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Localized left ventricular aneurysms with normal global function caused by myocarditis.
Left ventricular (LV) aneurysms usually result from coronary artery disease but may also occur in congenital,1 traumatic2,3 or infective heart diseases. LV aneurysms of infective origin are most often caused by Chagas's disease4 and infective endocarditis. Regional wall motion abnormalities have been occasionally observed during viral myocarditis.5 More recently Goudevenous et al6 reported a case of LV aneurysm during Coxsackie B4 virus infection but without histologic evidence of myocarditis. This study reports 2 cases of severe lymphocytic myocarditis presenting with ventricular tachycardia and LV aneurysm
Global biventricular dysfunction in patients with asymptomatic coronary artery disease may be caused by myocarditis
BACKGROUND: The causal role of asymptomatic critical coronary artery obstruction in patients presenting with severe global biventricular dysfunction but no evidence of myocardial infarction is uncertain. METHODS AND RESULTS: Among 291 patients aged >40 years undergoing a noninvasive (2-dimensional echocardiography) and invasive (catheterization, coronary angiography, and biventricular endomyocardial biopsy, 6 to 8 samples/patient) cardiac study because of progressive heart failure (New York Heart Association functional class III or IV) with global biventricular dysfunction and no history of myocardial ischemic events, 7 patients (2.4%; 7 men; mean age, 49+/-6.9 years) had severe coronary artery disease (3 vessels in 4 patients; 2 vessels in 1 patient, proximal occlusion of left anterior descending coronary artery in 2 patients). Left ventricular end-diastolic diameter and ejection fraction by 2-dimensional echocardiography were 73+/-10.5 mm and 23+/-6.5%, respectively, and right ventricular end-diastolic diameter and ejection fraction were 39+/-7 mm and 29+/-7.2%, respectively. Biopsy specimens showed extensive lymphocytic infiltrates with focal myocytolysis meeting the Dallas criteria for myocarditis in all patients (in 5 patients with and 2 patients without fibrosis). Cardiac autoantibodies were detected with indirect immunofluorescence in the serum of 2 patients with active myocarditis. The 2 patients with active inflammation received prednisone (1 mg. kg-1. d-1 for 4 weeks followed by 0.33 mg. kg-1. d-1 for 5 months) and azathioprine (2 mg. kg-1. d-1 for 5 months) in addition to conventional drug therapy for heart failure. At 8-month overall follow-up, cardiac volume and function improved considerably in immunosuppressed patients but remained unchanged in conventionally treated patients, of whom 1 died. CONCLUSIONS: Global biventricular dysfunction in patients with severe asymptomatic coronary artery disease and no evidence of previous myocardial infarction may be caused by myocarditis. Histologic findings may influence the treatment
Histologically proven myocarditis in patients with biventricular dysfunction and severe asymptomatic coronary artery disease.
The aim of our study was to investigate the pathogenesis of the global biventricular dysfunction observed in patients with critical coronary artery stenosis, but no evidence of myocardial ischemia or infarction. From January 1992 to January 1997, among consecutive patients undergoing invasive cardiac study including biventricular endomyocardial biopsy because of progressive heart failure (NYHA functional class III-IV) associated with biventricular dysfunction and no history of myocardial ischemic events, 7 patients had severe coronary artery disease (three vessel 4 patients; two vessel 1 patient, proximal occlusion of left anterior descending artery 2 patients). At two-dimensional echocardiography left and right ventricular end-diastolic diameter were 73 +/- 10.5 and 39 +/- 7 mm, respectively, left ventricular ejection fraction was 0.23 +/- 6.5 and right ventricular ejection fraction was 0.29 +/- 7.2. Histology showed extensive lymphocytic infiltrates with focal myocytolysis meeting the Dallas criteria for myocarditis in all patients. Two patients with active inflammation received prednisone and azathioprine in addition to conventional drug therapy for heart failure. At 6-month follow-up cardiac volume and function improved in immunosuppressed patients (left ventricular ejection fraction from 15 to 50% and from 20 to 38%, respectively) while they remained unchanged in conventionally treated patients. In conclusion, global biventricular dysfunction in patients with severe asymptomatic coronary artery disease and no evidence of previous myocardial infarction may be caused by myocarditis rather than by myocardial ischemia or hibernation
Psychological distress resulting from a mosaic of psycho-social variables as a risk factor for acute coronary syndromes
Brain natriuretic peptide in hypertrophic cardiomyopathy with and without systolic dysfunction
Young Survisors of apparently idiopathic cardiac arrest : results of bi-ventricular endomyocardial biopsy and specific treatment and meadle term follow-up.
[Psychological stress as precipitating factor of the acute manifestations of ischemic cardiopathy].
Psychological stress may play an important role as a risk factor for coronary heart disease (CHD). Psychological stress consists of different components whose diverse role in the onset of the acute manifestations of CHD is still not clear. We studied 80 patients with acute CHD (56 with unheralded myocardial infarction, 24 with unstable angina, mean age 55 +/- 9 years, 55 men) vs 80 controls (mean age 50 +/- 9 years, 52 men) admitted for an acute traumatic event. We proposed to both groups these questionnaires: a retrospective self and etero-evaluation of the degree of psychological stress; the modified Maastricht questionnaire (MMQ) that evaluates psychic and physical manifestations of psychological stress in the period preceding admission; the social support questionnaire (SSQ); the life event assessment that evaluates frequency and importance of life events in the year preceding admission. Psychological stress index was greater in patients (self-evaluation = 7.1 +/- 2.4; etero-evaluation = 7.4 +/- 2.3; MMQ = 91 +/- 30.8) than controls (self-evaluation = 4.3 +/- 2.3; etero-evaluation = 4.3 +/- 2.4; MMQ = 58.6 +/- 32.5; p < 0.001 for all questionnaires). The perception of strong social isolation was greater in patients (SSQ = 29.8 +/- 11.8) than controls (SSQ = 23.8 +/- 9.6; p < 0.001). Painful life events were more numerous in patients (10.7 +/- 2.3) than controls (8.2 +/- 3.4; p < 0.05) and perceived in a more negative way (patients = 12.7 +/- 4.1 vs controls = 10.2 +/- 3.8; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS
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