Successful management of harlequin syndrome due to pulmonary hemorrhage and atelectasis with VAV- ECMO.

INTRODUCTION: Pulmonary hemorrhage is a life-threatening complication of VA-ECMO occasionally presenting with Harlequin syndrome. CASE REPORT: We present a case of a VA-ECMO patient complicated with pulmonary hemorrhage, complete right lung atelectasis and differential hypoxia refractory to conventional treatment including optimal mechanical ventilation and bronchoscopy interventions. Patient was successfully managed by conversion of VA to VAV-ECMO. DISCUSSION: Pulmonary hemorrhage and atelectasis treatment in a VA-ECMO patient includes transfusion, hold and reversal of anticoagulation, bronchoscopy interventions and optimization of VA-ECMO and ventilator support. Differential hypoxia may ensue due to residual native cardiac function. If refractory to conservative treatment, a VAV-ECMO configuration may be utilized to improve upper body oxygenation by inserting an additional cannula to the superior vena cava. CONCLUSION: VAV-ECMO is an ECMO configuration support in patients at risk of Harlequin syndrome presenting with pulmonary hemorrhage.

Transthoracic Doppler echocardiography assessment of left anterior descending artery flow in patients with previous anterior myocardial infarction.

AIM: We tested the hypothesis that shortening of diastolic pressure half time (PHT) of left anterior descending (LAD) coronary flow in patients with old reperfused anterior myocardial infarction (MI) is related to the presence of permanent myocardial damage of the reperfused area. METHODS AND RESULTS: We studied 49 patients divided into: group A: 15 patients with previous anterior MI and evidence of myocardial scar; group B: 10 patients with previous anterior MI and no evidence of myocardial scar and group C: 24 patients without anterior MI. All patients underwent coronary angiography at least 6 months after an index event and any reperfusion procedure. Group A patients had lower PHT (199 +/- 62 ms) than group C (377 +/- 103 ms, p = 0.0001) and group B (316 +/- 154 ms, p = 0.029) patients. No other LAD flow velocity parameter differed among the 3 groups. A PHT value of 265 ms discriminated patients with scarred anterior wall with a sensitivity of 79% and a specificity of 94% (0.88, p < 0.001). CONCLUSION: Shortening of the LAD flow diastolic PHT in patients with remote, reperfused anterior MI reflects scarred myocardial tissue in the anteroapical wall while patients who maintain diastolic wall thickness after an acute coronary syndrome have PHT similar to patients without anterior MI.

Cardiac resynchronization therapy decreases the mitral coaptation point displacement in heart failure patients.

BACKGROUND: In patients with left ventricular (LV) dysfunction the mitral leaflet coaptation point (CPMA) is displaced towards the LV apex. The aim of our study was to estimate the value of CPMA measurement as a simple index regarding the acute effects of cardiac resynchronization therapy (CRT), which is coming to be an established method of treatment for congestive heart failure (CHF). METHODS: We studied 20 patients with CHF (NYHA III-IV) and LV ejection fraction (LVEF) 22 +/- 4%. All patients received CRT and an echocardiogram was performed within 24-48 hours. The echocardiographic indices LV end-diastolic diameter (LVEDD) and end-systolic diameter (LVESD), LVEF, mitral annulus diameter (MAD), and the degree of intraventricular desynchronization, were measured at CRT off and CRT on. The CPMA, the distance between the coaptation point of the mitral leaflets and the mitral annulus, was measured from the apical 4-chamber view in end-systole at both CRT on and CRT off. RESULTS: CRT improved both the contractility and dimensional indices in CHF patients. CPMA decreased from 11.3 +/- 2 mm at CRT off to 9.1 +/- 1.8 mm after CRT on (p < 0.001) and MAD from 38.9 +/- 3.9 mm at CRT off to 37.5 +/- 3.7 mm at CRT on (p < 0.002). LVEF improved from 24.5 +/- 5.7% at CRT off to 29.5 +/- 5.1% at CRT on (p < 0.001). There was an improvement in LV synchronization from 88 +/- 7 ms at CRT off to 48 +/- 3 ms at CRT on (p < .001). CPMA was correlated with MAD (r = 0.52, p < 0.05 and r = 0.59, p < 0.05 at CRT off and CRT on, respectively). Moreover, the absolute change in CPMA was correlated with LVESD (r = 0.68) and LVEDD (r = 0.65), both p < 0.05, with the time difference of the basal segments of the septal and lateral wall at CRT on (r = 0.68, p < 0.01), and inversely correlated with LVEF (r = -0.55, p < 0.05). CONCLUSION: In patients with severe LV systolic dysfunction and dilatation CRT was associated with an improvement in both CPMA and MAD.