Left ventricular endocardial longitudinal dysfunction persists after acute myocarditis with preserved ejection fraction.

BACKGROUND: The aim of present study was to assess left ventricular (LV) myocardial deformation and changes over time in patients with acute myocarditis (AM) with preserved ejection fraction detected by late gadolinium enhancement (LGE) magnetic resonance imaging. METHODS: Thirty-five male patients with AM diagnoses and preserved systolic function based on cardiac magnetic resonance imaging (MRI) were prospectively enrolled. On admission, echocardiography with measurements of global and segmental longitudinal (LS) strains was performed both at the endocardial (ENDO) and epicardial (EPI) levels. Findings were compared to 25 control subjects. Twenty-six patients were also monitored over a 22-month follow-up (FU group). RESULTS: On admission, global ENDO-LS was poorer in magnitude in AM (-19.2 ± 3.1) than in controls (-24.0 ± 1.05) (P < 0.0001), whereas EPI-LS was not different (-20.6 ± 3.4 vs -19.7 ± 6 P = NS). A functional increase in magnitude in both ENDO-LS (-20.8 ± 5.4, P = NS) and EPI-LS (-22.6 ± 4.6, P = 0.02) was found in FU vs AM patients. CONCLUSIONS: The present study demonstrates a steady ENDO-LS impairment in infarct-like AM during a 2-year follow-up period, despite a preserved LV ejection fraction.

Cardiovascular maladaptation to exercise in young hypertensive patients.

BACKGROUND: Impairment of the adaptive mechanisms that increase cardiac output during exercise can translate to a reduced functional capacity. We investigated cardiovascular adaptation to exertion in asymptomatic hypertensive patients, aiming to identify the early signs of cardiac and vascular dysfunction. METHODS AND RESULTS: We enrolled 54 subjects: 30 patients (45.1±11.9years, 19 males) and 24 age-matched healthy controls (44.4±9.6years, 14 males). Speckle-tracking echocardiography (STE) and echo-tracking were performed at rest and during exertion to assess myocardial deformation and arterial stiffness. RESULTS: E/E' increased from rest to peak exercise more in patients than in controls (peak stage: p=0.024). Global longitudinal strain increased significantly from rest to peak stage in controls (p=0.011) whereas it remained unchanged in patients (p=0.777). Left atrial (LA) reservoir was significantly increased throughout the exercise only in controls (p=0.001) whereas it was almost unchanged in patients (p=0.293). LA stiffness was significantly higher in patients than in controls both at rest (p=0.023) and during exercise (p<0.001). Beta index and pulse wave velocity (PWV) increased during exercise in both groups, showing higher values in patients in each step. CONCLUSIONS: Our study showed a more pronounced maladaptation during exercise, with respect to rest, of the cardiovascular system with impaired cardiac-vessel coupling in hypertensive patients compared to healthy subjects. Exercise echocardiography implemented by STE and echo-tracking is invaluable in the early detection of these cardiovascular abnormalities.

How to Understand Patent Foramen Ovale Clinical Significance - Part II: Therapeutic Strategies in Cryptogenic Stroke.

In the first part of this review, we reminded that patent foramen ovale (PFO) is a slit or tunnel-like passage in the interatrial septum occurring in approximately 25% of the population and that a number of conditions have been linked to its presence, the most important being cryptogenic stroke (CS) and migraine. We have also shown how, in the setting of neurological events, it is not often clear whether the PFO is pathogenically-related to the index event or an incidental finding, and therefore we thought to provide some useful key points for understanding PFO clinical significance in a case by case evaluation. The controversy about PFO pathogenicity has consequently prompted a paradigm shift of research interest from medical therapy with antiplatelets or anticoagulants to percutaneous transcatheter closure, in secondary prevention. Observational data and meta-analysis of observational studies previously suggested that PFO closure with a device was a safe procedure with a low recurrence rate of stroke, as compared to medical therapy. However, so far, published randomized controlled trials (CLOSURE I®, RESPECT® and PC Trial®) have not shown the superiority of PFO closure over medical therapy. Thus, the optimal strategy for secondary prevention of paradoxical embolism in patients with a PFO remains unclear. Moreover, the latest guidelines for the prevention on stroke restricted indications for PFO closure to patients with deep vein thrombosis and high-risk of its recurrence. Given these recent data, in the second part of the present review, we aim to discuss today treatment options in patients with PFO and CS, providing an updating on patients' management.

Extension to the Heart of Metastatic Lung Cancer Presenting as Acute Neurological Syndrome: The Key Role of Echocardiography.

Metastatic cardiac malignancies are significantly more common than primary cardiac tumors. Primary lung cancers often invade the heart locally and they can also spread to the heart via the blood, lymphatic system or both; in contrast, an extension to the left atrium from the pulmonary vein is very rare. Here, we report a case of a 79-year-old man with an acute neurological syndrome, in which an integrated multimodality imaging approach has allowed to discovery a lung cancer with cerebral embolism and intracavitary heart dissemination through the left superior pulmonary vein.

How to Understand Patent Foramen Ovale Clinical Significance: Part I.

Patent foramen ovale (PFO) is a remnant of fetal circulation commonly found in healthy population. However, a large number of clinical conditions have been linked to PFO, the most important being ischemic strokes of undetermined cause (cryptogenic strokes) and migraine, especially migraine with aura. Coexistent atrial septal aneurysm, size of PFO, degree of the shunt, shunt at rest, pelvic deep vein thrombosis, and prothrombotic states (G20210A prothrombin gene mutation, Factor V Leiden mutation, MTHFR: C677T, basal homocystine, recent surgery, trauma, or use of contraceptives) could enhance stroke risk in subjects with PFO. Owing to the complexity of this issue, for any individual presenting with a PFO, particularly in the setting of cryptogenic stroke, it is not clear whether the PFO is pathogenically related to the neurological event or an incidental finding. Thus, a heart-brain team, which individually plans the best strategy, in accordance with neuroimaging findings and anatomical characteristics of PFO, is strongly recommended. In the first part of this review, we discuss the embryologic and anatomic features of PFO, the diagnostic techniques for its identification and evaluation, and the relationship between PFO and neurological syndromes. A special attention is made to provide some key points, useful in a daily clinical practice, which summarize how better we understand PFO clinical significance.

In patients with post-infarction left ventricular dysfunction, how does impaired basal rotation affect chronic ischemic mitral regurgitation?

BACKGROUND: The aim of this study was to explore the contribution of left ventricular (LV) basal rotation to the mechanism of chronic ischemic mitral regurgitation (MR). METHODS: Fifty-seven patients (52 men; mean age, 68.3 ± 11.8 years) with postinfarction LV dysfunction (defined as an ejection fraction ≤ 45%) were prospectively enrolled. Each invariably had functional MR. To assess MR degree, the effective regurgitant orifice area (EROA) was quantified by echocardiography using the proximal isovelocity surface area method. Furthermore, mitral valve deformation (valve tenting and annular function) and LV global (systolic and diastolic volumes, function, and sphericity) and local remodeling (displacement of papillary muscles, regional strain, and rotation by speckle-tracking) were assessed. The patients were subsequently subdivided into two groups according to the absence (group A) or presence (group B) on transthoracic echocardiography of infarct area in the inferior and/or posterior basal segments. RESULTS: A larger EROA was found in group B than in group A (P = .034) and in subjects with asymmetric rather than symmetric tethering in either group (P = .036 and P = .040 for groups A and B, respectively). Basal radial (P = .009), circumferential (P = .042), and longitudinal (P = .005) strain and rotation (P = .021) were lower in group B than in group A. There was also a significant inverse correlation between EROA and basal rotation in group B (r = -0.75, P < .001). Furthermore, using multivariate linear regression analysis, we found that the independent determinants of EROA were end-diastolic volume (P < .001) and tenting area (P = .004) in group A and asymmetric tethering (P = .029) and basal rotation (P < .001) in group B. CONCLUSIONS: Impaired basal rotational mechanics occurring after an inferior-posterior myocardial infarction is associated with increased MR.

Perinatal asphyxia and cardiac abnormalities.

The most common etiologies of myocardial infarction in the perinatal period are congenital heart disease, coronary artery lesions, thromboembolism and perinatal asphyxia. Cardiac abnormalities in perinatal asphyxia include tricuspid regurgitation and mitral regurgitation associated with transient myocardial ischemia of the newborn. Patent foramen ovale is a frequent remnant of the fetal circulation. Persistent hypoxia sometimes causes pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. We describe a case of tricuspid regurgitation, mitral regurgitation, and patent foramen ovale in a 15-day-old newborn male infant with a history of perinatal asphyxia. Also this case focuses attention on the perinatal asphyxia.