Endothelin-1 levels in chronic congestive heart failure.

BACKGROUND: Endothelin-1 levels in patients with chronic congestive heart failure were evaluated with respect to the severity of cardiac dysfunction. The relationships between three neurohormones, brain natriuretic peptide (BNP), human atrial natriuretic peptide (HANP), and endothelin-1,were evaluated. METHODS: Forty patients (17 men and 23 women, aged 64-98 years) with chronic congestive heart failure were evaluated. Echocardiography was performed for each patient, and the left ventricular ejection fraction (EF) was calculated. Titers of HANP, BNP and endothelin-1 in serum were measured. Exclusion criteria included acute myocardial infarction, unstable angina, and renal dysfunction (serum creatinine >1.6 mg/dl). RESULTS: Endothelin-1 levels were correlated with HANP (r = 0.675, p < 0.0001) and BNP (r = 0.616, p < 0.0001) levels. Endothelin-1 levels were not correlated with the left ventricular ejection fraction or end-diastolic volume. BNP levels were correlated with the left ventricular ejection fraction (r = 0.315, p = 0.057). CONCLUSION: These findings indicate that endothelin-1 interacts with HANP and BNP in patients with chronic congestive heart failure. Endothelin-1 is suggested to play an important role in chronic congestive heart failure with preserved ejection fraction.

QRS voltages are transiently increased at the superacute stage of experimental myocarditis.

BACKGROUND: There are few reports on the precise electrocardiographic characteristics of acute myocarditis. The present study was focused on QRS voltage changes at the superacute stage of murine myocarditis. METHODS: Serial electrocardiograms were recorded during the acute stage of viral myocarditis in mice, and then the cardiac pathology was examined. After recording baseline electrocardiograms, mice (n=235) were inoculated intraperitoneally with the encephalomyocarditis virus, resulting in severe myocarditis. Electrocardiograms were serially recorded until nine days after virus inoculation (superacute stage, days 3 to 6; acute stage, days 7 to 9). Changes in heart rate and QRS voltages were analyzed. RESULTS: Serial electrocardiograms revealed that heart rates began to increase after day 3, and that the sum of the QRS voltages increased on day 3 and then decreased on days 7 to 9. Trivial mononuclear cell infiltrations and interstitial edema were most frequently found in mice at the superacute stage. CONCLUSIONS: Transient increase of the QRS voltages at the superacute stage of myocarditis was demonstrated, which may be due to an increase in ventricular mass caused by interstitial edema at this stage.

Relevance of inflammatory cell infiltrates for complete atrioventricular block in experimental murine myocarditis.

BACKGROUND: There are few systemic pathologic studies on myocarditis. This study aimed to clarify the pathologic characteristics of murine myocarditis. METHODS: We recorded serial electrocardiograms in experimental viral myocarditis in mice and then examined their cardiac pathology. After taking baseline electrocardiograms, we inoculated the mice intraperitoneally with the encephalomyocarditis virus. Electrocardiograms were serially recorded until 220 days after the virus inoculation. RESULTS: Serial electrocardiograms revealed ectopic beats, low voltage of the QRS complex, and the appearance of complete atrioventricular (AV) block. Corresponding myocardial lesions were found in the hearts of mice with these ectopic beats. Mononuclear cell infiltrations into the His bundle were most frequently found in mice with complete AV block. CONCLUSIONS: Inflammatory change with cellular infiltrations was the most common pathologic finding in mice with complete AV block. In clinical settings, anti-inflammatory therapy might be recommended for patients with myocarditis complicated with conduction disturbances.

Complete atrioventricular block in experimental murine myocarditis.

BACKGROUND: There were few reports on the pathological characteristics of the conduction system in myocarditis. This study was aimed to clarify the pathological characteristics of complete atrioventricular (AV) block in myocarditis. METHODS AND RESULTS: We studied serial electrocardiograms in experimental myocarditis in mice and also examined their cardiac pathology. After taking baseline electrocardiograms, mice were inoculated intraperitoneally with the encephalomyocarditis virus. Electrocardiograms were serially recorded until day 360. Serial electrocardiograms revealed the appearance of complete AV block. Myocardial lesions were found in the hearts of mice with these ectopic beats. Mononuclear cell infiltrations into the His bundle and necrotic lesions of the conduction system were found in 10.7% (18/168) of mice with complete AV block. However, 17.3% (29/168) of mice showed no evident pathological lesions except the edematous changes of AV node. CONCLUSIONS: The appearance of complete AV block in myocarditis may suggest not only significantly comparable pathological lesions of the conduction system but also the trivial edematous changes; in clinical settings, in the former case, permanent pacing therapy is necessary, and in the latter case, the disease may be transient and could be recovered from complete AV block. This study may shed light on the pathological characteristics of complete AV block in myocarditis.