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Desmin ( ) maintains the overall structure of cardiomyocytes and cytoskeletal organization within striated muscle cells. Mitochondrial thioredoxin reductase 2 ( ) is essential for mitochondrial oxygen radical scavenging. We describe a rare case of dilated cardiomyopathy (DCM) in an 18-year-old female with a heterozygous mutation involving both and genes.

Lower brain volume is associated with various cardiovascular (CV) risk factors, but less is known about the spinal cord (SC). Concomitant SC atrophy may contribute to motor weakness and slowness that are prominent features of frailty, known to increase mortality. The objectives of this study were to determine potential relations between SC size, age, individual CV risk factors, and overall CV risk.  Methods and results: We retrospectively reviewed 121 patients (age 60 ± 13 years, 75.2% females) who were referred to our institution for magnetic resonance imaging (MRI) of the cervical SC. Patients with known degenerative neurological or congenital disease were excluded from review. CV risk factors were obtained from medical records, and the Atherosclerotic Cardiovascular Disease (ASCVD) risk score was calculated. Cross-sectional SC area (SCA) was traced on each slice of the C2-C6 cervical images with electronic calipers and averaged. Mean SCA was inversely correlated with age (r = -.19; p = .04) and creatinine level (r = -.20; p = .03), but not with height (r = .04; p = .69), weight (r = .03; p = .72), or body mass index (r = .02; p = .80). There was a stepwise decrease in SCA in patients without hypertension (HTN) or diabetes mellitus (DM) (n = 23) compared to those with only HTN (n = 55) (84.4 ± 9.4 mm vs 79.6 ± 11.2 mm ) and to patients with DM and/or HTN (n = 43) (84.4 ± 9.4mm vs 76.6 ± 8.3mm  (p = .01). On multivariate regression, DM was an independent predictor of lower SCA (β = -4.4; p = 0.03), and there was a trend toward lower SCA in patients with only HTN (β = -4.0; p = 0.1) (p = 0.02 for the multivariate model after adjusting for age and creatinine). Among 74 patients with ASCVD risk scores, SCA had a moderate inverse correlation with the ASCVD score (r = -.42; p < 0.001), which remained an independent predictor of lower SCA on multivariate analysis (β = -2.9; p = 0.002).  Conclusion: Lower SCA appears related to existing DM and possibly HTN, as well as overall CV risk. SC atrophy in patients with CV disease and risk factors may contribute to frailty, which is associated with increased mortality. This study is subject to the limitations of a retrospective cross-sectional study of a relatively small sample size.

Exercise-induced ventricular tachycardia undergoes ischemia evaluation; however, it is important to identify idiopathic ventricular tachycardia in patients with concomitant coronary artery disease and radiofrequency ablations can be lifesaving. We report a case of exercise-induced right and left ventricular outflow tract ventricular tachycardia in a patient with triple vessel coronary artery disease.

BRASH syndrome involves the chain of events resulting from the collective effects of Bradycardia, Renal failure, Atrioventricular (AV)-nodal blockade, Shock, and Hyperkalemia. BRASH syndrome can rapidly progress to cardiac arrest. Early recognition is crucial. We present a case of transthyretin cardiac amyloidosis (ATTR-CA) in an elderly woman who presented with BRASH syndrome shortly after an AV-nodal blocker was prescribed for atrial fibrillation.

Lower body positive pressure (LBPP) treadmill activity might benefit patients with heart failure (HF). To determine the short-term effects of LBPP on left ventricular (LV) function in HF patients, LV ejection duration (ED), a measure of systolic function was prospectively assessed in 30 men with stable HF with LV ejection fraction ≤ 40% and 50 healthy men (N). Baseline measurements (100% body weight), including blood pressure (BP), heart rate (HR) and LVED, obtained via radial artery applanation tonometry, were recorded after 2 minutes of standing on weight support treadmill and after LBPP achieving reductions of 25%, 50%, and 75% of body weight in random sequence. Baseline, HR, and LVED (251 ± 5 vs 264 ± 4 ms; P = .035) were lower in the HF group. The LBPP lowered HR more (14% vs 6%, P = .009) and increased LVED more (15% ± 7% vs 10% ± 6%; P = .004) in N versus HF. Neither group had changes (Δ) in BP. On generalized linear regression, the 2 groups showed different responses (P < .001). Multivariate analysis showed %ΔHR (P < .001) and HF (P = .026) were predictive of ΔED (r 2 = 0.44; P < .001). In conclusion, progressive LBPP increases LVED in a step-wise manner in N and HF patients independent of HR lowering. The ΔLVED is less marked in patients with HF.

Type 2 diabetes mellitus (T2DM) is characterized by endothelial dysfunction, increased thrombogenicity, and inflammation. The soluble human F11 receptor (sF11R) and annexin A5 (ANXA5) play crucial roles in inflammatory thrombosis and atherosclerosis. We examined the relationship between circulating sF11R and ANXA5 and their impact on endothelial function. The study included 125 patients with T2DM. Plasma levels of sF11R and ANXA5 were quantified by ELISA. Microvascular function was assessed using the vascular reactivity index (VRI). Large artery stiffness was assessed by carotid-femoral pulse wave velocity (PWV). Carotid intima-media thickness (CIMT) was assessed by B-mode ultrasound imaging. The mean age of patients in the study was 59.7 ± 7.8 years, 78% had hypertension, 76% had dyslipidemia, and 12% had CKD. sF11R correlated positively with ANXA5 levels (β = 0.250, p = 0.005), and correlated inversely with VRI and total nitic oxide (NO), (β = −0.201, p = 0.024; β = −0.357, p = 0.0001, respectively). Multivariate regression analysis revealed that sF11R was independently associated with ANXA5 in the total population and in patients with HbA1c > 6.5% (β = 0.366, p = 0.007; β = 0.425, p = 0.0001, respectively). sF11R and ANXA5 were not associated with vascular outcome, suggesting that they may not be reliable markers of vascular dysfunction in diabetes. The clinical significance of sF11R/ANXA5 association in diabetes warrants further investigation in a larger population.

Dabigatran, the first novel oral anticoagulant (NOAC) with a reversal agent, heralded a paradigm shift in the treatment of nonvalvular atrial fibrillation. The potential for life-threatening hemorrhagic events with the use of NOACs has been highly debated since the effectiveness of reversal agents such as idarucizumab is based primarily on pharmacologic data. It is known that cancer patients are at an increased risk of bleeding with anticoagulation, though specific studies demonstrating the risks or efficacy of NOACs in this population are lacking. We provide the first report of hemopericardium resulting in multiorgan failure related to dabigatran use that was successfully reversed by idarucizumab in a man with prostate cancer on chemotherapy.

Because nearly half of BAV can be missed by transthoracic echocardiography,4 we also reviewed 1,069 transesophageal echocardiograms performed for an 18-month period (2006-2007) and found 3 cases of BAV (prevalence 0.11%, 95% CI 0.04%-0.25%). [...]the prevalence of BAV in African Americans may be lower than previously reported in other populations.2,3 Bicuspid aortic valve is viewed to be hereditary with linkages to regions of chromosomes 18q, 5q, and 13q.5 These linkages have not been well studied in African Americans, and the lower prevalence of BAV in African Americans merits further study.

Background: This meta-analysis assessed the relationship between obstructive sleep apnea (OSA) and echocardiographic parameters of diastolic dysfunction (DD), which are used in the assessment of heart failure with preserved ejection fraction. Methods: We searched the databases including Ovid MEDLINE, Ovid Embase, Scopus, Web of Science, Google Scholar, and EBSCO CINAHL from inception up to December 26, 2020. The search was not restricted to time, publication status, or language. Two independent investigators screened the identified studies and extracted the data in duplicate. We conducted a meta-analysis using RevMan v.5. The risk of bias was assessed using Cochrane collaboration tools. Comparisons were made between patients with OSA, diagnosed in-laboratory polysomnography or home sleep apnea testing, and patients without OSA in relation to established markers of DD. Results: Primary search identified 2,512 studies. A total of 18 studies including 2,509 participants were included. The two groups were free of conventional cardiovascular risk factors. Significant structural changes were observed between the two groups. Patients with OSA exhibited greater left atrial volume index (LAVI) (3.94 95% CI [0.8, 7.07]; p = 0.000) and left ventricular mass index (11.10 95% CI [2.56, 19.65]; p = 0.000) as compared to control group. The presence of OSA was also associated with more prolonged deceleration time (10.44 ms 95% CI [0.71, 20.16]; p = 0.04), isovolumic relaxation time (IVRT) (7.85 ms 95% CI [4.48, 11.22]; p = 0.000), and a lower ratio of early to late mitral inflow velocities (E/A) ratio (−0.62 95% CI [−1, −0.24]; p = 0.001) suggestive of early DD. The early mitral inflow velocity to mitral annular early diastolic velocity (E/e′) ratio (0.94 95% CI [0.44, 1.45]; p = 0.000) was increased. Linear correlation between severity of OSA and LAVI and IVRT parameters was observed but this association did not sustain for the E/A and E/e′. The ejection fraction was not significantly different between patients with OSA and healthy controls (−0.48 95% CI [−1.18, 0.23]; p = 0.18). Conclusion: An association between OSA and echocardiographic parameters of DD was detected that was independent of conventional cardiovascular risk factors. OSA may be independently associated with DD perhaps due to higher LV mass. Investigating the role of continuous positive airway pressure therapy in reversing or ameliorating DD is recommended.

Background. Takotsubo cardiomyopathy is defined as a transient left ventricular dysfunction, usually accompanied by electrocardiographic changes. The literature documents only two other cases of Takotsubo cardiomyopathy in the latter setting. Methods. A 78-year-old female presented to the ED with severe shortness of breath, hypertension, and tachycardia. On physical exam, heart sounds (S1 and S2) were regular and wheezing was noticed bilaterally. We found laboratory results with a WBC of 20.0 (103/μL), troponin of 16.52 ng/mL, CK-mb of 70.6%, and BNP of 177 pg/mL. The patient was intubated for acute hypoxemic respiratory failure. A chest X-ray revealed a large left-sided tension pneumothorax. Initial echocardiogram showed apical ballooning with a LVEF of 10–15%. A cardiac angiography revealed normal coronary arteries with no coronary disease. After supportive treatment, the patient’s condition improved with a subsequent echocardiogram showing a LVEF of 60%. Conclusion. The patient was found to have Takotsubo cardiomyopathy in the setting of a tension pneumothorax. The exact mechanisms of ventricular dysfunction have not been clarified. However, multivessel coronary spasm or catecholamine cardiotoxicity has been suggested to have a causative role. We suggest that, in our patient, left ventricular dysfunction was induced by the latter mechanism related to the stress associated with acute pneumothorax.