The present study reveals a novel genetic susceptibility locus that clearly underlines the role of genetically driven, inflammatory processes in the pathogenesis of idiopathic DCM.

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Spontaneous coronary artery dissection is a rare cause of ischemic heart disease. Incidence, etiology and optimal treatment are ill-defined. Between July 1995 and December 1997, we prospectively identified 42 patients (36 men, six women, mean age 59 +/- 12 years) with spontaneous coronary artery dissection among 3803 consecutive angiographic examinations in which the diagnosis of coronary artery disease was established for the first time (incidence 1.1%). In comparison to the remaining study population with stable angina pectoris (8 cases of spontaneous coronary artery dissection among 2852 patients; incidence: 0.3%), the incidence of spontaneous coronary artery dissection was significantly higher in the patient subgroups with acute myocardial infarction (13/450; 2.9%) and with unstable angina pectoris or postinfarction angina (21/501; 4.2%). Dissection was most frequently located in the left anterior descending coronary artery (19 cases), followed by the right coronary artery (15 cases) and the left circumflex coronary artery (8 cases). Because of an ambiguous angiographic lesion appearance intravascular ultrasound imaging was performed in 13 patients to confirm the diagnosis. The presumed etiology of spontaneous coronary artery dissection was atherosclerotic plaque rupture in 35 cases, heavy physical exercise in four cases and hormonal influences related to pregnancy and contraception in one case. In two cases, no obvious risk factor could be identified. Therapy consisted of intracoronary stenting in 24 patients (including ten patients with acute myocardial infarction), coronary artery bypass grafting (CABG) in 8 patients and balloon angioplasty (PTCA) in seven patients. Three patients were treated conservatively. During a mean follow-up period of 13.5 +/- 9.9 months, two patients died and 31 patients remained entirely asymptomatic, including all patients who were treated with CABG. Restenosis developed in three patients after stent implantation (restenosis rate: 12.5%). Following primary PTCA, spontaneous coronary artery dissection recurred in two patients, one of whom subsequently died.

ObjectiveTo evaluate the role of MRI in diagnosing acute myocarditis by correlation with immunohistological parameters.MethodsA total of 131 patients (85 men, 46 women; mean age, 44.9 years) with suspected acute myocarditis were examined by MRI. The relative water content of the left ventricular myocardium as well as relative and late enhancement was correlated with the immunohistological results in biopsy specimens.ResultsMyocardial inflammation was confirmed by immunohistology in 82 of the 131 patients investigated and ruled out in 49 patients. The sensitivity, specificity and accuracy for diagnosing myocarditis in patients with immunohistologically proven disease were 48.8%, 73.8% and 57.3%, respectively, for relative enhancement, 58.3%, 57.1% and 57.9% for relative water content, and 30.6%, 88.1% and 49.6% for late enhancement. A combination of all three parameters had 39,3% sensitivity and 91,3% specificity and 62,7% accuracy. Relative enhancement and late enhancement significantly correlated with the presence of myocarditis but relative oedema did not.ConclusionRelative and late enhancement significantly correlate with the presence of myocarditis, while there is no significant correlation for relative oedema. Myocarditis cannot be reliably diagnosed using any of the three MRI parameters alone but combinations of parameters will improve specificity.

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