Ventricular pacing-induced loss of contractile function and development of epicardial inflammation.

Perturbations in the normal sequence of ventricular activation can create regions of early and late activation, leading to dysynchronous contraction and areas of dyskinesis. Dyskinesis occurs across the left ventricular (LV) wall, and its presence may have important consequences on cardiac structure and function in normal and failing hearts. Acutely, dyskinesis can trigger inflammation and, in the long term (6 wk and above), leads to LV remodeling. The mechanisms that trigger these changes are unknown. To gain further insight, we used a canine model to evaluate transumural changes in myocardial function and inflammation induced by epicardial LV pacing. The results indicate that 4 h of LV suprathreshold pacing resulted in a 30% local loss of endocardial thickening. Assessment of neutrophil infiltration showed a significant approximately fivefold increase in myeloperoxidase activity in the epicardium versus the midwall/endocardium. Matrix metalloproteinase-9 activity increased ∼2 fold in the epicardium and ROS generation increased ∼2.5-fold compared with the midwall/endocardium. To determine the effects that electrical current alone has on these end points, a group of animals was subjected to subthreshold pacing. Significant increases were observed only in epicardial myeloperoxidase levels. Thus, the results indicate that transmural dyskinesis induced by suprathreshold epicardial LV activation triggers a localized epicardial inflammatory response, whereas subthreshold stimulation appears to solely induce the trapping of leucocytes. Suprathreshold pacing also induces a loss of endocardial function. These results may have important implications as to the nature of the mechanisms that trigger the inflammatory response and possibly long-term remodeling in the setting of dysynchrony.

The usefulness of adenosine deaminase in the diagnosis of tuberculous pericarditis.

The objective of this study was to evaluate the adenosine deaminase (ADA) activity usefulness in the diagnosis of tuberculous pericarditis (TP), comparing its value with pericardial effusions (PE) caused by other pericardial diseases. A retrospective case-control study was conducted with nine cases of TP and 39 other than TP diseases (12 neoplastic, 11 septic and 16 unknown origin). Every patient included in this study had PE samples submitted to ADA activity measures and microbiological analysis, and then had pericardial tissue samples submitted to microbiological and histopathological examination. Considering the value of 40 U/L as the cut-off for the diagnosis of TP, the specificity and sensitivity were respectively of 72% and 89%. The specificity of ADA activity for the TP was best applied in the differential diagnosis from PE of unknown origin. The present study demonstrates the clinical value of the measurement of ADA activity in PE in the diagnosis of TP.

The MB fraction of creatine phosphokinase. An indicator of myocardial involvement in acute pericarditis.

An elevated level of the MB fraction of creatine phosphokinase (CPK) with normal serum myoglobin and normal CPK values was found in a case of acute idiopathic pericarditis. The elevated serum CPK-MB isozyme is suggested to be an indicator of myocardial involvement accompanying acute pericarditis. The normal CPK and serum myoglobin values and the pattern of rapid decrease of CPK-MB level ruled out the possibility of acute myocardial infarction.

Serum creatine kinase MB isoenzyme activity in long-term hemodialysis patients.

Serum creatine kinase MB isoenzyme (CK-MB) activity was determined in 46 male long-term hemodialysis patients without evidence of myocardial infarction. Thirteen (28.3%) showed mild elevations. The abnormality persisted in seven of eight patients on repeated measurement at three- to eight-month intervals. There was a significant correlation between serum CK-MB and CK-MN activity, and the activity of both enzymes rose after intramuscular injection. The reason for the abnormality is not known. It is possible that skeletal muscle is the source of elevated enzyme activity. Caution should be exercised in the interpretation of serum CK-MB activity in the diagnosis of acute myocardial infarction in this patient population.

Elevation of plasma MB creatine kinase and the development of new Q waves in association with pericarditis.

A 64-year-old woman with an acute exacerbation of chronic relapsing pericarditis had initial clinical and ECG features that were consistent with an acute anterior myocardial infarction. Transient Q waves were observed in the precordial leads, and she also exhibited elevated plasma MB creatine kinase (MB CK) activity. However, the overall clinical and laboratory data, including angiographic and radionuclide studies, suggest that the myocardial damage was secondary to pericarditis per se, rather than ischemic myocardial infarction. This case emphasizes that Q waves and elevated MB CK activity can be seen in association with pericarditis, and this must be differentiated from myocardial infarction secondary to coronary artery disease.

New scoring system using tumor markers in diagnosing patients with moderate pericardial effusions.

We performed diagnostic and therapeutic pericardiostomy with drainage and biopsy in 51 patients with moderate to large pericardial effusions of different etiologies from August 1991 to July 1995. Patients were divided into 4 groups (group 1, tuberculous pericarditis; group 2, suspected tuberculous pericarditis; group 3, acute pericarditis; group 4, malignancy). The pericardial fluid adenosine deaminase level in tuberculosis (87 +/- 10 U/l) was significantly higher than that in malignancy or acute pericarditis (21 +/- 4 U/l, 23 +/- 7 U/l, respectively) (P = 0.0001). The mean pericardial fluid carcinoembryonic antigen level (1.8 +/- 0.3 ng/ml) in benign disease was significantly lower than that (170.7 +/- 46.4 ng/ml) in malignant disease (P = 0.0001). Follow-up study has been done. With a new scoring system (each score 1 for adenosine deaminase > or = 40 U/l, or carcinoembryonic antigen < or = 5 ng/ml) in 25 patients since November 1993, we could diagnose 5 among 7 patients (71%) with tuberculosis, 11 among 13 patients (85%) with malignancy (adenosine deaminase < or = 40 U/l, or carcinoembryonic antigen > or = 5 ng/ml) and 5 among 5 patients (100%) with acute pericarditis (adenosine deaminase < or = 40 U/l, or carcinoembryonic antigen < or = 5 ng/ml), respectively. Our long-term follow-up study suggests that with the new scoring system we can decrease complications or avoid unnecessary procedures or treatments of patients.

Detection of inducible nitric oxide synthase- and nitrotyrosine-positive cells in the lesions of pericarditis induced by porcine enterovirus serotype 3 infection.

The expression of inducible nitric oxide synthase (iNOS), an enzyme that produces nitric oxide, was examined in the hearts of pigs infected with porcine enterovirus serotype 3 (PEV3). Piglets orally infected with PEV3 developed tremors and paralysis 3-7 days post-infection. Affected animals had pericarditis and myocarditis. There were fibrin and inflammatory cell infiltrates (macrophages and neutrophils) in the pericardial sac and myocardium. Immunohistochemically, the majority of inflammatory cells in the pericardial sac were positive for iNOS and nitrotyrosine, an end product of nitric oxide. These results suggest that iNOS is upregulated in the pericardial lesion, and that increased nitric oxide production plays an important role in the development of PEV3-induced pericarditis and myocarditis.

[Myocardial disease in acute idiopathic pericarditis (author's transl)]. / Afección miocárdica en la pericarditis aguda idiopática.

Acute idopathic pericarditis can be accompanied by myocarditis, and in all types of acute pericarditis there are electrocardiographic signs of myocardial lesions. In order to determine the severity of the myocardial disease in acute idiopathic pericarditis, a prospective study has been carried out in a group of 25 patients with this diagnosis. The clinical evaluation included phonomecardiographic measurements of the systolic intervals, Weissler index in 24 cases, and echocardiographic study of the left ventricle in eight cases. Besides that, the serum levels of the myocardial enzymes (GOT, GPT, CPK, and LDH and its isoenzymes) were determined in all cases. The results showed a gallop rhythm in 8 percent of the cases, supraventricular arrhythmias in 4 percent, dysfunction of the left ventricle by systolic intervals and/or echocardiography in 32 percent, and increase of the myocardial enzymes in 24 percent, which represents a global incidence of myocardial disease of 44 percent. However, only three patients presented clinical manifestations of myocardial disease, although the congestive cardiac failure was always secondary to cardiac tamponade and not to myocardial failure. The increase of myocardial enzymes can determine important problems of differential diagnosis with an acute myocardial infarction. The clinical course was favourable in all of the cases, including the ones which showed myocardial disease.

Diagnosis of malignant pericarditis: a single centre experience.

BACKGROUND: Malignancy is the most common cause of effusive pericarditis with a haemodynamically significant amount of pericardial fluid. Early diagnosis and management of malignant pericarditis may significantly improve outcomes. AIM: To evaluate retrospectively the rate and clinical presentation of malignant pericarditis among patients undergoing invasive treatment, with a view to identification of optimal diagnostic modalities to distinguish this group among other patients. METHODS: We studied 191 patients (100 men and 91 women, median age 57 years, range 19-88 years) with effusive pericarditis who underwent invasive treatment in the National Institute of Tuberculosis and Lung Diseases in Warsaw in 1982- -2008 due to a significant amount of pericardial fluid and/or echocardiographic evidence of cardiac tamponade. Pericardiocentesis was performed in 93 cases, pericardioscopy in 61 cases, and substernal pericardiotomy in 37 cases. Pericardial fluid was sent for examination in all patients, and a pericardial specimen was obtained in 96 patients. The patients were divided into 3 groups: Group 1 included patients with malignant pericarditis (malignant cells found in the cytological examination of the pericardial fluid and/or neoplastic infiltration in the histological examination of the pericardial specimen), Group 2 included patients with probable malignant pericarditis (pericardial fluid without malignant cells with histologically confirmed malignancy at some other location), and Group 3 included patients with non-malignant pericarditis (negative cytological examination of pericardial fluid and histological examination of the pericardial specimen, with no evidence of malignancy during hospitalization and one-year follow-up). RESULTS: Malignancy was found in 111 (58%) of 191 patients, including 66 (35%) patients with definite malignant pericarditis and 45 (23%) patients with probable malignant pericarditis. Lung cancer, including adenocarcinoma, was the most common type of malignancy, present in 44 (67%) patients. Non-malignant pericarditis was found in 80 (42%) patients. Among patients with the diagnosis of malignancy (Groups 1 and 2), a positive result of the cytological examination of the pericardial fluid was obtained in 52 cases (sensitivity of 46%). Among patients without malignancy, a negative result of the cytological examination of the pericardial fluid was obtained in all 80 cases (specificity of 100%). Malignant infiltration was found in 20 of 44 patients with the diagnosis of malignancy (sensitivity of 46%) and in none among 52 patients without malignancy (specificity of 100%). Compared to patients with non-malignant pericarditis, patients with malignant pericarditis significantly more commonly presented with tachycardia of >100 bpm in a resting electrocardiogram (ECG) (in 77% of patients with malignant pericarditis vs. 43% of patients with non-malignant pericarditis, p = 0.01), low QRS amplitude (52% vs. 34%, respectively, p = 0.03), electrical alternans (19% vs. 3%, respectively, p = 0.001), echocardiographic evidence of cardiac tamponade (67% vs. 34%, respectively, p = 0.0001), enlarged mediastinal lymph nodes by chest computed tomography (CT) (90% vs. 29%, respectively, p <0.00001), pericardial thickness >8 mm by chest CT (62% vs. 16%, respectively, p <0.0001), and bloody pericardial effusion (94% vs. 43%, respectively, p <0.0001). Levels of carcinoembryonic antigen (CEA) and cytokeratin fragment-19 (CYFRA 21-1) in the pericardial fluid were higher in patients with malignant pericarditis compared to patients with non-malignant pericarditis, with median values of 40.8 ng/mL vs. 0.9 ng/mL, p <0.0001, and 162.85 ng/mL vs. 13.35 ng/mL, p <0.0001, respectively. CONCLUSIONS: 1. Malignancy was found in 58% of patients undergoing invasive treatment due to large pericardial effusion. 2. Cytological examination of the pericardial fluid and histological examination of a pericardial specimen showed high specificity (100%) but low sensitivity (46%) in the diagnosis of malignant pericarditis. 3. The most important predictors of malignant pericarditis included tachycardia of >100 bpm as revealed by the physical examination and ECG, echocardiographic evidence of cardiac tamponade, presence of enlarged mediastinal lymph nodes (>1 cm) and thickened pericardium (>8 mm) by chest CT, bloody pericardial effusion, and elevated levels of CEA (>5 ng/mL) and CYFRA 21-1 (>50 ng/mL) in the pericardial fluid.

[Leptospirosis with isolated cardiac manifestations]. / Leptospirose à manifestation cardiaque isolée.

A case of leptospirosis with isolated myocardial involvement is reported. Diagnostic problems set by this uncommon clinical picture are considered. The cause of the increase in CPK and MBCPK concentrations, reflecting myolysis, is discussed.

A case of lactate dehydrogenase (LDH)-IgG complex formation which causes low plasma LDH activity and an abnormal LDH isozyme pattern.

A case of an LDH-IgG complex formation which causes low plasma LDH activity and an abnormal LDH isozyme pattern was reported. A patient had pericarditis and myocardial hypertrophy of asymmetrical septal hypertrophy type. The same IgG was recognized in pericardial effusion. From a column chromatographic study, the molecular weight of LDH-IgG complex was estimated as being about 490,000. This complex was speculated as the IgG1-LDH2. The mechanism by which LDH-IgG is formed and the relationship between the complex itself and cardiac diseases remain unknown.

Detection of coronary disease patients at high risk for recurrent myocardial infarction by elevated plasma inactive creatine kinase B protein levels.

The diagnostic and prognostic significance of plasma inactive creatine kinase B protein (CK-Bi) levels measured by radioimmunoassay was determined in various ischemic myocardial syndromes. In 120 stable angina patients free of pain at time of blood sampling, mean CK-Bi level was 114 +/- 42 (SD) micrograms-equiv/ml; 195 micrograms-equiv/ml (95% confidence interval) represented upper limit of normal. In seven coronary artery disease (CAD) patients atrial pacing induced ischemia was not associated with increased coronary sinus CK-Bi. Of 201 consecutive patients with suspected acute infarction (AMI), 45 developed ECG criteria of transmural AMI with concomitant increased plasma CK-Bi levels (498 +/- 133, range 372-718 micrograms-equiv/ml). Elevated CK-Bi levels in evolving transmural AMI were detected before raised CK enzyme activity. Elevated plasma CK-Bi levels also occurred in acute pericarditis and in unstable angina. In the 84 patients not developing ECG changes or elevated plasma CK activity, their plasma CK-Bi levels were also normal and no coronary events occurred in the next 6 months. The remaining 55 patients had nontransmural AMI, with 15 also having elevated plasma CK and CK-Bi levels, of whom six developed re-AMI in the next 3 months. In the other 40 nontransmural AMI patients, plasma CK-Bi levels (350 +/- 65 micrograms/equiv/ml, range 228 to 445) increased significantly without associated CK activity rise, and 24 developed re-AMI (three fatal) in the next 6 months. These data suggest that: (1) plasma CK-Bi protein radioimmunoassay measurement provides a sensitive means for detecting myocardial necrosis or inflammation and (2) elevated plasma CK-Bi levels in coronary disease patients during myocardial ischemic pain may afford identification of a CAD clinical subset at high risk of subsequent AMI.

Endomyocardial biopsy findings in cases with pericarditis or perimyocarditis.

In order to determine the presence or absence of myocarditis in cases with viral or idiopathic pericarditis, a study was conducted as one of our series on endomyocardial biopsy. There were two groups of patients, pericarditis cases (n = 8), and patients with perimyocarditis (n = 6). In the former group, it was confirmed that cardiac sarcoplasmic enzymes were not released during the acute stage of the disease. In the latter, there was positive evidence of the enzyme release. Also, employing our method of categorizing the possibility of myocarditis at the histopathological level, we found that the category 'highly suggestive' of myocarditis was absent in all eight cases with pericarditis. However, in cases with perimyocarditis, this category was assigned in four out of six cases (67%), indicating a high incidence. The category, 'slightly suggestive', was seen in three cases of the former (38%) and two cases of the latter group (33%). It is concluded that in patients with pericarditis, the release of cardiac sarcoplasmic enzyme is an important diagnostic element in the diagnosis of perimyocarditis even if the clinical features reveal a predominance of pericarditis. In patients with perimyocarditis, progression to residual cardiac disease, such as conduction disturbance or congestive heart failure, is likely.

[Determination of creatine kinase and CK-MB in heart failure (author's transl)]. / Bestimmung der Creatinkinase und des Isoenzyms Creatinkinase-MB bei Herzinsuffizienz.

Serum activity of creatine kinase and creatine kinase-MB have been investigated in 129 patients of various etiology in overt heart failure. Elevations in CK-MB were found in 19 patients, most frequently in patients with inflammatory heart disease. We found no correlation between CK-MB activity in serum and the severity of heart failure. CK-MB elevation in patients with chronic heart failure may be interpreted as a sign of progressive as well as regressive processes in the myocardium.

A case of immunoglobulin G conjugated with lactate dehydrogenase, producing both loss of enzyme activity and an abnormal isoenzyme pattern.

We present a patient with an inhibitor of lactate dehydrogenase (LD; EC 1.1.1.27) in serum, who had pericarditis and myocardial hypertrophy. The patient's LD activity in serum was low and the LD isoenzyme pattern was abnormal. The relative molecular mass of this abnormal LD-IgG complex was approximately 490 000. The patient's IgG reacted with all five LD isoenzymes.

"Acute pericarditis": myocardial enzyme release as evidence for myocarditis.

The relationship between the serial ECG ST-T wave changes held to be characteristic of acute pericarditis and serum cardiac enzyme levels was studied in 18 young men with symptoms of acute infectious disease. Creatine kinase MB enzyme (CK-MB) was detected in 14 patients (78%); its peak levels were as high as 186 U/L during the first days of ST segment elevation. Normal values were only noted during the subsequent T wave inversion stage of the disease. ST segment elevation was more marked (p less than 0.01) and T wave inversions were deeper (p less than 0.01) and more prolonged (p less than 0.05) in the 12 patients with CK-MB levels over 10 U/L than in those with values under 10 U/L. Pericardial friction rub and/or pericardial effusion by echocardiography occurred in only one third of the patients. We conclude that the serial ECG changes of ST segment elevation, with subsequent T wave inversions in connection with acute infection, are caused by acute myocardial injury, myocarditis, as reflected by myocardial enzyme release.

[Acute pericarditis. Study of 50 consecutive cases]. / Les péricardites aiguës. Etude de 50 observations consécutives

50 consecutive cases of pericarditis were studied. Idiopathic and viral pericarditis made up 36 p. cent of all cases. The occurrence of tuberculous or rheumatic conditions was even lower than that reported in similar series in the literature. Amongst the clinical signs of these diseases, emphasis should be placed upon the frequency of chest pain which was increased by deep inspiration in only three out of four cases. Circulatory problems associated with the pericarditis were, on the whole, minimal. However, a fall in blood pressure was seen in 6 cases and true collapse in 3 more. The electrocardiogram showed, in addition to the classical signs, sagging of the PR interval in 36 p. cent and transient atrial fibrillation in 4 cases. As far as biological tests are concerned, it should be noted that elevation of creatine phospho-kinase to levels 4 times greater than normal may be seen, creating problems with the differential diagnosis from myocardial infarction. The course was in general favourable though two deaths occurred in this series (4 p. cent), one with tuberculous pericarditis and the other with idiopathic pericarditis.