Arrhythmogenic right ventricular cardiomyopathy or athlete's heart? Challenges in assessment of right heart morphology and function

The incidence of sudden cardiac death (SCD) in young athletes varies among studies, due to the disagreement in the definitions and the lack of information in this field

MitraClip after heart transplantation: A case report

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Prevalence and prognostic impact of non-cardiac co-morbidities in heart failure outpatients with preserved and reduced ejection fraction: a community-based study

Aim: To assess adverse outcomes attributable to non-cardiac co-morbidities and to compare their effects by left ventricular ejection fraction (LVEF) group [LVEF <50% (heart failure with reduced ejection fraction, HFrEF), LVEF 6550% (heart failure with preserved ejection fraction, HFpEF)] in a contemporary, unselected chronic heart failure population. Methods and results: This community-based cohort enrolled patients from October 2009 to December 2013. Adjusted hazard ratio (HR) and the population attributable fraction (PAF) were used to compare the contribution of 15 non-cardiac co-morbidities to adverse outcome. Overall, 2314 patients (mean age 77 \ub110 years, 57% men) were recruited [n = 941 (41%) HFrEF, n = 1373 (59%) HFpEF]. Non-cardiac co-morbidity rates were similarly high, except for obesity and hypertension which were more prevalent in HFpEF. At a median follow-up of 31 (interquartile range 16\u201341) months, 472 (20%) patients died. Adjusted mortality rates were not significantly different between the HFrEF and HFpEF groups. After adjustment, an increasing number of non-cardiac co-morbidities was associated with a higher risk for all-cause mortality [HR 1.25; 95% confidence interval (CI) 1.10\u20131.26; P < 0.001], all-cause hospitalization (HR 1.17; 95% CI 1.12\u20131.23; P < 0.001), heart failure hospitalization (HR 1.28; 95% CI 1.19\u20131.38; P < 0.001), non-cardiovascular hospitalization (HR 1.16; 95% CI 1.11\u20131.22; P < 0.001). The co-morbidities contributing to high PAF were: anaemia, chronic kidney disease, chronic obstructive pulmonary disease, diabetes mellitus, and peripheral artery disease. These findings were similar for HFrEF and HFpEF. Interaction analysis yielded similar results. Conclusions: In a contemporary community population with chronic heart failure, non-cardiac co-morbidities confer a similar contribution to outcomes in HFrEF and HFpEF. These observations suggest that quality improvement initiatives aimed at optimizing co-morbidities may be similarly effective in HFrEF and HFpEF

Renal Insufficiency in Non-Diabetic Subjects: Relationship of MTHFR C677t Gene Polymorphism and Left Ventricular Hypertrophy

Association of methylenetetrahydrofolate reductase (MTHFR) 677CT gene polymorphism with hyperhomocysteinemia, renal failure, and cardiovascular events is controversial. We investigated the relationship of MTHFR 677CT polymorphisms with left ventricular hypertrophy (LVH) and renal insufficiency.Glomerular filtration rate (GFR) and left myocardial ventricular mass/m2 were assessed in 138 non-diabetic subjects (age, 50.93 ± 14.85 years; body mass index, 27.95 ± 5.98 kg/m(2)), 38 no-mutation wild MTHFR C677CC, 52 heterozygous MTHFR C677CT, and 48 homozygous MTHFR C677TT, all with adequate adherence to current international healthy dietary guidelines. Serum homocysteine, insulin resistance, high-sensitivity C-reactive-protein (hsCRP), parathyroid hormone, and renal artery resistive index (RRI) were challenged by odds ratio analysis and multiple linear regression models.MTHFR 677CT polymorphism showed higher GFR (73.8 ± 27.99 vs. 58.64 ± 29.95; p= 0.001) and lower renal failure odds (OR, 0.443; 95% confidence interval, 0.141-1.387) in comparison with wild MTHFR genotype. A favorable effect on GFR of MTHFR polymorphism is presented independently by the negative effects of LVH, increased intra-renal arterial resistance, and hyperparathyroidism; GFR is the significant predictive factor to LVH.Renal insufficiency in non-diabetic subjects is explained by interactions of MTHFR C677T polymorphism mutation with LVH, hsCRP, intact parathyroid hormone (iPTH), and RRI. Sign of these predictive effects is opposite: subjects with MTHFR 677CT polymorphism have lower likelihood of renal insufficiency; differently, wild-type MTHFR genotype subjects have lower GFR and greater hsCRP, iPTH, RRI, and LVH

Effect of uric acid serum levels on carotid arterial stiffness and intima-media thickness: A high resolution Echo-Tracking Study

Serum uric acid (UA) has been shown to be a predictor of cardiovascular (CV) morbidity and mortality, and it may play a role in the pathogenesis of CV disease affecting vascular structure and function. However, there is limited evidence of its specific association with carotid artery stiffness and structure. The aim of our study was to evaluate whether UA is associated with early signs of atherosclerosis, namely local carotid arterial stiffness and intima-media thickening. We evaluated 698 consecutive asymptomatic patients, referred to the Cardiovascular Department for risk factors evaluation and treatment. All patients underwent carotid artery ultrasonography with measurement of common carotid intima-media thickness (IMT) and echo-tracking carotid artery stiffness index Beta. Patients with hyperuricemia (defined as serum uric acid ≥7 mg/dL in men and ≥6 mg/dL in women) had higher IMT (0.97±0.22 vs 0.91±0.18, p<0.001) and stiffness index Beta (8.3±3.2 vs 7.5±2.7, p=0.005). UA levels correlated with both IMT (r=0.225; p<0.001) and stiffness index Beta (r=0.154; p<0.001); the correlations were statistically significant in males and females. In a multivariate model which included age, arterial pressure, serum glucose and LDL-cholesterol, serum UA emerged as an independent explanatory variable of IMT and stiffness index Beta. Carotid IMT and local arterial stiffness are related to UA independently of established CV risk factors; UA may play a role in the early development of atherosclerosis

Management of oral anticoagulant therapy after intracranial hemorrhage in patients with atrial fibrillation

Intracranial hemorrhage (ICH) is considered a potentially severe complication of oral anticoagulants (OACs) and antiplatelet therapy (APT). Patients with atrial fibrillation (AF) who survived ICH present both an increased ischemic and bleeding risk. Due to its lethality, initiating or reinitiating OACs in ICH survivors with AF is challenging. Since ICH recurrence may be life-threatening, patients who experience an ICH are often not treated with OACs, and thus remain at a higher risk of thromboembolic events. It is worthy of mention that subjects with a recent ICH and AF have been scarcely enrolled in randomized controlled trials (RCTs) on ischemic stroke risk management in AF. Nevertheless, in observational studies, stroke incidence and mortality of patients with AF who survived ICH had been shown to be significantly reduced among those treated with OACs. However, the risk of hemorrhagic events, including recurrent ICH, was not necessarily increased, especially in patients with post-traumatic ICH. The optimal timing of anticoagulation initiation or restarting after an ICH in AF patients is also largely debated. Finally, the left atrial appendage occlusion option should be evaluated in AF patients with a very high risk of recurrent ICH. Overall, an interdisciplinary unit consisting of cardiologists, neurologists, neuroradiologists, neurosurgeons, patients, and their families should be involved in management decisions. According to available evidence, this review outlines the most appropriate anticoagulation strategies after an ICH that should be adopted to treat this neglected subset of patients

Cardiac transplantation in transthyretin amyloid cardiomyopathy: Outcomes from three decades of tertiary center experience

Aims: Transthyretin cardiac amyloidosis (ATTR-CM) is a progressive and fatal cardiomyopathy. Treatment options in patients with advanced ATTR-CM are limited to cardiac transplantation (CT). Despite case series demonstrating comparable outcomes with CT between patients with ATTR-CM and non-amyloid cardiomyopathies, ATTR-CM is considered to be a contraindication to CT in some centers, partly due to a perceived risk of amyloid recurrence in the allograft. We report long-term outcomes of CT in ATTR-CM at two tertiary centers. Materials and methods and results: We retrospectively evaluated ATTR-CM patients across two tertiary centers who underwent transplantation between 1990 and 2020. Pre-transplantation characteristics were determined and outcomes were compared with a cohort of non-transplanted ATTR-CM patients. Fourteen (12 male, 2 female) patients with ATTR-CM underwent CT including 11 with wild-type ATTR-CM and 3 with variant ATTR-CM (ATTRv). Median age at CT was 62 years and median follow up post-CT was 66 months. One, three, and five-year survival was 100, 92, and 90%, respectively and the longest surviving patient was Censored > 19 years post CT. No patients had recurrence of amyloid in the cardiac allograft. Four patients died, including one with ATTRv-CM from complications of leptomeningeal amyloidosis. Survival among the cohort of patients who underwent CT was significantly prolonged compared to UK patients with ATTR-CM generally (p < 0.001) including those diagnosed under age 65 years (p = 0.008) or with early stage cardiomyopathy (p < 0.001). Conclusion: CT is well-tolerated, restores functional capacity and improves prognosis in ATTR-CM. The risk of amyloid recurrence in the cardiac allograft appears to be low

A Large Ostium Secundum Atrial Septal Defect in an 88-Year-Old Asymptomatic Woman

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Pathogenesis

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