Myocardial delayed enhancement in patients with pulmonary hypertension and right ventricular failure: evaluation by cardiac MRI.

In this study, we evaluated patients with pulmonary arterial hypertension (PAH) and impaired right ventricular function. We used cardiac MRI for the detection of myocardial delayed enhancement (MDE) and its possible association with other clinical variables. 20 patients (6 males and 14 females, aged 44.5+/-11 years; 15 New York Heart Association class III, 5 class IV) with known PAH (13 idiopathic, 7 resulting from chronic pulmonary embolism) were evaluated for the detection of MDE. Short-axis cine images of the heart were made for ventricular function assessment using a steady-state free precession sequence. For MDE evaluation, a short-axis phase-sensitive inversion recovery sequence was performed 10 min after intravenous administration of 0.2 mmol kg(-1) gadodiamide. Right ventricle (RV) systolic dysfunction, RV enlargement and RV hypertrophy were present in 20 patients (RV ejection fraction, 21.5+/-7.2%; RV diastolic diameter, 5.97+/-0.79 cm; RV wall thickness, 0.73+/-0.10 cm). 13 of the 20 patients (65%) were positive for MDE (10 anterior, 12 inferior). All 13 positive patients with MDE demonstrated small hyperintense areas at the insertion points of the RV free wall in the interventricular septum. We found no significant correlation between MDE and ejection fraction or other haemodynamic variables. In this study, MDE correlated positively only with the duration of disease. We found that septal MDE can be present in patients with PAH and impaired ventricular function. However, further studies are necessary to investigate this possible association and its prognostic implication.

Case report. Isolated left ventricular myocardium non-compaction: MR imaging findings from three cases.

The purpose of this study is to report three cases of left ventricular myocardium non-compaction (LVNC), with emphasis on the MRI findings. From May 2006 to February 2007, three patients -- 2 females (6 years and 42 years of age) and 1 male (18 years of age) -- presented to our radiology department, two of them with fatigue, shortness of breath and episodes of syncope and arrhythmia, for further investigation by cardiac MRI because an apparent asymmetrical pattern of hypertrophy of the left ventricular myocardium was suspected by transthoracic echocardiography. The 18-year-old patient was only experiencing arrhythmia, and arrhythmogenic right ventricular dysplasia was suspected. The images (produced by a 1.5T MRI system) were interpreted by two experienced radiologists and post-processed with Argus software (Siemens, Germany) for ejection fraction calculation. In all three patients, MRI aided in the correct identification of prominent ventricular myocardial trabeculations and deep intertrabecular recesses communicating with the ventricular cavity, as well as areas of hypokinesia with depressed systolic function, and showed the absence of myocardial delayed enhancement and other structural heart defects. In conclusion, cardiac MRI was useful for correctly identifying this rare congenital heart disorder and appears to increase diagnostic accuracy. Although considered a rare anomaly, radiologists should be capable of recognizing LVNC, as current non-invasive imaging methods have increased the frequency of this diagnosis and timely detection is vital in considering early-stage transplantation.

Cholinergic stimulation with pyridostigmine, hemodynamic and echocardiographic analysis in healthy subjects.

OBJECTIVE: Growing evidence suggests that sudden death after an acute myocardial infarction (AMI) correlates with autonomic nervous system imbalance. Parasympathomimetic drugs have been tested to reverse these changes. However, their effects on ventricular function need specific evaluation. Our objective was to analyze pyridostigmine's (PYR) effect on hemodynamic and echocardiographic variables of ventricular function. METHODS: Twenty healthy volunteers underwent Doppler echocardiographic evaluations, blood pressure (BP), and heart rate (HR) assessment at rest, before and 120 min after ingestion of 30 mg PYR or placebo, according to a double-blind, placebo-controlled, crossed and randomized protocol, on different days. RESULTS: PYR was well tolerated and did not cause alterations in BP or in ventricular systolic function. A reduction in HR of 10.9 +/- 1.3% occurred (p < 0.00001). There was an A wave reduction in the mitral flow (p < 0.01) and an E/A ratio increase (p < 0.001) without changes in the other diastolic function parameters (p > 0.05). CONCLUSION: PYR reduces HR and increases E/A ratio, without hemodynamic impairment or ventricular function change.