distal tip of the bare wire and sewn to the overlying parietal pericardium. In the bilateral thoracotomy group, atrial defibrillation thresholds (defined as < 90% and > 10% successful defibrillation of 20 shocks at a given delivered energy) were obtained in anesthetized dogs using the wire electrodes with the chest closed and open and using two transvenously placed catheters with coil electrodes in the distal 6 cm (one in the coronary sinus and the other in the right atrial appendage) with the chest open. In the median sternotomy group, thresholds were obtained in minimally sedated animals without reopening the chest. A 25% increase above threshold shock was also used to determine a new percent success. After 4 days, the wire electrodes were removed by pulling on the external ends. At the time of removal, blood pressure and heart rate were monitored for 30 min, after which dogs were killed and their hearts sent for histopathologic study. For all dogs, chest radiographs were obtained postoperatively and on study days. RESULTS: Atrial defibrillation using the wire electrodes was successful in all dogs at a mean (+/- SE) voltage of 112 +/- 9 V, with an energy level of 0.46 +/- 0.07 J and an impedance of 59.3 +/- 5 ohms. The mean percent success at the atrial defibrillation threshold was 36 +/- 5%. The 25% increase in defibrillation voltage improved the mean percent success to 73% (mean energy 0.66 +/- 0.19 J). No clinical or hemodynamic complications were observed during shock delivery, and no ventricular arrhythmias were induced during the shocks. No complications followed wire electrode removal. Histopathologic analysis showed no structural damage. CONCLUSIONS: The atrial defibrillation threshold obtained using temporary epicardial wire electrodes for atrial defibrillation is < 1 J in dogs. Atrial defibrillation using temporary epicardial wire electrodes can be performed safely, quickly and reliably without the need for anesthesia or antiarrhythmic agents. The wire electrodes can be removed without adverse hemodynamic or structural consequences. These data provide a basis for testing atrial defibrillation using epicardial wire electrodes in patients after open heart surgery.
There are many causes of acute pericarditis (inflammation of the pericardium) and diagnosis is often difficult owing to the dynamic nature of the disease. History and physical examination, augmented by radiographic and ECG studies, will allow the diagnosis to be made in the majority of cases. The ECG typically undergoes a four-stage evolution, and frequent reassessment of the patient is essential. Outpatient treatment is usually successful, although a subgroup of these patients require hospitalization.
SETTING: Large academic medical center in Tanzania. OBJECTIVES: To determine the etiologies and outcomes of large pericardial effusions in HIV-infected and uninfected patients. DESIGN: Prospective cohort study of patients admitted with new large pericardial effusions, confirmed echocardiographically. Patients had pericardial biopsies and drainage with extensive analysis of tissue and fluid specimens, and were followed with clinical and echocardiographic examinations. RESULTS: Of 28 patients with large pericardial effusions, 19 were infected with HIV-1. 22 had invasive diagnostic procedures: 14 of 14 HIV-infected patients, but only 4 of 8 non-HIV-infected patients, had tuberculous pericarditis (P = 0.01). All but 1 of the HIV-infected patients had strongly positive tuberculin skin tests, and short-term outcomes were similar in the 2 groups. CONCLUSION: TB is the predominant cause of large pericardial effusion in HIV-infected patients in this setting; non-HIV-infected patients are more likely to have other etiologies. These patients were at an early stage of HIV infection and responded well to treatment. In settings where microbiological studies are not routinely available, HIV-infected patients with large pericardial effusions may be treated empirically for tuberculosis and monitored for improvement. If improvement does not follow within 2-4 weeks further studies are indicated. HIV-negative patients should undergo diagnostic evaluation initially.
A case of complete debridement of a calcified pericardium in a patient with constrictive pericarditis is reported. The use of an ultrasonic surgical aspirator facilitated disintegration of calcium without damaging the adherent epicardium and myocardium.
From 1970 to 1990, 71 consecutive patients (51 men and 20 women) had pericardectomy for chronic constrictive pericarditis. The mean age was 44.2 +/- 16.1 years. In the preoperative state 2.8% were in NYHA class I, 18.3% in II, 43.6% in III and 35.2% in IV. The operative approach was median sternotomy in 93% and left anterolateral thoracotomy in 7%. The early mortality rate (within 30 days after operation) was 5.6%. All four early deaths were female (P < 0.001), in the preoperative state the patients were classified as NYHA class IV (P < 0.01). These patients had a significantly higher preoperative mean right atrial pressure then survivors (21.5 +/- 8.5 mmHg vs 13.6 +/- 5.6 mmHg, P < 0.005). Follow-up was obtained for 65 patients (91.5%) and averaged 11 +/- 5.8 years (the longest period was 21.5 years). Actuarial survival at 5, 10, 15 and 20 years for all patients was 84.6% +/- 4.5%, 80.1% +/- 5.3%, 70.5% +/- 6.9% and 65.8% +/- 7.9%, respectively. In the preoperative state 10 of the 12 late deaths (83%) were classified NYHA class IV and the remaining ones class III. Of the 49 patients alive 23% belong to NYHA class I, 42% to II and 35% to III; none is in class IV. Negative predictors of survival were found to be preoperative NYHA class IV (P < 0.01), low-voltage electrocardiogram (ECG) (P < 0.01), ascites (P < 0.01), dyspnea at rest (P < 0.05) and hyperbilirubinemia (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
In a case of CPPD crystal deposition disease of the pseudorheumatoid type and of long duration, calcified constrictive pericarditis developed and was surgically treated. Analysis of the calcium deposit in the pericardium was carefully made by infrared absorption, x-ray diffraction, and thermogravimetry. It revealed that the deposit was composed of B-type carbonated apatite. Previously, both calcium pyrophosphate dihydrate (CPPD) and apatite crystals, either in the same place or in different tissues, have been reported in the same patient. These observations raise the possibility that the same metabolic error might lead to both types of crystal deposition.
BACKGROUND: Adenosine deaminase (ADA) activity in pericardial fluid is a valuable aid in the diagnosis of tuberculous pericarditis (TP), but there is no systematic review performed to evaluate the benefits of ADA activity as an adjunctive test for TP diagnosis. The objective of this systematic review was to evaluate the utility of ADA activity as a diagnostic marker of TP on patients presenting with pericardial effusion. METHODS: MEDLINE, LILACS and Cochrane Library databases (1980-2005) searches to identify articles related to adenosine deaminase activity on TP diagnosis. Articles with patients with at least one TP diagnostic criteria were included. The controls were patients with other pericardial diseases with moderate or large pericardial effusion. To calculate the sensitivity, specificity, as well as positive and negative likelihood ratios we extracted the total number of confirmed TP cases over all patients with pericardial effusion as well as the number of cases with ADA activity values of 40 U/L and over. RESULTS: Thirty one studies met our initial inclusion criteria and five articles were selected. The heterogeneity limited the specificity analysis (p=0.004). The method yielded a sensitivity and specificity of 88% and 83%, respectively. The SROC curve presented an area with a tendency towards 1 (value of 0.9539) and corroborates the diagnostic value of ADA activity. CONCLUSIONS: The present study confirms the clinical value of ADA activity as adjunctive diagnostic marker of TP among other causes of pericardial effusion.
Mitral annular velocities are reportedly useful in diagnosing constrictive pericarditis (CP); however, their exact efficacy in larger clinical settings remains unevaluated. This study reexamined the role of longitudinal tissue Doppler imaging in diagnosing CP in clinical practice. Tissue velocity imaging (GE Vingmed System Five) was performed in 122 subjects (87 referred with clinically suspected CP and 35 age- and sex-matched controls). Of the 87 subjects with suspected CP, 45 (51.7%) had CP confirmed at surgery, 11 (12.6%) had restrictive heart disease, 20 (23.0%) had right heart failure due to cor pulmonale, and the other 11 (12.6%) had old pericardial effusions and no hemodynamic evidence of constriction on follow-up echocardiography. Of the 45 patients with CP, mitral early diastolic (Ea) annular velocities from septal and lateral regions were normal (>/=8 cm/s) in 40 (88.9%) and decreased (<8 cm/s) in 1 or both regions in 5 (3 with left ventricular systolic dysfunction, 2 with extensive mitral annular calcification). Of 11 patients with restrictive cardiomyopathy, 8 (72.7%) had reduced Ea (<8 cm/s) and 3 showed normal Ea velocity in 1 or both corners of the mitral annulus. All except 2 patients with right-sided heart failure from cor pulmonale and those with previous pericardial effusion had normal Ea velocities. A normal Ea velocity improved recognition of CP, particularly in the presence of nondiagnostic 2-dimensional or transmitral flow-Doppler imaging. The overall sensitivity and specificity for diagnosing CP using tissue Doppler incrementally with M-mode, 2-dimensional, and transmitral flow Doppler were 88.8% and 94.8%, respectively. Mitral annular velocities help with diagnosis and differentiation of CP in most cases, except in the presence of extensive annular calcification, left ventricular systolic dysfunction, or segmental nonuniformity in myocardial velocities.
We report a case of group F streptococcal pericarditis, the source of which was found to be an esophagomediastinal fistula arising from a midesophageal diverticulum. The patient presented subacutely and had no preexisting symptoms of esophageal disease. Antibiotic therapy, surgical drainage, pericardiectomy, and esophageal myotomy led to a successful outcome.
Gastropericardial fistula, purulent pericarditis, and cardiac tamponade developed 7 years after laparoscopic Nissen fundoplication. The patient was successfully managed through a thoracotomy by open drainage of the pericardium, excision and closure of the fistula, and an omentum flap.
The pericardium envelopes the cardiac chambers and under physiological conditions exerts subtle functions, including mechanical effects that enhance normal ventricular interactions that contribute to balancing left and right cardiac outputs. Because the pericardium is non-compliant, conditions that cause intrapericardial crowding elevate intrapericardial pressure, which may be the mediator of adverse cardiac compressive effects. Elevated intrapericardial pressure may result from primary disease of the pericardium itself (tamponade or constriction) or from abrupt chamber dilatation (eg, right ventricular infarction). Regardless of the mechanism leading to increased intrapericardial pressure, the resultant pericardial constraint exerts adverse effects on cardiac filling and output. Constriction and restrictive cardiomyopathy share common pathophysiological and clinical features; their differentiation can be quite challenging. This review will consider the physiology of the normal pericardium and its dynamic interactions with the heart and review in detail the pathophysiology and clinical manifestations of cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy.
BACKGROUND: In most primary myocardial diseases, early diastolic mitral annulus velocity (E') decreases with disease progression. To our knowledge, constrictive pericarditis (CP) is the only condition without this phenomenon. OBJECTIVE: This study was performed to evaluate the diagnostic and pathophysiologic role of mitral annulus velocity in patients with CP. METHODS: In all, 17 patients with CP (9 men; mean age 46.5 +/- 14.3 years), 8 patients with cardiac tamponade (Tamp) (2 men; mean age 44.5 +/- 15.0 years), and age- and sex-matched control subjects for CP and Tamp were recruited for the study. Early mitral inflow velocity and E' were obtained while simultaneously recording respiration. In 8 patients with CP and in all patients with Tamp, these measurements were repeated after the relief of constrictive physiology or after pericardiocentesis. RESULTS: In patients with CP, E' was significantly higher than it was for control subjects (12.9 +/- 3.0 cm/s vs 9.8 +/- 2.4 cm/s, P <.01). An E' of 2 cm/s higher than the predicted normal E' could differentiate patients with CP from control subjects with a sensitivity of 76% and specificity of 82%. In 12 of 17 patients (71%), inspiratory E' was higher than expiratory E'-the opposite of mitral inflow variation. In 8 patients, E' decreased significantly after the relief of constrictive physiology (13.8 +/- 2.5 cm/s vs 9.3 +/- 3.1 cm/s, P <.05). In contrast, E' in the Tamp group was significantly lower than in the control group (6.8 +/- 1.6 cm/s vs 10.2 +/- 2.5 cm/s, P <.01), did not show significant respiratory variation, and increased significantly after pericardiocentesis (6.8 +/- 1.6 cm/s vs 9.5 +/- 3.0 cm/s, P <.05). CONCLUSION: E' is exaggerated in CP, which is helpful for diagnosis. The opposite phenomenon was noted in Tamp, a dissimilarity that might contribute to different hemodynamics.
We report the case of a 30-year-old man with acute pericarditis in whom effusive-constrictive physiology developed rapidly in less than 2 weeks. Serial echocardiography demonstrated a dramatic change in the appearance of the pericardial effusion and the pericardial space. The patient underwent pericardiectomy with symptom relief. The findings at operation included a markedly thickened and inflamed pericardium. The case highlights the role of echocardiography in the evaluation of patients with pericardial disease and the echocardiographic features that prompted early surgical intervention.