Acute hypoxic pulmonary hypertension associated with right heart failure.

COPD is a cause of chronic pulmonary hypertension, with increased pressure during exacerbations. But acute right ventricular failure is very rare in this condition. We reported two cases in which exacerbation and hypoxaemia have induced an acute severe pulmonary hypertension complicated by right ventricular failure and cardiogenic shock. The supportive treatment and the correction of hypoxaemia have rapidly solved the clinical situation.

An Aspergillus myocardial abscess diagnosed by echocardiography.

This is a rare case of Aspergillus myocardial abscess in 19-year-old woman with acute lymphoblastic leukemia treated by chemotherapy. During pancytopenia she developed invasive aspergillosis with myocardial abscess. The presence of specific antigen in the pericardial effusion was diagnostic. She died despite vigorous antifungal therapy.

Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease.

Valvular heart disease, inducing valvular regurgitation, has been described in users of drugs such as anorectic agents and ergot derivates. 3,4-Methylenedioxymethamphetamine (MDMA; "ecstasy") also leads in vitro to the proliferation of cardiac valvular interstitial cells by activation of the 5-hydroxytryptamine 2B receptor. The aim of this study was to determine the occurrence of valvulopathy in young adults taking MDMA. Twenty-nine subjects using or having used MDMA and 29 gender- and age-matched controls were blindly evaluated with echocardiography. Eight subjects (28%) who took MDMA had abnormal echocardiographic results using the United States Food and Drug Administration's criteria for appetite suppressant-induced valvular heart disease, compared with none in the control group (p = 0.0045). Six (21%) subjects had mitral regurgitation of 1/4 and 4 (14%) of > or =2/4, compared with none in the control group (p = 0.002). The mean mitral regurgitant area ratios (jet/atrium) were 12 +/- 9.8% and 5 +/- 1.3%, respectively (p = 0.007). Tricuspid regurgitation > or =2/4 was present in 13 MDMA users (45%) and absent in controls (p <0.001). The mean tricuspid regurgitant area ratios were 19 +/- 9.5% and 9 +/- 4.5%, respectively (p <0.001). Four MDMA users (14%) had mild aortic regurgitation (p = 0.11). Valvular "strands" were present in 6 MDMA users (21%) and in none of the controls (p = 0.02). In conclusion, MDMA may lead to mild to moderate valvular heart disease and valvular strands.

Role of myocardial bridging in the apical localization of stress cardiomyopathy.

BACKGROUND: The apical ballooning syndrome is precipitated by emotional or physical stress but the underlying mechanism remains poorly understood. The contribution of myocardial bridging on the aetiology and the onset of the syndrome is not known. METHODS: We observed 8 patients with chest pain, T-wave inversion in several leads of the ECG, transient left ventricular apical ballooning and no significant angiographic stenosis. RESULTS: There were 7 women and I man. The median age was 67.5 years. Seven patients had an intense emotional or physical stress (87.5%). All patients presented with chest pain and aT-wave inversion in the precordial leads. The median elevation of creatine-kinase was 171 IU. In all patients, echocardiography showed an alteration of the left ventricular function with a very extensive apical akinesia. Left ventricular hypertrophy was observed in 7 patients. A myocardial bridging in the mid segment of the left anterior descending coronary artery was observed in 5 patients (62.5%). Recovery was complete in all patients. During follow-up, no patient showed recurrence. CONCLUSIONS: Our data suggest that myocardial bridging possibly enhanced by catecholamines during stress may contribute, in association with left ventricular hypertrophy, to the preferential apical localization of the apical ballooning syndrome. Further investigations are necessary to confirm