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Objectives: The purpose of this study was to assess whether medical management may alter the severity of functional mitral regurgitation (FMR) and its prognosis in patients who have heart failure with reduced ejection fraction (HFrEF)., Background: FMR in patients who have HFrEF is associated with a worse prognosis. It is uncertain to what extent medical management may alter the severity of FMR and its prognosis., Methods: The extent of FMR was assessed at baseline and after a median follow-up period of 50 months in 163 consecutive HFrEF patients (left ventricular ejection fraction <40%). Severe FMR was defined as mitral regurgitation (MR) grade 3-4. All of the patients received the maximal tolerable doses of their heart failure (HF) medications. Major adverse cardiac events were defined as a composite of all-cause death and the need for heart transplantation or hospitalization for HF and/or malignant arrhythmias., Results: A total of 50 (31%) patients had severe MR at baseline. During the follow-up period, 38% of the severe FMR patients showed an improvement to nonsevere FMR (MR grade <3), whereas 18% of the nonsevere FMR patients developed severe FMR despite optimal HF treatment. Cox regression analysis revealed that the presence of sustained severe FMR or worsening of FMR was the most important independent prognostic determinant with an adjusted odds ratio of 2.5 (95% confidence interval: 1.5 to 4.3, major adverse cardiac events 83% vs. 43%). In addition, those patients showed a 13% increase in left ventricular end-diastolic volume index (LVEDVI), whereas the patients with improvement in their severe MR showed a 2% decrease in LVEDVI (p = 0.01)., Conclusions: Severe FMR was successfully treated with medication in almost 40% and was associated with prevention of left ventricular adverse remodeling and with an improved long-term prognosis., (Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: To contribute to the protocol development of exercise training in LVAD supported patients by reviewing the exercise programs for those patients in the ESC affiliated countries., Methods: A subset of data from 77 (26 countries) LVAD implanting centers that participated in the Extra-HF survey (170 centers) was analyzed., Results: Of the 77 LVAD implanting centers, 45 (58%) reported to have a functioning exercise training program (ETP) for LVAD patients. In 21 (47%) of the 45 ETP programs in LVAD implanting centers, patients begin their ETP during their in-hospital post-operative recovery period. Most centers (71%) have an early post-discharge program for their patients, and 24% of the centers offer a long-term maintenance program. The professionals involved in the ETPs are mainly physiotherapists (73%), psychologists, cardiac rehab nurses (22%), or cardiologists specialized in rehabilitation (22%). Not all programs include the treating cardiologist or surgeons. Most of the ETPs (84%) include aerobic endurance training, mostly cycling (73%), or walking (62%) at low intensity intervals. Some programs apply resistance training (47%), respiratory muscle training (55%), or balance training (44%). Reasons for the absence of ETPs are referral of patients to another center (14 centers) and lack of resources (11 centers)., Conclusion: There is a great variance in ETPs in LVAD implanting centers. Not all the implanting centers have an ETP, and those that do have adopted a local protocol. Clear guidance on ETP supplied by LVAD implanting centers to LVAD supported patients and more evidence for optimal modalities are needed., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Because of the current donor shortage, organ selection criteria are being progressively liberalized. We present a case of carbon monoxide poisoning in a multiorgan donor that led to primary cardiac allograft failure. A biventricular assist device was used as a bridge to recovery.

This report describes the diagnostic difficulty encountered in a young female patient presenting with neurologic symptoms, atrial fibrillation and severe left ventricular systolic dysfunction, eventually leading to cardiac transplantation. The scrutiny used in the evaluation of the particular aspect of the left ventricle, and the integration of the information obtained from echocardiography, angiography and magnetic resonance imaging, led to the diagnosis of a rare and mostly unknown cause of cardiac failure. The correct identification of this entity is mandatory because enhanced risk of thromboembolism and malignant arrhythmia should be anticipated. A review of the literature revealed only 6 patients in whom isolated non-compaction of the left ventricle was treated by heart transplantation.

This case report describes the devastating consequences of spontaneous coronary dissection in a 36-year-old female patient. Surgical revascularization was attempted, but diffuse myocardial infarction developed. The patient was bridged to heart transplantation but died secondary to multiple organ failure. To our knowledge, this is the only reported case of spontaneous dissection of the three main coronary arteries due to severe cystic medial necrosis.

We report a patient in whom presumed vasospasm of an angiographically normal coronary artery led to severe transmural myocardial ischemia. To our knowledge, this is the first case in which an allergic reaction to locally applied chlorhexidine caused such a severe reaction.

Pulmonary vascular reactivity was assessed during diagnostic heart catheterization in two patients with pulmonary hypertension unexplained by pulmonary or cardiac disease and in five patients with atypical chest pain and normal coronary arteriograms. Acetylcholine, an endothelium-dependent vasodilator that also has a direct contracting effect on vascular smooth muscle cells, was infused in the right atrium in a step-wise increasing dose in order to obtain final blood concentrations in the pulmonary circulation ranging from 10(-6) mol/L to 10(-4) mol/L. In the five control patients, acetylcholine induced a dose-related decrease of pulmonary vascular resistance (-52 percent +/- 9 percent). In the patients with primary pulmonary arterial hypertension, however, acetylcholine caused a paradoxic increase of pulmonary arterial pressure and of pulmonary vascular resistance. Thus, it appears that endothelium-dependent vasodilation is impaired in the pulmonary circulation of patients with primary pulmonary arterial hypertension. Endothelial dysfunction in the pulmonary circulation may play a role in the pathophysiology of this disease.

The findings in a 40-year-old man with Kartagener's triad (sinusitis, bronchiectasis, and situs inversus) and corrected transposition of the great vessels are presented. Electron microscopy revealed normal ultrastructure of the axoneme in both respiratory cilia and sperm tails. Light microscopic evaluation of the spermatozoa showed 50 percent motility, suggesting normal fertility. This assumption is confirmed, as the patient has two children. We suggest that an abnormal, uncoordinated motility pattern of the ultrastructurally normal respiratory cilia results in improper mucociliary clearance. This coordination is not needed in swimming spermatozoa, which could explain the apparent paradox between bronchopulmonary symptoms and normal fertility in our patient.