Differentiation of heart failure related to dilated cardiomyopathy and coronary artery disease using gadolinium-enhanced cardiovascular magnetic resonance.

BACKGROUND: Heart failure treatment depends partly on the underlying cause of the disease. We evaluated cardiovascular magnetic resonance (CMR) for the problem of differentiating dilated cardiomyopathy (DCM) from left ventricular (LV) dysfunction caused by coronary artery disease (CAD). METHODS AND RESULTS: Late gadolinium enhancement with CMR was performed in 90 patients with heart failure and LV systolic dysfunction (63 patients with DCM and unobstructed coronary arteries and 27 with significant CAD at angiography). We also studied 15 control subjects with no coronary risk factors and/or unobstructed coronary arteries. None (0%) of the control subjects had myocardial gadolinium enhancement; however, all patients (100%) with LV dysfunction and CAD had enhancement, which was subendocardial or transmural. In patients with DCM, there were 3 findings: no enhancement (59%); myocardial enhancement indistinguishable from the patients with CAD (13%); and patchy or longitudinal striae of midwall enhancement clearly different from the distribution in patients with CAD (28%). CONCLUSIONS: Gadolinium CMR is a powerful technique to distinguish DCM from LV dysfunction related to CAD and yields new insights in DCM. These data suggest that using the coronary angiogram as the arbiter for the presence of LV dysfunction caused by CAD could have lead to an incorrect assignment of DCM cause in 13% of patients, possibly because of coronary recanalization after infarction. The midwall myocardial enhancement in patients with DCM is similar to the fibrosis found at autopsy; it has not previously been visualized in vivo and warrants further investigation. CMR may become a useful alternative to routine coronary angiography in the diagnostic workup of DCM.

DANAMI-2: is primary angioplasty superior to thrombolysis in acute MI when the patient has to be transferred to an invasive centre?

Primary angioplasty is superior to thrombolysis in acute myocardial infarction when performed in a timely manner but the benefits are unknown when inter-hospital transfer is required for angioplasty. On the 20th March 2002 at the American College of Cardiology 51st Annual Scientific Session, the results of the Danish Multicentre Randomized Trial on Thrombolytic Therapy versus Acute Coronary Angioplasty in Acute Myocardial Infarction (DANAMI-2) were presented. 1,572 patients were randomized to front loaded tPA or angioplasty on presentation within 12 h of acute myocardial infarction; 1,129 from hospitals requiring transfer for up to 3 h for angioplasty. The trial was stopped early since there was a 40% relative reduction in the composite primary end-point of death, disabling stroke or reinfarction within 30 days (absolute reduction 13.7 to 8%, p=0.0003) with primary angioplasty. This appeared to be driven by a significant reduction of reinfarction from 6.3 to 1.6%. Ambulance transfer was shown to be safe but time to angioplasty was approximately 60 min longer than time to thrombolysis. No data are as yet available on the relative infarct sizes or left ventricular function in the two groups. The management of acute myocardial infarction is an area of missed opportunities. Patients present late to hospital, up to 30% of eligible patients do not receive reperfusion therapy and door to needle time is longer than is ideal. Whilst we await the full details of the trial and long term follow-up, we should not forget the challenges of conventional management of acute myocardial infarction.

Detection of apical hypertrophic cardiomyopathy by cardiovascular magnetic resonance in patients with non-diagnostic echocardiography.

OBJECTIVE: To investigate the role of cardiovascular magnetic resonance (CMR) in a series of patients with ECG repolarisation changes and normal echocardiography. PATIENTS AND DESIGN: 10 patients with anterolateral T wave inversion for which there was no obvious pathological cause who had normal routine echocardiography without contrast for the exclusion of hypertrophic cardiomyopathy (HCM) also had CMR that was diagnostic of apical HCM. RESULTS: Apical HCM detected by CMR could be morphologically severe with wall thickness up to 28 mm, or mild. The extent of repolarisation abnormalities did not correlate to the morphological severity. CONCLUSIONS: In patients with unexplained repolarisation abnormalities, a normal routine echocardiogram without contrast does not exclude apical HCM. Further imaging with CMR or contrast echocardiography may be required. The reliance on routine echocardiography to exclude apical HCM may have led to underreporting of this condition.