Coronary vasospasm as the underlying cause for chest pain in patients with PVB19 myocarditis.

OBJECTIVE: To evaluate the incidence of coronary vasospasm as a possible pathophysiological mechanism causing chest pain symptoms in patients with clinically suspected myocarditis. DESIGN AND SETTING: Prospective study in a teaching hospital. PATIENTS: 85 patients who presented at hospital with atypical chest pain and demonstrated clinical signs suggestive of myocarditis. MAIN OUTCOME MEASURES: Incidence of coronary vasospasm demonstrated by intracoronary acetylcholine (ACh) testing. METHODS: The combined procedure of intracoronary ACh testing and endomyocardial biopsy (EMB) was performed after ruling out significant coronary artery disease (CAD). EMBs were analysed for myocardial inflammation by immunohistological methods and for virus genome persistence. RESULTS: Pathological biopsy results, including myocardial inflammation or detection of viral genomes, or both, were found in 55 (64.7%) patients while 30 (35.3%) patients showed neither cardiac inflammation nor viral genomes and were defined as the control group. Coronary vasospasm was demonstrated in 39/55 (70.9%) patients with pathological results compared with only 12/30 (40.0%) with normal biopsy results (p = 0.01). Patients with isolated PVB19 infection (n = 22) demonstrated a significantly higher incidence of coronary vasospasm than both those with isolated HHV6 infection (86.4% vs 46.7%; p = 0.025) and those with normal biopsy results (86.4% vs 40.0%; p<0.001). Univariate and multivariate logistic regression analysis showed that only PVB19 infection was independently correlated with coronary vasospasm (OR = 4.9, 95% CI 1.56 to 15.28, p = 0.006). CONCLUSIONS: Coronary vasospasm is one of the main reasons for atypical chest pain in patients with clinical signs of myocarditis and biopsy-proven PVB19 myocarditis in the absence of significant CAD.

Cardiac magnetic resonance in myocardial disease.

For a number of patients it is difficult to diagnose the cause of cardiac disease. In such patients cardiac magnetic resonance is useful for helping to make a differential diagnosis between ischaemic and dilated cardiomyopathy; identifying patients with myocarditis; diagnosing cardiac involvement in sarcoidosis and Chagas' disease; identifying patients with unusual forms of hypertrophic cardiomyopathy and those with continuing myocardial damage; and defining the sequelae of ablation treatment for hypertrophic obstructive cardiomyopathy.

Transient left ventricular dysfunction with apical ballooning (tako-tsubo cardiomyopathy) in Germany.

AIMS: A peculiar type of an acute coronary syndrome is characterised by acute onset of chest pain, STsegment changes, elevated troponin I levels and a transient balloon-like apical left ventricular dysfunction, but without significant coronary artery disease. We sought to assess this syndrome in German patients. METHODS AND RESULTS: A total of 22 females and 1 male with acute transient left ventricular dysfunction were identified during an interval of 2 years and were investigated clinically and angiographically. All patients presented without obstructive coronary artery disease. In 16 patients (70%) ST-segment elevations were observed mimicking acute myocardial infarction, whereas the remaining patients (30%) revealed only negative T waves. Deep negative Twaves were characteristically seen during the course of recovery in all patients. Elevated troponin I levels>2.0 microg/l (upper level of normal) were measured in all patients (mean 18+/-26.5 microg/l, range from 2.2-135.7 microg/l). Creatine kinase rose up to a mean of 282+/-236 IU/l (upper level of normal 180 U/l). Emotional or physical stress situations associated with the onset of the symptoms were observed in 16 patients (70%). Other suspected trigger factors were gastrointestinal infection and in one case a surgical intervention. In four patients a trigger factor could not be identified. Left ventriculography showed an ejection fraction of 53+/-15%. After an interval of 7+/-2 days after the first angiogram, ejection fraction had increased from 48+/-11% to 64+/-11% in eight controlled patients by repeated ventriculography. Coronary spasm with a lumen reduction>75% could be provoked using acetylcholine in 10 of 17 tested patients (59%) with reproduction of the symptoms. Within 14 days the LV dysfunction returned to normal in all patients. The ECG abnormalities disappeared completely as early as 3 months (74%) and were not seen in any patient after 6 months. CONCLUSION: Tako-tsubo cardiomyopathy is not exclusively a Japanese or Northern American phenomenon. Despite increased patient reports the exact underlying cause and pathophysiology of this syndrome remain unclear. However, despite the initial dramatic presentation of this disease the prognosis is good.

New non-invasive approaches for the diagnosis of cardiomyopathy: magnetic resonance imaging.

Cardiac magnetic resonance imaging (CMR) permits a detailed look at the myocardium in patients with recent onset heart failure. Late-enhancement CMR provides information that is similar to that obtained by the naked eye of a pathologist. Myocardial scarring is endocardial in myocardial infarction, but it is epicardial in myocarditis and intramyocardial in hypertrophic cardiomyopathy. Thus, the distinction between these entities is possible by depicting scar via late-enhancement CMR and observing myocardial function by cine magnetic resonance imaging. Moreover, non-invasive follow-up--and hence observation of the healing or remodelling process--can be achieved using CMR. New CMR pulse sequences also permit depiction of myocardial oedema, which may occur early in patients with myocarditis and may be the only sign of the disease in the absence of necrosis. It is anticipated that cardiac MRI will become a standard diagnostic technique in patients with new onset of heart failure, left-ventricular hypertrophy or clinical symptoms suggestive of myocarditis.

Evaluation of aortic stenosis by cardiovascular magnetic resonance imaging: comparison with established routine clinical techniques.

OBJECTIVE: To evaluate whether direct planimetry of aortic valve area (AVA) by cardiac magnetic resonance (CMR) imaging is a reliable tool for determining the severity of aortic stenosis compared with transthoracic echocardiography (TTE), transoesophageal echocardiography (TOE), and cardiac catheterisation. METHODS: 44 symptomatic patients with severe aortic stenosis were studied. By cardiac catheterisation AVA was calculated by the Gorlin equation. AVA was measured with CMR from steady state free precession (true fast imaging with steady state precession) by planimetry. AVA was also determined from TOE images by planimetry and from TTE images by the continuity equation. RESULTS: Bland-Altman analysis evaluating intraobserver and interobserver variability showed a very small bias for both (-0.016 and 0.019, respectively; n = 20). Bias and limits of agreement between CMR and TTE were 0.05 (-0.35, 0.44) cm2 (n = 37), between CMR and TOE 0.02 (-0.39, 0.42) cm2 (n = 32), and between CMR and cardiac catheterisation 0.09 (-0.30, 0.47) cm2 (n = 36). The sensitivity and specificity of CMR to detect AVA < or = 0.80 cm2 measured by cardiac catheterisation was 78% and 89%, of TOE 70% and 70%, and of TTE 74% and 67%, respectively. CONCLUSION: CMR planimetry is highly reliable and reproducible. Further, CMR planimetry had the best sensitivity and specificity of all non-invasive methods for detecting severe aortic stenosis in comparison with cardiac catheterisation. Therefore, CMR planimetry of AVA with steady state free precession is a new powerful diagnostic tool, particularly for patients with uncertain or discrepant findings by other modalities.