Improved diastolic function in type 2 diabetes after a six month liraglutide treatment

AbstractAimsTo investigate whether liraglutide improves diastolic function in type 2 diabetes.MethodsThirty-seven patients with type 2 diabetes who began liraglutide therapy between June 2013 and May 2014 were enrolled in this observational, prospective study. 26 patients received liraglutide therapy for at least 6months. The remaining 11 patients withdrew from liraglutide therapy during the first month, were started on other hypoglycaemic therapies and formed the control group. Anthropometric, metabolic and echocardiographic parameters including pulsed wave tissue Doppler imaging were evaluated at baseline and at 6months.ResultsIn the liraglutide group the early diastolic mitral annulus velocity on the lateral (e-lat) and medial (e-med) sides of the mitral annulus increased from 9.2±3.4 to 11.6±4.7cm/s (p<0.001) and from 6.9±1.7 to 8.4±2.6cm/s (p<0.003), respectively. The ratio of early-to-late velocities on the lateral and medial sides of the mitral annulus increased from 0.7±0.3 to 0.9±0.4 (p<0.001) and from 0.5±0.1 to 0.6±0.1 (p<0.02), respectively. The ratio of early diastolic mitral inflow velocity to early diastolic myocardial relaxation velocity decreased from 10.7±4.3 to 8.5±2.5 (p<0.005). No improvements in diastolic function was detected in the control group. Glucose control improved similarly in both groups: HA1bc −1.5% (−17mmol/mol) vs −1.3% (−14mmol/mol), p=0.67.ConclusionsIn patients with type 2 diabetes, 6months liraglutide treatment was associated with a significant improvement in diastolic function

Case Report: An Unusual Case of Biventricular Thrombosis in a COVID-19 Patient With Ischemic Dilated Cardiomyopathy Assessment of Mass Mobility and Embolic Risk by Tissue Doppler Imaging

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein binds to angiotensin-converting enzyme 2 (ACE2) receptor on vascular cells. As a consequence, patients with COVID-19 have an increased incidence of thromboembolic complications of the SARS-CoV-2 infection and subsequent endothelial cell damage with consequence of development of systemic vasculitis and diffuse intravascular coagulation. The present case describes a COVID-19 female patient with ischemic dilated cardiomyopathy, who presented with congestive heart failure and echocardiographic evidence of biventricular apical thrombi. The peak antegrade longitudinal velocity (Va) of each thrombotic mass was measured by pulsed wave tissue Doppler imaging (PW-TDI). Both left ventricular and right ventricular apical thrombi were found with a TDI-derived mass peak Va &lt; 10 cm/s. There was no clinical evidence of neither systemic nor pulmonary embolization, probably due to the hypomobility of both left and right ventricular masses

Charlson comorbidity index, neutrophil-to-lymphocyte ratio and undertreatment with renin-angiotensin-aldosterone system inhibitors predict in-hospital mortality of hospitalized COVID-19 patients during the omicron dominant period

Purpose: To investigate the clinical predictors of in-hospital mortality in hospitalized patients with Coronavirus disease 2019 (COVID-19) infection during the Omicron period. Methods: All consecutive hospitalized laboratory‐confirmed COVID-19 patients between January and May 2022 were retrospectively analyzed. All patients underwent accurate physical, laboratory, radiographic and echocardiographic examination. Primary endpoint was in-hospital mortality. Results: 74 consecutive COVID-19 patients (80.0 ± 12.6 yrs, 45.9% males) were included. Patients who died during hospitalization (27%) and those who were discharged alive (73%) were separately analyzed. Compared to patients discharged alive, those who died were significantly older, with higher comorbidity burden and greater prevalence of laboratory, radiographic and echographic signs of pulmonary and systemic congestion. Charlson comorbidity index (CCI) (OR 1.76, 95%CI 1.07-2.92), neutrophil-to-lymphocyte ratio (NLR) (OR 1.24, 95%CI 1.10-1.39) and absence of angiotensin-converting enzyme inhibitors (ACEI)/angiotensin II receptor blockers (ARBs) therapy (OR 0.01, 95%CI 0.00-0.22) independently predicted the primary endpoint. CCI ≥7 and NLR ≥9 were the best cut-off values for predicting mortality. The mortality risk for patients with CCI ≥7, NLR ≥9 and not in ACEI/ARBs therapy was high (86%); for patients with CCI &lt;7, NLR ≥9, with (16.6%) or without (25%) ACEI/ARBs therapy was intermediate; for patients with CCI &lt;7, NLR &lt;9 and in ACEI/ARBs therapy was of 0%. Conclusions: High comorbidity burden, high levels of NLR and the undertreatment with ACEI/ARBs were the main prognostic indicators of in-hospital mortality. The risk stratification of COVID-19 patients at hospital admission would help the clinicians to take care of the high-risk patients and reduce the mortality

The influence of chest wall conformation on myocardial strain parameters in a cohort of mitral valve prolapse patients with and without mitral annular disjunction

Purpose To evaluate the possible influence of chest wall conformation on myocardial strain parameters in a cohort of mitral valve prolapse (MVP) patients with and without mitral annular disjunction (MAD). Methods All consecutive middle-aged patients with MVP referred to our Outpatient Cardiology Clinic for performing two- dimensional (2D) transthoracic echocardiography (TTE) as part of work up for primary cardiovascular prevention between March 2018 and May 2022, were included into the study. All patients underwent clinic visit, physical examination, modified Haller index (MHI) assessment (the ratio of chest transverse diameter over the distance between sternum and spine) and conventional 2D-TTE implemented with speckle tracking analysis of left ventricular (LV) global longitudinal strain (GLS) and global circumferential strain (GCS). Independent predictors of MAD presence on 2D-TTE were assessed. Results A total of 93 MVP patients (54.2 ± 16.4 yrs, 50.5% females) were prospectively analyzed. On 2D-TTE, 34.4% of MVP patients had MAD (7.3 ± 2.0 mm), whereas 65.6% did not. Compared to patients without MAD, those with MAD had: 1) significantly shorter antero-posterior (A-P) thoracic diameter (13.5 ± 1.2 vs 14.8 ± 1.3 cm, p < 0.001); 2) significantly smaller cardiac chambers dimensions; 3) significantly increased prevalence of classic MVP (84.3 vs 44.3%, p < 0.001); 4) significantly impaired LV-GLS (-17.2 ± 1.4 vs -19.4 ± 3.0%, p < 0.001) and LV-GCS (-16.3 ± 4.1 vs -20.4 ± 4.9, p < 0.001), despite similar LV ejection fraction (63.7 ± 4.2 vs 63.0 ± 3.9%, p = 0.42). A-P thoracic diameter (OR 0.25, 95%CI 0.10–0.82), classic MVP (OR 3.90, 95%CI 1.32–11.5) and mitral annular end-systolic A-P diameter (OR 2.76, 95%CI 1.54–4.92) were the main independent predictors of MAD. An A-P thoracic diameter ≤ 13.5 cm had 59% sensitivity and 84% specificity for predicting MAD presence (AUC = 0.81). In addition, MAD distance was strongly influenced by A-P thoracic diameter (r = − 0.96) and MHI (r = 0.87), but not by L-L thoracic diameter (r = 0.23). Finally, a strong inverse correlation between MHI and both LV-GLS and LV-GCS was demonstrated in MAD patients (r = − 0.94 and − 0.92, respectively), but not in those without (r = − 0.51 and − 0.50, respectively). Conclusions A narrow A-P thoracic diameter is strongly associated with MAD presence and is a major determinant of the impairment in myocardial strain parameters in MAD patients, in both longitudinal and circumferential directions

Molecular Approaches and Echocardiographic Deformation Imaging in Detecting Myocardial Fibrosis

The pathological remodeling of myocardial tissue is the main cause of heart diseases. Several processes are involved in the onset of heart failure, and the comprehension of the mechanisms underlying the pathological phenotype deserves special attention to find novel procedures to identify the site of injury and develop novel strategies, as well as molecular druggable pathways, to counteract the high degree of morbidity associated with it. Myocardial fibrosis (MF) is recognized as a critical trigger for disruption of heart functionality due to the excessive accumulation of extracellular matrix proteins, in response to an injury. Its diagnosis remains focalized on invasive techniques, such as endomyocardial biopsy (EMB), or may be noninvasively detected by cardiac magnetic resonance imaging (CMRI). The detection of MF by non-canonical markers remains a challenge in clinical practice. During the last two decades, two-dimensional (2D) speckle tracking echocardiography (STE) has emerged as a new non-invasive imaging modality, able to detect myocardial tissue abnormalities without specifying the causes of the underlying histopathological changes. In this review, we highlighted the clinical utility of 2D-STE deformation imaging for tissue characterization, and its main technical limitations and criticisms. Moreover, we focalized on the importance of coupling 2D-STE examination with the molecular approaches in the clinical decision-making processes, in particular when the 2D-STE does not reflect myocardial dysfunction directly. We also attempted to examine the roles of epigenetic markers of MF and hypothesized microRNA-based mechanisms aiming to understand how they match with the clinical utility of echocardiographic deformation imaging for tissue characterization and MF assessment

Idiopathic Pulmonary Fibrosis for Cardiologists: Differential Diagnosis, Cardiovascular Comorbidities, and Patient Management

The presence of rare comorbidities in patients with cardiovascular disease (CVD) presents a diagnostic challenge to cardiologists. In evaluating these patients, cardiologists are faced with a unique opportunity to shorten diagnosis times and direct patients towards correct treatment pathways. Idiopathic pulmonary fibrosis (IPF), a type of interstitial lung disease (ILD), is an example of a rare disease where patients frequently demonstrate comorbid CVD. Both CVD and IPF most commonly affect a similar patient demographic: men over the age of 60 years with a history of smoking. Moreover, IPF and heart failure (HF) share a number of symptoms. As a result, patients with IPF can be misdiagnosed with HF and vice versa. This article aims to increase awareness of IPF among cardiologists, providing an overview for cardiologists on the differential diagnosis of IPF from HF, and describing the signs and symptoms that would warrant referral to a pulmonologist with expertise in ILD. Once patients with IPF have received a diagnosis, cardiologists can have an important role in managing patients who are candidates for a lung transplant or those who develop pulmonary hypertension (PH). Group 3 PH is one of the most common cardiovascular complications diagnosed in patients with IPF, its prevalence varying between reports but most often cited as between 30% and 50%. This review summarizes the current knowledge on Group 3 PH in IPF, discusses data from clinical trials assessing treatments for Group 1 PH in patients with IPF, and highlights that treatment guidelines recommend against these therapies in IPF. Finally, this article provides the cardiologist with an overview on the use of the two approved treatments for IPF, the antifibrotics pirfenidone and nintedanib, in patients with IPF and CVD comorbidities. Conversely, the impact of treatments for CVD comorbidities on patients with IPF is also discussed.Funding: F. Hoffmann-La Roche, Ltd.Plain Language Summary: Plain language summary available for this article.status: publishe